Secondary cleft surgery [1 ed.]

Table of contents :
Preface
Facial and dental relationships in individuals with cleft lip and/or palate
Scar revision of the cleft lip
Correction of the short upper lip in the cleft patient
Rhinoplasty in adolescent cleft patients
Orthodontic approach in the treatment of the cleft patient
Secondary grafting in the alveolar cleft patient
Surgical correction of midface deficiency in cleft lip and palate malformation
Intraoral bone transport in clefting
Secondary cleft surgery and speech
Velopharyngeal insufficiency in patients with cleft palate
The management of oronasal fistulas in the cleft palate patient
Cumulative Index 2002

Citation preview

Oral Maxillofacial Surg Clin N Am 14 (2002) ix

Preface

Secondary cleft surgery

Orrett E. Ogle, DDS Guest Editor

This issue of Oral and Maxillofacial Surgery Clinics of North America is devoted to secondary cleft surgery. Not many nonacademic oral and maxillofacial surgeons are currently involved in primary cleft repair, but secondary cleft surgery is an area in which we play an important role. Rehabilitation of the child with a cleft is truly a team effort in which expertise in one discipline complements the other and no particular specialty alone can achieve all of the desired goals of the child’s rehabilitation. Each specialty brings something unique to the table, and as such, we have included articles by plastic surgeons, oral and maxillofacial surgeons, speech therapists, and orthodontists. We also have included wellrespected authors from outside the United States who offer a wider perspective. Primary cleft surgery calls on every aspect of surgical skill and aesthetic sense. The goal of the primary repair is to achieve as normal an appearance as possible with satisfactory function of speech and mastication. The desired goals are not always achieved, and unplanned secondary procedures are often required. Some of these procedures are covered in articles on scar revision of the cleft lip, surgery to correct the short lip, repair of palatal fistulas, and velopharyngeal incompetence. Not all secondary cleft surgery is unplanned, however, but is staged. These staged surgeries include alveolar bone grafting and orthognathic surgery. The recent innovation of dis-

traction osteogenesis to manage the cleft patient is included and shows great promise. Two disciplines that are essential to the total rehabilitation of the cleft patient are speech therapy and orthodontics. The effect of surgical procedures on speech is discussed in detail, and the role of orthodontics is included so as to give the surgeon a better understanding of orthodontic treatment. The surgeon also must understand the effects of surgery on the growth and development of the face, jaws, and dentition. This view is presented as a comparison to cleft palate patients who never had surgery. The contributing authors are all experienced with cleft patients and have provided effective solutions to the varied presentations that we may encounter in secondary cleft surgery. I wish to thank all of the authors for agreeing to participate in this project, which was so dear to me, and for providing the quality articles included in this issue. I sincerely hope that readers will find this issue useful and enjoyable. Orrett E. Ogle, DDS Department of Dentistry Oral and Maxillofacial Surgery Woodhull Medical and Mental Health Center 760 Broadway, Room 2B-320 Brooklyn, NY 11206, USA E-mail address: [email protected]

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 5 1 - 1

Oral Maxillofacial Surg Clin N Am 14 (2002) 411 – 424

Facial and dental relationships in individuals with cleft lip and/or palate Samir E. Bishara, BDS, DDS, MS Department of Orthodontics, College of Dentistry, University of Iowa, 219 Dental Science S, Iowa City, IA 52242, USA

Management of individuals with clefts of the lip or palate or both is a complex procedure. The complexity is a result of the variation among different cleft types and individual variation within the same cleft type. All this is superimposed on various techniques by which different craniofacial centers or individual specialists treat their patients surgically, orthodontically, and otherwise. Many investigators [1 – 20] have concluded that the dentofacial relationships of individuals with repaired clefts differ from those of persons without clefts. Many factors can interplay to cause such differences: 1. Changes in the facial structures could be part of a syndrome that includes other manifestations, such as cranial deformities. 2. Changes in the facial structures could be part of a response to the mechanical presence of a defect (ie, when there is a tissue deficiency, various structural compensations are needed to improve function). 3. Changes in the facial structures could be the result of the different management procedures, such as surgery and orthodontics. 4. Individuals with clefts possess their own genetic and acquired potential to develop into a Class I, II, or III dental or skeletal patterns. This fact explains why the dentofacial relationship in two individuals with similar clefts can look significantly different from each other despite having

E-mail address: [email protected]

obtained essentially the same type of treatment from the same group of specialists. The purpose of this article is to describe and explain the facial and dental relationships in individuals with different cleft types with and without a surgical repair. An attempt is made to outline the different variables that must be considered in the study of the craniofacial growth of the cleft face.

Facial characteristics of individuals with different types of unrepaired and repaired clefts In the attempt to better understand facial growth in cleft lip and palate patients, it may be helpful to answer the following questions systematically: 1. Does the unoperated cleft individual have the same facial growth potential as the noncleft individual? 2. Do all unoperated cleft types have the same growth potential? 3. What effects does cleft management have on facial and dental growth? The logic behind these questions is obvious, because it is important to determine how an ‘‘unrepaired cleft face’’ looks before attempting to determine the effect of management. The following discussion encompasses the following descriptions: (1) the cephalometric relationships of the dentofacial structures (ie, maxilla, mandible, maxilla-mandible, and dentition, and (2) the dental arch relationships of the anterior and posterior segments.

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 4 3 - 2

412

S.E. Bishara / Oral Maxillofacial Surg Clin N Am 14 (2002) 411–424

Background Numerous studies consistently demonstrated that the facial and dental relationships of individuals with repaired clefts differ from those of noncleft individuals. Most of these differences have, until recently, been blamed on the lip and palatal surgery and on other rehabilitative procedures. Findings on individuals with isolated clefts of the palate precipitated a reevaluation of the understanding of the relationship between surgical management, clefting, and facial growth. How did this happen? One of the initial questions raised was how do individuals with isolated clefts of the palate (CPO) differ from normals? In an attempt to answer this question, 20 female subjects with CPO were compared to 25 noncleft female subjects [2]. Female subjects were chosen because this type of cleft occurs more frequently in the female gender. To minimize the effect of growth on the interpretation of the results, it was decided to include only individuals who were age 16 years or older. The comparisons between the cleft and noncleft groups indicated the presence of significant differences in the maxillary and mandibular relationships between the two groups. Specifically, the maxilla and mandible were relatively retruded as compared to the normal subjects; however, the maxilla and mandible were in an acceptable relationship to each other as indicated by the positive maxillary-mandibular apical base relationship (ANB) angle. Similar results were reported earlier by Dahl [8]. The cause of these differences between the cleft group and normal group traditionally has been attributed to palatal surgery. The next question was: Why should palatal surgery cause mandibular retrusion? The author examined a sample of individuals with isolated clefts of the palate, but some of these subjects were obturated, whereas others were operated [2]. The two groups were then compared cephalometrically. Surprisingly, there were no significant differences between the two groups in their cephalometric skeletal facial relationship. Both groups were found to have a similarly retruded maxilla and mandible, a steep mandibular plan, and upright mandibular incisors. Data from earlier studies by Hagerty and Hill in 1963 on Puerto Ricans [11] and Dahl in 1970 on the Danish cleft population [8] confirmed these results. What is the significance of all these findings? Does it mean that palatal surgery as performed on these subjects had no effects on the anteroposterior and vertical growth of the facial skeleton? If this is true,

then why did the maxilla and mandible become relatively retruded in the obturated group? One also may interpret these findings to mean that the skeletal changes observed are, at least in part, related to the presence of the cleft itself rather than the effect of palatal repair. These observations are specifically related to the skeletal facial structures. Palatal surgery has definite unfavorable effects on the maxillary dental arch dimensions and on the occlusion, because palatal surgery causes constriction of the maxillary arch and an increase in the incidence of anterior and posterior cross-bites [8]. Animal research helped provide important information. Cheirici et al, in 1973, created palatal clefts in otherwise normal Rhesus monkeys [7]. They found that the induced palatal clefts caused the maxilla and mandible to become retrusive. From these findings one can assume that the changes in facial relationships in the unrepaired individuals are a response to a tissue deficiency (ie, biomechanical compensations to the presence of the palatal cleft). One always should be cautious as to interpreting the findings from animal experimentation and their direct application to humans. However, the cumulative findings from human and animal observations partly explain the differences between individuals with and without palatal clefts. More importantly, it points to the need for a reexamination of the understanding of the unoperated cleft face. Without such knowledge it becomes difficult to infer that the facial relationship and the occlusal discrepancies in the repaired cleft face are exclusively the result of surgical management.

Dentofacial characteristics of different types of cleft faces before and after surgical repair For this discussion to have a perspective, the effects of the presence of the cleft and the effect of surgery are presented for the three most commonly occurring cleft types, starting with the less severe clefts, in the following order: Individuals with unilateral cleft lip and alveolus Individuals with cleft palate only Individuals with complete unilateral cleft lip and palate It is important to remember that within each cleft type, various degrees of malrelationship are expressed. In each individual, clefting of the lip or

S.E. Bishara / Oral Maxillofacial Surg Clin N Am 14 (2002) 411–424

413

Table 1 Effects of surgical management on cephalometric dentofacial relationships in individuals with unilateral cleft of the lip and alveolus Cephalometric findings Maxilla

Mandible Maxilla-mandible

Dentition Upper incisors Lower incisors

Unrepaired UCLA vs. normals [3,5]

Operated UCLA vs. normals [8]

Tendency for maxillary protrusion in UCLA Greater maxillary depth in UCLA Both are believed to be the result of the forward rotation of the non-cleft segment No difference in size and relationship Larger ANB and angle of convexity in UCLA because of the maxillary protrusion

No difference in relationship Smaller maxillary depth in UCLA

The influence of lip surgery caused recontouring of the premaxilla

No difference in size and relationship No difference in relationship

No influence

Inclined lingually in UCLA Inclined lingually in UCLA

Lip surgery caused the incisors to tip lingually No influence

No difference Inclined labially in UCLA

Effect of surgery

The influence of the lip surgery on the maxilla improved maxillary-mandibular relationship

Abbreviations: ANB, Maxillary-mandibular apical base relationship; UCLA, unilateral cleft of the lip and alveolus.

palate or both is superimposed on the genetic and epigenetic potential of the particular individual, which is a finding that has been observed repeatedly in normal populations [21 – 28]. Within each cleft group there is a large range of variation, and the following descriptions serve as general characterizations for each cleft type.

Persons with unilateral cleft lip and alveolus Unrepaired unilateral cleft lip and alveolus Skeletal relationship [3,5]: There is a tendency for maxillary protrusion in the unrepaired clefts as compared to the noncleft subjects (Tables 1, 2). The

mandibular relationship, however, does not seem to be influenced significantly by the presence of an alveolar cleft of the primary palate (Fig. 1). Dental relationship: When the maxillary dental arch is viewed occlusally (Fig. 2A), the anterior part of the noncleft segment has a tendency to be rotated forward, hence the increased overjet, as a result of incisor protrusion. The cleft segment has a tendency to rotate slightly medially, however, so there is a tendency for the canines to be edge to edge and sometimes in cross-bite. When viewed labially (Fig. 2B), the teeth on either side of the cleft have a tendency to roll superiorly, which results in these teeth being in infraocclusion with a localized openbite tendency. In summary, the effects of the cleft of the lip and alveolus are limited to that part of the

Table 2 Effects of surgical management on dental relationships in individuals with unilateral cleft of the lip and alveolus Dental findings

Unrepaired UCLA

Operated UCLA (%)

Effect of surgery

Incisor inversion Mandibular overjet Posterior cross-bite UniBi-

12.5% None

18.5 5.6

Increased incidence of anterior cross-bite

12.5% None

23.6 14.5

Increased incidence of posterior cross-bite

Abbreviation: UCLA, unilateral cleft of the lip and alveolus.

414

S.E. Bishara / Oral Maxillofacial Surg Clin N Am 14 (2002) 411–424

incisor inclination and an increased incidence of anterior and posterior cross-bites (Tables 1,2). Surgical and orthodontic implications

Fig. 1. Skeletal relationships of the maxilla and mandible in individuals with unrepaired cleft lip and alveolus.

dentofacial complex that surrounds the cleft area (Fig. 3). Effects of lip repair on the skeletal structures in unilateral cleft lip and alveolus [8] Maxilla: Lip repair has a molding effect on the anterior maxilla that results in a reduction of the maxillary protrusion to a more normal relationship. Mandible: No significant changes in either the mandibular relationship or dimension occurred as a result of the lip repair. Maxillary-mandibular relationship: The improvement in this relationship after surgery was reflected as a reduction in the relatively large ANB angle. This is the result of the decrease in the protrusion of the anterior part of the maxilla after lip repair. In summary, as a result of lip surgery, the skeletal structures of individuals with unilateral cleft lip and alveolus have been restored to a relationship that for all practical purposes can be described as similar to noncleft individuals (Tables 1, 2).

The description of the unoperated face provides an explanation of some of the differences in the dentofacial relationships between individuals with repaired clefts of the lip and alveolus and normal individuals [3,5,8] As an example, in individuals with unilateral cleft lip and alveolus, the presence of the intact secondary palate minimizes the effect of the lip surgery on the maxillary skeletal base. Dahl [8] found that at the end of the growth period, the maxillary-mandibular relationships in operated individuals with unilateral cleft lip and alveolus were comparable to those in noncleft individuals. Lip surgery can improve substantially the increased overjet caused by the rotation of the noncleft segment and also improve the maxillarymandibular skeletal anteroposterior relationship. On the other hand, lip surgery can cause or accentuate dental discrepancies, such as cross-bites [8]. Most of these dental discrepancies in individuals with unilateral cleft lip and alveolus can be treated successfully orthodontically. The stability of the orthodontic correction is influenced to a degree by some of the dental tendencies that have been observed in the ‘‘unrepaired’’ cleft face (eg, teeth in infraocclusion) (Fig. 2A – D). A prolonged period of retention or even permanent retention for severely affected teeth on either side of the cleft may have to be considered. In summary, lip surgery by itself has little detrimental effect on skeletal facial growth; it actually might have a beneficial effect on the protruding noncleft segment. On the other hand, lip repair results in an increased incidence of anterior and posterior cross-bites.

Persons with isolated clefts of the palate Effects of lip repair on the dental structures Unrepaired isolated clefts of the palate [2,8] Incisor inclination: In the repaired unilateral cleft lip and alveolus, the maxillary incisors were relatively protrusive, and lip repair caused maxillary and mandibular incisors to become more upright. The uprighting tendency was greater for the maxillary teeth and resulted in a decrease in the overjet and an increase in the incidence of anterior cross-bite. Posterior transverse relationship: There was an increase in the incidence of unilateral and bilateral posterior cross-bites as a result of lip repair. In summary, cleft lip repair results in a decrease in

Skeletal relationships: The presence of a palatal cleft seems to be associated with the retrusion of the maxilla and mandible in relation to the cranial base, but they remain well related to each other (Fig. 4). The mandibular plane is rotated backward and downward. Dental relationships: The mandibular incisors are inclined lingually. Dental arches: The presence of an unrepaired palatal cleft does not seem to influence the maxillary dentition adversely (Fig. 5).

S.E. Bishara / Oral Maxillofacial Surg Clin N Am 14 (2002) 411–424

415

Fig. 2. (A) Occlusal view of the dental arches in an individual with cleft lip and alveolus. (B) Frontal view of the occlusal models, which shows the tendency of the teeth to roll superiorly on each side of the cleft. Lateral view of the models on the noncleft (C) and cleft (D) sides.

Effects of palatal surgery on the skeletal structures of isolated clefts of the palate Individuals with isolated clefts of the palate present an attractive model to study the exclusive effects of palate surgery on facial and dental growth because the influence of the presence of a lip and alveolar cleft and the effect of lip repair are all eliminated

(Tables 3, 4). By comparing repaired with unrepaired (obturated) individuals with isolated clefts of the palate, one can assume that existing differences, for the most part, could be attributed to the surgical management of the palate. Maxilla: No significant changes in the anteroposterior relationship of the maxilla were present between the operated and obturated groups. Posterior

416

S.E. Bishara / Oral Maxillofacial Surg Clin N Am 14 (2002) 411–424

Fig. 5. Maxillary dentition of an individual with an unrepaired cleft palate only.

Fig. 3. Facial view of an individual with an unrepaired cleft of the lip and alveolus.

maxillary height was shorter in the operated group, which indicates that palatal surgery has affected the posterior descent of the palate. Mandible: No differences were present in the mandibular skeletal relationship or dimensions, except that the mandibular plane was steeper in the group with obturated isolated clefts of the palate.

Maxillary-mandibular relationship: There was a reduced ANB angle in the group with operated isolated clefts of the palate group. In summary, one can conclude that palate repair has only a subtle effect on the skeletal relationship of the maxilla and mandible because most cases in the group with repaired isolated clefts of the palate maintained a positive but smaller than normal ANB angle. On the other hand, the effect of the combined reduction of the ANB angle with the mandibular forward rotation that occurs after palatal repair should be considered as disadvantageous. This is because the combined effects of these changes might predispose some individuals to have a concave facial profile and an increase in the incidence of anterior cross-bites. Effects of palatal repair on the dental structures Incisor inclinations: Palatal repair caused a slight decrease in the angulation of the upper incisors and an increase in the incidence of anterior cross-bite. Posterior transverse relationship: Comparisons between the operated and obturated cleft groups indicated that there was a marked increase in unilateral and bilateral posterior cross-bites in the operated group [8]. Surgical considerations

Fig. 4. Skeletal relationships of the maxilla and mandible in individual with unrepaired cleft palate only.

In general, palatoplasty in individuals with isolated clefts of the palate does not result in gross anteroposterior skeletal maxillary-mandibular discrepancies. In persons with an inherent tendency for maxillary retrusion, however, the palatoplasty possibly could accentuate the maxillary retrusion, leading to an unfavorable maxillary-mandibular relationship. On the other hand, palatal surgery has a more pronounced

S.E. Bishara / Oral Maxillofacial Surg Clin N Am 14 (2002) 411–424

417

Table 3 Effects of surgical management on the cephalometric dentofacial relationships in individuals with cleft of the palate only [2,8] Operated CPO Cephalometric findings vs. normals

Unoperated CPO vs. operated CPO

Maxilla

Maxillary retrusion in the CPO Maxillary depth shorter and maxillary apical base width narrower — posterior face height shorter

Mandible

Mandibular retrusion in the CPO Steep mandibular plane in CPO The ANB angle is smaller but not significantly different from normals

Maxillary relationship similar All dimensions are the same except for a decreased posterior face height in the operated group (i.e, possible maxillary backward rotation) Mandibular relationship similar Steepness of MP more in the unoperated

Maxilla-mandible

Effect of surgery Little effect on the anteroposterior skeletal relationship or dimensions for the maxilla

Palatoplasty may decrease the tendency for a steep MP and increase the forward rotation

Reduced ANB angle as a result of the subtle changes in the maxilla and mandible, but the ANB angle is still positive

Causes reduction in the ANB angle

No significant effects on incisor inclination

Dentition Upper incisors

More upright in CPO

Similar inclination

Lower incisors

More upright in CPO

Similar inclination

Abbreviations: ANB, Maxillary-mandibular apical base relationship; CPO, cleft of the palate only; MP, Mandibular plane.

effect on the maxillary dental arch, which leads to the increased incidence of posterior and anterior crossbites in the surgically treated subjects. In summary, palatal repair in individuals with isolated clefts of the palate has a more significant effect on the dentition compared to the skeletal structures. The size and location of the surgical wound relative to the anterior and posterior teeth have an influence on the severity of the dental changes. The larger and closer the contracting wound is to the teeth, the more adverse are the dental changes.

Persons with unilateral cleft lip and palate Unrepaired unilateral cleft lip and palate Individuals with unilateral cleft lip and palate express the combined effects of (1) the presence of a cleft of the lip and alveolus, in which the premaxilla on the noncleft side is rotated forward [3,5] and (2) the presence of a cleft palate, which causes the maxilla and mandible to be relatively retrusive (Tables 5, 6) [2,7,8].

Table 4 Effects of surgical management on dental relationships in individuals with cleft of the palate only Dental findings Incisor relationship Normal Incisor inversion Mandibular overjet Extreme maxillary overjet Transverse occlusion Normal Unilateral cross-bite Bilateral cross-bite

Unoperated CPO (%)

Operated CPO (%)

Effect of surgery

90.9 0 0 9.1

70 10 15 5

Increase in anterior cross-bite

80 10 10

51.3 20.5 28.2

Dramatic increase in posterior cross-bite

Abbreviation: CPO, cleft of the palate only.

418

Unoperated UCLP Cephalometric findings vs. normal

UCLP with operated lip only vs. normals

UCLP with operated lip and palate vs. UCLP with operated lip only

Maxilla

No difference in relationship and dimension

Maxillary retrusion

Greater maxillary retrusion than with lip surgery only Maxillary apical base width is smaller in the group with operated palate

Mandible

Similar relationship

Maxilla-mandible

Mandibular retrusion in the UCLP and steep mandibular plane No difference in relationship

No difference in relationship

Similar relationship, but the MP is less steep in the group with operated palate Negative ANB relationship

Dentition Upper incisors

No difference in inclination

More upright than normals

No difference

More upright than the normals

More upright than normals

No difference

Lower incisors

Abbreviations: ANB, Maxillary-mandibular apical base relationship; MP, Mandibular plane; UCLP, unilateral cleft of the lip and palate.

Effect of lip/palatal surgery The lip surgery causes the molding of the anterior part of the maxilla and makes the maxilla slightly retruded Lip and palatal surgeries cause the maxilla to be further retruded Palatal surgery may decrease the steepness of the MP Lip surgery decreases the ANB angle, but the palatal surgery further decreases the ANB angle to a negative value Lip surgery causes the upper incisors to upright Lower incisors are upright in the unoperated and operated UCLP when compared to normals

S.E. Bishara / Oral Maxillofacial Surg Clin N Am 14 (2002) 411–424

Table 5 Effects of surgical management on the cephalometric dentofacial relationships in individuals with unilateral cleft of the lip and palate [3,5,8]

S.E. Bishara / Oral Maxillofacial Surg Clin N Am 14 (2002) 411–424

419

Table 6 Effects of surgical management on dental relationships in individuals with unilateral cleft of the lip and palate [8] Dental findings

Unoperated CLP (%)

CLP with operated lip only (%)

CLP with operated lip and palate (%)

Incisor relationship Normal

83

64.3

30.5

17

35.7

32.2

0

0

37.3

46

52.9

9

Unilateral cross-bite

27

41.2

50

Bilateral cross-bite

9

5.9

41

Inversion of incisors

Mandibular overjet Transverse occlusion Normal

Buccal cross-bite

18

0

0

Effect of surgery Lip surgery increases the inversion of upper incisors Lip and palatal surgeries also create an increased incidence of mandibular overjet

Most of the unilateral cross-bites are on the cleft side. Lip surgery increases the incidence of cross-bite slightly. Lip and palatal surgery increases incidence greatly. Buccal cross-bite is only present in the unoperated group.

Abbreviations: CLP, cleft lip and palate; UCLP, unilateral cleft of the lip and palate.

Skeletal relationships: The result of these opposing influences on the unoperated maxilla is that it maintains a ‘‘normal’’ relationship to the cranial base. The mandible, on the other hand, is rotated backward as a result of the presence of the palatal cleft (Fig. 6). Dental relationships: Occlusal view: In the maxillary arch, the relationship of the cleft segment to the noncleft segment varies from normal to different degrees of medial collapse, particularly in the canine area (Fig. 7A,B). This relationship causes an in-

creased incidence of cross-bite [1,3,5]. On the noncleft side, the premaxillary segment has a tendency to rotate forward and laterally, which increases the incidence of Brophy’s syndrome in the premolar area (ie, maxillary premolars with buccal overjet) (Fig. 7C) [5]. Lateral view: There is a tendency toward infraocclusion of the teeth on either side of the cleft defect (Fig. 7D), which is similar to what is seen in individuals with unrepaired unilateral cleft lip and alveolus [3,5].

Effects of surgery in unilateral cleft lip and palate

Fig. 6. Skeletal relationships of the maxilla and mandible in individuals with unrepaired unilateral complete cleft lip and palate.

It is often assumed that all the disturbances in the facial growth of individuals with repaired clefts of the lip or palate or both are the result of the effects of lip and palatal surgeries. But is the surgery the only explanation of the patient clinical picture, or is it the combined effect of surgery and the presence of the cleft? Earlier in this article, the effect of lip surgery on individuals with unilateral cleft lip and alveolus and the effects of palatal surgery on individuals with isolated clefts of the palate were outlined. It is important to remember that in each of these two groups either the primary or secondary palates were intact. As a result, in these two cleft types there is a partial anatomic support for the dentition and alveolar

420

S.E. Bishara / Oral Maxillofacial Surg Clin N Am 14 (2002) 411–424

Fig. 7. (A) Occlusal view of the dental arches in an individual with unilateral complete cleft of the lip and palate. (B) Notice the lingual cross-bite tendency on the cleft side. (C) Notice the buccal cross-bite tendency on the noncleft side. (D) The teeth on either side of the cleft have a tendency to be in infraocclusion.

processes from the constricting influence of the scar tissues that accompany lip or palatal repair. On the other hand, individuals with complete unilateral cleft lip and palate are deprived of this partial supportive bony mechanism (Fig. 8). To simplify this part of the presentation, the findings on individuals with unilateral cleft lip and palate who had lip repair but no palatal repair are

presented first. From a purely experimental point of view, it would have been ideal if one could find a group of individuals with unilateral cleft lip and palate who had palatal surgery but no lip surgery. Such an approach is, to say the least, hard to justify, however. The question can be indirectly addressed by examining individuals with unilateral cleft lip and palate who had lip and palatal repair and compare

S.E. Bishara / Oral Maxillofacial Surg Clin N Am 14 (2002) 411–424

421

smaller in magnitude compared to that of individuals with unoperated clefts or normal subjects, but the angle was still positive. These findings indicate that the effects of lip surgery on the maxillary skeletal structures in unilateral cleft lip and palate are not similar to its effects on individuals with unilateral cleft lip and alveolus. Two factors help explain the differences in the effect of lip repair in these two cleft types: (1) The presence of the palatal cleft causes maxillary and mandibular retrusion in the unilateral cleft lip and palate group. (2) The presence of an intact secondary palate in individuals with unilateral cleft lip and alveolus minimizes the retrusion of the maxilla after lip surgery. In summary, lip repair in individuals with unilateral cleft lip and palate has a molding effect on the maxilla, which causes a decrease in the SNA and ANB angles (Tables 5, 6). The presence of the palatal cleft enhances the effects of lip repair, which causes the maxilla to retrude further as compared to individuals with unilateral cleft lip and alveolus who had lip repair [11,15]. Effects of lip surgery on the dentition

Fig. 8. Facial view of an individual with an unrepaired unilateral complete cleft of the lip and palate. Notice the lack of any bony support for either the anterior or posterior parts of the palate.

them to individuals with unilateral cleft lip and palate who had lip repair only.

Upper incisors: Lip surgery causes the maxillary incisors to be more upright and decreases the overjet, but generally it does not cause an increase in the incidence of anterior cross-bite on the noncleft side (Tables 5, 6). Posterior cross-bite: There is an increased incidence of unilateral posterior cross-bite on the cleft side as a result of lip surgery [8].

The combined effects of lip and palatal repair Effects of lip surgery in individuals with unilateral cleft lip and palate Unilateral cleft lip and palate with lip repair only versus unrepaired unilateral cleft lip and palate Skeletal structures Maxilla: The anteroposterior relationship of the maxilla (SNA) in individuals with unrepaired unilateral cleft lip and palate was similar to noncleft individuals. On the other hand, individuals with unilateral cleft lip and palate who had lip repair have a maxilla that is more retrusive than that of individuals with unoperated clefts. Mandible: Lip surgery had no apparent effects on mandibular size or relationship. Maxilla-mandibular relationship: The ANB angle in unilateral cleft lip and palate with lip repair is

To evaluate the added effects of palatal surgery, two groups with unilateral cleft lip and palate must be compared, one group that had their lip repaired but not their palate, whereas in the other group, both the clefts of the lip and palate were repaired. For such a comparison to have validity, both groups should have an identical lip surgery [8]. Effects on the skeletal structures Maxilla: The added effect of palatal surgery caused the maxilla to be further retrusive and the maxillary apical base to be more constricted than with lip repair only. The cumulative effects of lip and palatal surgeries on the maxilla are relatively more severe than the separate effects of lip surgery in unilateral cleft lip and alveolus and palatal surgery

422

S.E. Bishara / Oral Maxillofacial Surg Clin N Am 14 (2002) 411–424

in individuals with isolated clefts of the palate. This is because of the lack of any continuity in either the primary or secondary palates (Table 6). Mandible: Palatal repair resulted in a decrease in the steepness of the mandibular plane. This finding is similar to the effect of palatal repair in individuals with isolated clefts of the palate. Maxilla-mandibular relationship: Palatal repair caused a maxillary retrusion and a decrease in the steepness of the mandibular plane. The combined effects produced a negative ANB relationship in individuals with unilateral cleft lip and palate who had lip and palatal repair. Lip repair in unilateral cleft lip and palate causes the maxilla to be retrusive. The presence of a palatal cleft also causes further maxillary retrusion. Finally, the palatal repair causes the mandibular plane to be less steep (ie, rotate forward). This forward mandibular rotation is considered favorable in most orthodontic situations, except in cases with a negative ANB angle. When the maxilla is already retruded, the decrease in the steepness of the mandibular plane helps increase the incidence of anterior cross-bite. In summary, the combined effects of lip and palatal repair significantly influenced the skeletal relationship of the maxilla and mandible, which caused the ANB relationship to be negative. Effects on the dentition Upper incisor relationship: There was no difference in the incisor inclination between individuals who had their lip and palate repaired when compared to individuals who had lip surgery only. The lingual inclination of the maxillary incisors in both groups seems to be primarily the result of lip repair. There was a sharp increase in the incidence of anterior cross-bites (in more than one third of the individuals) after lip repair (Table 6). Posterior cross-bite: The added effect of palatal surgery increases the incidence of posterior cross-bite. Surgical and orthodontic implications The surgical and orthodontic implications of lip and palatal surgery are as follows: 1. The combined effects of lip and palatal surgeries cause the maxilla to be relatively retrusive; hence, the increased incidence of anteroposterior discrepancies in the maxillarymandibular relationships. 2. The lack of continuity of the primary and secondary palates in individuals with unilateral

cleft lip and palate allows the effects of the lip and palatal surgeries to be expressed fully and negatively influence the growth of the maxilla in a significant manner. As a result, individuals with operated unilateral cleft lip and palate have an increased incidence of maxillarymandibular discrepancies, as evidenced by the significant reduction in the ANB angle [8]. Similar discrepancies are not frequently observed in the ‘‘unoperated’’ faces of individuals with unilateral cleft lip and palate [3,5]. 3. The combined effects of lip and palatal surgery caused an overall and dramatic increase in the incidence of anterior and posterior cross-bites as compared to the incidence in cases with unilateral cleft lip and palate or those who had lip surgery alone [3,5,8]. 4. The incidence of abnormal skeletal and dental relationships in most of the studies reported earlier were obtained from cleft populations that did not receive surgical or orthodontic treatment. Orthodontic and orthopedic treatment can improve significantly the maxillary-mandibular relationship and the incidence of anterior and posterior cross-bites that occur after the surgical repair of the clefts. The orthodontist should note the tendency for the alveolar processes adjacent to the cleft to roll superiorly and the teeth to be in infraocclusion in the unoperated clefts, which could explain the tendency for these teeth to move in the same direction after their position is corrected orthodontically. Permanent retention of these teeth helps to stabilize them in their proper position.

Summary of facial characteristics of individuals with unrepaired clefts Numerous studies on unrepaired clefts indicated that significant differences in dentofacial relationships are present between the different cleft types when compared to each other and to matched normal individuals [1 – 20]. For individuals with unrepaired clefts, the main differences in the relationship of the facial skeletal structures of the three most frequently occurring clefts can be summarized as follows: Relative maxillary protrusion with normal mandibular relationship in the unilateral cleft lip and alveolus group Maxillary and mandibular retrusion with a steep mandibular plane in the cleft palate only group

S.E. Bishara / Oral Maxillofacial Surg Clin N Am 14 (2002) 411–424

Normal maxillary relationship with relative mandibular retrusion and steep mandibular plane in the unilateral cleft lip and palate group An explanation of these facial changes in the unrepaired cleft individuals includes the following points: 1. In the cleft lip and alveolus group, the defect either allows the noncleft segment to rotate in a lateral and anterior direction or allows it to ‘‘overgrow.’’ This results in a larger SNA angle and the appearance of a relative maxillary skeletal protrusion with an increase in the ANB angle. This is also associated with overjet and an increase in maxillary length (Figs. 1 – 3). 2. When individuals with isolated clefts of the palate were compared to normal subjects, it was found that in the unoperated cleft group, the maxilla and mandible were relatively retruded but in good relationship to each other, and the mandibular plane was relatively steep. Maxillary and mandibular retrusion is associated with the presence of a palatal cleft (Figs. 4,5). 3. The facial skeletal relationship of individuals with unilateral complete lip and palate is a reflection of the cumulative characteristics of the dentofacial findings of individuals with cleft lip and alveolus and those with an isolated cleft palate. The normality of maxillary relationship is caused by the combination of the tendency for maxillary protrusion present with the lip and alveolus and the tendency for maxillary retrusion present in the cleft palate only group (Figs. 6 – 8). 4. On average, all individuals with an unrepaired palatal cleft have a tendency for mandibular retrusion, a steep mandibular plane, and upright lower incisors. This finding was consistent in individuals with isolated clefts of the palate and unilateral cleft lip and palate. These findings tend to indicate that part of the maxillary and mandibular characteristics of individuals with repaired clefts are related to the presence of the cleft itself. It can be concluded that different cleft types have different skeletal and dental characteristics and that part of what is considered as ‘‘bad effects of surgical management’’ (eg, maxillary and mandibular retrusion) are expressed in the unrepaired cleft face. These characteristics must be recognized because they can influence our under-

423

standing of the effects of the surgical repair and the planning of orthodontic treatment.

References [1] Atherton JD. Morphology of facial bones in skulls with unoperated unilateral cleft palate. Cleft Palate J 1967;4: 18 – 30. [2] Bishara SE. Cephalometric evaluation of facial growth in operated and non-operated individuals with isolated clefts of the palate. Cleft Palate J 1973;3:239 – 46. [3] Bishara SE, Krause JC, Olin WH, Weston D, Van Ness J, Felling C. Facial and dental relationships of individuals with unoperated clefts of the lip and/or palate. Cleft Palate J 1976;13:238 – 52. [4] Bishara SE, Olin WH, Krause CJ. Cephalometric findings in two cases with unrepaired bilateral cleft lip and palate. Cleft Palate J 1978;15:233 – 8. [5] Bishara SE, Sosa-Martinez R, Patron-Vales H, Jakobsen JR. Dentofacial relationships in individuals with unoperated clefts: comparisons between three cleft types. Am J Orthod 1985;87:481 – 507. [6] Bishara SE. Maxillofacial growth and development: the method of analysis. In: Morris HL, editor. The Bratislava project: some results of cleft palate surgery. Iowa City: University of Iowa Press; 1978. p. 74 – 82. [7] Chierici G, Harvold E, Vargervik K. Morphogenetic experiments in cleft palate: mandibular response. Cleft Palate J 1973;10:51 – 61. [8] Dahl E. Craniofacial morphology in congenital clefts of the lip and palate. Acta Odontol Scand 1970; 28(Suppl):57. [9] Davis AD. Unoperated bilateral complete cleft lip and palate in the adult. Plast Reconstr Surg 1951;7: 482 – 91. [10] Graber TM. An appraisal of the developmental deformities in cleft palate and cleft lip individuals. Quarterly Bulletin, Northwestern University Medical School 1949;23:153. [11] Hagerty RF, Hill MJ. Facial growth and dentition of the unoperated cleft palate. J Dent Res 1963;42:412 – 21. [12] Huddard AG, Bodenham RS. The evaluation of arch form and occlusion in unilateral cleft palate subjects. Cleft Palate J 1972;9:194 – 209. [13] Innes CO. Some observations on unrepaired hare-lips and cleft palates in adult members of the Dusan tribe of North Borneo. Br J Plast Surg 1962;15:173 – 81. [14] Law FE, Fulton JT. Unoperated oral clefts at maturation. Am J Public Health 1959;49:1517 – 24. [15] Mestre JC, DeJesus J, Subtelny JD. Unoperated oral clefts at maturation. Angle Orthod 1960;30:78 – 85. [16] Ortiz-Monasterio F, Rebel AS, Valderramo M, Cruz R. Cephalometric measurements on adult patients with nonoperated cleft palates. Plast Reconstr Surg 1959; 24:54 – 61. [17] Ortiz-Monasterio F, Serrano A, Barrera G, RodriquesHoffman H, Vinageras E. A study of untreated adult

424

[18] [19] [20]

[21] [22]

[23]

S.E. Bishara / Oral Maxillofacial Surg Clin N Am 14 (2002) 411–424 cleft palate patients. Plast Reconstr Surg 1966;38: 36 – 41. Pitanguy J, Franco T. Non-operated facial fissures in adults. Plast Reconstr Surg 1967;39:569 – 77. Pruzansky S. Factors determining arch form in clefts of the lip and palate. Am J Orthod 1955;41:827. Ross M. Comparison of model analysis of untreated cleft palate adults and normal adults. Am J Orthod 1962;48:63 – 4. Bjork A. The face in profile. Svensk Tandlak Tidskr 1947;40(Suppl):5b. Downs WB. Variation in facial relationships: their significance in treatment and prognosis. Am J Orthod 1948;34:812 – 40. Krogman W, Sassouni V. A syllabus in roentgenographic cephalometry. Philadelphia: Philadelphia Center for Research in Child Growth; 1957.

[24] Riedel RA. A cephalometric roentgenographic study of the relation of the maxilla and associated parts to the cranial base in normal and malocclusion of the teeth [Master’s thesis]. Chicago: Northwestern University; 1948. [25] Riolo ML, Moyers RE, McNamara JA, Hunter WS. An atlas of craniofacial growth: cephalometric standards from the University School Growth Study. Ann Arbor: University of Michigan; 1974. [26] Steiner CC. Cephalometrics for you and me. Am J Orthod 1953;39:729 – 55. [27] Tweed CH. Was the development of the diagnostic facial triangle as an accurate analysis based on fact or fancy? Am J Orthod 1962;48:823 – 40. [28] Wylie WL. Rapid evaluation of facial dysplasia in the vertical plane. Angle Orthod 1952;22:165 – 82.

Oral Maxillofacial Surg Clin N Am 14 (2002) 425 – 437

Scar revision of the cleft lip Ladi Doonquah, DDS, MDa,b,*, Orrett E. Ogle, DDSc a

Section of Otorhinolaryngology, Department of Surgery, University Hospital of the West Indies, Kingston, Jamaica b Private Practice, Oral and Maxillofacial Surgery, Suite 230, 3490 Piedmont Road, Atlanta, GA 30305, USA c Department of Dentistry and Oral and Maxillofacial Surgery, Woodhull Hospital, 760 Broadway, Brooklyn, NY 11206, USA

The repair of cleft lip and palate deformities continues to be one of the more challenging areas of surgery. Despite a plethora of new techniques and various refinements, residual deformities continue to be a recurring feature in cleft patients [1 – 15]. Among these deformities, defects of the lip figure prominently. The high visibility of the lip complex makes even minor defects readily apparent. In this area of surgery, as in no other, the adage ‘‘by your scars you will be judged’’ is particularly suitable [16]. To this end, an article devoted to scar revision of the lip is appropriate. Revisionary surgery in any area is often more challenging than the initial surgery. Secondary cleft lip surgery is no different, despite the relatively small anatomic unit represented. The decision to revise the scar in the repaired cleft lip should not be taken lightly. Several factors contribute to an unacceptable scar in the lip of a cleft patient. The operating surgeon must be familiar with them and how to alter them in the revision process. The surgeon must communicate clearly to the patient that scars do not disappear but that they merely exchange one scar for hopefully a more acceptable one. Unrealistic expectations should be determined and addressed before surgery. An undesirable scar is a result of complex factors that must be understood completely. The pathophysiology of wound healing, along with the relevant anatomy peculiar to the lip, must be known thor-

* Corresponding author. Suite 230, 3490 Piedmont Road, Atlanta, GA 30305. E-mail address: [email protected] (L. Doonquah).

oughly. Correct surgical techniques, proper tissue handling, and good surgical principles must be adhered to, along with proper perioperative care. Adjunctive procedures, such as dermabrasion, collagen injection, and dermal micrografting should be included in the surgeon’s arsenal [17].

Anatomy A brief review of the anatomy, especially the muscular infrastructure of the lip upper complex (Fig. 1), is important to the understanding of secondary lip defects. Improper restoration of segments of the muscular substructure of the lip is a major cause of postsurgical lip deformities. (The outer landmarks of the upper lip are addressed later). The lip complex comprises the skin anteriorly and the oral mucosa posteriorly. There is a ring of muscles between these two layers, the major one being the orbicularis oris, which extends in a circumoral fashion from commissure to commissure. It consists of a horizontal band, oblique band, and an incisive band, which extends from the nasal sill to the region of the modiolus. Laterally the orbicularis oris inserts in and around the region of the modiolus. The horizontal band functions to close the interlabial opening and appose the lip against the dentoalveolar region. The oblique and incisive bands elevate the upper lip and assist in forward projection. Arising from the underlying midfacial skeletal complex in a radial fashion is the upper facial ring of muscles and a smaller perinasal group that arises primarily from the anterior alveolar process of the maxilla and inserts into various elements around the

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 4 7 - X

426

L. Doonquah, O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 425–437

Fig. 1. Muscles of the perioral region.

nasal septum and nasal floor. Both groups have fibers that insert into and around the orbicularis muscle. The upper facial ring group of muscles that starts from the midline comprises the transversus nasalis that arises from the nasal dorsum and extends inferiorly around the nasal alae and floor and inserts into the incisal crest and superior medial aspect of the upper lip. The levator labi superior alaeque nasi arises from the lateral superior aspect of the nasal bone and the frontal aspect of the maxilla and inserts into and around the nasal alae and upper lip. The levator labi superior arises from the infraorbital region of the maxilla and inserts around the nasal alae and upper labial vestibular mucosa. The levator anguli oris arises from the canine fossa and inserts laterally into the outer aspect of the orbicularis oris. The zygomaticus minor arises from the medial aspect of the body of the zygoma and inserts medially into the orbicularis. The zygomaticus major arises from the lateral aspect of the body of the zygoma and inserts into the modiolus. The risorius muscle extends from the lateral aspect of the cheek and inserts into and around the modiolus. The smaller set of muscles that arises from the anterior alveolar process of the maxilla inserts into the area around the nasal septum and floor. It consists of the alaris, the depressor septi, and the myrtiformis,

and it serves to anchor the superior aspect of the lip to the floor of the nose. Both groups of muscles, along with the obicularis oris complex, make up an important substructure that is disrupted in complete clefts. Detailed attention to the surgical restoration of the form and function of these muscles is critical in primary and secondary repair of the cleft lip [18,19]. The muscles provide an important scaffold for the overlying scar and contribute to or detract from its cosmesis. Improper alignment of these muscles negatively affects lip movement and, by extension, the range of lip functions, including facial expression and speech [20].

Skeletal framework With the greater concentration on the scar itself and the surgical emphasis placed on the dissection and reorientation of the muscles in secondary repairs of the cleft lip, the contribution of the osseous understructure to the appearance of the lip is sometimes overlooked. Considerations must be given to the skeletal infrastructure when planning revision procedures of the lip [20,21]. The lack of projection of the nasomaxillary and dentoalveolar skeletal complex, for example, can accentuate deformities of the lip

L. Doonquah, O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 425–437

and render a careful soft tissue repair ineffectual. Rotation of one side of the anterior maxilla also can make a repaired lip appear asymmetrical, with an apparent lack of bulk on one side. Frequently, osseous repositioning or reconstruction can be accomplished simultaneously through the same surgical incision used to correct the lip deformity. Careful attention, however, must be given to the management of the soft tissue flaps when this is done. The osseous repair segment of the operation should not last too long because the edema in the lip may distort the soft tissue anatomy sufficiently, to preclude precise reorientation of the flaps during surgery.

Assessment Any surgical intervention to revise the scar in the cleft lip must be based on a complete analysis of the problem. Evaluating lip deformities is highly subjective and should take into account ethnic variations, the original deformity, and the previous surgical method of primary repair. A systematic approach to the assessment of secondary lip deformity is critical, and many authors have attempted to develop methods to classify these secondary defects of the cleft lip [22]. Unfortunately, many of these methods have been cumbersome and overly detailed. Two authors, Wilson in 1985 and Assuncao in 2000, have designed two relatively simple and transferable methods for the evaluation of postsurgical lip deformities [23,24]. Wilson looked at six different aspects of the lip:    

Amount of lip tissue Freedom of movement of the upper lip Equality of bulk over its length Cupid’s bow position and presence of all components  Philtral structures width, direction of scars, and relocation of ridges  Alignment of circumoral muscles

427

No particular numbering system is ascribed to this method. Assuncao described a VLS (vermilion, lip, scar) system that ascribed various numbers (Vo – V7, Lo – L6, So – S5) to the specific types of deformities. Whatever method is chosen by the surgical team, it should be simple, complete, and easily reproducible. The authors’ assessment of lip deformities categorizes them into three broad areas: lip volume, mobility, and architecture. Lip volume defects include discrepancies that involve the height, thickness, or length of the lip. Mobility defects refer to lack of mobility, asymmetric movements, and horizontal tightness of the upper lip with attendant loss of the labial sulcus. Lip architectural deficiencies refer to deficiencies in position and presence of various lip landmarks, especially the philtrum and its components, cupid’s bow and its components, and the vermilion border. No numbering system is ascribed, because it is thought of as a guide to look at all the various components involved in creating an aesthetic, mobile, and functional unit (Table 1). In the process of examining and identifying the defects, one must be guided by sound anatomic knowledge of the area and the general principles that are involved in primary cleft surgery. This approach enables the surgeon to identify not only the defects but also their probable cause. By approaching the problem with this mindset, a solution can be created that is tailored to suit each particular situation.

Lip volume defects Volume discrepancies, such as redundancy or deficiency, manifest themselves as thick or thin lateral areas, asymmetry of the lip, and lip length discrepancies. Many of these defects are associated with the vermilion and are often related to the underlying musculature from which the lip receives its bulk. A discussion of abnormalities of the vermilion and the underlying musculature follows.

Table 1 Lip deformities Lip volume defects

Lip mobility defects

Lip architectural discrepancies

Lip thickness Lip height Lip length Lip projection Increased projection Decreased projection

Lip tightness/pressure of labial sulcus Decrease mobility Asymmetric mobility

Gross asymmetry Mismatch of vermilion border Notching of vermilion border Asymmetry of tubercle Philtrum/philtral ridge distortion Cupid’s bow presence and position Orientation and nature of existing scar

428

L. Doonquah, O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 425–437

Vermilion abnormalities Several types of defects are associated with the vermilion in cleft lip patients, but in this section we will focus on those related to volume. Many vermilion deformities exhibit muscular defects as the major underlying cause of the deformity. Patients with wide unilateral or bilateral clefts exhibit more severe defects. Vermilion border discrepancies include notching and whistle deformity. Notching is a result of inadequate muscle support caused by improper attachment of the underlying muscle or lack of wound eversion at time of closure. The whistle deformity is caused by inadequate bulk in the central lip area as a result of muscular diastasis.

Orbicularis oris abnormalities The orbicularis oris consists of three bands: horizontal, oblique, and incisal. The horizontal band runs medially from the region of the modiolus, where it decussates and meets just below the philtrum with its counterpart from the contralateral side. The oblique band extends from the lateral aspect in the area of the modiolus to the upper philtral region, whereas the incisive band starts in the same area but inserts into the nasal spine. In the cleft lip the main fibers of the orbicularis oris are believed to run parallel to the cleft margin upward toward the nose. Other smaller fibers insert into the overlying dermis and underlying mucosa. It is readily apparent that this muscle is severely disrupted in cleft lip patients. The resultant defect contributes to various aspects of lip abnormalities, such as, but not limited to, the following:     

Abnormal thickness of the philtrum Wide philtrum Lateral bunching Abnormal vermilion thickness Vermilion/lip asymmetry

Abnormal thickness of the philtrum is usually caused by placement of the orbicularis muscle on the cleft side too far medially. A wide philtrum is caused by inadequate attachment of the orbicularis to the philtrum or lateral placement in relation to the philtral ridges. This is seen more frequently in bilateral clefts and wide unilateral clefts [25]. Lateral bunching, an abnormality that is seen more clearly in attempts to whistle, again is caused by improper placement of the medial aspect of the orbicularis on the cleft side. Abnormal thickness may be caused by

excessive overlap of the orbicularis oris between the cleft and noncleft side.

Lip mobility defects Lip mobility defects are also multifactorial. A tight upper lip may be caused by a wide cleft, overprojection of the premaxilla, severe rotation of the maxilla on the noncleft side, abnormal scarring, infection and subsequent loss of tissue, and improper closure of the oral musculature. Asymmetrical lip movements can be caused by various factors. Chief among them, however, is improper alignment of the free edges of the dissected orbicularis, which explicitly illustrates the major role that the orbicularis plays in normal form and function of the lip and how improper realignment contributes to myriad lip abnormalities [26]. In 1990, Schendel et al examined the histology of the orbicularis oris muscle in patients who had primary repair of the cleft lip [27]. They reported a significant amount of scarring beyond the repaired cleft margins, with connective tissue scattered throughout the muscle fibers. They also noted varying extent of muscular fiber abnormalities with resultant muscle atrophy, some of which they postulated was caused by surgical denervation injury. If this study is accepted, then it further illustrates the importance of careful dissection and proper reorientation of muscle groups in the cleft patient [28,29].

Lip architecture Because of different interpretations of lip landmarks in various aspects of the cleft lip literature, it is important that one review the overlying surface anatomy [30]. The external lip complex (Fig. 2A,B) consists of the mucosal region, which is bounded above by the vermilion border (white roll in light complexioned individuals and a red to pale brown roll in darker individuals) and below by the wet line. The center projection of the vermilion is the tubercle. Cupid’s bow is that central portion of the vermilion border at the inferior aspect of the philtrum. The philtrum is the central groove that extends from cupid’s bow to the base of the columella. It is approximately one fourth of the width of the upper lip and is bordered on both sides by the philtral ridges. Lip architectural deformities mainly refer to malposition of various aspects of cupid’s bow, the philtrum, philtral ridges, and the vermilion border.

L. Doonquah, O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 425–437

429

Fig. 2. (A,B) Surface land marks of the lip.

From a purely cosmetic standpoint, lip architecture, both at rest and in function, is governed by the position of these various lip landmarks and their relation to each other. In consideration of these lip landmarks and the deviation from normal, it is critical to remember normal ethnic variations. The various landmarks divide the lip into cosmetic subunits that function interdependently. They rest on muscular foundations that must be properly in place. The basic goal from a cosmetic perspective is to have a lip with symmetrical vermilion show; normal vermilion border, tubercle centered with normal dimension and projection; cupid’s bow with all components present and in position; philtrum with

proper length and direction of the philtral ridges and correct width of the philtral column; normal lip height throughout the length of the lip; and labial scar that is positioned in such a way as to replicate the philtral ridge on one or both sides [31]. Lip landmark deficiencies of necessity must be understood in the context of deviation from the norms. The cleft lip patient may show one or more of the following deformities: discontinuity defect of the vermilion border with cranial displacement of the medial margins, absence of one or more philtral ridges, loss of part of cupid’s bow, abnormal projection of cupid’s bow in the separated prolabium, superiorly displaced tubercle, or decreased projection of the cleft side. These landmark discrepancies,

430

L. Doonquah, O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 425–437

however, are just manifestations of deeper problems and should be viewed as such.

Volume defects Vertical deficiency

Surgical techniques The surgical techniques that are used secondarily to correct abnormal defects in the cleft lip patient depend on the defect that is present. The technique varies from patient to patient and cannot rely totally on any set approach but must depend on the ingenuity and experience of the surgeon. The authors note that although they categorize the defects into three categories, more than one problem may exist in the same patient (eg, volume and mobility defects may be seen in the same lip). Planning the surgery requires careful analysis of the deformity and the fabrication of a problem list. The lip revision must be designed to correct the specific problem as it affects the skin, muscles, and mucosa. This section presents guidelines that should be helpful to the surgeon.

Unilateral cleft lip. Vertical deficiency in the unilateral cleft (Fig. 3A) results from several factors. The components of the defect are manifested in all three layers. Some of the causes include inadequate rotation of the noncleft segment, wound dehiscence with healing by secondary intention and subsequent vertical scar contraction, abnormal scar contraction in cases in which straight line or slightly curved incisions were used in the primary repair, and inadequate dissection and horizontal lengthening of the orbicularis muscle. An inadequate muscle repair often results in a vertically deficient lip. In this type of defect a total secondary repair gives the best results, although V-Y closures may be used for small defects. The surgical goals consist of conservative excision of the scar, further rotation of cupid’s bow, readjustment of the lateral segment, and adequate interdigitation of the orbicularis oris musculature.

Fig. 3. (A) Vertical scar contraction with inadequate rotation of Cupid’s bow. (B) Preoperative identification of anatomic landmarks. (C) Planned surgical incisions showing back cut and scarred area that will be removed. (D) Postoperative view at 1 week.

L. Doonquah, O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 425–437

Fig. 4. Bilateral cleft with vertical lip defect.

Before any incisions are made, the standard anatomic landmarks (Fig. 3B) should be identified, particularly cupid’s bow, and measurements recorded as in the primary repair of the cleft lip. These measurements guide the surgeon in planning the incisions, deciding the amount of scar tissue that may be removed (Fig. 3C), and aiding in the repositioning of the flaps (Fig. 3D). Starting the incision at the wet/dry line, extending it across the base of the columella, and using a back cut to increase the downward rotation achieve the desired rotation of the noncleft side. The back cut should be on the contralateral philtrum line or just adjacent to it to mask the scar. Care must be taken to dissect adequately the muscular layer on the cleft side and properly align the edges during the closure. The surgeon should make every effort to be sure that the cupid’s bow is centered. Vicryl 4-0 is used for deep closure, whereas nylon 6-0 or 5-0 sutures are used to approximate the skin margins. The skin sutures are

431

removed in 3 to 4 days and the lip scar is supported with Steri-Strips (3M, St. Paul, MN) during the first 10 days and then at night for another 2 weeks. If necessary, the nose also may be narrowed at the same time or additional corrections made in the general contour of the nose. The authors believe that the rotation-advancement revision should be used to correct vertical problems (Fig. 3A), ignoring scars from other techniques (eg, LeMesurier, Tennyson). The additional scars produced from adding the incision for the rotation method to quadrangular or triangular flap repairs are minimal, and the quality of the result is significantly improved. Bilateral cleft lip. A vertically short upper lip in the bilateral cleft (Fig. 4A) is most probably a result of a short prolabium that could not be stretched to match the lateral lip segments during the primary repair. Minor to moderate defects may be managed Fig. 5A – C). More often than not, however, it is necessary to reopen the cleft and reclose the lip. Molding of the alveolus by the primary repair along with soft tissue growth often provides an environment in which a good secondary repair can be performed. When this is not the case, lengthening of the lip without sufficient local tissue requires an Abbe´ flap. (This flap is discussed in the article by Juri et al elsewhere in this issue.) The authors do not advocate routine use of the Abbe´ flap, however. Horizontal deficiency Unilateral cleft lip. A horizontal deficiency in the unilateral cleft lip (Fig. 6A,B) may be caused by a

Fig. 5. (A – C) Lengthening of the short bilateral lip with a V-Y procedure. (A) The design of the incisions enables lengthening of the midportion of the lip and narrowing of the alar bases. (B) Incisions are carried through all lip layers, and a hook is inserted at the midline to pull the lip inferiorly, lengthening the midportion and approximating the lateral lip elements. (C) Completed procedure. (From Bardach J, Salyer KE. Surgical techniques in cleft lip and palate. Chicago: Year Book Medical Publishers; 1987; with permission.)

432

L. Doonquah, O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 425–437

Fig. 6. (A,B) Horizontal lip defect secondary to a retrusive maxilla, unrepaired alveolar cleft, and dentoalveolar abnormalities on the cleft side.

tight upper lip from closing a wide cleft, sacrifice of excessive soft tissue during the primary repair, orbicularis oris defects, an unrepaired alveolar cleft that involves the nasal floor, or maxillary retrusion. It is important to determine if the flat upper lip is caused by soft tissue problems or an underlying skeletal

abnormality. In most cases of skeletal abnormality, the upper lip profile is restored or improved by maxillary advancement at the Le Fort I level and repair and bone grafting of the alveolar cleft. In profile, the upper lip should be full and should protrude slightly beyond the lower lip (see Fig. 2B).

Fig. 7. (A,B) Male patient with vertical and horizontal lip defects who was first treated with maxillary advancement before the lip was revised.

L. Doonquah, O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 425–437

Flattening of the lip on the cleft side only may be caused by one or more of the following: maxillary hypoplasia on the cleft side with a deficient alveolus, medial rotation of the maxilla on the cleft side, palatal inclination of the teeth (canine and premolars), or orbicularis oris abnormalities. Careful analysis is required. Correction of the skeletal and dental support should correct the flattened upper lip appearance and should be addressed before soft tissue procedures are considered (Fig. 7A,B). Orbicularis oris abnormalities An orbicularis oris abnormality often manifests itself as a widened scar that results from lateral tension on the skin suture line. There is a depression under the repair with bunching in the lateral portion of the upper lip. In this type of defect the widened scar should be excised completely, the entire cleft reopened, the muscle groups identified, and the cleft repaired in three separate layers: mucosa, muscle, and skin. Dissection and repositioning of the muscle fibers horizontally across the lip with horizontal lengthening and interdigitation are essential. A thin lip on the cleft side in which there is atrophy of the orbicularis oris muscle and the subcutaneous tissues with resultant loss of volume may be augmented with allogeneic dermis. To augment the lip with allogeneic dermis (AlloDerm, Life Cell Corp., The Woodlands, TX) two 7-mm incisions are

433

made starting at the junction of the wet/dry line and extending up the labial mucosa toward the vestibule at either ends of the area that requires augmentation. Tunnels are then created in the submucosal plane, into which the determined size of rolled allogeneic dermis is placed. The allograft is not sutured in place so as to prevent puckering. In addition to lost volume, the normal projection of the upper lip is frequently reduced and may require mucosal flap advancement to improve the projection. A V-Y closure may be performed to increase lip projection in addition to the augmentation (Fig. 8A – D). Bilateral cleft lip. In the bilateral cleft, a wide prolabium, prominent premaxilla, inadequate orbicularis oris repair, skeletal defects, and a tight upper lip secondary to excision of excess tissue during the initial closure are the most common horizontal abnormalities seen. Most revisions of the bilateral cleft require complete reopening of the cleft. In the case of a wide prolabium, the lip scar is completely reopened and the prolabium narrowed to 15 to 16 mm at the cupid’s bow. In cases in which the columella is short, tissue may be left in the prolabium for later fork flap lengthening of the short columella. For cases in which the orbicularis oris is inadequately repaired, the complete cleft is reoperated, the prolabial flap is elevated and pedicled to the base of the columella (Fig. 9), and the muscles are adequately

Fig. 8. (A – D) Whistle-style defects of the vermilion may be corrected by a V-Y advancement as shown. (From Jackson IT, Fasching MC. Secondary deformities of cleft lip, nose and cleft palate. In: McCarthy JG, editor. Plastic surgery. Philadelphia: WB Saunders; 1990; with permission.)

434

L. Doonquah, O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 425–437

Fig. 9. Surgery for scar revision of a bilateral cleft shows the prolabium pedicled to the columella as the orbicularis oris muscle is horizontalized and closed in the midline. The prolabium will be repositioned over the muscle repair.

dissected and brought across the clefts to be interdigitated and sutured in the midline. When enough local tissue is not available, midline insertion of an Abbe´ flap should be used to increase the horizontal length of the upper lip. The insertion of this flap produces good philtrum lines and lip tubercle. Orthognathic surgery to advance the midface also must be considered and skeletal problems addressed before the final soft tissue revision (see Fig. 7A,B).

construction of all the muscle elements are impossible. Fibrosis within the musculatures from previous repair [27] also makes the functional result less than would be desired, but there definitely are improvements within the lip. Orbicularis oris defects are common in bilateral clefts, particularly in babies with wide clefts that did not benefit from presurgical molding of the maxilla or patients who had their cleft closed later than normal, as is frequently seen in lesser developed countries. The wide cleft or a severely protruding premaxilla makes it impossible for the surgeon to join the muscles from the lateral segments in the midline. A clinical examination reveals an absence of muscle in the prolabium, with bulging above the vermilion on the lateral aspects of the upper lip that becomes more prominent on pouting or facial animation. Secondary correction of orbicularis oris defects in the bilateral cleft requires full reopening of the clefts, separation of the muscle from its vertical attachment to the alar base (Fig. 10), horizontal rotation, and advancement across the clefts to be closed in the midline.

Lip architectural discrepancies The most significant architectural characteristics of the upper lip are the two philtral columns, the central depression between these columns, and the

Lip mobility abnormalities Functional abnormalities of the lip are the result of orbicularis oris defects and may be the result of muscle atrophy or deficiency, malpositioning of the muscle during the primary repair, or discontinuities. An inadequate muscle repair results in a lip that does not function properly during facial expression, speech, sucking, or mastication. Observing the patient’s lips while pouting can assess muscle function within the lip. Lack of a complete circumoral muscular ring makes whistling difficult or impossible. Attempting to whistle accentuates the deformity and results in a depression below the repair and excessive bunching in the lateral aspect of the lip. Asymmetrical movements of the lip also may be apparent. These functional defects most often require a total secondary repair and should be performed even if the lip contour and scar appear good in the static position. The cleft should be reoperated and the muscle properly dissected and carefully reapproximated. The surgeon and patient must be aware that not all lip functions are restored, because the anatomy of the area is complex, and accurate identification and re-

Fig. 10. Bilateral cleft that shows insertion of the cleft ends of the orbcularis oris muscle inserted vertically into the ala.

L. Doonquah, O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 425–437

V-shaped cupid’s bow. Lip architectural discrepancies may involve, among other things, the loss of the philtrum, problems with cupid’s bow, vermilion discrepancies, and notching. Table 1 catalogs most of these defects. Cupid’s bow defects are common and most often related to poor alignment of the points on the vermilion during the primary repair. This can be corrected by a localized Z-plasty to realign the vermilion border at the lateral aspect of the cupid’s bow (Fig. 11A,B). Notching at the vermilion may be corrected by a single V-Y (see Fig. 8A – D) or double V-Y procedures. In larger defects, the entire labial sulcus may be released, as in a Le Fort I osteotomy, and advanced forward and down into the area of the vermilion defect. In severe defects, an anteriorly based tongue flap may be used, but the aesthetic aspect is not good because of texture and color differences between tongue and vermilion. A better technique devised by Juri et al is discussed elsewhere in this issue. The hypertrophic scar on the skin in a lip without other defects may be excised using a slightly zigzag incision (only skin is excised). The incision should not be too ‘‘wavy’’ because it leaves a saw tooth scar in an area that should have a straight philtrum line. The skin is undermined toward the cleft side and closed. Triamcinolone acetonide, 10mg/mL per 1 cm length of scar [32], is injected immediately post-

Fig. 11. (A,B) Z-plasty for correction of a step deformity of the vermilion border (white roll ) of the upper lip. (From Jackson IT, Fasching MC. Secondary deformities of cleft lip, nose and cleft palate. In: McCarthy JG, editor. Plastic surgery. Philadelphia: WB Saunders; 1990; with permission.)

435

operatively into the edges of the wound. Sutures are removed in 5 days and the wound supported with Steri-Strips for up to 10 days. The authors prefer to cover the wound with a silicone cream (Kelocote) for 12 h/d at night for up to 6 weeks.

Wound management The different surgical techniques previously outlined do not achieve the desired goal if the surgical site is not managed properly. Correct management of the surgical wound is of paramount importance. The pathophysiology of wound healing and the ultimate formation of a scar is a complex constellation of biologic events. Many factors can be controlled by the surgical team, whereas others—such as the patient’s age, preexisting medical conditions, and social environment—are beyond the ambit of the health care provider. Revision of any scar and the ultimate result of this intervention are governed by how well this complex constellation of biologic events is managed. Wound healing involves three main phases: substrate phase, proliferative phase, and remodeling phase. The substrate phase begins at the time the wound is sustained and lasts for approximately 5 to 6 days. During this time there is tremendous recruitment of leukocytes and macrophages to the area. They provide cellular de´bridement functions and encourage the formation of fibroblasts and additional leukocytes and macrophages. The proliferative phase is, as the name suggests, a massive proliferation of fibroblasts, myofibroblasts, and attendant collagen synthesis. It proceeds from day 5 to 2 weeks after the injury. The remodeling phase begins at 2 weeks and goes on for a year or more. There is concomitant deposition and lysis of collagen as the wound itself remodels and the scar matures. Hypertrophic scars and keloids are believed to result from an imbalance of collagen synthesis during this time [32]. The surgeon can enable a smooth and rapid progression through these phases and ultimately obtain a good result by abiding by simple, timeproven tissue handling principles. The methods that are outlined herein seem pedantic; however, when they are not adhered to, poor scar formation results. Keeping this in mind helps to minimize complications and maximize good results. The incision should be placed in an area that can be camouflaged by an existing anatomic unit (eg, the philtral ridges or at the alar base). It should be only as long as first estimated because additional length always can be obtained. The incision plane should

436

L. Doonquah, O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 425–437

be perpendicular to the surface of the skin unless otherwise planned. The tissue margins and flaps should be handled in an atraumatic fashion. The choice of instrumentation is important. Delicate tooth-holding forceps and skin hooks provide an excellent manner of manipulating the subunits, but the operator must remember consistently to handle the tissues gently. Proper muscle identification, adequate undermining of skin or mucosa where needed, and tension-free closure are critical for good apposition of the wound margins. Tissue conservation is important, especially in the cleft lip, where prior intervention often has resulted in less tissue volume with undesirable scar tissue. Proper suturing is an art form, and in primary or secondary cleft surgery it is a skill of immense importance. The practice of passing the suture in an accurate direction and at the desired height on the first attempt should be acquired. This is a basic surgical tenet, but when ignored, it results in tissue edges that are macerated by repeated careless attempts at passing the needle through the tissue. The knot should be placed to approximate and slightly evert the wound margins but not strangulate the tissue. One of the more important complications (although uncommon in the cleft lip) that good surgical techniques should avoid is a hematoma [33]. In general, hematomas present a multiplicity of problems to the healing cleft lip. The collection of blood under the skin or oral mucosa may disrupt the neovascularization of the overlying flaps. The increased volume within the wound places tension along the margins, which can strangulate tissue at the wound edges and ultimately promote wound dehiscence or severe scarring in the vestibule. Collected blood is also an excellent medium for bacterial growth and easily can become infected. In either circumstance the result is increased fibrosis and a more unsightly scar. Hemostasis must be achieved before would closure. Postoperative management of the wound is equally important. The incision line should be kept clean and dry. Sutures should be removed atraumatically and the margins should be supported after suture removal. In children and infants, postoperative restraints should be used sparingly and then discarded once the patient is fully awake [34]. Most children do not touch the area operated on because of the associated pain. Restrained children tend to be more combative, which increases the potential for damage to the repaired lip. Basic surgical precepts have been outlined for the management of the surgically created wound. The

concepts are simple and widely known but frequently overlooked. Adhering to these simple time-honored concepts helps to ensure consistently good outcomes in the management of cleft lip patients.

Summary Scar revision surgery in the cleft lip patient requires a systematic approach. The secondary defect noted in the cleft patient is a result of the coalescence of several factors, which must be clearly delineated and understood. Despite the fact that the abnormal scar manifests itself primarily in the integumentary structures, the correction cannot be limited to the design and execution of various skin flaps. The skin is simply a soft tissue drape overlying important functional musculature, which in itself is upheld by the midfacial skeletal complex and the dentoalveolar region. These units are interdependent, and restoration of one aspect cannot be achieved properly without addressing the others. To that end the deficient nasomaxillary complex must be reconstructed appropriately via osteotomies, distraction osteogenesis, or grafts. The dental complex must be rebuilt via orthodontic methods with or without dental orthopedic intervention, prosthodontic appliances, and, in some cases, endosteal implants. The cartilaginous framework of the nasal complex must be reoriented properly and augmented if necessary by secondary rhinoplasty. In secondary lip repairs the muscles of the region must be dissected out thoroughly, identified, and placed in their proper anatomic position. Accomplishing the preceding tasks provides outward cosmesis and good oral and facial function. Only when all of these tasks are accomplished can the cutaneous aspect of the scar be truly revised. Even with the best primary repair of the cleft lip, secondary deformities continue to haunt us. The psychological, aesthetic, and functional challenges that beset these patients have wide effects not only on themselves but also their family and society as a whole. Continuous assessment and refinements of surgical management is critical to affording these patients the best care possible.

Acknowledgment The authors wish to thank Dr. Hope Wettan for illustrations in Figs. 1 and 2A,B and Miss Tricia Jagrop for Fig. 10.

L. Doonquah, O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 425–437

References [1] Crawford BS. An attempt to reduce the visible scar in primary cleft hip repair. Br J Plast Surg 1976;29: 113 – 5. [2] Dussen FN. The Egyedi flap in secondary cleft lip repair. J Craniomaxillofac Surg 1991;19:311 – 3. [3] Figueroa AA, Reisberg AJ, Polley JW, Colon M. Intra oral appliance modification to retract the premaxilla in patients with bilateral cleft lip. Cleft Palate Craniofacial J 1996;33:497 – 500. [4] Gur E, Zeker RM. The diamond vermilion flap: a new technique for augmentation in cleft repair. Cleft Palate Craniofacial J 2000;37:123 – 4. [5] Hovey LM. Secondary unilateral cleft lip repair: combining rotation advancement principles with a cross lip muscle flap. Ann Plast Surg 1979;3:241 – 9. [6] Kai S. Secondary correction of the cleft lip and nose deformity: a new technique for revision of whistling deformity. Cleft Palate J 1985;22:290 – 5. [7] Kawai T, Mukai Y, Natsume N. Philtrum creation in secondary unilateral cleft lip repair. Int J Oral Maxillofac Surg 1996;25:345 – 50. [8] Nakajima T, Yoshimura Y, Konech K, Nakanishi Y. Primary repair of an incomplete unilateral cleft lip: avoiding an elongated lip and achieving a straight suture line. Br J Plast Surg 1998;51:511 – 6. [9] Onizuka T. Philtrum formation in the secondary cleft lip repair. Plast Reconstr Surg 1975;56:522 – 6. [10] Park BY, Roh TS. Rectangular flap for horizontal upper tightness in secondary cleft lip deformity. Plast Reconstr Surg 1999;104:1976 – 81. [11] Rodgers CM, Mulliken JB. Deepithelialized muscosalsubmucosal flaps to correct the ‘‘whistling lip’’ deformity. Cleft Palate J 1989;26:136 – 40. [12] Sagelasli N. Cleft lip repair by soft tissue expansion. Ann Plast Surg 1992;29:164 – 9. [13] Sadove AM, Epphey BL. Correction of secondary cleft lip and nasal deformities. Clin Plast Surg 1993;20: 793 – 801. [14] Tange I. The Lambda flap for secondary cleft lip repair. Cleft Palate Craniofacial J 1997;34:357 – 61. [15] Uhm K, Shin KS, Lee YH, Lewi JD. Nostril sill augmentation in secondary cleft lip. Ann Plast Surg 1987;19:391 – 9. [16] Fitz Gibbons GM, Gillies HD. The commandments of Gillies. Br J Plast Surg 1968;21:226. [17] Chen YR, Yeow VK. Cleft lip camouflage using dermal micrografts. Plast Reconstr Surg 1999;103:1250 – 3.

437

[18] Schafer ME, Goldnasser MS. On the importance of muscle repair in secondary cleft lip deformity. Clin Plast Surg 1984;11:761 – 71. [19] Schendel SA. Unilateral cleft lip repair: state of the art. Cleft Palate Craniofacial J 2000;37:335 – 41. [20] Kinnebrew NC. Secondary rhinocheiloplasty. Oral Maxillofacial Surg Clin N Am 1991;3:671 – 91. [21] Tessier P, Tulasne JF. Secondary repair of cleft lip deformity. Clin Plast Surg 1984;11:747 – 60. [22] Amaratunga NA. A comparison of Millard’s and Le Mesurier’s methods of repair of the complete unilateral cleft lip using a new symmetry index. J Oral Maxillofacial Surg 1988;46:353 – 6. [23] Assuncao AG. The VLS classification for secondary deformities in the unilateral cleft lip. Br J Plast Surg 1992;45:288 – 92. [24] Wilson LF. Correction of residual deformities of the lip and nose in repaired clefts of the primary palate (lip and alveolus). Clin Plast Surg 1985;12:719 – 32. [25] Henkel K, Gundlach KH, Saka B. Incidence of secondary lip surgeries as a function of cleft type and severity: one center’s experience. Cleft Palate Craniofacial J 1998;35:310 – 2. [26] Meijer R. Secondary repair of the bilateral cleft lip deformity. Cleft Palate J 1984;21:86 – 91. [27] Schendel SA, Pearl RM, De Armond SJ. Pathophysiology of cleft lip muscles following the initial surgical repair. Plast Reconstr Surg 1991;88:197 – 200. [28] Lazamis DD, Hudson DA, Zyl JE, Fleming AN, Fernandes D. Repair of unilateral cleft lip: a comparison of five techniques. Ann Plast Surg 1998;41: 587 – 94. [29] Park CG, Ha B. The importance of accurate repair of the orbicularis oris muscle in the correction of unilateral cleft lip. Plast Reconstr Surg 1995;96:780 – 8. [30] Sando WL, Jurkiewicz MJ. Cleft lip: plastic surgery principles and practice. St. Louis: CV Mosby; 1990. [31] Gundlach KK, Schmitz R, Maerker R, Bull HG. Late results following different methods of cleft lip repair. Cleft Palate J 1982;19:167 – 71. [32] Ogle OE. Keloids and hypertrophic scars. Oral Maxillofacial Surg Clin N Am 1998;10:1 – 12. [33] McGregory IA. Fundamental techniques of plastic surgery and their surgical applications. 8th edition. New York: Churchill-Livingstone; 1989. [34] Johnson HA. The immediate postoperative care of a child with cleft lip: time proved suggestions. Ann Plast Surg 1979;2:430 – 3.

Oral Maxillofacial Surg Clin N Am 14 (2002) 439 – 451

Correction of the short upper lip in the cleft patient Jose´ Juri, MDa,b,c,*, Marı´a Fernanda Valotta, MDc, Susana Letiz, MDc a

Medical Sciences School, Interamerican University, Chacabuco 90 3r piso, Capital Federal, Buenos Aires, Argentina 1069 AAB b Medical Sciences School, University of Buenos Aires, Paraguay 2155, Capital Federal, Buenos Aires, Argentina 1121 c Clı´nica Juri de Cirugı´a Pla´stica, Cervin˜o 3251, Capital Federal, Buenos Aires, Argentina 1425 AGB

Although the recent advances in surgical techniques and orthopedic management for cleft patients have lessened the severe sequelae seen in the past, perfection still remains difficult to achieve in one single operation, and revisional procedures must be considered part of the treatment plan. Vertical shortening of the lip is commonly seen in unilateral and bilateral clefts. In many cases, this deformity, besides affecting the patient from an aesthetic point of view, is functionally responsible for labial incompetence. To make an adequate surgical planning, the surgeon must determine if the short lip is caused by a short vermilion only (whistling deformity) or if the cutaneous portion is also involved. To make a correct diagnosis, one must consider 13 to 20 mm as being the normal height of the cutaneous portion of the lip measured from the base of the columella to the cupid’ s bow. The whistling deformity as an isolated entity is most commonly seen in unilateral clefts. The combination of both, often associated with a tight lip, is a frequent stigma of bilateral cases.

on V-Y mucosal advancements for restoration of the median tubercle [1 – 3]. In the authors’ experience, these techniques have proved to be partially effective only in mild cases. Even tongue flaps have been used for this purpose [4 – 6]. In 1971, Kapetansky published an ingenious method for correcting the whistling deformity in bilateral clefts. It consisted of two triangular flaps of lateral vermilion, which are approximated and sutured end to end at the midline [7]. Not satisfied with the shape achieved in the central part of the lip with this technique, the authors performed a modification of the Kapetansky’s pendulum flaps, which was published in 1976 [8]. By incorporating additional tissue at the midline, they achieved a complete restoration of the central tubercle. This technique then became the procedure of choice. The authors use it whenever a whistling deformity exists, extending its indications to unilateral clefts, or for tissue deficiencies caused by other problems such as bites and burns.

Correction of the short upper lip caused by vermilion insufficiency

Kapetansky-Juri advancement flaps Step-by-step operative technique

Many techniques have been described for the treatment of vermilion insufficiency, mostly based

* Corresponding author. Cervin˜o 3251, CP 1425 AGB, Capital Federal, Buenos Aires, Argentina. E-mail address: [email protected] (J. Juri).

Flap design. The authors mark two lateral flaps that include most of the lateral lip segments, with rounded central edges. The superior border of the flap runs 1 or 2 mm inferior to the mucocutaneous junction, and the inferior border runs where the dry vermilion meets the wet mucosa (Fig. 1A,B).

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 4 6 - 8

440

J. Juri et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 439–451

Fig. 1. (A) Intraoperative marking and (B) design of Kapetansky- Juri advancement flaps. The superior border of the flap runs 1 to 2 mm. from the mucocutaneous junction superiorly, and in the interface between dry and wet mucosa inferiorly, with rounded central edges.

Flap dissection. The flaps are nourished by wide superior pedicles of orbicularis muscle. The dissection is performed in a subdermal plane superficially and in a submucous fashion (Fig. 2) that reaches the base of the nose superiorly and the nasolabial folds laterally. To achieve an adequate mobilization, the lateral tip of the flap must be freed from its attachments. In some cases, this maneuver implies sectioning the superior labial artery that nourishes the Kapetansky’s flaps as originally described. Taking into account the changes that occur in blood vessel patterns in cleft lips [9], the flaps are nourished by the rich anastomosis network present in this region between the superior labial and the angular arteries (Fig. 3A,B). Flap mobilization. To allow for rotation of the lateral flaps, the central triangular vermilion flap is raised. The lateral flaps are rotated inward past the midline to a downward direction in a 90° angle. The central triangular flap is brought down and sutured over the ‘‘shoulders’’ of the L-shaped flaps (Fig. 4A,B). Flap suture. The flaps are sutured carefully with separate stitches of 6 or 7-0 nylon, which are removed on the third postoperative day to prevent stitch marks (Fig. 5A,B). One of the authors (J.J.) has been performing this flap procedure for more than 25 years. Some clinical cases are presented to appreciate fully the extent of the procedure (Figs. 6 – 9).

Correction of the short upper lip caused by cutaneous and vermilion insufficiency Many methods that use regional tissues, with different designs, have been proposed for the treatment of this deformity [10]. The authors believe that adding scars to an already scarred and usually tight lip is of no benefit in this kind of patients and does not contribute to creating a philtrum of normal appearance. Besides being scarred, this tissue usually lacks adequate bulk. This issue becomes more evident in the profile view and accentuates the usual retroposition of the maxilla. Even if the occlusion has been corrected, the surgical result of the maxillary advance still can be concealed because the soft tissue deficit has not been addressed properly. The authors believe that the Abbe´ flap fulfills all the requirements needed for the correction of this deformity. Traditionally, the first lip switch flap reported in the literature is attributed to Pietro Sabattini, who published it in 1938 [11]. He used a flap from the lower lip to cover a defect from the upper lip left by a wide scar excision. In 1948, Stein reported the use of two flaps from the upper lip to reconstruct the lower lip after the excision of a large tumor [12]. In 1865, Estlander rotated a flap from the upper lip to the lower lip, including the oral commissure. This flap was published in 1872 in German and in 1877 in French [13]. In 1898, Robert Abbe´ from New York was the first to use a lip switch flap from the lower lip to the upper lip in a cleft patient [14]. All four

J. Juri et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 439–451

441

surgeons seem to have performed their operations independently from each other. Recently, extensive research conducted by Jacques Vrebos from Belgium [15] found an earlier description of a lip switch flap published by Hierzel, a Swedish surgeon, in 1756 [16]. He rotated a V-shaped flap of full thickness of the corner of the lower lip into an extensively damaged upper lip. He even designed special instruments to perform the full-thickness section of the lip easier. Despite history and because of custom and habit, the lip switch flap is universally known as the Abbe´ flap. He deserves the credit as being the first to use the lip switch flap in a cleft patient. Abbe´ flap: step-by-step operative procedure

Fig. 2. Kapetansky-Juri advancement flap dissection. The flaps are nourished by wide superior pedicles of orbicularis muscle. The dissection is performed in a subdermal plane superficially and in a submucous fashion, reaching the base of the nose superiorly and the nasolabial folds laterally.

Flap design This flap has two key points, one of which is flap design. One must keep in mind that the philtrum is anatomically a tiny structure. A normal philtrum has the form of a trapezoid and measures 13 to 15 mm in length, 1 to 1.2 mm at the level of the cupid’s bow and 0.5 to 0.7 mm at the columellar base. It is common to find wide Abbe´ flaps that look awkward on a patient’s face. A small philtrum looks natural and blends with the rest of the anatomic features. The location of the flap on the lower lip depends on the arc of rotation of the pedicle. It must be positioned in a way that when the rotation takes place, the flap fits perfectly in the recipient bed (Fig. 10A,B). If the scarred tissue from the upper lip exceeds the limits of the philtrum, the authors perform two cresecent-shaped advancement flaps around the alar bases to provide

Fig. 3. (A) A wide dissection of the orbicularis pedicles can be fully appreciated in this intraoperative picture. Notice the lateral tips of the flaps totally freed from its attachments, to allow for a complete rotation of the flap. (B) The flaps are adequately nourished in spite of section of the orbicularis artery at the tip of the flap. This is due to the rich anastomosis network present in this region between the superior labial and the angular arteries.

442

J. Juri et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 439–451

Fig. 4. Kapetansky-Juri advancement flap mobilization. (A) The flaps are freed and totally rotated past the midline. (B) The central portion of the flaps are rotated 90 degrees, allowing for suture of the ‘‘shoulders’’ of the flaps in the midline. This is how the projection of the median tubercle is enhanced.

for unscarred skin and adjust the recipient bed to the anatomic dimensions of the normal philtrum (Fig. 11A – D). Flap dissection The flap includes the three planes of the lip: mucosa, muscle, and skin. To identify the pedicle safely, it is convenient first to visualize the exact location of the orbicularis artery on the contralateral side. No hemostasis is accomplished (Fig. 12A,B).

Flap inset The other key point of this operation is a complete 180° rotation of the flap. To accomplish this, the flap must be held only by the orbicularis pedicle with no additional tissue (Fig. 13A,B). Flap suture The surgical maneuvers allow for an exact mucocutaneous junction coaptation. The suture is performed with separate stitches of 6-0 nylon (Fig.14A,B).

Fig. 5. Kapetansky-Juri advancement flap suture. (A) intraoperative image at the end of the operation. The final suture is performed with 6-0 or 7-0 nylon. (B) In the drawing, notice how the central flap which was raised to allow for inset of the lateral portions, is sutured in a more upward position.

J. Juri et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 439–451

443

Fig. 6. (A) A 3-year-old boy presented for consultation regarding correction of his vermilion insufficiency caused by secondary bilateral cleft lip. In the postoperative view (B), one can appreciate not only the adequate shape of the central tubercle but also the acquisition of lower lip tone caused by an adequate lip seal.

Fig. 7. (A) An 18-year-old patient sought correction of his whistling deformity as a sequela of unilateral right cleft lip. (B) Postoperative view at 1 year shows complete correction of the deformity.

Fig. 8. (A) A 22-year-old man with inadequate upper lip length and asymmetric lateral components. (B) Six months after the operation, a good shape of the central tubercle is obtained, together with symmetry of the lateral lip components.

444

J. Juri et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 439–451

Fig. 9. (A) A 55-year-old woman presented with an asymmetric upper lip. She had a scar properly located from the primary repair of a left unilateral cleft lip. (B) Together with the Kapetansky-Juri flaps, an asymmetric resection of the white portion of the lip was performed to achieve a better shape at the vermilion border.

Pedicle division If the flap is correctly inset and sutured, it establishes vascular communication with the adjacent tissues in a short period of time. Traditionally, pedicle division is performed at 2 or 3 weeks [17,18]. Other authors admit that division can be accomplished safely at 6 to 8 days [19]. The abundant blood supply in this region makes it pointless to maintain

the pedicle much longer. Based on the authors’ clinical experience, they section the pedicle on day 5 (Kitaro Ohmori, MD, personal communication, 1980). This early division of the pedicle greatly improves the morbidity of the procedure and minimizes the period of inadequate intake and limited oral hygiene (Fig. 15A,B). Figures 16, 17 and 18 illustrate some examples of clinical cases to dem-

Fig. 10. (A,B) Abbe´ flap design. The location of the flap on the lower lip depends on the arc of rotation of the pedicle. It must be positioned in such a way that when the rotation takes place, the flap fits perfectly in the recipient bed.

J. Juri et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 439–451

445

Fig. 11. (A) When the scarred lip goes beyond the boundaries of the philtrum, two lateral crescent-shaped flaps are designed around the alar nostrils to advance intact skin. (B) The scarred tissue is resected. (C) The flaps are dissected as far as the nasolabial sulcus to allow for advancement without any tension. The flaps are advanced to the level of the lateral philtral columns. (D) Notice the absence of tension at the suture lines to prevent widening of the scars in the postoperative period.

onstrate the type of result that can be achieved with this technique. After trying many different methods to correct the same problem, the authors believe that the result of experience is choosing the optimal surgical technique. The Kapetansky-Juri procedure is, in the authors’ opinion, the most versatile method that allows correction of inadequate vermilion bulk at the level of the central tubercle. The Abbe´ flap allows for resection of all cicatricial tissue in the midline, which corrects any kind of deficit of white lip and vermilion. It also provides adequate mucosal cover when absence of labial sulcus is observed in extremely short lips. The reconstruction achieved is

not only aesthetic but also functional. Return to normal sensory and motor functions in an Abbe´ flap is fully restored within a 2-year period [19]. After trying hundreds of different methods for treating this condition, the authors conclude that these two techniques provide the most satisfactory results in the correction of this difficult deformity.

Acknowledgment The authors express thanks to Lorena Martinez, MD, for her valuable help in creating the medical illustrations in this article.

446

J. Juri et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 439–451

Fig. 12. Abbe´ flap dissection. (A) Intraoperative picture showing individualization of the orbicularis artery on the contralateral side of the pedicle. This is a safe maneuver tha can be done to avoid inadvertent section of the pedicle’s artery. (B) The orbicularis artery runs in the submucous plane, in the intersection between dry and wet mucosa.

Fig. 13. Abbe´ flap inset. (A,B) In order to achieve a complete 180 degree rotation, the flap is held by the orbicularis artery only to allow for unrestricted movement.

J. Juri et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 439–451

Fig. 14. Abbe´ flap suture. (A, B) The narrow pedicle allows for a perfect coaptation of the mucocutaneous junction. The final suture is made with 6-0 nylon.

Fig. 15. Abbe´ flap pedicle division. (A) 5- day postoperative view showing the pedicle immediately before section. All stitches have been removed at this point. (B) Drawing representing the final result.

447

448

J. Juri et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 439–451

Fig. 16. (A) A 20-year old patient presented with a severely scarred upper lip caused by a secondary bilateral cleft lip. (B) One year after the Abbe´ flap, the lip acquired adequate fullness. (C) Notice the severity of the retruded upper lip on the profile view caused by tissue insufficiency. (D) To improve lip contour, a small resection of the white lip is performed to provoke eversion of the vermilion. On the profile view, balance between upper and lower lip is nicely achieved.

J. Juri et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 439–451

449

Fig. 17. This is not a case of short lip, but it can demonstrate clearly how an Abbe´ flap can replace tissue regardless of its previous quality. An excellent result can be achieved despite the severity of the previous deformity. This 16-year-old patient had a severe sequela of bilateral cleft lip, in which the prolabium was surrounded by the two lateral lip elements, with absence of the central tubercle. (A – C) This is an unpleasant result of a primary repair. (B) The authors decided to replace all misplaced tissue and reconstruct the philtrum and the central tubercle with new tissue, brought by the Abbe´ flap. (D) On the profile view, good anteroposterior projection is achieved.

450

J. Juri et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 439–451

Fig. 18. (A) A 25-year-old patient presented with a superior maxillary retrusion and soft tissue deficit caused by a unilateral cleft lip sequela from the left side. (B) She denied orthognathic surgery, so an Abbe´ flap was offered to add bulk and contour to the upper lip. (C) On the profile view, the recessed maxilla is masked by the soft tissue gain. (D) A vermilion eversion also was performed by resecting a portion of white lip to achieve a better contour.

J. Juri et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 439–451

References [1] Bardach J, Noordhoff MS. Correction of secondary bilateral cleft lip deformities. In: Bardach J, Salyer KE, editors. Surgical techniques in cleft lip and palate. 2nd edition. St. Louis: Mosby-Year Book; 1991. p. 176. [2] Robinson DW, Ketchum L, Masters FW. Double V-Y procedure for whistling deformity in repaired cleft lips. Plast Reconstr Surg 1970;46:241 – 4. [3] Sadove AM, Eppley BL. Correction of secondary cleft lip and nasal deformities. Clin Plast Surg 1993;20: 793 – 801. [4] Cohen SR, Kawamoto Jr HK. The free tongue graft for correction of secondary deformities of the vermilion in patients with cleft lip. Plast Reconstr Surg 1991;88: 613 – 9. [5] Guerrerosantos J. Use of a tongue flap in secondary correction of cleft lips. Plast Reconstr Surg 1969; 44:368 – 71. [6] Guerrerosantos J, Dicksheet S, Ruiz-Razura A. Free tongue composite graft for correction of a vermilion defect. Plast Reconstr Surg 1985;76:451 – 4. [7] Kapetansky DI. Double pendulum flaps for whistling deformities in bilateral cleft lips. Plast Reconstr Surg 1971;47:321 – 3. [8] Juri J, Juri C, de Antueno J. A modification of the Kapetansky technique for repair of whistling deformities of the upper lip. Plast Reconstr Surg 1976;57:70 – 3. [9] Slaughter WB, Henry JW, Berger JC. Changes in blood vessel patterns in bilateral cleft lip. Plast Reconstr Surg 1960;26:160 – 79. [10] Bardach J, Noordhoff MS. Correction of secondary bilateral cleft lip deformities. In: Bardach J, Salyer

[11]

[12]

[13]

[14]

[15] [16]

[17] [18]

[19]

451

KE, editors. Surgical techniques in cleft lip and palate. 2nd edition. St. Louis: Mosby-Year Book; 1991. p. 183 – 90. Sabattini P. Cenno storico dell’ origine e progressi della rinoplastica e cheiloplastica, seguita della descrizione di queste operazioni praticamente eseguite sopra un solo individuo. Bologna: Belle Arti; 1838. Stein SAV. Lip repair (cheiloplasty) performed by a new method [in Danish]. Hospitals Meddelelser 1848;1:212. [Reprinted in Plast Reconstr Surg 1974;53:332.] Estlander JA. Eine neue methode aus der einen lippe substanzverluste der anderen zu ersetzen. Arch Klin Chir 1872;14:622. In: McDowell F, editor. The source book of plastic surgery. Baltimore: William and Wilkins; 1997. p. 335 – 40. Abbe´ R. A new plastic operation for the relief of the deformity due to double harelip. Med Rec 1898; 53:477. [Reprinted in Plast Reconstr Surg 1968; 42:341.] Vrebos J, Dupuis C, Hierzel JG. A lip-switch flap in 1756. Plast Reconstr Surg 1994;93:201 – 4. Hierzel JG. Bera¨ttelse om en lyckelingen fo¨rra¨ttad operation pa˚ en piga, hvars la¨ppar til en stor del voro ba¨ rtsra¨ tta. Kongl. Svenska Vetenskapsacademiens Handlingar 1756;4:270 – 6. Jackson IT. Local flaps in head and neck reconstruction. St. Louis: Mosby-Yearbook; 1985. p. 360. Zide BM. Deformities of the lips and cheeks. In: McCarthy JG, editor. Plastic surgery. Philadelphia: WB Saunders; 1990. p. 2018. Smith JW. Clinical experiences with the vermilion bordered lip flap. Plast Reconstr Surg 1961;27:527 – 43.

Oral Maxillofacial Surg Clin N Am 14 (2002) 453 – 461

Rhinoplasty in adolescent cleft patients Deodatta V. Bendre, MD, FACS*, Ferdinand A. Ofodile, MD, FACS Division of Plastic Surgery, Harlem Hospital Center, 506 Lenox Avenue, New York, NY 10037, USA

It is universally accepted that correction of cleft lip nose deformity remains a formidable challenge. Despite early correction of cleft lip nose deformity, one is often faced with an adolescent patient who has an acceptable upper lip but has a deformed nose. Usually, these patients come from underdeveloped countries to the United States for correction of nasal deformities. The nose forms a prominent part of the face. Ironically, a masterly executed cleft lip repair directs the beholders’ eyes from the deformed lip to the deformed nose. Real progress has been made in the treatment of cleft lip and palate in the last four decades. Preoperative dental orthopedics and appliances have progressed to produce a near normal maxillary dental arch. In the bilateral cleft lip and palate, positioning of a protruding premaxilla in the dental arch results in superior cleft lip repair. Many techniques have been designed to correct cleft nose deformity; however, the technical improvements in cleft nose repair have lagged behind the progress in cleft lip and palate repair. More and more cleft surgeons are beginning the correction of cleft nose at the time of cleft lip repair; however, several of the patients still require correction of cleft lip nose deformity later in life.

Unilateral cleft lip nose deformity A deformed nose that results from unilateral cleft of the lip and palate is likened to a tent whose one * Corresponding author. Division of Plastic Surgery, Harlem Hospital Center, 506 Lenox Avenue, New York, NY 10037. E-mail address: [email protected] (D.V. Bendre).

side is depressed (see box). The nasal tip is supported by the central pole of the tent (columella and septum) and the sides (alae) are supported by its bony floor (the maxilla). When one side of this floor (the maxilla) is depressed and hypoplastic, the ala is pulled to that side, and the columella and septum are tilted toward the normal side, which results in classic deformity of the nose [1]. There is much controversy regarding the causation of cleft lip nasal deformity. Many investigators [2 – 4] believe that the deformity of the nose is produced by the malpositioning of essentially normal structures, whereas others [5] contend that intrinsic defects in nasal structures result in cleft nasal deformity. Depressed and hypoplastic bony scaffolding is the most important aspect of cleft nose deformity.

Pathologic anatomy Nasal deformities of unilateral clefts have multiple components that require correction. The base of the columella is deviated toward the noncleft side. The cartilaginous septum is convex on the cleft side, which produces airway obstruction. The tip of the nose and the septum is deviated to the noncleft side. On the cleft side, the angle between medial and lateral crura is excessively obtuse, which results in depressed dome. The cartilage on the cleft side may be smaller and thinner than the normal side. The cleft-side nostril may have a web close to the pyriform aperture.

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 4 8 - 1

454

D.V. Bendre, F.A. Ofodile / Oral Maxillofacial Surg Clin N Am 14 (2002) 453–461

Characteristics of unilateral cleft nose deformities  A nasolabial fistula may be present  The premaxilla and maxillary











     

segments are displaced on the noncleft side The nasal pyramid is tilted to the cleft side, the turbinate on the cleft side is hypertrophied The curved nasal septum and hypertrophied turbinate result in airway obstruction The columella is short on the cleft side and its base is deviated to the noncleft side The lateral crux of the lower lateral cartilage, on the cleft side, is longer. Its base is attached backwards and downwards The dome of the lower lateral cartilage is displaced lower and to the cleft side, which results in bifid tip and excessive skin on the dome of lower lateral cartilage on cleft side Larger ala forms S-shaped curve or is flat The nasal tip is asymmetrical The nostril sill may be small or wide The nostril is smaller or larger on cleft side The entire nostril may be retropositioned The whole nose on the cleft side may be longer as measured from Radix to the alar margin

examination of the nose, lip, and palate may reveal the following characteristics: Deformity of the dental arch, including a tooth in the cleft A shortened and deviated columella Deviated and displaced septum and hypertrophied turbinate Irregularity, depression, bifidity of the tip Deformity of the ala, ala-cheek angle Nasolabial fistula Webbing of the vestibule on the cleft side Smaller or larger vestibule The objectives of corrective surgery are to (1) restore the symmetry of alar cartilages, (2) produce a cosmetically acceptable nose and a harmonious relationship between the repaired lip and the nose, (3) create a nasal sill, nasal floor, and columella of equal size on both sides, and (4) produce an ala without flare and a vestibule without webbing.

Timing of surgery The controversy that existed about timing of corrective surgery for cleft nose deformity seems to have diminished in recent years. More cleft surgeons

The nostril on the cleft side may be smaller or larger than the noncleft side. The cleft side ala buckles inward. The base of the ala is caudally displaced on the cleft side. The ala-facial angle is flattened. The nasal floor on the cleft side may be wide or narrow.

Surgical procedures In an adolescent patient, a detailed history should be obtained. Details about the previous surgery and any orthodontic treatment should be noted. Physical

Fig. 1. Alar unit rotations. (A) Blair. (B) Joseph. (C) Gillies Kilner. (D) Berkeley. (From Converse and McCarthy, Reconstructive Plastic Surgery, 2nd Edition, Philadelphia: W.B. Saunders Company, with permission.)

D.V. Bendre, F.A. Ofodile / Oral Maxillofacial Surg Clin N Am 14 (2002) 453–461

455

Fig. 2. Correction of the narrow nostril floor. (A) Design of flap taken from the area lateral to the ala. (B) The flap has been transposed into the floor of the vestibule. (From Converse and McCarthy, Reconstructive Plastic Surgery, 2nd Edition, Philadelphia: W.B. Saunders Company, with permission.)

are correcting nasal deformities at the time of lip repair [6 – 8]. The lip repair includes (1) closing the primary palate, (2) correcting flared ala, (3) correcting tip deformities by elevating the depressed dome on the cleft side to more normal position, and (4) augmenting the alar platform. The procedures that produce excellent results in early years of life may not retain their earlier promise as the face grows and matures. In the past, Peet and Paterson and others [9 – 12] recommended delayed nasal repair. They suggested that altering the cartilages would complicate future corrective surgery, and altering nasal cartilages may complicate future nasal surgery. McIndoe and others [13 – 15], however, have advocated that correcting nasal deformity at the same time as cleft lip repair results in normal development of nasal structures.

Fig. 3. Correction of wide alar base. (A) An incision is made along the caudal border of the alar cartilage and a parallel incision is made higher in the nostril. The tissues between these incisions are undermined and detached medially, leaving a flap of skin that includes the ala. Scar tissue in the floor of the nostril is excised, as is a V of redundant labial skin, and the medial site is prepared for the alar flap. (B) The alar flap is transferred medially and sutured in place, narrowing the floor of the nostril and improving the contour. (From Converse and McCarthy, Reconstructive Plastic Surgery, 2nd Edition, Philadelphia: W.B. Saunders Company, with permission.)

Fig. 4. The Striath technique for the removal of the web of tissue that veils the apex of the naris. (A) Outline of the incision. (B) A skin flap has been raised exposing the cartilage. (C) The exposed alar cartilage is excised, and the remaining mucosal flap is incised, rotated anteromedially, trimmed, and sutured to the columella. The skin flap is rotated into the vestibule and sutured to the lateral wall. (D) Cartilage may be added to increase the projection dome of the alar cartilage. (From Converse and McCarthy, Reconstructive Plastic Surgery, 2nd Edition, Philadelphia: W.B. Saunders Company, with permission.)

In an adolescent patient, correction of nasal deformity could be performed with closed or open technique. The dental arch should be established and maxillary hypoplasia should be corrected before correction of the nasal deformity. The following deformities may require correction in a particular case: The lip may have unacceptable scarring. The columella on the cleft side may be short and the caudal end of nasal septum may be protruding on the normal side. Caudal septum may be displaced on the normal side and deviated to the cleft side. The dome of the alar cartilage may be depressed, which may result in bifid and depressed tip. The alar facial angle may be flat. The nostril on the cleft side may be large or small. There may be webbing of the skin in the vestibule.

Surgery Procedure for correction of cleft lip nasal deformity fall in to two categories: (1) correction of ala as one unit and (2) correction of alar soft tissue and

456

D.V. Bendre, F.A. Ofodile / Oral Maxillofacial Surg Clin N Am 14 (2002) 453–461

Fig. 5. Correction of webbing in the lateral vestibule. (A) Z-plasty. (B) V-Y advancement. (C) Medial advancement (arrow) of a medially based flap of vestibular skin and alar cartilage in a unilateral cleft lip and nose deformity. A full-thickness skin graft is placed in the resulting lateral defect. (From Rees TD, Guy CL, Converse JM. Repair of the cleft lip nose: addendum to the synchronous technique with full thickness skin grafting of the nasal vestibule. Plast Reconstr Surg 1966;37:47; with permission.)

cartilaginous framework separately. Cartilagenous framework can be repositioned using either intranasal or extranasal incisions.

Cartilaginous septum The cartilaginous nasal septum may be dislocated from the vomerine groove, the caudal end may be displaced to the normal nostril, and the septum may be deviated to the normal side, which produces nasal obstruction. Submucous resection of septal cartilage may be adequate to correct septal deviation in most patients. In some patients other methods of septal alterations may be required: (1) scoring of septal cartilage on appropriate side, (2) excision of caudal part of septum that protruding in the nostril, and (3) placing the caudal septum on the nasal spine if it is dislocated.

Fig. 6. (A) Outline of the inverted V forked flap and small wedges in the nostril floors and at the vermilion borders. (B) Wound closed after the forked flap is advanced to elevate the nasal tip with formation of the Cupid’s bow. (From Millard DR. Columellar lengthening by a forked flap. Plast Reconstr Surg 1958;22:454; with permission.)

Nasal tip The dome on the cleft side must be elevated to the normal side and sutured in the elevated position. To give more definition to the tip, a tip graft with a columellar strut support may be necessary. Columella The columella may need lengthening using one of the many methods described in Fig. 1. A short columella on the cleft side is difficult to correct. A simple V-Y plasty from the tip might suffice. Nostril sill The alar base excision may be necessary for alar flare. To widen the nasal floor, a flap from the lateral aspect of the alar base may need to be transposed to the nostril sill. Conversely, to narrow the wide nasal

Fig. 7. (A,B) Outline of two triangular flaps from the scarred borders of the prolabium. (C) Rotation and interdigitation of the flaps to lengthen the columella. (From Marcks KM, Trevaskis AE, Payne MJ. Elongation of columella by flap transfer and Z-plasty. Plast Reconstr Surg 1957;20:466; with permission.)

D.V. Bendre, F.A. Ofodile / Oral Maxillofacial Surg Clin N Am 14 (2002) 453–461

457

dome on the cleft side. She underwent revision of the scarred lip, and during open rhinoplasty, elevation of the dome on the cleft side, a columellar strut, and cartilage graft for the tip projection were performed. Preoperative, intraoperative, and immediate postoperative photographs are presented (Fig. 12).

Fig. 8. Lengthening the columella. Method of correcting the flat nasal tip with short columella. (A) Bipedicle flaps of skin and subcutaneous tissue in the floor of the nostrils are based medially on the columella and laterally on the alae. A wedge of skin removed from the lower part of each ala diminishes the vertical length of the ala. (B) Freely mobilized flaps are advanced medially and sutured together in the midline to provide the desired increase in the length of the columella. Triangles of skin on the upper lip, as shown in (A), have been resected because redundant skin is present on the lip when the alae are transferred medially. (From Cronin TD. Lengthening columella by use of skin from nasal floor and alae. Plast Reconstr Surg 1958;21:417; with permission.)

floor a flap from the nasal floor may be transposed to the lateral aspect of the alar base. Case 1 shows an 18-year-old woman who had her lip repaired in childhood. Note the short columella, the deformity of alar cartilage, and the depressed

Bilateral cleft nose deformity The bilateral cleft nose deformity (see box) depends on the severity of the cleft. The more deformed the dental arch, the more pronounced the nasal deformity. A partial cleft lip and symmetrical cleft spares the nose of profound nasal deformity; however, many bilateral cleft lip deformities are asymmetrical.

Features of bilateral cleft nasal deformity  Medial crura are displaced laterally







 

with bases partially submerged in the prolabium Alar domes are laterally displaced, and the angle between medial and lateral crura is obtuse, which results in broad and bifid tip The lateral crura are displaced downward, which causes hooding of the nostril. Alar cartilage may protrude in the vestibule Alar bases are displaced laterally, which causes bilateral flattening of alar-facial angle and wide nostril floor Nasolabial fistulas may be present The position of cartilaginous septum depends on the asymmetry of the cleft deformity

A patient who presents in adolescence for repair of bilateral cleft lip nose deformity can pose a problem. Usually these patients have the cleft lip and palate repaired in childhood. Three basic areas must be addressed in these patients:

Fig. 9. (A) Diamond-shaped excision. (B) V-Y advancement of the tip. (C) Bilateral alar wing flaps. (From Converse and McCarthy, Reconstructive Plastic Surgery, 2nd Edition, Philadelphia: W.B. Saunders Company, with permission.)

1. The columella may be short or nonexistent in the horizontal direction. 2. The nostril floor is wide, and there may be an oronasal fistula. 3. The nasal tip needs projection and definition.

458

D.V. Bendre, F.A. Ofodile / Oral Maxillofacial Surg Clin N Am 14 (2002) 453–461

An adolescent cleft nose deformity that remains after cleft lip surgery can be treated at any time a patient presents. Prerequisites include having a premaxilla and lateral maxillary segment that are stable and in an arch with good occlusion with the mandibular arch, ensuring that the upper and lower lips are in harmonious relation, and ensuring adequate orbicularis oris muscle approximation. A plan should be made for each individual patient and it should be carried out in a sequence (Figs. 2 – 13). Columella A short columella may be lengthened by several methods. When the lip scar requires revision, the Millard technique using a forked flap gives excellent results. Cronin and Upton recommended a composite graft from the ear to lengthening of columella. When tissue at the nasal tip is adequate but the floor of the nose is deficient, flaps from alar rims can be advanced in the columella. Most of the lengthened columella requires columellar strut for support. Nostrils The nostril sill may require narrowing. The same procedures for correcting a flared nostril can be used for this purpose with excellent results. Increasing the width of the nostril floor can be accomplished by

Fig. 11. Correction of the wide flaring nostrils. (A) Flap b is raised from the floor of the nasal vestibule. An incision frees the alar base. (B) The alar base flap is rotated and the resulting defect is repaired by the transposition of flap b and a V-Y closure. (From Converse and McCarthy, Reconstructive Plastic Surgery, 2nd Edition, Philadelphia: W.B. Saunders Company, with permission.)

transferring tissue from the lateral aspect of the alar base to the nostril floor. Bifid nasal tip The open rhinoplasty technique is best suited for correcting a bifid tip. The domes should be sutured together and the tip graft should be added if tip projection must be improved. The caudal part of the septum may protrude in one of the nostrils, which may require resection. Deviation of the bony pyramid may require formal rhinoplasty. In case 2, an 18-year-old woman presented for correction of bilateral cleft nose deformity. She underwent several procedures to correct her lip deformity in the past. She had a short columella and

Fig. 10. Lengthening the columella. (A) Flat nose due to a short columella in a patient with bilateral cleft lip. (B) Flaps outlined on each nostril floor. (C,D) Flaps are elevated and advanced medially. (E) Suturing of the columella and closure of the secondary defects. (From Converse JM. Corrective surgery of the nasal tip. Laryngoscope 1957;67:16; with permission.)

D.V. Bendre, F.A. Ofodile / Oral Maxillofacial Surg Clin N Am 14 (2002) 453–461

459

Fig. 12. 18 yr old female. (A-F) Cleft lip repaired in childhood, shows short columella, deformed alar cartilage and depressed dome on cleft side. Revision of scarred lip, elevation of dome columellar strut, and tip graft.

460

D.V. Bendre, F.A. Ofodile / Oral Maxillofacial Surg Clin N Am 14 (2002) 453–461

Fig. 12 (continued ).

Fig. 13. 18 yr old female. (A-D) Several procedures for correction of bilateral cleft lip deformity. After Abbe´ flap, forked flap for columella and tip graft.

D.V. Bendre, F.A. Ofodile / Oral Maxillofacial Surg Clin N Am 14 (2002) 453–461

461

Fig. 13 (continued ).

depressed tip. The Abbe´ flap for correction of tight upper lip was performed, and forked flaps from the upper lip were used to lengthen the columella. A columellar strut and tip graft were used for tip projection. Preoperative and postoperative photographs are presented (Fig. 13).

Summary The cleft lip nose deformity is a difficult surgical problem to correct. It is necessary to individualize a treatment plan to achieve optimum results. A spate of articles on this subject in the latter part of last century reveals that there is no simple surgical procedure to obtain a harmonious relation between lip and nose.

Acknowledgment The authors gratefully acknowledge technical assistance provided by Hugh Lawrence, PA-C, Harlem Hospital Center Surgery Service.

References [1] Hogan VM, Converse JM. Secondary deformities of unilateral cleft lip and nose. In: Grabb WC, Rosenstein SE, Bzoch KR, editors. Cleft lip and palate. Boston: Little, Brown & Company; 1971 Chapter 47, p. 2178.

[2] Peyton WT, Ritchie HP. Quantitative studies on congenital clefts of the lip. Arch Surg 1936;33:1046. [3] Coupe TB, Subtelny JD. Cleft palate deficiency or displacement of tissue. Plast Reconstr Surg 1960; 26:600. [4] Huffman WC, Lierle D M. Studies on the pathological anatomy of the unilateral harelip nose. Plast Reconstr Surg 1949;4:225. [5] Stark RB, Kaplan JM. Development of the cleft lip nose. Plast Reconstr Surg 1973;51:413. [6] Salyer KE. Primary correction of the unilateral cleft lip nose: a 15-year experience. Plast Reconstr Surg 1986;77:559. [7] Bardach J, Salyer KE. Surgical techniques in cleft lip and palate. Chicago: Year Book Medical Publishers; 1987. [8] McComb H. Primary correction of unilateral cleft lip nasal deformity: a 10 year review. Plast Reconstr Surg 1985;75:791. [9] Peet EW, Patterson TJS. The essentials of plastic surgery. Oxford: Blackwell Scientific; 1963. [10] Blair VP. Nasal deformities associated with congenital cleft of the lip. JAMA 1925;84:185. [11] Gillies H, Kilner TP. Hare lip: operation for correction of secondary deformities. Lancet 1932;2:1369. [12] Marcks KM, Trevaskis AE, Berg EM, Puchner G. Nasal defects associated with cleft lip deformity. Plast Reconstr Surg 1964;34:176. [13] McIndoe AH. Correction of alar deformity in cleft lip. Lancet 1938;1:607. [14] Brown JB, McDowell F. Secondary repair of cleft lips and their nasal deformities. Ann Surg 1941;114:101. [15] O’Conner GB, McGregor MW, Tolleth H. The nasal problems in cleft lips. Surg Gynecol Obstet 1968; 116:503.

Oral Maxillofacial Surg Clin N Am 14 (2002) 463 – 476

Orthodontic approach in the treatment of the cleft patient Rosa Carolina Marcovitch, H, DDSa,b,* a

Center for Craniofacial Anomalies and Maxillofacial Surgery, Sercom, Unidad Odontolo´gica Especializada, Local 8, Av. Ppal. Urb., Los Samanes c/c Calle Ro´mulo Gallegos, Maracay, Edo. Aragua, Venezuela b Private Practice, Calle Vargas. Resid. Galil III Apt. 601 Maracay. Edo. Aragua. Venezuela

Clefts of the orofacial structures are among the most common of all congenital malformations. Clefts of the lip can be unilateral or bilateral and often involve the alveolar ridge. Clefts of the palate vary in length and width. Some may involve all of the hard and soft palate, some only part of the hard and soft palate, and others may be limited to the soft palate (Fig. 1A – D). As a result of the communication between the nasal and oral cavities, a wide range of functions, including speech, may be impaired [1]. Children with cleft lip or palate or both require the coordinated services of many specialists during the years of treatment. For this reason many parents seek care for their children at a cleft palate or craniofacial treatment center. At such a center the cleft team may appropriately evaluate the deformity, coordinate a plan of care, and offer the best attention to the patient. The team is usually formed by a group of professionals in the fields of plastic surgery, pediatrics, speech therapy, pediatric dentistry, orthodontics, oral and maxillofacial surgery, and prosthodontics, among others. The role of the orthodontist in the treatment of children with clefts is significant. Over the years of treatment that cleft patients require, the orthodontist is involved in all stages of care to achieve optimal dental and jaw relationships. Record keeping is critical for long-term orthodontic care and should include the patient’s health and genetic history, serial clinical examination, photographs, study casts, and

* Calle Vargas, Resid. Galil III. Apto. 601 Maracay, Edo. Aragua ZP 2101 Venezuela. E-mail address: [email protected]. (R.C. Marcovitch, H).

radiographs. When there is a combination of orthodontic and orthognathic surgical treatment, the orthodontist must have an overview of the total treatment plan and guide the orthodontic treatment toward the surgical objectives. Good coordination between the oral and maxillofacial surgeon and the orthodontist is important for the development of a satisfactory occlusion because they plan the management of the bony defect in the maxillary arch that results from the cleft and the final orthognathic surgery where needed. Another important role of the orthodontist is to prepare the upper jaw for a bone graft of the alveolar cleft. The orthodontic treatment of the cleft patient is directed not only toward children but also to adults who have concerns about the appearance of their lip and nose, their ability to speak clearly, and the final appearance and function of their teeth.

Goals of treatment The orthodontic treatment of the cleft patient presents some special challenges. The goals of the treatment are to counteract the forces that inhibit development of the maxillary alveolus, minimize the retardation of forward maxillary growth, provide for adequate relationships of the jaws, and establish and maintain the position of the maxillary segments [2]. When orthognathic surgery is planned in conjunction with orthodontic treatment, the goals must be expanded to include elimination of dental compensations and alignment of the teeth on a proper position in their bony bases. The sequencing of surgical procedures is as important as the procedures themselves, and continuous evaluation is required to

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 4 4 - 4

464

R.C. Marcovitch / Oral Maxillofacial Surg Clin N Am 14 (2002) 463–476

Fig. 1. (A) Unilateral incomplete cleft lip. (B) Unilateral complete cleft lip. (C) Bilateral cleft lip. (D) Cleft palate.

R.C. Marcovitch / Oral Maxillofacial Surg Clin N Am 14 (2002) 463–476

465

orthodontic intervention were not appreciably different [6]. In the case of a wide bilateral cleft that would prevent an aesthetic and functional lip repair, however, it was still used. An elastic band placed over the premaxilla and anchored to the head of the baby was used, and by pressure it retracted the premaxilla enough to facilitate surgery.

The molding alveolar plate

Fig. 2. Clinical view of a feeding plate showing dental floss attached to the plate to assist in retrieval of the plate.

monitor the changing needs and problems as the patient grows and different surgical interventions are planned. If the patient does not receive the appropriate orthodontic attention during the various stages of surgery, he or she may develop a nonfunctional occlusion, teeth eruption into the cleft area, oronasal fistulas that permit escape of nasal secretions to the mouth and food going into the nose, defects of pronunciation, nasal deformity, and unaesthetic physical appearance. Two key areas that the orthodontist always must address are protrusion of the premaxilla in the bilateral cleft and the progressive increase in the constriction of the dental arches. This constriction of the maxillary segments, even in the absence of surgical intervention, is a result of the absence of an intact palate between the two maxillary processes [3].

First stage of treatment: presurgical orthopedics The concept of presurgical orthopedic treatment was introduced in the 1950s by McNeil [4], who used an intraoral appliance that resulted in the proper alignment of the maxillary segments in a relatively short time in patients with unilateral complete clefts. This treatment resulted in a reduction of cleft width in skeletal and soft tissues, and this method of treatment was accepted for a period of time. In the 1960s, surgeons combined the procedure with a primary bone graft. This combination was studied by Pruzansky, who reported failures several years after presurgical orthopedic treatment and bone grafting had been used [5]. The use of presurgical infant orthopedics began to decline in the 1970s because it was found that the results obtained with presurgical orthopedics and no

In the treatment protocol used by the author, ‘‘feeding plates’’ are used from the first week of life and continue until the child is able to control the position of the tongue and can prevent food from entering the nasal area. It allows the child to swallow efficiently, especially with bottle feeding, and prevents suffocation while the baby is being fed. Parents frequently report incidents of their baby gasping for air during bottle feeding when the child does not use any device to obturate the palatal cleft. This observation is caused by the communication between oral and nasal cavities, which allows free flow of liquid between each cavity. The feeding plate is a simple acrylic plate that is made from impressions taken shortly after birth and delivered the same day (Fig. 2). An individualized impression tray should be prepared if the clinician does not have special prefabricated trays for infants (Fig. 3). An individualized custom tray can be made using a warm thermoplastic modeling material that is placing into the baby’s mouth with the fingers and held with enough pressure to get a good copy of the palatal tissues. After the modeling material has lost its warmth, it is removed from the mouth and poured with gypsum stone to make the working cast. Acrylic is adapted to the cast to make an individualized

Fig. 3. Prefabricated pediatric dental impression trays.

466

R.C. Marcovitch / Oral Maxillofacial Surg Clin N Am 14 (2002) 463–476

Fig. 4. Custom-made tray for taking an alginate impression in the cleft palate infant.

impression tray (Fig. 4). Holes should be placed in the custom acrylic tray to allow outflow of excess alginate during the taking of the impression. The trays should extend anteriorly from the maxillary frenum at the cleft lip site posteriorly past the end of the alveolar ridges into the palate and laterally to include the lateral mucobuccal fold. It is important that the tray be able to capture the important anatomic areas that are critical for appliance construction. Assuming the tray is already available, the first step is to take an alginate impression that covers the premaxilla and the entire hard palate. The child should be on the mother’s lap and held in a vertical position and should not be laid flat. The filled tray is placed and gently guided into the oral cavity. Once the impression has been taken, the oral and nasal cavity must be examined carefully and all residual particles of alginate removed. The clinician must scrutinize carefully the impression to ascertain that the entire

defective area along with the vestibular areas has been captured. The impression is poured with orthodontic stone to obtain the final cast on which the acrylic plate is fabricated (Fig. 5A). All the lateral borders of the alveolus must be marked on the cast to ensure that the plate extends only to the vestibule (Fig. 5B). In bilateral cleft appliances, the finish line is not placed in the anterior area. The bilateral segments are supported uniformly from the lateral position, which allows the premaxilla to drift evenly posteriorly with lip pressure [7]. On the cast, anatomic areas that can cause unwanted extension of the acrylic must be waxed out. They usually are the anterior cleft area and the superior aspect of the nasal passage. The plate is made from autopolymerizing acrylic with the powder-liquid method. The flanges must be contoured and trimmed so as to be certain that they are not overextended. The palatal plate must have a uniform thickness and the borders should be smooth. It is recommended that a small hole be placed in the front area of the plate with a round bur to tie dental floss to the appliance (Figs. 2, 6). This allows parents to feel secure when the plate is in place and makes it easily retrievable. Retention is rarely a problem, and the patient accepts it quickly. The parent must be instructed to clean the appliance after every feeding and gently clean the mouth. The appliance must be reconstructed as maxillary growth takes place. The author has observed that it must be replaced every 2 or 3 months, but this requirement may vary. The device is used until the time of palatoplasty and then discontinued. Cephalometric findings suggest that there is no restriction of anterior maxillary growth after the use of a passive alveolar molding appliance before 4 years of age. Facial growth parameters (except for

Fig. 5. (A) Stone cast made from an alginate impression of an infant with cleft palate. (B) Stone cast with vestibular markings to show extent of buccal flange of a feeding/orthopedic plate.

R.C. Marcovitch / Oral Maxillofacial Surg Clin N Am 14 (2002) 463–476

467

sella-nasion-point B angle (SNB)) appear normal, and dental parameters are not affected [7]. It is the author’s opinion that the plate at this stage is not acting as an expansion appliance and does not have any other function other than serving as a feeding device. It does serve as a passive mechanism to permit growing and molding of the alveolar segments and avoiding the tongue pressure on the cleft during the first weeks of life, however, which would make the cleft wider. After primary repair of the cleft lip the appliance keeps the tongue out of the cleft palate and limits its expansion from the forces applied by the strong tongue muscles. Limiting expansion of the cleft from tongue pressure makes a tension-free closure of the lip or palate easier to achieve. Having a good initial closure prevents the need for secondary surgical procedures caused by palatal fistulas or badly scarred lips.

The lip closure stage

Fig. 6. Feeding plate inserted into the mouth of cleft palate infant. Note dental floss attached to the plate.

Surgical reconstruction of the lip (Fig. 7A,B) has a great influence on the final position of the maxillary segments. The repaired lip exerts a marked orthopedic force on the cleft maxilla that results in rapid

Fig. 7. (A,B) Surgical reconstruction of the lip of patient shown in Fig. 1B. Primary closure assists in molding the anterior portion of the alveolar cleft and has a great influence on the final position of the maxillary segments.

468

R.C. Marcovitch / Oral Maxillofacial Surg Clin N Am 14 (2002) 463–476

improvement of the originally displaced maxillary segments [8,9]. The function of the repaired perioral musculature achieved from the primary lip closure assists in the contouring of the alveolus by placing forces on the separated arch segments. These muscular forces help to mold the segments into an adequate position that improves not only the dental area but also the overall facial aesthetics. Reconstruction of the nasal floor and upper portion of the lip initiates pressure on the maxillary basal bone and nasal septum, whereas the reconstruction of the lower portion of the lip establishes pressure on the dentoalveolar structures [10]. When the continuity of the orbicularis oris and the buccinator muscles is established, it provides a more normal functional matrix to influence maxillary growth. The surgical procedure usually preserves lip tissue for aesthetics, restores the separated lip elements, and allows the nasal base to be narrowed (Fig. 8). It is important that early evaluation of the relationship of the maxillary segments and the maxilla to the mandible be conducted by the orthodontist to avoid inappropriate axial eruption of the incisors and collapse of the posterior arch, which interferes in the adequate function of the masticatory system. Children and adults with repaired cleft lip and palate do not have a normal functional occlusion unless orthodontic treatment has been completed successfully. The earlier the orthodontic intervention, the better the final results in the permanent dentition. Reports in the literature indicate that surgery has little influence on facial growth but does influence dental occlusion [11]. It is believed that the most successful closure of the lip is achieved when the procedure is performed in two stages. First, an early lip adhesion is performed with no attempt to produce definitive aesthetic closure. Later a definitive procedure for final closure is performed [12]. The final closure of the cleft lip

Fig. 8. Primary lip repair showing narrowing of the nasal base.

is usually done when the baby is approximately 3 months old. The contemporary consensus is that lip surgery should be performed when the baby is 10 to 12 weeks of age, weighs 10 pounds, and has a hemoglobin of 10 g. Allowing the nose and lip to grow before lip closure makes the surgery technically easier. After 10 to 12 weeks, other problems are more likely to have been identified if they exist. The immune system also is better developed and the risk of infection is less [6].

Palatal closure To get better results toward maxillary growth it is recommended that palatal surgery be performed in two steps. With an emphasis on speech development, velar closure is performed early. This intervention is characterized by elevation of mucosal flaps only [13] and exposure of velar muscular bundles, which are severed from their attachments on the posterior palatal shelf and sutured in the midline to form a sling [14]. Other techniques may involve a double reversing Z-plasty (furlow). Only the soft palate is closed, and the objectives of the surgery are to join the cleft palatal edges, lengthen the soft palate, and repair the levator palatini muscle. Most children with a cleft palate have the soft palate repaired between ages 18 and 24 months [6]. The timing of closure of the hard palate depends on speech proficiency and development of occlusion. As a rule, it is postponed until 6 to 8 years of age to allow correct intercuspation of the first permanent molars to become established before the intervention [15]. In the interim between closure of the soft palate and the hard palate at age 8, the palatal defect is managed with an obturator. The timing of closure of the secondary palate is a point of disagreement because it seems clear that the acquisition of normal speech is aided by an intact palate, and at the time that speech is developing rapidly (early in the second year of life), not having an intact palate may create severe articulation problems that may require years of speech therapy to correct. Because of this disagreement, some experts recommend complete palatal closure by the age of 12 months [16]. On the other hand, it seems that the later the secondary palate is closed, the less tendency toward medial collapse of the maxillary arches and the retardation of growth that is usually seen in children with surgically repaired palatal clefts [17]. The age at which the palate is repaired seems to influence maxillary growth directly, and in the author’s practice it is noticed that more maxillary collapse results from early rather than later surgery.

R.C. Marcovitch / Oral Maxillofacial Surg Clin N Am 14 (2002) 463–476

469

After the palate is repaired, active orthodontic treatment is not usually needed until the child is in the mixed dentition. After palatoplasty most patients are able to achieve velopharyngeal closure and do not have the escape of air through the nose that produces ‘‘cleft-palate speech.’’

Primary dentition stage During the primary dentition stage the only orthodontic treatment that is frequently indicated is the correction of an anterior or posterior cross-bite by expansion of the maxillary segments (Fig. 9). Crossbites are caused by the collapse of the maxillary segments after palatal repair. Cross-bite can be unilateral or bilateral, anterior or posterior, and may involve one tooth, the segment, or the complete maxillary arch. When one tooth is involved the treatment can be delayed. The cross-bite can be corrected by moving the maxillary segments with an orthopedic appliance because of the lack of bone between them. A quad-helix, a plate with an expander crew, or any expansor device may be used (Fig. 10). If there are occlusal interferences, an acrylic bite plane can be worn on the mandibular posterior teeth to let the upper arch expand as desired. After the expansion to correct the cross-bite has been achieved, the expansion must be maintained with a retainer. Relapse after expansion is always rapid if long-term retention is not used, and the retention must be kept until the patient receives a bone graft to consolidate the maxillary arch. The orthodontist must ensure that the retainer does not interfere with speech. Patients treated with surgery of the lip and palate often develop midfacial retrusion (Fig. 11). Once retrusion becomes apparent, clinical options include (1) allowing abnormal facial development to continue with surgical intervention after growth is com-

Fig. 9. Cross-bite in the primary dentition.

Fig. 10. Quad helix device for maxillary expansion.

pleted and (2) treating it immediately with extraoral traction to the maxilla. The latter choice minimizes the amount of therapy that is necessary as the patient matures [18]. This therapy can be used if the discrepancy is mild. The literature substantiates that protraction of the maxilla is possible, that it increases growth at the circummaxillary sutures, and that it produces favorable results in noncleft subjects. This appliance applies an orthodontic force to the underdeveloped maxilla and is anchored on the forehead and chin. The long-term stability of maxillomandib-

Fig. 11. Profile view of cleft patient showing deficient horizontal maxillary growth.

470

R.C. Marcovitch / Oral Maxillofacial Surg Clin N Am 14 (2002) 463–476

ular relations after face mask therapy has not been documented in large series of patients, although individual case reports have appeared in the literature [19]. Face mask therapy can be undertaken at any age when the maxillary arch seems to be developing a retrusive relationship. It also might be helpful in cases in which bone grafts have been placed at an early age and there is a noticeable reduction in maxillary growth [9]. Face mask therapy has a high tendency for relapse. The excessive bone apposition that is needed in the tuberosity area for stabilization of the forward displacement of the maxilla cannot take place for two reasons. First, there is the counterpressure from a tight lip 24 hours a day (which already has brought about the condition to be treated by inhibiting normal forward/downward displacement of the maxilla with growth). Second, scarring in the pterygomaxillary region after extensive tissue mobilization for palate closure hampers bone apposition [20]. If the orthodontist decides to use this procedure to improve the relationship between the jaws, he or she must anticipate that even if the cross-bite has been corrected at that moment it will not be maintained. As the normal growth of the mandible occurs, the maxillary arch remains underdeveloped because of the effects of the surgical treatment. As the permanent dentition replaces the deciduous dentition, the lack of vertical growth of alveolar process becomes apparent [21]. The characteristic features of these patients are (1) medial collapse of the maxilla, (2) maxillary or mandibular retrognathism or both, (3) lack of vertical development of the maxilla, and (4) disturbed airway caused by the diminished size of the nasopharynx [22]. These deformities, which are seen in most cleft lip and palate patients, are not caused by reduced growth potentials and can be attributed to a change in maxillary bone position and a concomitant inhibition of vertical alveolar growth [21]. It seems that the best way to address the deficient growth of the maxilla is to defer treatment until the first permanent molars and permanent incisors have erupted. Every child with a cleft should be referred to a pediatric dentist between 2.5 and 3 years of age. Primary teeth should be preserved and retained until the permanent teeth erupt, except when the orthodontist recommends removal of certain teeth to prevent a crowding situation in the permanent dentition. Early radiographs are recommended to evaluate dental caries and missing and malformed teeth. In this period the patient also may present with problems associated with the surgical procedures, such as scarred lip or palatal fistulas, and the pedo-

dontist should consult with the surgeon regarding the need for secondary surgery.

Transitional dentition stage There are two major goals to be achieved during the transitional stage: the alignment of the erupting incisors and bone grafting of the alveolar defect. The malposition of the maxillary incisors is common in the cleft patient, especially incisors that are close to the defect. These teeth usually erupt palatally, are excessively rotated and poorly inclined, and frequently are in cross-bite (Fig. 12A,B). The upper lateral incisor is the most susceptible to having abnormalities in number, size, shape, undesirable positions, timing of formation, and eruption (Fig. 13A). Supernumerary teeth in the cleft area are usually found. Normal alignment is not frequently seen and the dental midline is often affected. The literature shows an association between clefting and dental anomalies. The upper lateral incisor is the most susceptible to being affected in the area of the cleft in deciduous and permanent dentitions. The prevalence of hypodontia increases strongly with the severity of the cleft. Hypodontia is similarly prevalent in subjects with isolated cleft palate with and without a positive family history of clefts. Premolars constitute another group of frequently missing teeth, and the incidence reported is approximately 6.6% in the general population [23]. In the permanent dentition, the timing of tooth formation is delayed in children from all cleft groups compared to noncleft children. Enamel defects and abnormalities in shape and size of both dentitions are far more common in children and fetuses affected with cleft than in normal subjects. No differences have been observed between the sides of the cleft and the sexes in the variations of the lateral incisor situated in the cleft area [24]. Some investigators have found that the formation of permanent teeth in children with cleft lip or palate or both was delayed approximately 6 months [25]. The goals of this stage of treatment are mainly the correction of incisor malalignment and displaced teeth, placement of anterior teeth to resolve anterior cross-bite if present, and achieving the best possible arch form before bone graft. Orthodontic fixed appliances should not be placed on rotated incisors until root development is almost complete. This precaution avoids incomplete root formation and root resorption. Fixed appliances, such as bands on the first molars and bonded edgewise

R.C. Marcovitch / Oral Maxillofacial Surg Clin N Am 14 (2002) 463–476

471

Fig. 12. (A,B) Typical occlusion seen in the cleft patient after closure of the palate. Malposition of the central incisor close to the cleft is frequently seen.

brackets on the incisors and some cuspids, are usually used. Progressive arch series then are used to restore arch form (Fig. 13B,C). In cleft patients a correct midline relationship of the maxillary arch to the mandibular arch sometimes may be impossible to achieve. It may not be possible

to move an incisor adjacent to a cleft in the direction of the cleft because of the inadequacy of bone to maintain tooth support; this could lead to the exposure of the root surface and loss of the tooth [9]. Lateral expansion of posterior segments also can be treated at this time by using fixed palatal arches,

Fig. 13. (A) Abnormal lateral incisor in a cleft patient. (B,C) Fixed orthodontic appliance are used to restore arch form.

472

R.C. Marcovitch / Oral Maxillofacial Surg Clin N Am 14 (2002) 463–476

quad helix (see Fig. 10), or screw expanders. It is important to use a retainer for posterior expansion and incisor alignment. It can be a bonded wire on the palatal surface of affected teeth or a removable retainer used at nights until the next stage of comprehensive orthodontic treatment begins. Cleft patients often receive speech therapy by the time they begin primary school. Cleft patient speech is a characteristic nasal emission on some consonants sounds. The goal of the initial speech therapy is to correct the articulation errors while maintaining and reinforcing velopharyngeal adaptive mechanisms to prevent nasal escape of air. In some children, malpositioned maxillary incisors may make correct tongue positioning more difficult, which becomes another reason for orthodontic treatment at age 7 to 8 years [6]. Speech is a major consideration, and correcting incisor malalignment shortly after the eruption of the incisors may improve the potential for good tonguetip contact and enhance the adequate development of skills needed for articulation [9]. The other important goal at this stage is the alveolar bone grafting and the surgical and orthodontic management of the cleft maxilla. The orthodontist and the surgeon must collaborate in determining the time and sequence of secondary alveolar bone grafting. Bone grafting of the cleft allows subsequent eruption of the unerupted tooth (usually the permanent lateral incisor and/or the cuspid) into the dental arch in its proper position. Even the supernumerary teeth that are often found in clefts can be brought into the arch if the length of its root permits it. It is recommended that the alveolar bone graft be completed before the eruption of the permanent canines, which allows the canine to erupt into a well-formed alveolus with stable maxillary segments. The graft is customarily placed when the root of the canine is approximately two-thirds to three-fourths formed, which is usually around 9 to 11 years of age. Cancellous bone taken from the iliac crest seems to afford the most desirable results. The author’s center does not advocate primary bone graft at the time of the lip closure because of the effect on future growth [26,27]. If the alveolar defect is not corrected, there is a tendency for loss of bone on the surface of roots close to the defect and the central or lateral incisor, and the canines adjacent to the cleft are at risk of periodontal pocketing and ultimate loss. Any bone graft serves merely as a matrix for the induction of new bone and is replaced as the area is remodeled and new bone is formed [6]. The stability of the reconstructed alveolus depends on the presence of teeth in the area of the graft [28]. Retention is

important at this stage. If a retention appliance is not placed, constrictive pressure forces could reduce or even preclude bone formation. Another important goal, besides closing the cleft area, is to obtain appropriate periodontal conditions for the teeth within and adjacent to the cleft. In some patients with cleft lip and palate, reduced marginal bone height, inadequate facial attached gingiva, and gingival recession of the teeth next to the cleft have been demonstrated after bone grafting [29,30]. Studies have demonstrated that osseous grafting before canine eruption resulted in clinically satisfactory periodontal support for the canine, however [31]. It is expected that the canine can erupt into the graft with the periodontal fibers necessary to maintain the viability and existence of alveolar bone [32] and can even induce alveolar bone formation [33].

Orthodontic treatment stage The final stage of orthodontic treatment includes the use of fixed appliances, which consist of bonded brackets and full banded molars. The stage begins almost at the same time that noncleft patients would receive their orthodontic treatment, usually when they are in their teens. The goals at this stage are to obtain an adequate arch form and alignment, get the best occlusion and function, maintain or improve sagittal and transverse relationship between arches, avoid or correct cross-bites, and prepare for orthognathic surgery if needed or receive a prosthetic restoration (Fig. 14A,B). A common situation that the orthodontist faces when treating cleft patients during this period is the decision that must be made regarding the lateral incisor. If the lateral incisor is present and it is viable to take its place within the arch after alveolar bone grafting, every attempt to preserve it should be made. In the case of a missing lateral incisor, the orthodontist may decide to move the cuspid into the place of the lateral incisor or prepare or maintain the space for a prosthetic replacement in the future. The prosthesis may be implant borne if there is adequate bone to place an endosseous implant. The lateral incisor should be replaced with a fixed prosthesis if the cuspid in the cleft side is in a functional Class I relationship, when the cuspid anatomy is not suitable to a good occlusion with lower teeth, or the gingival contour of the cuspid does not allow sufficient movement to cover the lateral incisor space. Extraction of teeth to improve dental alignment should not be done until after the eruption of all permanent teeth. In cases in which upper bicuspids

R.C. Marcovitch / Oral Maxillofacial Surg Clin N Am 14 (2002) 463–476

473

Fig. 14. (A,B) Use of prosthetic appliance to replace a missing lateral incisor at the site of alveolar bone graft.

will be extracted to align the teeth because of a lack of space, the specialist must evaluate the midface profile and should anticipate that an underdeveloped maxilla will appear more pronounced when this is done. Regarding the mandible arch, bicuspid extractions should be made in the case of crowding in which the problem cannot be resolved easily by stripping the incisors to achieve a better alignment of the anterior teeth. During the adolescent stages of development when maxillary retrusion is mildly evident, it may be advisable to extract the mandibular bicuspids to retroposition the lower incisors lingual to the upper incisors to achieve adequate anterior overbite and overjet relationships and desirable lip contour and lip relationships [9]. When evaluating children between the ages of 9 and 10 years and face mask therapy is being considered, it should be initiated at the beginning of the adolescent growth spurts because this is the stage at which the greatest changes in development of the maxillary region might be anticipated. It must be emphasized, however, that it might not be possible to correct excessive midface retrusion by face mask therapy alone, and in many cases the adjunctive help of orthognathic surgery may be required [9]. Class III elastics have been shown to be useful in complementing orthodontic treatment, especially in cleft patients with vertical and sagittal deficiencies. The result of using the elastics is elongation of the upper molars. After its movement, the mandible rotates downward and back. The elastics must be worn for several months to achieve a desirable result. After a functional occlusion and a better overall facial appearance have been obtained, the next step is retention. Because the cross-bite tendencies and relapse of rotated teeth are greater in cleft patients,

full retention must be used as the final step of treatment. A removable retainer or a palatal bonded wire of anterior teeth is recommended at least for a full year, and after that the patient should be wearing the removable appliance at least at night.

Orthognathic surgery stage When the proper maxillomandibular relationship is not obtained in cleft patients with conventional orthodontic methods and the requirements of the case exceed the limits of orthodontic treatment, orthognathic surgery is indicated. It has been estimated that 25% to 60% of all patients born with complete unilateral cleft lip and palate require maxillary advancement to correct the maxillary hypoplasia and improve aesthetic facial proportions [34]. In some cleft patients who seem to have been treated successfully by conventional orthodontia during adolescence, the author has observed that after finishing the full fixed appliance orthodontic treatment, there is relapse of anterior and lateral cross-bites from what seems to be continuous mandible growth. This is not caused by the excessive growth of the mandible itself, however, but the less sagittal or vertical growth of the maxillary bone. In these cases the orthodontist should not prolong orthodontic treatment but recommend surgical advancement of the maxilla at the Le Fort I level as the final stage of treatment. Sometimes mandibular setback is also required in patients who have a real mandibular prognathism. The timing of orthognathic surgery must be planned carefully by the surgeon and the orthodontist. The surgery is usually performed at approximately 17 years of age for girls and 18 to 20 years for men, when active facial growth is decreasing. Before

474

R.C. Marcovitch / Oral Maxillofacial Surg Clin N Am 14 (2002) 463–476

surgery, new cephalometric radiographs and tracings, clinical pictures, and dental casts should be obtained to assess the current position of maxillary and mandible bones and the existing occlusion. Controversies exist about the timing of the osteotomies in adolescent patients. Freihofer found that the only osteotomies that could be performed in adolescents without great likelihood of relapse were anterior maxillary segmental retropositioning and mandibular advancement. All other procedures, including maxillary advancement and mandibular retropositioning, were subject to unacceptable frequency of relapse when performed before the age of 16 years. The main reason for the clinically unacceptable results is continued forward growth of the mandible [35]. On the other hand, there are other reports of successful osteotomies performed before adolescence, and these clinicians recommend only waiting until the maxillary permanent dentition has erupted to avoid damaging them during maxillary advancement. Their patients ranged between 14 and 17 years of age [36]. It is the author’s opinion that to achieve more secure results and avoid relapse after orthognathic surgery, timing of the procedure should wait until active facial growth has decreased (at approximately the ages stated previously). In the past, it was common for the mandible to be set back to produce a normal occlusion with the retropositioned maxilla (this was mainly because of fear of devitalizing a scarred maxilla from the surgery), but this produced a flat, unaesthetic facial appearance. Currently, the standard treatment is a Le Fort I maxillary advancement. If the patient has a small chin or if an extensive setback of the mandible is required, an advancement genioplasty can be performed during the same operation to maintain an acceptable throat length. If the chin is excessively long, it can be reduced in vertical height at the same time [37]. If the patient has an alveolar cleft that has not been grafted when the maxillary osteotomy is planned, the two procedures may be performed simultaneously [38]. Distraction osteogenesis is also an effective procedure to achieve maxillary advancement. Figueroa and Polley [39] treated 14 patients using a rigid external distraction device and concluded that maxillary distraction osteogenesis after complete osteotomy with the rigid external distraction technique is a highly effective treatment modality to manage cleftrelated maxillary hypoplasia. The technique allows for vector control of the osteomized maxilla throughout the distraction process. It has been used, with minimal morbidity, in children as young as 5 years of

age, adolescents, and adults. In all patients treated with the device, the initial negative skeletal convexity and dental overjet were satisfactorily corrected with the associated favorable soft tissue changes.

Prosthetic considerations Because the absence of a lateral incisor in the cleft area is common, the restoration of the tooth should be included in the treatment plan in cases in which the orthodontist decides not to replace it with the cuspid (Fig. 1A,B). Prosthetic restoration should be planned after surgical-orthodontic treatment has been completed. A transpalatal retainer with an acrylic tooth can be used to aid in maintaining the surgical result and provide a better dental appearance. If desired, 6 months after surgery a fixed prosthetic appliance can be used. A four-unit fixed bridge can be used, but an implant-borne prosthesis in a bone grafted alveolus gives the best result. Bone grafting of the alveolar cleft in cases in which the lateral incisor is missing should be performed with the aim of providing enough bone for a dental implant. The orthodontist should create the space that is needed for the prosthesis; the space should not be too small. After implant placement and final prosthetic restoration, residual spacing can be closed by orthodontic movement of teeth within the maxillary arch.

Summary Successful orthodontic treatment of the cleft patient constitutes a challenge that requires long-term commitment from the orthodontist, who works in conjunction with surgeons of various specialties to produce a patient with a functional dentition and good facial aesthetic results. Presurgical orthodontic treatment is a cornerstone to ensuring a successful surgical result and preventing relapse. Communication between the surgeon and the orthodontist becomes essential to guide the appropriate therapy and improve results. Growth and development of the cleft patient should be understood because they play an important role during treatment. A sequence of regular stages of treatment used to resolve many of the characteristic problems seen in cleft patients has been presented. Variations should be made to solve specific troubles in some cases. Every effort should be made to enable the patient to obtain a better shape and function of the occlusion and an aesthetically pleasing appearance.

R.C. Marcovitch / Oral Maxillofacial Surg Clin N Am 14 (2002) 463–476

Acknowledgments Special thanks to Dr. Julio Linares, staff oral maxillofacial surgeon, and Dr. Carmita Alvarez, who collaborated in the treatment of some of the patients whose photographs are presented in this article.

References [1] Pruzansky S, Aduss H. Journal of Clinical Orthodontics interviews: Dr. Samuel Pruzansky, Howard Aduss on cleft lip and palate. Journal of Clinical Orthodontics 1976;May:380 – 95. [2] Vargervik K. Orthodontic management of unilateral cleft lip and palate. Cleft Palate J 1981;18:256 – 9. [3] Bishara S, Da Silva FO, et al. Upper dental arch morpholgy of adult unoperated complete bilateral cleft lip and palate. Am J Orthod Dentofacial Orthop 1998;114: 154 – 61. [4] McNeil CK. Orthodontic procedures in the treatment of congenital cleft palate. Dent Rec 1950;79:126. [5] Pruzansky S. Presurgical orthopaedics and bone grafting for infants with cleft lip and palate: a dissent. Cleft Palate J 1964;1:154. [6] Proffit WR, White Jr RP. Special problems in cleftpalate patients. Surgical-orthodontic treatment. St. Louis: Mosby-Yearbook; 1991. p. 625 – 39. [7] Huebener D, Marsh J. Alveolar molding appliances in the treatment of cleft lip and palate infants: Multidisciplinary management of cleft lip and palate. 1990;74: 601 – 7. [8] Pruzansky S, Aduss H. Prevalence of arch collapse and malocclusion in complete unilateral cleft lip and palate. Trans Eur Orthod Soc 1967;43:365 – 82. [9] Subtelny JD. Orthodontic principles in treatment of cleft lip and palate. In: Bardach J, Morris HL, editors. Multidisciplinary management of cleft lip and palate. Philadelphia: WB Saunders Co; 1990. p. 615 – 36. [10] Ross RB. Facial growth in cleft lip and palate. Head Neck 1989;42:2012. [11] Davies AD. Unoperated bilateral complete cleft lip and palate in the adult. Plast Reconstr Surg 1951;7:482. [12] Hamilton R, Graham WP, Randall P. A lip adhesion operation in cleft lip surgery. Cleft Palate J 1988;25: 53 – 7. [13] Widmaier W. A surgery procedure for the closure of palatal clefts: Treatment of patients with clefts of lips, alveolus, and palate. Symposium Hamburg 1966; 87 – 9. [14] Braithwaite F, Maurice JG. The importance of the levator palati muscle in cleft palate closure. Br J Plast Surg 1968;21:60 – 2. [15] Hotz M, Gnoinski W, et al. Early maxillary orthopedics in CLP cases: guidelines for surgery. Cleft Palate J 1978;15:305 – 411. [16] Riski JE, Millard RT. The processes of speech: evaluation and treatment. In: Cleft palate and cleft lip: A team

[17]

[18]

[19]

[20]

[21]

[22] [23] [24]

[25]

[26]

[27]

[28]

[29]

[30]

[31]

[32]

[33]

[34]

475

approach to clinical management and rehabilitation of the patient. Philadelphia: WB Saunders Co; 1979. p. 415 – 8. Mazaheri M, Harding RL, Nanda S. The effects of surgery on maxillary growth and cleft width. Plast Reconstr Surg 1967;40:22 – 9. Buschang PH, Porter C. Pace mask therapy of preadolescents with unilateral cleft lip and palate. Angle Orthod 1994;2:145 – 50. Subtelny JD. Oral respiration: facial maldevelopment and corrective dentofacial orthopedics. Angle Orthod 1980;50:147 – 64. Gnoinski W. Infant orthopedics and later orthodontic monitoring for unilateral cleft lip and palate patients in Zurich. Multidisciplinary management of cleft lip and palate. WB Saunders 1990;71:578 – 85. Kerr M, Welch C. Functional regulator therapy for cleft palate patients. Am J Orthod Dentof Orthop 1981; Nov.:508 – 24. Borden GH. Mandibular growth in the cleft palate infant [Thesis]. Chicago: University of Illinois; 1953. Valinoti Jr JR. The congenitally absent premolar problem. Angle Orthod 1958;28:36 – 8. Ranta R. Tooth formation in children with cleft lip/palate. Am J Orthod Dentof Orthop 1986;Jul.: 11 – 8. Menius JA, Largent MD, Vincent CJ. Skeletal development of cleft palate children as determined by hand-wrist roentgenographs: a preliminary study. Cleft Palate J 1966;3:67 – 75. Lynch JB, Wisner HK, Evans RM, et al. Cephalometric study of maxillary growth five years after alveolar bone grafting of cleft palate infants. Plast Reconstr Surg 1970;46:564 – 7. Jolleys A, Robertson N. Early bone grafting in complete clefts of the lip and palate. Br J Plast Surg 1972; 25:229 – 37. Figueroa A, Polley J, Cohen M. Orthodontic management of the cleft lip and palate patient. Clin Plast Surg 1993;20:733 – 53. Stenstro¨m SJ, Thilander BL. Bone grafting in secondary cases of cleft lip and palate. Plast Reconstr Surg 1963;32:353 – 60. Helms JA, Speidel MT, Denis KL. Effect of timing on long-term clinical success of alveolar cleft bone grafts. Am J Orthod Dentofacial Orthop 1987;92:232 – 40. Eldeeb M, Hinrichs J, Waite D, Bandt C, Bevis R. Repair of alveolar cleft defects with autogenous bone grafting: periodontal evaluation. Cleft Palate J 1986; 23:126 – 36. Boyne PJ, Sands NR. Combined orthodontic-surgical management of residual palato-alveolar cleft defects. Am J Orthod 1976;70:20. Abyholm FE, Bergland O, Semb G. Secondary bone grafting of alveolar clefts: A surgical/orthodontic treatment enabling a non-prosthodontics rehabilitation in cleft lip and palate patients. Scand J Reconstr Surg 1981;15:127 – 40. Ross RB. Treatment variables affecting facial growth

476

R.C. Marcovitch / Oral Maxillofacial Surg Clin N Am 14 (2002) 463–476

in complete unilateral cleft lip and palate: an overview of treatment and facial growth. Cleft Palate J 1987;24: 71 – 7. [35] Freihofer Jr HPM. Results of osteotomies of the facial skeleton in adolescence. J Maxillofac Surg 1977; 5:267 – 9. [36] Braun TW, Sotereanos GC. Orthognathic and secondary cleft construction of adolescent patients with cleft palate. J Oral Surg 1980;38:425. [37] Munro IR, Salyer KE. Orthognathic surgery for pa-

tients with cleft lip and palate: Multidisciplinary management of cleft lip and palate. WB Saunders 1990;63: 500 – 8. [38] Tideman H, Stoelinga P, Gallia L. Le Fort I advancement with segmental palatal osteotomies in patients with cleft palates. J Oral Surg 1982;40:721. [39] Figueroa A, Polley JW. Management of severe cleft maxillary deficiency with distraction osteogenesis: Procedure and results. Am J Orthod Dentof Orthop 1999;Jan:115.

Oral Maxillofacial Surg Clin N Am 14 (2002) 477 – 490

Secondary grafting in the alveolar cleft patient Amin Kazemi, DMD, MDa, Jeffrey W. Stearns, DMD,MDa, Raymond J. Fonseca, DMDa,b,* a

Department of Oral and Maxillofacial Surgery, Hospital of the University of Pennsylvania, 5th Floor White Building, 3400 Spruce Street, Philadelphia, PA 19104, USA b University of Pennsylvania School of Dental Medicine, 4001 Spruce Street, Philadelphia, PA 19104, USA

Historical perspective The initial attempts at the treatment of alveolar cleft defects date back to 1901, when Von Eiselberg used pedicled bone to fill an alveolar defect [1]. Since that time, the complex management of a cleft patient has advanced tremendously. These progressions have been made possible by the visionary work of multiple clinicians (Table 1). It is important to recognize that these advancements were achieved in the face of strong antagonists, who advocated no treatment of the alveolar cleft defect. Continued surgical advancements and refinement in techniques have brought about controversies in the timing of repair and the source of graft material. These controversies however, have not detracted from the goal of this treatment, which includes closing of the oronasal fistula, establishing continuity between the cleft segments, constructing proper alveolar contour, preventing tooth loss caused by lack of periodontal bone support, providing proper support for eruption of teeth and orthodontic tooth movement, and creating firm support for the nasal floor [2]. Although the repair of the alveolar cleft may be one of the last considerations in the global treatment of a cleft patient, if these goals are achieved, it provides

* Corresponding author. School of Dental Medicine, Hospital of the University of Pennsylvania, 4001 Spruce Street, Philadelphia, PA 19104. E-mail address: [email protected] (R.J. Fonseca).

tremendous enhancement of oral function and aesthetics for a cleft patient. By reviewing the incidence, etiology, indications for treatment, timing, source of graft material, patient evaluation and assessment, presurgical orthodontics, surgical techniques, postoperative care, and complications, the authors hope to provide the reader with a comprehensive understanding of alveolar clefts and their repair. This is an exciting area of oral and maxillofacial surgery that allows for integration and participation with multiple clinicians from other specialties who are also intimately involved in the care of the cleft patient. Proper communication, understanding, and coordination with these clinicians allows for optimum treatment of these unique individuals.

Incidence and etiology Among the many congenital birth defects, there have been more than 250 different types of facial clefting disorders described in the literature. The most frequently reported defect is clefting of the palatine bone and the alveolar process of the maxilla [3,4]. The overall incidence of cleft lip and palate is reported at 1:750 live births in the United States [5]. Stratified between the different ethnic groups the incidence is as follows: African Americans, 1:2000; whites, 1:1000; and Asians, 1:500 live births [6,7]. The location of the clefting is usually on the left side of the maxilla (left:right:bilateral 6:3:1). Out of the various combinations of isolated cleft lip, isolated cleft palate, and cleft lip and palate, the cleft lip and palate is the most

1042-3699/02/$ - see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 4 2 - 0

478

A. Kazemi et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 477–490

Table 1 Historical perspective Date

Author

Contribution

1908 1914 1931

Lexer [79] Drachter [80] Veau [81]

1955

Nordin et al

1968

Jolley [28]

1972

Boyne and Sands [82] Wolfe et al [74]

Free bone grafts Bone grafts to alveolar cleft Classification and attempt at tibial graft to cleft palate Early alveolar cleft repair with autogenous bone Detrimental effects of early bone grafts on maxillary growth Protocol for secondary bone graft Favorable results with calvarial bone Alveolar graft with allogenic bone

1983 1987

Nique, Fonseca [66]

common in occurrence (see box) [7]. In 75% of the cleft lip and palate occurrences, the cleft runs through the alveolar ridge. It is currently believed that less than 40% of the clefts of the lip and palate are of genetic origin [5,6]. Mutations in specific collagen genes in Stickler syndrome [8,9], homeodomain-containing protein PAX3 in Waardenburg’s syndrome [10], and sonic hedgehog in midline craniofacial defects are examples of direct genetic correlation with cleft lip and palate [11,12]. Environmental factors play a clear role in gene expression, which affects the phenotype [13]. For example, Hwang et al report direct correlation between maternal smoking and clefting [14]. Tolarova and Harris found a decrease in clefting recurrence in mothers who took multivitamins (either the subjects had a child with asyndromic cleft lip and palate or they or their partner had a cleft lip and palate) [15]. Antiepileptic drugs also have been linked to clefting [16]. Maternal alcohol consumption has been under extensive debate as an etiologic factor [17]. Infections (rubella and toxoplasmosis) and growth factor deficiency are among other environmental factors [18].

Incidence of cleft lip and palate Cleft 0.29 Cleft 0.31 Cleft 0.48

lip per 1000 palate per 1000 lip and palate per 1000

The evaluation of the etiologic sources is important, especially a genetic evaluation. The lack of attention to associated anomalies may bring about improper genetic counseling and treatment.

Treatment goals and objectives The functional and aesthetic problems associated with cleft lip and palate depend on the size of the cleft and whether it is unilateral or bilateral. The patient’s quality of life can be affected in many ways. Some of the more common complaints include [19]            

Food/fluids coming out of the nose An inability to blow balloons or suck a straw A persistent smell or discharge from the nose Poor speech An inability to clean the teeth in the cleft area Decayed or deformed teeth in the cleft area Missing or supernumerary teeth in the area Lack of bone support for teeth adjacent to the defect Poor alignment of the teeth of the lesser and greater segments Mobility and overgrowth of the premaxilla in the bilateral case Lack of support for the alar base of the nose and lip in the unilateral case Lack of support for the alar base, columella, and lip in the bilateral case.

These complaints allow the surgeons to create a list of surgical goals that would alleviate these aesthetic and functional issues. The following list has been amassed from the available literature [2,19 – 21]: 1. Close vestibular and palatal oronasal fistula 2. Restore physiologic continuity of the dental arch to enable oral and dental health to be maintained 3. Provide bone for stability and continuity of the dental arch and premaxilla 4. Allow eruption of the permanent teeth or placement of dental implants through bone graft 5. Provide support for the lateral ala of the nose 6. Allow for the orthodontic alignment of the teeth 7. Facilitate nasolabial muscle and soft tissue reconstruction 8. Establish functional nasal airway 9. Provide support for the lip

A. Kazemi et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 477–490

10. Prevent tooth loss caused by lack of periodontal bone support. It serves the practitioner well to have this list in mind while constructing a unique surgical plan for a unique cleft patient, thus providing an exceptional treatment that satisfies most of the patients’ functional, aesthetic, and psychosocial needs.

Timing of alveolar cleft grafting To comprehend better the various ideologies concerning the timing of the alveolar cleft grafting, one first should have a firm grasp of its classification:  Primary (0 – 2.5 years, usually at the time of

lip repair)  Early secondary (2 – 5 years, before the eruption

of permanent incisors)  Secondary (6 – 13 years, before the eruption of

the permanent canines)  Late ( > 13 years, after the eruption of the per-

manent canines) Select clinicians believe that primary bone grafting has a vital role. It is their belief that with refinement in surgical skills, the advent of bone morphogenetic protein, and improvement in management of scar tissue, the alveolar cleft grafting is sensible during the primary time period [22 – 36a]. These studies seem to have limited their focus to isolated components of the deformity, however (asymmetry [36b], just narrow clefts [37], and condition of adjacent teeth [38]). Most studies of primary bone grafting indicate an impedance on anterior and inferior growth of the maxilla and poor angulations of the teeth and the premaxilla [22 – 29,31 – 35]. Jolley et al, in a study of the early bone grafting of alveolar cleft, reported not only an anteroposterior growth limitation but also a higher propensity for cross-bites as a result [23]. The most common time to perform this surgery is during secondary bone grafting. Numerous studies have shown the efficacy of this procedure in satisfying the previously mentioned goals [39 – 45]. The main advantages of performing the surgery during this time period are providing a high likelihood of success (up to 98% in one study), providing excellent periodontal attachment for the adjacent teeth, allowing for eruption of the canine, allowing for orthodontic alignment, and ensuring minimal impedance on facial growth [39 – 45]. Posnick also mentions that waiting allows maximum transverse (posterior) growth of the maxilla

479

to occur before bone grafting [21]. Ninety-five percent of the anteroposterior and transverse growth of the maxilla is completed by the age of 8 [21]. It is critical to remember that in the case of cleft lip and palate the sequence of eruption is usually delayed. Most surgeons agree that the preferred age of treatment is contingent on the dental age rather than the chronologic age. Based on the limited studies in alveolar cleft grafting during the early secondary period, it is difficult to justify performing the bone graft on this age group [46]. Boyne advocated alveolar cleft grafting during this time period in cases in which the permanent lateral or central incisors seem to be erupting into the cleft, causing severe malposition of the tooth and decreasing periodontal support of the erupting tooth [47]. Although many studies have proved the late period as a suboptimal age group to perform alveolar cleft grafting, this group should not be excluded from such treatment. The potential for successful surgery still exists and in some situations one even could include the alveolar cleft grafting with the patient’s orthognathic (Le Fort I) procedure. In adult patients the chance of successfully bone grafting an alveolar cleft is less than in the adolescent. The main objective with this population is to achieve oronasal closure, provide continuity and stability of the maxillary arch, and allow for possible implant restoration [48]. The fact that controversy exists in this area indicates that much investigation still remains to be done. As progression is made with better understanding of maxillary growth, improvement and enhancement of grafting materials, and refinement in surgical technique, one must reassess the success of this procedure in the different age groups.

Grafting material and donor sites Numerous variables affect the decision-making process in choosing an appropriate donor site for alveolar cleft bone grafting, including factors such as the size of the cleft, the volume of bone needed, whether teeth will erupt through the graft material, the health of the donor site, and the healing potential of the patient. Table 2 includes the various donor sites and grafting materials along with their advantages and disadvantages [25,49 – 75]. It is beyond the scope of this article to discuss each of these in great detail, so the Table 2 has been provided as a summary. To enhance the osteoinductive ability of the graft material, one can use platelet-rich plasma. This plasma provides the graft material with more factors to

480

A. Kazemi et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 477–490

Table 2 Advantages and disadvantages of various graft material Donor site / grafting material

Advantages

Disadvantages

Autogenous: greatest number of viable osteoprogenitor cells, which allow for early revascularization (osteogenic, osteoconductive, osteoinductive) Iliac crest Adequate quantity (uni- and bi-) Questionable effects on growth Easily condensed and placed Possible gait disturbance Proven successful results Postoperative hematoma Little donor site morbidity Donor site morbidity Two-team approach Tibia Adequate volume (uni- and bi-) Concern with ambulation and Quality similar to iliac crest epiphyseal injury Predictable results Two-team approach Rib For infants Donor site morbidity Two-team approach Unpredictable results Cranial bone Adequate quantity (uni- and bi-) Donor site aesthetics/defect (corticocancellous block graft) Less resorption (membranous bone) Stigma and fear for patient Rapid vascularization Less cellular component Predictable quality Two-team approach Mandibular symphysis Quantity adequate for uniLimited amount of bone Less resorption (membranous bone) No external scars Allogenic: derived from a genetically unrelated member of same species (osteoconductive, osteoinductive) Comparable to autogenous No osteogenic potential Allows for eruption of teeth Delayed incorporation Avoids donor site morbidity Alloplastic: inert foreign body material (osteoconductive, osteoinductive) Avoids donor site morbidity Delayed healing Inability of teeth to erupt

enhance the progenitor cell transformation to osteoblasts. If the graft survives the early complications of infection and integrates into the cleft defect, the only variable that remains is the volume of bone that resorbs over time. This becomes an important factor, especially when prosthetic reconstruction, such as implant placement, comes into play. It is necessary to perform a secondary bone grafting procedure before implant placement to provide for adequate bulk and contour.

malpositioned teeth in the region of the cleft, crossbites, caries, oral hygiene, position and mobility of the premaxilla, and the adequacy of the soft tissue for tension-free closure [46,76]. If this evaluation reveals that the patient has lateral or central incisors whose eruption is in jeopardy secondary to large cleft defects, the patient must undergo grafting earlier to salvage these teeth. At this stage the surgeon must choose an appropriate flap design and grafting material along with possible donor site based on the evaluation. Radiographic evaluation includes panoramic, occlusal, and periapical films of the cleft region.

Patient evaluation and assessment A patient with an alveolar defect should be evaluated for the repair of the alveolar cleft in the late primary and early mixed dentition period. The evaluation of a cleft patient starts with a thorough history and physical examination, along with all the past anesthetic and surgical history. The focused examination should evaluate the previous repairs, any oronasal fistula, the alar support, the size of the alveolar defect,

Presurgical orthodontic care Two major orthodontic considerations intimately integrate with the timing of the alveolar cleft grafting: the correction of cross-bites and the alignment of the anterior teeth [77,78]. If posterior cross-bites exist secondary to narrowed transverse dimension of the maxilla, maxillary expansion may be performed

A. Kazemi et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 477–490

before grafting [76]. If the graft is performed before the expansion of the maxilla, a 3-month period must elapse before this expansion. If a bilateral cleft exists with a premaxilla, the maxilla must be expanded first before distalization of the premaxilla to ensure proper space. The Quadhelix and Hyrax appliances that are

481

usually used for maxillary expansion should be left in place for at least 3 months postoperatively to help prevent relapse. It is critical that the orthodontic alignment of the anterior teeth be attempted with great care to avoid root exposure through the thin alveolar bone in the cleft region [2].

Fig. 1. Case of a unilateral alveolar cleft. (A,B) A unilateral cleft in the area of the left maxilla. (C,D) Patient 2 weeks after operation from a secondary alveolar bone grafting procedure (autogenous cancellous bone). (E,F) Patient 3 months after operation.

482

A. Kazemi et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 477–490

Surgical technique Three basic surgical principles must be satisfied for the successful treatment of the alveolar cleft grafting: (1) closure of oronasal fistula, (2) adequate volume of graft material, and (3) water tight and tension-free closure. The preprocedural considerations by the surgeon should include the amount of mucosa available for closure, the best flap design to maintain adequate blood supply and tension-free closure, the extent of the oronasal communication, the level of support needed for the alar base, and the donor site evaluation. Once these decisions have been made by the surgeon, he or she can approach the surgery with confidence and focus on accomplishing individual steps efficiently and completely. General anesthesia is the most common choice of anesthesia for the repair of the alveolar cleft, especially if a donor site is involved. Nasal intubation on the unaffected side is preferred; however, an oral endotracheal tube tucked to the opposite side may be adequate. The presence of a pharyngeal flap should be determined before intubation. Placement of a throat pack prevents passage of excess blood into the stomach, which minimizes the chance of postextubation emesis and possible aspiration. Irrigation of the oral cavity with chlorhexidine solution is advised to decrease the chance of immediate postoperative infection. Injection with local anesthesia with epinephrine not only aids with postoperative pain control and intraoperative hemostasis but also allows the surgeon to identify the margins of the bony cleft and the oronasal communication. If the graft material allows for a two-team approach, it is more convenient to choose the donor site opposite the side of the cleft to decrease the amount of interference between the two teams and possible cross-contamination of the donor site field. Once the local anesthesia has been applied, an incision is made through the mucosa overlying the cleft down to the bony margins to allow the vertical portion of the cleft to be used for the closure of the nasal floor. There is usually adequate amount of tissue present within the oronasal fistula, which leaves one with enough tissue to achieve an oral closure. The area of the pyriform aperture creates a unique problem

because there are no bony margins. In this area, the soft tissue is divided into two layers to create adequate tissue for the closure of the most superior and anterior aspect of the oronasal fistula. A periosteal elevator is used to elevate the mucosa within the cleft, which allows for the closure of the oronasal fistula and full exposure of the bony walls of the cleft. All excess soft tissue should be trimmed from this area to allow for maximum contact of native bone with the bone graft. The ideal position for the inverted suture line and the knots of the oronasal fistula closure is toward the nasal side. Once the soft tissue flap design is carried out and the tissue is elevated, the bone graft material can be placed in the area of the alveolar cleft and the final closure initiated (Figs. 1,2). At this juncture the flap design that was chosen preoperatively must be implemented. Three main soft tissue flap designs are described in the literature. Posnick [21] points out two important factors that must be considered in choosing a flap design: (1) preserving the vestibular architecture and (2) providing the maximum attached mucosa in the area of the alveolar cleft to allow for development of a normal periodontal sulcus and attachment of erupting canine. The buccal finger flap has an excellent blood supply and provides adequate soft tissue for the closure over the bone graft. It does not satisfy the two factors mentioned previously, however. It shortens the buccal vestibule and provides nonkeratinized tissue in the area of eruption of the canine. The lateral sliding flap is raised on the lesser segment with a broad base and has an excellent blood supply. It brings adjacent attached gingiva to the area of the alveolar cleft. It leads to shortening (although less) of the buccal vestibule, however. Another negative factor associated with this type of flap is the reliance on secondary healing of the mucosa in the denuded area adjacent to the alveolar cleft. This flap design provides for an excellent tension-free closure and decreases the chance of dehiscence. The oblique sliding flap is a modification of the Moczair flap. The adjacent attached mucosa from the lesser and the greater segments are brought to the alveolar cleft site, thus covering the newly formed ridge. It provides more than adequate attached gingival for tension-free closure of wide alveolar clefts. There is a minor decrease in the vestibular depth. This same

Fig. 2. The repair of a unilateral alveolar cleft. (A,B) Incision line for an oblique sliding flap (dashed line). (C) The closure of the nasal mucosa and the introduction of the bone graft to the alveolar defect. (D) Depiction of the nasal mucosa flap along with the closure of the oral mucosa. (E) Final mucosal closure of the oblique sliding flap. (F) A palatal splint placed over the closure area to prevent formation of a hematoma and stabilize the bone graft.

A. Kazemi et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 477–490

483

484

A. Kazemi et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 477–490

Fig. 3. Case of a bilateral alveolar cleft. (A) Preoperative view of the bilateral cleft defect. (B) Postoperative view of the closure of the oblique sliding flap. (C,D) Two-year and 2-month postoperative palatal and labial view.

approach is carried out with the palatal tissue, and there may be reliance on healing by secondary intention at the distal release sites. The four corners of the flap are closed with a horizontal mattress suture. This is the authors’ flap of choice (Figs. 3,4). The palatal flap with posterior release allows for anterior advancement of the palatal attached mucosa to the alveolar cleft site. The obvious danger of damage to the greater palatine neurovascular bundle detracts from such flap design, however. With such significant mobilization of the adjacent mucosa and the placement of the bone graft, it is advisable to place a palatal splint (fabricated preoperatively) to provide maximum immobilization of the bone graft and support the palatal tissue. The splint also may play a role in minimizing the formation of hematoma. Care must be taken to avoid tight pressure points on the palatal mucosa, because it creates added postoperative pain and discomfort for the patient and may decrease the blood flow to the flap edges (Fig. 5).

In the case of a bilateral alveolar cleft, the technique is essentially the same, with the precaution that the premaxilla cannot provide significant tissue for advancement. The adjacent sites must provide the soft tissue coverage. The greatest challenge in the closure of such cases occurs in the area directly posterior to the premaxilla. Postoperatively, a liquid diet, avoidance of trauma to the site, and avoidance of activities such as swimming are recommended for 5 to 7 days (or until the first postoperative visit). The patient is placed on antibiotics and nasal decongestants after the operation and for at least 1 week postoperatively. Meticulous oral hygiene with chlorhexidine mouth wash rinses is essential in minimizing the chance of infection. Hospital stays with these procedures depend on the individual patient, choice of donor site, and other miscellaneous factors that necessitate further careful observation of the patient. Complications of the alveolar cleft grafting with primary oral and nasal closure can include infection,

A. Kazemi et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 477–490

485

Fig. 4. The repair of a bilateral alveolar cleft using an oblique sliding flap technique. (A) A bilateral alveolar cleft palate. (B) Needle palpation of the bony edges of the alveolar cleft while injecting local anesthesia. (C) The incision line (dashed line). (D) Elevation of the nasal mucosa on the left and closure of the nasal mucosa on the right. Placement of the bone graft over the closed nasal mucosa. (E,F) Palatal depiction of the movement of the adjacent mucosa in the oblique sliding flap technique. (G) Mucosal closure in a bilateral alveolar cleft. (H,I) Final closure of the bilateral alveolar cleft repair using a oblique sliding flap technique.

486

A. Kazemi et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 477–490

Fig. 4 (continued ).

wound dehiscence, loss of the graft, and incomplete closure of the oronasal fistula. An infection is the most detrimental complication that may occur in this surgery. Observance of the following steps can aid in reducing the rate of infection and avoiding the creation of a larger defect and a larger oronasal fistula: 1. Preoperative oral hygiene 2. Appropriate intraoperative and postoperative antibiotics 3. Excellent postoperative oral hygiene 4. Nasal decongestants 5. Prompt recognition and treatment of upper respiratory infection.

Summary Although many controversies exist regarding the timing, choice of graft material, or even flap design, this procedure has provided a predictable means of resolving a unique and debilitating problem for the cleft patient. Considering that these patients are exposed to numerous surgical procedures, it is the surgeons’ obligation to plan operations carefully and provide individualized treatment that allows for the best results for individual patients. With the best interest of the cleft patients in mind, we must strive forward to create better techniques and materials to repair alveolar clefts. Because this subject

Fig. 5. Clinical presentation of the posterior release palatal advancement technique. (A,B) Labial and palatal view of a palatal cleft. (C) Reflection of the posterior palatal flap, exposing the palatal cleft. (D) Placement of the autogenous cancellous bone graft in the area of the palatal defect. (E) Closure of the palatal mucosa overlying the palatal defect. (F) Final closure of the palatal flap with posterior release. (G) Six-month postoperative view of the palatal flap.

A. Kazemi et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 477–490

487

488

A. Kazemi et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 477–490

involves many variables and is not conducive to prospective and randomized studies, it will take considerable communication and sharing on the parts of the clinicians involved to advance the science of alveolar cleft grafting.

[16]

[17]

References [18] [1] Koberg WR. Present view of bone grafting in cleft palate [review]. J Maxillofac Surg 1973;1: 185 – 93. [2] Zeitler D. Alveolar cleft grafts. In: Fonseca R, editor. Oral and maxillofacial surgery. Philadelphia: WB Saunders; 2000. p. 75 – 86. [3] Jones MC. Facial clefting: etiology and development pathogenesis. Clin Plast Surg 1993;20:599 – 608. [4] Vanderas AP. Incidence of cleft lip, cleft palate, and cleft lip and palate among races: a review. Cleft Palate J 1987;24:216. [5] Fraser FC. The genetics of cleft lip and palate. Am J Hum Genet 1970;22:336 – 52. [6] Fraser FC. Research revisited: the genetics of cleft lip and cleft palate. Cleft Palate J 1989;26:255 – 7. [7] Tolarova M, Cervenka J. Classification and birth prevalence of orofacial clefts. Am J Med Genet 1998;75: 126 – 37. [8] Ahmad NN, McDonald-McGinn DM, Zackai EH, et al. A second mutation in the type II Pro collagen gene (COL2AI) causing Stickler syndrome (arthroophthalmoopathy) is also a premature termination codon. Am J Hum Genet 1993;52:39 – 45. [9] Brunner HG, van Beersum SE, Warman ML, et al. A Stickler syndrome gene is linked to chromosome 6 near the COL11A2 gene. Hum Mol Genet 1994;3: 1561 – 4. [10] Tassabehji M, Newton VE, Leverton K, et al. PAX3 gene structure and mutations: close analogies between Waardenburg syndrome and the splotch mouse. Hum Mol Genet 1994;3:1069 – 74. [11] Belloni E, Muenke M, Roessler E, et al. Identification of sonic hedgehog as a candidate gene responsible for holoprosencephaly. Nat Genet 1996;14:353 – 6. [12] Roessler E, Belloni E, Gaudenz K, et al. Mutations in the human Sonic Hedgehog gene cause holoprosencephaly. Nat Genet 1996;14:357 – 60. [13] Vargervik K, Ferrari C. Embryogenesis and comprehensive management of the cleft patient. In: Fonseca R, editor. Oral and maxillofacial surgery. Philadelphia: WB Saunders; 2000. p. 3 – 13. [14] Hwang SJ, Beaty TH, Panny SR, et al. Association study of transforming growth factor alpha (TGF alpha) Tag I polymorphism and oral clefts: indication of geneenvironment interaction in a population-based sample of infants with birth defects. Am J Epidemiol 1995; 141:629 – 36. [15] Tolarova M, Harris J. Reduced recurrence of orofacial clefts after periconceptional supplementation with

[19]

[20]

[21]

[22]

[23]

[24]

[25]

[26]

[27]

[28]

[29]

[30]

[31]

high-dose folic acid and multivitamins. Teratology 1995;51:71 – 8. Dravet C, Jutian C, Legras C, et al. Epilepsy, antiepileptic drugs and malformations in children of women with epilepsy: a French prospective cohort study. Neurology 1992;42(Suppl 5):75 – 82. Jones KL, Smith DW, Ulleland CN, et al. Pattern of malformations in offspring of chronic alcoholic mothers. Lancet 1973;1:1267 – 71. Wyszynski DF, Beaty TH. Review of the role of potential teratogens in the origin of human non-syndromic oral clefts. Teratology 1996;53:309 – 17. Stassen L. Alveolar bone grafting: how I do it. In: Booth P, Schendel S, Hausamen J, editors. Oral and maxillofacial surgery. New York: Churchill-Livingstone; 1999. p. 1047 – 57. Hawkins J. Secondary bone grafting for unilateral alveolar clefts. Chicago: University of Illinois at Chicago, Grand Rounds; 2000. Posnick J. The staging of cleft lip and palate reconstruction: infancy through adolescence. In: Rose A, Ross A, editors. Craniofacial and Maxillofacial Surgery in Children and Young Adults. Philadelphia: WB Saunders; 2000. p. 785 – 815. Freide H, Johanson B. A follow-up study of cleft children treated with primary bone grafting. Part I: orthodontic aspects. Scand J Plast Reconstr Surg 1974;8: 88 – 103. Jolleys A, Robertson NRE. A study of the effects of early bone grafting in complete clefts of the lip and palate: 5 year study. Br J Plast Surg 1972;25:229 – 37. Molsted K, Dahl E, Skovgaard LT, et al. A multicentre comparison of treatment regimens for unilateral cleft lip and palate using a multiple regression model. Scand J Plast Reconstr Surg Hand Surg 1993;27:277 – 84. Prickrell K, Quinn G, Massengill R. Primary bone grafting of the maxilla in clefts of the lip and palate. Plast Reconstr Surg 1968;41:438 – 43. Pruzansky S. Presurgical orthopedics and bone grafting for infants with cleft lip and palate: a dissent. Cleft Palate J 1964;1:229 – 37. Rehrmann AH, Koberg WR, Koch H. Long-term postoperative results of primary and secondary bone grafting in complete clefts of lip and palate. Cleft Palate J 1970;7:206 – 21. Robertson NRE, Jolleys A. Effects of early bone grafting in complete clefts of lip and palate. Plast Reconstr Surg 1968;42:414 – 21. Rosenstein SW, Monroe CW, Kernahan DA, et al. The case for early bone grafting in the cleft lip and palate. Plast Reconstr Surg 1982;70:297 – 307. Rosenstein SW, Dado DV, Kernahan DA, et al. The case for early bone grafting in cleft lip and palate: a second report. Plast Reconstr Surg 1991;87:644 – 54. Sameshima GT, Banh DS, Smahel Z, et al. Facial growth after primary periosteoplasy versus primary bone grafting in unilateral cleft lip and palate. Cleft Palate Craniofac J 1996;33:300.

A. Kazemi et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 477–490 [32] Smahel Z, Mullerova Z, Nejedly A, et al. Changes in craniofacial development due to modifications of the treatment of unilateral cleft lip and palate. Cleft Palate Craniofac J 1998;35:240 – 7. [33] Smahel Z, Mullerova Z, Horak I. Facial development in unilateral cleft lip and palate prior to the eruption of permanent incisors after primary bone grafting and periosteal flap surgery. Acta Chir Plast 1996;38:30 – 6. [34] Spyropoulos MN, Linder-Aronson S. Evaluation of facial features in two groups of cleft lip and palate patients receiving centralized and non-centralized treatment regimens. Eur J Orthod 1997;19:411 – 22. [35] Suzuki A, Goto K, Nakamura N, et al. Cephalometric comparison of craniofacial morphology between primary bone grafted and nongrafted complete unilateral cleft lip and palate adults. Cleft Palate Craniofac J 1996;33:429 – 35. [36a] Pickrell K, Quinn G, Massengill R. Primary bone grafting of the maxilla in clefts of the lip and palate. Plast Reconstr Surg 1968;41:438 – 43. [36b] Molsted K, Dahl E, Brattstrom V, et al. A six center international study of treatment outcome in patients with clefts of the lip and palate: evaluation of maxillary asymmetry. Cleft Palate Craniofac J 1993;30:22. [37] Keese E, Schmelzle R. New findings concerning early bone grafting procedures in patients with cleft lip and palate. J Craniomaxillofac Surg 1995;23: 296 – 301. [38] Dado DV, Rosenstein SW, Alder ME, et al. Longterm assessment of early alveolar bone grafts using three-dimensional computer-assisted tomography: a pilot study. Plast Reconstr Surg 1997;99:1840 – 5. [39] Andlin-Sobocki A, Eliasson LA, Paulin G. Periodontal evaluation of teeth in bone grafted regions in patients with unilateral cleft lip and cleft palate. Am J Orthodont Dentofacial Orthop 1995;107:144 – 52. [40] Hall HD, Posnick JC. Early results of secondary bone grafts in 106 alveolar clefts. J Oral Maxillofac Surg 1983;41:289 – 94. [41] Jia YL, James DR, Mars M. Bilateral alveolar bone grafting: a report of 55 consecutively-treated patients. Eur J Orthod 1998;20:299 – 307. [42] Kalaaji A, Lilja J, Friede H, et al. Bone grafting in the mixed and permanent dentition in cleft lip and palate patients: long-term results and the role of the surgeon’s experience. J Craniomaxillofac Surg 1996; 24:29 – 35. [43] Lee C, Crepeau RJ, Williams HB, et al. Alveolar cleft bone grafts: results and imprecisions of the dental radiograph. Plast Reconstr Surg 1995;96:1534 – 8. [44] Ramstad T, Semb G. The effect of alveolar bone grafting on the prosthodontic/reconstructive treatment of patients with unilateral complete cleft lip and plate. Int J Prosthodont 1997;10:156 – 63. [45] Troxell JB, Fonseca RJ, Osborn DB. A retrospective study of alveolar cleft grafting. J Oral Maxillofac Surg 1982;40:721 – 5. [46] Clark J, Zeitler DL. Outcome of alveolar grafting in cleft patients of different ages. J Oral Maxillofac Surg 1996;54(Suppl 3):117.

489

[47] Boyne PJ. Bone grafting in the osseous reconstruction of alveolar and palatal clefts. Oral Maxillofac Surg Clin N Am 1991;3:589 – 97. [48] Posnick JC, Tompson B. Cleft orthognathic surgery: complications and long-term results. Plast Reconstr Surg 1995;96:255. [49] Allard RHB, Lekkas C, Swart JGN. Autologous versus homologous bone grafting in osteotomies, secondary cleft repairs and ridge augmentations: a clinical study. Oral Surg Oral Med Oral Pathol 1987;64:269 – 74. [50] Ames JR, Ryan DE, Maki KA. The autogenous particulate cancellous bone marrow graft in alveolar clefts. J Oral Surg 1981;51:588 – 91. [51] Canaday JW, Zeitler DL, Thompson SA, et al. Suitability of the iliac crest as a site for harvest of autogenous bone grafts. Cleft Palate Craniofac J 1983;30: 579 – 81. [52] Catone GA, Reimer BL, McNeir D, et al. Tibial autogenous cancellous bone as an alternative donor site in maxillofacial surgery: a preliminary report. J Oral Maxillofac Surg 1992;50:1258. [53] Craft PD, Sargent LA. Membranous bone healing and techniques in calvarial bone grafting. Clin Plast Surg 1989;16:11 – 9. [54] Feinberg SE, Vitt M. Effect of calcium phosphate ceramic implants on tooth eruption. J Oral Maxillofac Surg 1988;46:121 – 7. [55] Georgiade NC, Pickrell KL, Quinn GW. Varying concepts in bone grafting of alveolar palatal defects. Cleft Palate J 1964;1:438 – 43. [56] Harsha BC, Turvey TA, Powers SK. Use of autogenous cranial bone grafts in maxillofacial surgery. J Oral Maxillofac Surg 1986;44:11 – 5. [57] Horwell BB, ElDeeb M. Nonporous hydroxyapatite in the repair of alveolar clefts in a primate model: clinical and histological findings. J Oral Maxillofac Surg 1989;47:946 – 52. [58] Kaban LB, Mulliken JB, Glowacki J. Treatment of jaw defects with demineralized bone implants. J Oral Maxillofac Surg 1982;40:623 – 6. [59] Kartebein MJ, Nelson CL, Sadove AM. Retrospective analysis of 135 secondary alveolar cleft grafts using iliac or calvarial bone. J Oral Maxillofac Surg 1991; 49:493 – 8. [60] Koole R. Ectomesemchymal mandibular symphysis bone graft: an improvement in alveolar cleft grafting. Cleft Palate Craniofac J 1994;31:217. [61] Kraut RA. The use of allogenic bone for alveolar cleft grafting. J Oral Surg 1987;64:278 – 82. [62] Kusiak JF, Zins JE, Whitaker LA. The early revascularization of membranous bone. Plast Reconstr Surg 1985;76:510 – 6. [63] LaRossa D, Buchman S, Rothkopf DM, et al. A comparison of iliac and cranial bone in secondary grafting of alveolar clefts. Plast Reconstr Surg 1995;96: 789 – 99. [64] Marx RE, Miller RI, Ehler WJ, et al. A comparison of particulate allogenic and particulate autogenous bone

490

[65]

[66]

[67]

[68]

[69]

[70]

[71]

[72]

[73]

A. Kazemi et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 477–490 grafts in maxillary alveolar clefts in dogs. J Oral Maxillofac Surg 1984;42:3 – 9. Matthews DE, Broomhead I, Grossman W, et al. Early and late bone grafting in cases of cleft lip and palate. Br J Plast Surg 1970;23:115 – 29. Nique T, Fonseca RJ, Upton LG, et al. Particulate allogenic bone grafts into maxillary alveolar clefts in humans. J Oral Maxillofac Surg 1987;45:386 – 92. Rudman RA. Prospective evaluation of morbidity associated with iliac crest harvest for alveolar cleft grafting. J Oral Maxillofac Surg 1997;55:219 – 23. Sadove AM, Nelson CL, Eppley BL, et al. An evaluation of calvarial and iliac donor sites in alveolar cleft grafting. Cleft Palate J 1990;17:225 – 9. Sindet-Pedersen S, Enemark H. Reconstruction of alveolar clefts with mandibular or iliac crest bone grafts: a comparative study. J Oral Maxillofac Surg 1990;48: 554 – 8. Sindet-Pedersen S, Enemark H. Mandibular bone grafts for reconstruction of alveolar clefts. J Oral Maxillofac Surg 1988;46:533 – 7. Smith JD, Aramson M. Membranous versus endochondral bone autografts. Arch Otolaryngol 1974;99: 203 – 5. So LL, Lui WW. Alternative donor site for alveolar bone grafting in adults with cleft lip and palate. Angle Orthod 1996;66:9 – 16. Tan AES, Brogan WF, McComb HK, et al. Secondary

[74]

[75]

[76]

[77]

[78]

[79]

[80] [81] [82]

alveolar bone grafting: 5 year periodontal and radiographic evaluation in 100 consecutive cases. Cleft Palate Craniofac J 1996;33:513. Wolfe SA, Berkowitz S. The use of cranial bone grafts in the closure of alveolar and anterior palatal clefts. Plast Reconstr Surg 1983;72:659 – 71. Zins JE, Whitaker LA. Membranous versus endochondral bone: implications for craniofacial reconstruction. Plast Reconstr Surg 1983;72:778 – 84. Boyne PJ, Sands NR. Combined orthodontic-surgical management of residual palato-alveolar cleft defects. Am J Orthod 1976;70:20 – 37. Moore RN. Orthodontic management of the patient with cleft lip and palate. Ear Nose Throat J 1986;65: 356 – 7. Shaw WC, Semb G. Current approaches to the orthodontic management of cleft lip and palate. J R Soc Med 1990;83:30 – 3. Lexer E. Die verwendung der freien knochenplastik nebst versuchen u¨ber gelenkversteifung und gelenktvansplantation. Langenbecks Arch Chir 1908;86:939. Drachter R. Die gaumenspalte und deren operative behandlay. Dtsch Z Chir 1914;131:1. Veau V. Division palatine; anatomic Chirurgie, phonetique. Paris: Masson; 1931. Boyne PJ, Sands NR. Secondary bone grafting of residual alveolar and palatal clefts. J Oral Surg 1972;30: 87 – 92.

Oral Maxillofacial Surg Clin N Am 14 (2002) 491 – 507

Surgical correction of midface deficiency in cleft lip and palate malformation Timothy A. Turvey, DDSa,c,*, Ramon L. Ruiz, DMD, MDa,b,c,d, Bernard J. Costello, DMD, MDe,f,g a

Department of Oral and Maxillofacial Surgery, University of North Carolina at Chapel Hill, Brauer Hall, CB #7450, Chapel Hill, NC 27599-7450, USA b Department of Pediatrics, University of North Carolina at Chapel Hill, Brauer Hall, CB #7450, Chapel Hill, NC 27599-7450, USA c Children’s Hospital of North Carolina, Chapel Hill, NC, USA d University of North Carolina Craniofacial Center, Chapel Hill, NC, USA e Departments of Oral and Maxillofacial Surgery, Pediatric Dentistry, and Pediatric Surgery, University of Pittsburgh Medical Center, Pittsburgh, PA, USA f Magee-Women’s Hospital, Pittsburgh, PA, USA g Children’s Hospital of Pittsburgh, Pittsburgh, PA, USA

Facial disproportion is commonly seen in patients with cleft lip and palate malformation. This dysmorphology is partially caused by the inherent cleft defect, the hypoplastic tissue adjacent to the cleft defect, and the effect of the cleft on subsequent development. Patients who have undergone cleft palate repair during infancy often exhibit some degree of maxillary growth restriction. Extensive literature suggests that this disproportionate jaw growth is the biologic consequence of prior surgical intervention for closure of the soft tissues and is not related to the congenital cleft deformity [1 – 28]. Other authors have reported maxillary hypoplasia severe enough to produce a clinically significant dentofacial deformity with negative effects on speech and occlusion in 25% of cases [4]. Essentially all patients who have clefts that involve the maxilla or palate have a degree of hypoplasia that results in facial asymmetry, at least

* Corresponding author. Department of Oral and Maxillofacial Surgery, University of North Carolina at Chapel Hill, Brauer Hall, CB# 7450, Chapel Hill, NC 27599-7450. E-mail address: [email protected] (T.A. Turvey).

on the margins of the cleft or in the region of the cleft. Although not all patients with clefts are candidates for undergoing skeletal reconstruction, most can benefit. Although the degree of midface deficiency in some patients is small enough to permit adequate orthodontic compensations, the deficiency of skeletal support in the region of the cleft may be enough to warrant surgery to improve the projection. The successful correction of these secondary skeletal deformities frequently requires treatment protocols, which include orthognathic surgery in conjunction with the final phase of orthodontic treatment. Appreciation that a cleft represents interruption of tissue development that affects all layers in the area is critical to understanding the importance of skeletal reconstruction. This tissue deficiency must be comprehended in all three dimensions, especially for skeletal construction. Cleft lip and palate repair requires multiple staged procedures to achieve optimal results. Addressing midface deficiency in the presence of cleft malformation represents only one stage of reconstruction of the defect. Primary lip and palate closures, rhinoplasty, bone grafting, lip revisions, and other procedures cannot be viewed as isolated events. They all have a place in the correction of the cleft malformation, and

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 4 9 - 3

492

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

most affect growth and development of the associated structures around the cleft site. Facial skeletal disproportion may be addressed two ways: (1) osteotomy with repositioning or (2) contour bone grafting [27,28]. Both techniques are useful, have separate indications, and are commonly used together for patients with cleft malformations. Osteotomies and repositioning of skeletal units are reserved for patients with deficiency of entire aesthetic units, such as the maxilla, orbit, or nose. Bone grafting is commonly used to alter the morphology of a skeletal unit, which may be positioned adequately but poorly shaped.

Timing of surgery The decision for the timing of surgery is governed by the biologic and psychosocial concerns of each patient. The best time to reconstruct disproportionate facial skeletal conditions is when the patient is adequately prepared physically and psychologically. It is prudent to delay surgery of the facial bones until complete maturation is achieved. This delay improves the predictability of treatment and reduces the risks of outgrowing the correction. Informing patients of the relevancies of facial growth issues and explaining the risks of undergoing surgery before maturation are important to the decision-making process. A decision to proceed with surgery before maturation should not be taken lightly because there is the possibility of requiring additional surgery once growth has reached its adult level. The omen of outgrowing the skeletal correction and requiring additional surgery is tempered by the lessening morbidity of repeat surgery in contemporary settings. The postoperative course for facial skeletal surgery is becoming more benign because bone plates and screws have nearly eliminated the need for intermaxillary fixation, steroids and antibiotics have controlled swelling and infection, and alternatives to homologous blood transfusion (autologous blood banking and the use of recombinant erythropoietin) are used effectively. These arguments aside, skeletal surgery before maturation should not be used for the convenience of the impatient surgeon or orthodontist. Another biologic consideration that affects the timing of surgery is the eruption of the permanent dentition. Delaying surgery until the canine and second molars have erupted minimizes the risk of injury to the teeth during osteotomy. Third molars usually can be removed at the time of the osteotomy, and their presence should not be a major concern. The patient,

parents, and treating doctors participate in the decision of when to proceed with surgery. The patient’s chief complaint and desires should be weighed with the greatest priority. Improvement of self-concept and image in cleft patients almost always follows surgery to address facial skeletal disproportion, and this important factor cannot be overlooked in the timing of surgery. Improving facial appearance by addressing the skeletal disproportion often results in dramatic and complementary changes. The patient normally perceives these changes positively, and the surgical effort sends a clear message that someone cares and is helping. Exceptions to this generalization may be observed in persons who use the stigma as an excuse for dependency. Trying to identify such individuals before surgery is not easy, and involving a psychologist who is familiar with children with clefts is helpful.

Presurgical counseling As with any patient with a congenital facial malformation, cleft patients are psychologically different from most patients with acquired deformities [29]. Cleft patients have had their problem since birth and have had to adapt to multiple changes from previous surgical procedures. Many cleft patients are acquainted with the disappointment of previous attempts at soft tissue revisions with the hope of erasing the scar on the lip and correcting the nasal asymmetry. For others, expectations from skeletal surgery are completely unrealistic. These patients should be identified and referred for counseling. Adolescents are under enormous pressures to conform to peers, especially in the United States. At no other time in life is someone exposed to more self and peer criticism about appearance differences. Many adolescent patients with clefts are victimized by ridicule, and this is accompanied by low self-esteem and difficulty with socialization. Social withdrawal is another issue that results from the pressures felt by many adolescents, especially those with facial disfigurement. Although counseling can help, the patient still must cope with the problem, which may be improved with surgery.

Surgical reconstruction Surgeons who care for children with cleft lip and palate deformities must proceed with a firm understanding of three-dimensional regional anatomy, the extent of the hard and soft tissue defects, and the

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

complex interplay between surgery and subsequent maxillofacial growth. This understanding allows a clinician to formulate and sequence appropriately the staged surgical treatment of patients with cleft lip and palate deformities from the initial consultation in infancy through adulthood. The goals of skeletal reconstruction in the patient with clefts include improvement of skeletal proportion and balance, improvement of occlusion, closure of residual defects and fistulas, and improvement of the soft tissue position by providing the foundation for support. Skeletal surgery does not erase the lip scar of adjust a landmark mismatch. It provides an opportunity to improve the skeletal support for the soft tissue drape. It can help improve the asymmetry of the lip and nasal base and may support the nasal tip. In providing skeletal support, the stigma of the cleft defect may be reduced so that soft tissue revision may not be needed or desired. By providing skeletal support, the lip assumes a more normal contour and the reflection of light on the scar changes so that the scar may be less obvious. Although the intention of some lip repair techniques is to place the scar where the philtral column should be, the result often falls short. The scar commonly falls on a flat, unsupported position on the lip, which is obvious. Appropriate skeletal support often moves the scar to an area of greater curvature, which reflects light differently and is less conspicuous. Patients should be counseled that the skeletal surgery sets the stage for definitive lip and nasal revisions in the future. Residual skeletal deformities present in patients with unilateral cleft lip and palate come in many varieties. Reconstruction of these defects and deformities requires accurate diagnosis, thoughtful treatment planning, and precise surgical execution of the defined plan. This reconstructive effort typically involves multiple practitioners who have varying degrees of involvement based on the patient’s growth and development and the specific functional and aesthetic issues confronting the patient. The common deformities of the unilateral cleft lip and palate child and adult patient are listed in the box. Patients with bilateral cleft lip and palate have similar deformities but also may present with additional anatomic (skeletal and dental) discrepancies that require consideration (see box). If the maxilla has been grafted successfully so that there is bony continuity without fistula, then a traditional Le Fort I osteotomy (with or without mandibular surgery) may be performed. Even with a maxilla that has been grafted successfully, segmental osteotomies can be more complicated in the bilateral cleft lip and palate

493

Residual dysmorphology in the child and adult unilateral cleft lip and palate patient Residual cleft lip and nose scarring Nasal cartilage distortion Deviated septum Hypertrophied nasal turbinates Unrepaired or residual oronasal fistulas associated with the primary palate cleft (alveolus) Cleft dental gap Missing or malformed teeth Dental crowding Complex malocclusion Periodontal disease Inflammation of the soft tissue surrounding oronasal fistulas. Defects or hypoplasia involving the piriform rim, nasal floor, and alveolus Maxillary hypoplasia (anteroposterior, vertical, and transverse) Maxillary canting and asymmetry Compensatory mandibular asymmetry Mandibular growth disturbance

patient because of palatal scarring, incomplete graft consolidation, and concerns related to the vascular pedicle of the premaxillary segment [4,16,22,27,28].

Specific technical considerations In contemporary cleft team settings, most cleft patients undergo bone grafting to the cleft maxilla and palate at developmentally appropriate times [5 –

Additional dysmorphology in the child and adult bilateral cleft lip and palate patient Ectopically positioned premaxilla Continuous oronasal fistula from the incisive foramen forward to the maxillary clefts on both sides Exaggerated curve of Spee and occlusal plane discrepancies Reduced vascularity of the premaxillary segment requiring modified vestibular incision design and osteotomies through tunneling procedures

494

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

Fig. 1. The circumvestibular incision can be used in most cleft patients and provides the best visualization for conducting the osteotomy.

9]. This procedure provides a bony matrix for support of the erupting permanent teeth, establishes continuity of the nasal floor and maxilla, closes the residual oronasal fistula, and stabilizes the premaxilla in bilateral cases. When this occurs, midface advancement surgery is relatively straightforward. Unfortunately, some patients may not have had successful bone grafting procedures performed so that residual fistulas with dental gaps at the cleft site and skeletal defects remain. For patients who have not benefited from previous bone grafts, the situation is more complex. In both circumstances, the general principles of flap design for maxillary advancement must be followed, which ensures adequate perfusion to the mobilized maxilla. Maxillary advancement in the presence of a cleft is different from the noncleft situation because of the absence of tissues and the effects of multiple previous surgical attempts to close the defects. Perfusion of the mobilized maxilla is from vessels that come from the overlying soft tissues, predominantly the palatal tissues. In cleft patients this tissue is commonly scarred and fibrotic. Care must be exercised when designing the incisions to perform the osteotomy. With few exceptions, almost all can be treated by Le Fort I osteotomy via the circumvestibular incision and down-fracture approach. For persons with severe palatal scarring, persons who have previous-

Fig. 2. An anterior pedicle incision limits visualization and access but provides additional perfusion to the maxilla. It should be used in cleft patients with significant palatal scars and in patients with bilateral clefts.

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

ly undergone an island palatal repair, and persons with bilateral clefts of the maxilla, an anterior buccal pedicle should be maintained to provide adequate perfusion to the mobilized premaxillary segment [27,28]. Technically, this is a more challenging operative procedure. In the standard approach for midface advancement at the Le Fort I level, a circumvestibular incision is made from the zygomaticomaxillary buttress to the opposite side, high in the mucobuccal fold (Fig. 1). Subperiosteal dissection exposes the entire lateral wall of the maxilla from the piriform aperture to the pterygomaxillary junction and from the alveolus, above the roots of the teeth, to the inferior orbital rim. The broad exposure permits excellent visualization of all osteotomies. At the time of mobilization, this incision permits the maxilla to be down-fractured and entirely pedicled to the palatal tissues and the

495

remaining buccal tissues below the incision. Visualization and ease of mobilization are the major advantages of this approach. Hemorrhage control is performed with direct visualization and ligation of vessels. When an anterior buccal pedicle remains, the operation is more difficult (Fig. 2). Visualization is reduced and mobilization by down-fracturing is not possible. Mobilization of the midface is achieved by in-fracturing combined with anterior traction. For most cleft palate patients, the area of greatest resistance to mobilizing the maxilla is the vertical portion of the palatine bone, located in the posterior medial aspect of the maxillary sinus. The bone is thick and access is limited, especially when down-fracturing is not possible. Compounding this problem is the presence of the greater palatine vessels, which descend from the sphenopalatine fossa to the posterior maxilla. The vessels run

Fig. 3. (A – C) Osteotomies for cleft patients should be designed for the circumstance. Creativity is encouraged.

496

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

Fig. 4. (A,B) An 8-year-old child with a repaired cleft lip and palate who is already demonstrating maxillary deficiency.

through the canal in this bone and are prone to rupture during mobilization. Hemorrhage control is at times difficult and usually limited to maneuvers that involve the use of packing and injecting local anesthesia that contains a vasoconstrictor (epinephrine 1:100,000).

The surgical techniques used for these approaches have been described in detail previously, and interested readers are referred to more detailed references dealing with technique [27,28]. In patients whose maxillas have not been previously bone grafted, residual oronasal fistulas are

Fig. 5. (A,B) Anterior cross-bite, malrotations, and ectopic eruption of teeth into the cleft. Oronasal fistulas are present on the buccal and palatal.

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

497

the use of the osteotome to further weaken the structure is advisable before beginning mobilization. Segmenting the maxilla of cleft patients is often tempting to improve occlusal relationships. Segmenting the maxilla in this population should be undertaken cautiously, however, with consideration of the compromised vascularity and tissue scarring. Accepting posterior cross-bite and other occlusal compromises may be judicious rather than risk necrosis of small segments.

Fig. 6. The panorex demonstrates a missing lateral incisor and developing cuspid on the cleft side with minimal periodontal support for the malrotated central incisor adjacent to the cleft. It is important that the orthodontist not attempt to rotate the tooth before placement of the bone graft. Once a periodontal defect occurs, as almost surely will if correction of the malrotation before grafting is undertaken, the bone graft cannot eliminate it.

common. Also, patients who have had gingivo periosteoplasty in infancy may lack the volume of bone necessary to support the lateral incisor or the canine or may present with residual fistulas. Incision design should be used that permits simultaneous closure of oronasal fistulas and plans for additional bone grafting if necessary. Of great importance is the construction of the nasal floor, which is created by using the tissues that line the fistula. Creativity and care are the important elements for surgery to correct midface deficiency in patients with clefts. Because the skeleton is always asymmetrical in cleft patients, osteotomy design is important for maximum improvement of aesthetics (Fig. 3). Sometimes even subtle differences between the osteotomy designs on the cleft side reflect positive soft tissue changes. Adequate mobilization is a key element of success when performing midface osteotomies in the presence of a cleft. The scarring and thickness of bone (particularly the vertical portion of the palatine bone) are two major obstacles. The posterior medial aspect of the maxillary sinus is unusually thick in cleft patients and it must be cut or fractured to permit adequate mobilization. This is usually accomplished with a small osteotome tapped along the thin lateral nasal walls. Adequately weakening the structure is occasionally accompanied by hemorrhage from the descending palatine vessels. Control is by direct visualization and ligation. Failure to weaken the posterior structures before mobilization may result in an unfavorable fracture extending to the skull base or orbit, which can result in blindness [30,31]. If excessive forces are required to mobilize the maxilla, repeating

Bone grafting There are three important reasons for using bone grafts in cleft patients when performing midface advancement. The bone graft can be wedged into the defects in the lateral maxillary walls, which helps maintain the position of the maxilla during healing. The bone graft also encourages bone healing and reduces the risks of the fibrous union. The third use of bone grafts in midface advancement is to contour the middle face. In cleft patients the midface is not just retruded, it is also malformed, and altering the skeletal morphology is important for aesthetic enhancement. Augmenting the cheek projection, the infraorbital regions, the paranasal regions, the nasal bridge, or chin is commonly used at the time of midface advancement. These maneuvers are helpful and easily performed at the time of surgery, and their importance should not be overlooked. There are many bone donor sources, including the ilium, cranium, tibia, mandible, ribs, and zygoma. Although harvesting bone requires more surgical time and has associated morbidity, the predictability

Fig. 7. The cephalometric radiograph demonstrates maxillary deficiency, anterior cross-bite, and the mixed dentition.

498

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

Fig. 8. (A) The bone graft was placed at age 8, and a preliminary stage of orthodontics was initiated after the graft to align, level, and maintain adequate space for eruption of the cuspid adjacent to the central incisor. (B) This radiograph taken at age 11 demonstrates eruption of the cuspid into the grafted bone.

Fig. 9. At age 14, the patient demonstrates progressive maxillary deficiency and a protrusive lower lip. The amorphous facial appearance results not only from maxillary deficiency but also from contour deficiencies of the cheeks and the infraorbital regions.

Fig. 10. At age 14, the patient demonstrates progressive maxillary deficiency and a protrusive lower lip. The amorphous facial appearance results not only from maxillary deficiency but also from contour deficiencies of the cheeks and the infraorbital regions.

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

Fig. 11. Anterior cross-bite is present. A maxillary left premolar was removed to facilitate eruption of the left cuspid. Notice the excellent periodontal health and the absence of fistulas facilitated by the bone graft.

of the result easily justifies its use. No bone substitute has the same success in cleft patients as fresh autogenous bone. The morbidity of bone harvest can be reduced with good surgical technique and should not be an excuse for using allogeneic bone or other alternative. The bone graft material of choice for use in cleft surgery is always fresh autogenous bone. The iliac crest is frequently used to graft residual defects of the anterior maxilla and alveolus. Cancellous bone and corticocancellous blocks are used for filling defects in the alveolus or lateral maxillary walls. The authors’ preference for bone grafts to contour the middle face is split-thickness calvarium. For the chin,

Fig. 12. The cephalometric radiograph confirms maxillary deficiency.

499

Fig. 13. At the time of surgery, split-thickness cranial bone grafts were to be placed in the osteotomy defects and support the cheek prominence and infraorbital region.

a pedicled bone graft from the inferior border of the mandible is used. Cancellous grafts generally can be condensed into maxillary defects and are self-retained. Block grafts or only grafts should be secured with a screw(s) to promote healing, reduce resorption, and reduce the risk of infection.

Stabilizing the operated maxilla The development of more rigid fixation devices permits improvement of the results of cleft skeletal surgery. Originally stainless steel plates and screws and then titanium alloy systems were used instead of the traditional stainless steel wires to secure the position of the maxilla. The many benefits of using more rigid fixation include the reduced time for intermaxillary fixation and better assurance of the position of the midface during healing [12]. Improved long-term stability results from bone plates and screws, although a true comparison study has not been published [15,32,33]. Long-term stability can be improved by understanding the biologic constraints of facial skeletal surgery and by adhering to the principles of not stretching the major muscles of mastication as a result of displacing the facial skeleton. A single disadvantage of the use of metallic bone plates and screws is the reduced ability to manipulate toothbearing segments with elastic traction during the postoperative period. Polymer engineers are credited with developing the next potential improvement in cleft surgery. Biodegradable bone plates and screws are currently available for use in the midface and mandible. Each product is formulated and manufactured differently,

500

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

Fig. 14. The surgery performed was maxillary advancement, mandibular set back and augmentation genioplasty, and bone grafts to contour the cheeks and maxilla. The genioplasty was performed to improve the balance.

and care must be exercised when choosing a system for use in cleft patients. Strength, degradation, inflammatory response, purity of the manufacturing process, and ease of use must be considered. The authors’ experience has been with a self-reinforced polylactate system that has acceptable characteristics and high patient appeal. Short-term results have been promising [34].

Velopharyngeal considerations One of the complexities of the cleft palate is the function of the velopharyngeal sphincter. Under normal circumstances, sealing the nasal cavity from the oral cavity occurs by simultaneous elevation of the soft palate and contraction of the lateral pharyngeal walls and associated musculature to produce a sphincter,

Fig. 15. (A,B) The postsurgical panorex and cephalometric radiographs.

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

501

Fig. 16. Facial views at age 15.

Fig. 17. Facial views at age 15.

which separates the nasal and oral cavities [35]. In many patients with repaired cleft lip and palate, the apparatus is altered and the patient has learned to overcome a short or scarred palate that does not move well by recruiting extra efforts from adjacent structures. Passavant’s ridge (hypertrophy of tissue in the posterior pharyngeal wall) is an example of a compensatory effort that many cleft patients have developed to overcome the insufficiency of velar movement and stretch. Some patients develop compensatory reserve to overcome the change in position of the soft palate that results from maxillary advancement. A few cleft patients are not able to tolerate even small degrees of maxillary displacement, and the velopharyngeal function may deteriorate [36,37]. This

potential cannot be overlooked and patients should be counseled appropriately. A complete speech evaluation by an experienced speech pathologist who is familiar with cleft palate speech is necessary before advancement of the maxilla. Almost all cleft patients have some element of hypernasality immediately after surgery. Among the patients who develop significant hypernasality after maxillary advancement, however, the number of persons who require surgical correction with a pharyngeal flap or sphincteroplasty is low. Fortunately, resolution gradually occurs with time so that, for most patients, returning to baseline speech by 6 months after surgery is typical. Delaying subsequent pharyngeal surgery to reduce nasality for at least 6 months

502

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

Fig. 18. Oral views at age 18 demonstrating cuspid substitutions for lateral incisors and no need for prosthetic management.

after maxillary advancement is advisable. This delay allows natural compensation to occur and permits bone healing to proceed without introducing more scarring, which may contribute to relapse. In some patients with pharyngeal flaps in place who did not have velopharyngeal adequacy before midface advancement, reduced nasality was noted after surgery. Although sibilant distortions and articulation errors secondary to malocclusion are expected to improve, reduction of hypernasality after maxillary advancement is a paradox. This observation is

Fig. 19. Oral views at age 18 demonstrating cuspid substitutions for lateral incisors and no need for prosthetic management.

Fig. 20. Demonstration of good stability and maintenance of the result. No lip or nasal revisions have been performed.

explained by the altered dynamics of the sphincter that result after surgery. Stretching the flap and its positional change apparently improves the dynamics of the velopharyngeal mechanism enough so that improved speech occurs in some patients. This observation is not predictable and patients must be cautioned appropriately. When a pharyngeal flap is in place and maxillary advancement is undertaken, the flap should be removed only if it does not permit adequate mobilization of the maxilla. When the flap is in place, nasal intubation can be difficult, and the anesthesiologist must be prepared to use endoscopic assistance with endotracheal tube insertion [38]. The usefulness of distraction osteogenesis in cleft habilitation cannot be overlooked but is beyond the scope of this article [39 – 47]. The preciseness and predictability of orthognathic surgery, combined with low morbidity, reduced treatment time, and immediate changes, make it attractive when considering alternative methods of advancing the cleft skeleton, such as distraction osteogenesis. Although proponents of distraction osteogenesis suggest minimal surgical intervention and morbidity, there is mounting evidence to the contrary [46,47]. Its efficacy in the management of the cleft facial skeleton and its indications for use should be studied further by prospective randomized clinical trials. Two case reports (Figs. 4 – 29) exemplify the role of maxillary advancement in cleft habilitation.

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

503

Fig. 21. The 16-year-old patient with a bilateral cleft lip and palate previously had undergone bone grafting to the maxilla bilaterally. Notice the deficient projection of the entire middle face, especially the paranasal regions. Also notice the relatively protrusive lower lip.

Fig. 22. The 16-year-old patient with a bilateral cleft lip and palate previously had undergone bone grafting to the maxilla bilaterally. Notice the deficient projection of the entire middle face, especially the paranasal regions. Also notice the relatively protrusive lower lip.

Fig. 23. Orthodontic preparation included advancing the cuspid on the left adjacent to the central. Attempts to open space on the right for a prosthetic lateral incisor are in progress.

Fig. 24. Orthodontic preparation included advancing the cuspid on the left adjacent to the central. Attempts to open space on the right for a prosthetic lateral incisor are in progress.

504

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

Fig. 25. The right posterior maxilla was mobilized independently and an ostectomy at the right lateral incisor space was performed. The posterior segment was advanced a greater distance than the left, so the cuspid was placed adjacent to the central incisor. It is desirable to eliminate prosthetic treatment when possible. Feasibility model surgery demonstrated that closure of the lateral incisor space on the right could be performed without compromise. The major advantages of doing this were eliminating prosthetic needs and improving occlusal symmetry.

Fig. 26. The segments were stabilized with bone plates.

Fig. 27. Inlay and onlay cranial bone grafts were placed to facilitate bone consolidation and contouring of the midface.

Fig. 28. (A,B) Improved skeletal support permitted soft tissue and nasal revisions 9 months after maxillary advancement and bone grafting.

506

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

Fig. 29. Final occlusion without the need for prosthetic care.

References [1] Sulik KK. Craniofacial development. In: Turvey TA, Vig KL, Fonseca RJ, editors. Facial clefts and craniosynostosis: principles and management. Philadelphia: WB Saunders; 1996. [2] Semb G, Shaw WC. Facial growth in orafacial clefting disorders. In: Turvey TA, Vig KL, Fonseca RJ, editors. Facial clefts and craniosynostosis: principles and management. Philadelphia: WB Saunders; 1996. [3] Schendel SA, Tessier P, Tulasane JF. Facial clefting disorders and craniosynostosis considerations. In: Turvey TA, Vig KL, Fonseca RJ, editors. Facial clefts and craniosynostosis: principles and management. Philadelphia: WB Saunders; 1996. [4] Ross RB. Treatment variables affecting facial growth in complete unilateral cleft lip and palate: VII. An overview of treatment and facial growth. Cleft Palate J 1987;24:33. [5] Rehrmann AH, Koberg WH, Koch H. Long-term postoperative results of primary and secondary bone grafting in complete clefts of the lip and palate. Cleft Palate J 1970;7:206. [6] Rehrmann AH. The effects of early bone grafting on growth of the upper jaw in cleft lip and palate in children: a computer evaluation. Minerva Chir 1971; 26:874. [7] Copeland M. The effect of very early palatal repair on speech. Br J Plast Surg 1990;43:676. [8] Jolleys A. A review of the results of operations on cleft palates with reference to maxillary growth and speech function. Br J Plast Surg 1954;7:229. [9] Turvey TA, Vig KW, Hoke J, Moriarty J, et al. Delayed bone grafting in the cleft maxilla and palate: a retrospective multidisciplinary analysis. Am J Orthod Dentofacial Orthop 1984;86:243 – 56. [10] Fonseca RJ, Turvey TA, Wolford LM. Orthognathic surgery in the cleft patient. In: Fonseca RJ, Baker SJ, Wolford LM, editors. Oral and maxillofacial surgery. Philadelphia: WB Saunders; 2000; p. 87 – 146.

[11] Braun TW, Sotereanos GC. Orthognathic and secondary cleft reconstruction of adolescent patients with cleft palate. J Oral Surg 1980;38:425. [12] Drommer R, Luhr HG. The stabilization of osteotomized maxillary segments with Luhr miniplates in secondary cleft surgery. J Maxillofac Surg 1981;9:166. [13] Poole MD, Robinson PP, Nunn ME. Maxillary advancement in cleft lip and palate patients: a modification of the LeFort I osteotomy and preliminary results. J Maxillofac Surg 1986;14:123. [14] Stoelinga PJ, Haers PE, Lennen RJ, et al. Late management of secondary grafted clefts. Int J Oral Maxillofac Surg 1990;19:97. [15] Eskenazi LB, Schendel SA. An analysis of LeFort I maxillary advancement in cleft lip and palate patients. Plast Reconstr Surg 1992;90:779. [16] Tideman H, Stoelinga P, Gallia L. LeFort I advancement with segmental palatal osteotomies in patients with cleft palates. J Oral Surg 1980;38:196. [17] West RA. Orthognathic surgery: an adjunct for correcting secondary cleft deformities. Oral Maxillofac Surg Clin N Am 1991;3:641. [18] Westbrook Jr MT, West RA, McNeill RW. Simultaneous maxillary advancement and closure of bilateral alveolar clefts and oronasal fistulas. J Oral Maxillofac Surg 1983;41:257. [19] Posnick JC. The staging of cleft lip and palate reconstruction: infancy through adolescence. In: Craniofacial and maxillofacial surgery in children and young adults. Philadelphia: WB Saunders; 2000; p. 785 – 826. [20] Posnick JC. Cleft lip and palate: bone grafting and management of residual oro-nasal fistula. In: Craniofacial and maxillofacial surgery in children and young adults. Philadelphia: WB Saunders; 2000; p. 827 – 59. [21] Posnick JC. Cleft-orthognathic surgery: the unilateral cleft lip and palate deformity. In: Craniofacial and maxillofacial surgery in children and young adults. Philadelphia: WB Saunders; 2000; p. 860 – 907. [22] Posnick JC. Cleft-orthognathic surgery: the bilateral cleft lip and palate deformity. In: Craniofacial and

T.A. Turvey et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 491–507

[23]

[24]

[25]

[26]

[27]

[28]

[29]

[30]

[31]

[32]

[33]

[34]

maxillofacial surgery in children and young adults. Philadelphia: WB Saunders; 2000; p. 908 – 50. Posnick JC. Cleft-orthognathic surgery: the isolated cleft palate deformity. In: Craniofacial and maxillofacial surgery in children and young adults. WB Saunders; 2000; p. 951 – 78. Posnick JC, Tompson B. Cleft-orthognathic surgery: complications and long-term results. Plast Reconstr Surg 1995;96:255 – 66. Wolford LM, Cooper RL. Orthognathic surgery in the growing cleft patient and its effect on growth [abstract]. Presented at the American Association of Oral and Maxillofacial Surgeons Annual Scientific Sessions. Anaheim, CA, September 1987. Wolford LM, Cooper RL, El Deeb M. Orthognathic surgery in the young cleft patient and the effect on growth [abstract]. Presented at the American Cleft Palate-Craniofacial Association Annual Meeting. St. Louis, May 1990. Wolford LM, Cottrell DA. End-stage reconstruction in the complex cleft lip/palate patient. In: Turvey TA, Vig KL, Fonseca RJ, editors. Facial clefts and craniosynostosis: principles and management. Philadelphia: WB Saunders; 1996; p. 504 – 96. Turvey TA, Vig KW, Fonseca RJ. Maxillary advancement and contouring in the presence of cleft lip and palate. In: Facial clefts and craniosynostosis: principles and management. Philadelphia: WB Saunders; 1996. Broder HL. Psychosocial considerations in habilitation of patients with facial deformity: a developmental perspective. In: Turvey TA, Vig KL, Fonseca RJ, editors. Facial clefts and craniosynostosis: principles and management. Philadelphia: WB Saunders; 1996; p. 143 – 52. Lo LJ, Hung KF, Chen YR. Blindness as a complication of LeFort I osteotomy for maxillary disimpaction. Plast Reconstr Surg 2002;109:688 – 98. DeZutter A, Deconinck H, Rodesch G, et al. Neuroophthalmic complication after maxillary surgery. Bulletin de la Societe Belge d Ophthalmologie 1999;271: 39 – 42. Posnick JC, Dagys AP. Skeletal stability and relapse patterns after LeFort I osteotomy fixed with miniplates: the unilateral cleft lip and palate deformity. Plast Reconstr Surg 1994;94:924. Posnick JC, Taylor M. Skeletal stability and relapse patterns after LeFort I osteotomy using miniplate fixation in patients with isolated cleft palate. Plast Reconstr Surg 1994;94:51 – 8. Turvey TA, Bell RB, Tejera TJ, Proffit WR. The use of self-reinforced biodegradable bone plates and screws in orthognathic surgery. J Oral Maxillofac Surg 2002; 60:59 – 65.

507

[35] Mason R, Turvey TA, Warren DW. Speech considerations with maxillary advancement procedures. J Oral Surg 1980;38:752 – 8. [36] Watzke I, Turvey TA, Warren DW, Dalston R. Alterations in velopharyngeal function after maxillary advancement in cleft palate patients. J Oral Maxillofac Surg 1990;48:685 – 9. [37] Hung KF, Chen PKT, Lo LJ, Yun C, Wang R. Alteration of the velopharyngeal functions after rigid midface distraction [abstract]. Presented at the International Society of Craniofacial Surgery 8th International Congress. Taipei, Taiwan, November 1999. [38] Kopp VJ, Rosenfield MH, Turvey TA. Nasotracheal intubation in the presence of a pharyngeal flap. J Anesthesiol 1995;82:1063 – 4. [39] Cohen SR, Rutrick RE, Burstein FD. Distraction osteogenesis of the human craniofacial skeleton: initial experience with a new distraction system. J Craniofac Surg 1995;6:368. [40] Cohen SR, Burstein FD, Stewart MB, Rathburn MA. Maxillary-midface distraction in children with cleft lip and palate: a preliminary report. Plast Reconstr Surg 1997;99:1421. [41] Polley JW, Figueroa AA. Rigid external distraction: its application in cleft maxillary deformities. Plast Reconstr Surg 1998;102:289 – 311. [42] Polley JW, Figueroa AA, Charbel FT, et al. Monoblock craniomaxillofacial distraction osteogenesis in a newborn with severe craniofacial synostosis: a preliminary report. J Craniofac Surg 1995;6:421. [43] Figueroa AA, Polley JW. Management of severe cleft maxillary deficiency with distraction osteogenesis: procedure and results. Am J Orthod Dentofacial Orthop 1999;115:1 – 12. [44] Polley JW, Figueroa AA, Hohlastos MS. Management of secondary orofacial cleft deformities. In: Goldwyn RM, Cohen MN, editors. The unfavorable result in plastic surgery: avoidance and treatment. 3rd edition. Philadelphia: Lippincott Williams & Wilkins; 2000. [45] Chen PKT, Liou EJW, Hung KF, Huang CS, Chen YR. Lengthening of hypoplastic maxilla in cleft patients using interdental distraction osteogenesis and rapid orthodontic tooth movement. Presented at the International Society of Craniofacial Surgery 8th International Congress. Taipei, Taiwan, November 1999. [46] Costello BJ, Bowman CJ, Stanton DC, Silverstein KE. Distraction osteogenesis for the reconstruction of traumatic defects. J Craniomaxillofac Trauma 2000; 6:47 – 52. [47] Rieger J, Jackson IT, Topf JS, Audet B. Traumatic cranial injury sustained from a fall on the rigid external distraction device. J Craniofac Surg 2001;12:237 – 41.

Oral Maxillofacial Surg Clin N Am 14 (2002) 509 – 523

Intraoral bone transport in clefting Cesar A. Guerrero, DDS Santa Rosa Oral and Maxillofacial Surgery Center, Centro Integral Santa Rosa #105, Caracas 1061, Venezuela

Distraction osteogenesis is a surgical technique based on the principle of ‘‘tension-stress’’ that allows bone and soft tissue lengthening through a progressively controlled fracture separation [1,2]. Since its introduction in the field of oral and maxillofacial surgery [3 – 12], the research has been oriented to decreasing the surgical insult by better instrumentation, miniaturizing the distraction devices, developing multidirectional distractors, and using the intraoral route to avoid facial scars and social inconvenience [13 – 19]. All new technology requires a time of introduction during which surgeons cautiously await refinements, improved instrumentation, variation on surgical techniques, and, most importantly, well-analyzed postoperative data. The latest research on biology and biomechanics has been oriented to speeding up the healing process by means of finding ideal surgical management and the use of products (eg, bone morphogenetic proteins, platelet-rich plasma, and particulate bone grafts) that might help the healing process. In terms of biomechanics, smaller but stronger intraoral distractors have been developed, unidirectional, bidirectional, and multidirectional vector appliances are on the market, and some of the devices could be changed easily from one direction to a corrected one as the occlusion requires. All the recent efforts in distractor development and design have been designed to return patients to regular activities 2 to 3 weeks after surgery on a soft to regular diet and without being cosmetically impaired (Figs. 1 – 19). In cleft patients, distraction osteogenesis can play a role in certain deficiency situations with high failure rate, as in bone grafting in adult alveolar clefts. Alveolar clefts in untreated patients after the age of 8 to 11 years are difficult to treat. The teeth next to

E-mail address: [email protected]

the cleft are partially erupted and are often poorly aligned in the alveolus, which limits the possibility to place a bone graft successfully and adequately create a watertight buccal, palatine, and nasal surfaces closure. The saliva and bacteria could contaminate the graft through the periodontal ligament or through the wound, which produces partial or total graft failure. The indications for alveolar reconstruction are maxillary discontinuity, lack of adequate alveolar bone, oronasal fistulas, lack of nasal base support, unstable orthodontic treatment, and unpleasant gingival contour when smiling. The possibility of using distraction osteogenesis to treat alveolar clefts after the age of 13 years seems attractive to avoid all the complications related to bone grafts or the use of fixed prostheses. Two publications open the door to this new field of distraction osteogenesis [20,21]. Currently, surgeons, orthodontists, periodontists, and prosthodontists are working to define the precise indications of distraction osteogenesis over traditional surgery. When and how to obtain the maximum benefit from existing distraction techniques, the long-term stability, and predictability and quantifying the need for overcorrection is being investigated. Several scientific articles already have been written on the healing variables that may alter the final clinical outcome, most common complications, and their management [22 – 28].

Intraoral bone transport The pioneering work of Costantino et al [29] demonstrated the possibility of reconstructing the mandible in dogs and in humans based on the surgical principles of Ilizarov. An osteotomy is performed in a nontreated area, and a bony segment is transported through soft tissue guided by a distraction device

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 5 2 - 3

510

C.A. Guerrero / Oral Maxillofacial Surg Clin N Am 14 (2002) 509–523

Fig. 1. (A) Preoperative frontal view of a 12-year-old boy with left alveolar cleft. (B) Intraoral frontal view.

until there is an abutment between the transported bone or disc to the docking site (bone host), which creates bone continuity by the distraction healing process. Other researchers [30,31] used different extraoral devices to repeat the mandibular reconstruction obtained by Costantino. A major step forward

was to obtain similar clinical results with the use of internal distractors [32,33]. Some clinical situations proved difficult to manage, however. Because of the shape of the mandible, it was difficult to achieve the width and height that were needed in the reconstruction for dental implant placement in long segment

Fig. 2. (A,B) Diagrams show the alveolar defect and the treatment planning by intraoral bone transport.

C.A. Guerrero / Oral Maxillofacial Surg Clin N Am 14 (2002) 509–523

511

Fig. 3. (A,B) The alveolar defect and the segmental osteotomy design to perform the alveolar bone transport for reconstruction.

reconstruction. It was also understood that the distraction osteogenesis process happens from the point of origin to the point of destination. When the disc was transported along a curve, the collagen fibers within the distraction site that eventually would mineralize always followed a straight line pattern.

Another important issue was the reconstruction of long defects. Ilizarov confronted this situation in the treatment of the limbs. Because the bone segments travel a long way, the patients and animal research subjects showed a contraction of the periosteum that eventually would form thinner bone, which creates a

Fig. 4. (A) A small vertical incision is made deep in the sulcus to osteotomize the transport disk. The bone cut starts with a 701 bur in the cortical bone above and high between the dental roots under abundant irrigation. (B) A spatula osteotome is used through the small incision to complete the osteotomy. (C) Left maxillary segment repositioning with orthognathic surgery and rigid fixation to close the open bite. (D) Intraoral distractor placement after the osteotomies are completed and wounds are closed. Note the superior arms fixed with bicortical screws to gain bone anchorage and the inferior arms interdentally attached with the use of wires and acrylic.

512

C.A. Guerrero / Oral Maxillofacial Surg Clin N Am 14 (2002) 509–523

required, and as an alternative for high surgical costs and long hospitalizations.

Surgical technique in the cleft patient

Fig. 5. After a 7-day latency period the appliance is activated 1 mm per day until the desired movement is achieved. Acrylic is placed on top of the device to resume regular diet.

problem called hourglass deformity. This would be the weakest point in the healed bone. A possible remedy for larger segments or a way to go around a curve is to create two discs that come into the midline using the same surgical principles of distraction. This procedure is called bifocal or trifocal bone transport according to the clinical situation, and it was possible to use two different distraction vectors to obtain a particular bone shape as needed. The intraoral bone transport technique has been used to treat patients after gunshot wounds, benign and malignant tumor removal, osteomyelitis, and malunion. It is indicated as the first surgical alternative in patients with a poor prognosis or reinterventions, for medically compromised individuals when minimal surgery and no bone grafts are

Patients should undergo orthodontic treatment when teeth are aligned and leveled in segments and rectangular arch wires are placed. The mechanics are not oriented to move the anterior teeth into the alveolar cleft if the root is exposed to the cleft because saliva and bacteria infiltrate, which causes chronic periodontal disease and a poor environment for grafting. A surgeon’s biggest challenge is to adequately create a three-dimensional soft tissue envelope to locate the grafting material properly. Even if this goal is achieved with delicate and meticulous surgery, saliva and bacteria contaminate the graft through the periodontal ligament. Using bone transport, the surgeon can decrease the size of the recipient site and enlarge the soft tissues around the site. The metabolic activity of the distraction process also augments the local blood supply, stem cells, and nutrients. A small incision at the depth of the vestibule is made through the mucosa, muscles, and periosteum. The soft tissues are carefully elevated and small retractors are used to expose the bone adequately. An interdental osteotomy is performed under abundant irrigation. Bone overheating should be avoided at all times. The bony segment is completely separated with the use of a spatula osteotome. The surgical wound is closed carefully. The periosteal layer, which is responsible for most of the bone

Fig. 6. (A,B) Docking site surgery. Once the distraction disk has reached the objective area, the epithelium between the bone surfaces is removed. A 701 bur is used to drill holes and make the bone bleed, cancellous autologous bone grafts are obtained either from the chin or the tuberosity, and the grafts are placed over the docking area. Finally, a posterior sliding flap is elevated and advanced and a water-tight closure is performed.

C.A. Guerrero / Oral Maxillofacial Surg Clin N Am 14 (2002) 509–523

513

Fig. 7. (A – C) An occlusal view shows a severe bone discontinuity on the left side and its alveolar reconstruction after bone transport. A palatal splint was used to maintain the orthognathic surgery on the left segment. A plastic pontic is placed over the distraction area awaiting the mineralization for implant positioning. The palatal fistula was closed using a lateral palatal flap during the docking site surgery.

healing process, must be reunited meticulously. A miniaturized distraction device is used to separate the osteodental segment from its original position progressively, which decreases the size of the alveolar cleft because the distractor is activated. The device must be attached firmly to the bone disc and to the

Fig. 8. Dental photograph shows the alveolar reconstruction using bone transport.

maxilla. Too much motion between the fragments results in the development of fibrous and cartilaginous tissue. Minimal micromotion is obtained by cutting the distractor arms to the smallest size possible. The device is fixed to the basal bone with long screws, and at the tooth level interdental wires covered with dental resin or acrylic for rigidity are used. The wiring avoids any damage to the dental structures by screws. A latency period of 7 days is enacted before activation begins at 0.5 mm twice a day. Activation is continued until the mucosa of the two fragments meets. When the disc or bullet arrives at the target area, the patient is scheduled for the second stage surgery. Once the two segments are together a second surgery, called ‘‘the docking site surgery,’’ is needed. In the orthopedic literature there are reports about activating the appliance after the disc or bullet has approached the docking site to create a fusion between the two segments. The fragments in the maxilla are so small, however, that they cannot fuse. Because of this inability, the following steps are taken: removing the epithelium between the two bone

514

C.A. Guerrero / Oral Maxillofacial Surg Clin N Am 14 (2002) 509–523

Fig. 9. (A – C) Panoramic radiographs show the defect, the appliance positioning, and appearance 12 days after activation.

fragments, preparing the two borders by removing the cartilage-like tissue that develops as the disc travels through the softer tissues, perforating the bony edges with a 701 bur to produce internal bleeding, and obtaining bone graft either from the chin or tuberosity areas, which is placed over the joining bones. After the cartilage-like tissue is removed, a space is created, usually between 4 and 6 mm. The distractor should be activated to consolidate bone fragments together by an immediate movement and not the usual 1 mm a day. An alternative possibility could be the use of one or two lighter plates. Different soft tissue designs can be used to cover the docking site area properly, especially after the placement of intraoral bone grafts. Advancing, sliding, or three-dimensional flaps could be used. Improper management of this surgical stage ends in malunion, fibrous union, or bone segment dislocation, which happens if the docking site is wide or if the bone graft is contaminated with saliva and bone resorption occurs. Clinical judgment is needed to determine the best approach for the particular reconstruction and choose from the different ways to consolidate the two bony fragments. The distraction process ends once the mineralization process is completed, usually 10 to 12 months after surgery.

Important variables that may modify the surgical outcome include age of the patient, amount of movement, quality and quantity of bone, surgical technique (clean cuts under abundant irrigation), and adequate wound closure without gaps that allows postoperative contamination of saliva and food. The presence of an infection in the distraction site partially or completely stops the healing process and creates a situation that ranges from a nonunion to partial mineralization. These clinical situations are accompanied by correspondent radiologic findings, which were reported by Samchukov. Although the oral cavity is well vascularized and infections are rarely seen after distraction osteogenesis, the surgical principles must be kept in mind to avoid surgical complications.

Summary The advantages of this technique over the traditional alveolar reconstruction are as follows: no need for bone grafts, which involve a donor site, minimal surgical time, no hospitalization, progressive improvement with excellent psychological adaptation, bone height and width that are similar to the neighboring alveolus with excellent possibilities for

C.A. Guerrero / Oral Maxillofacial Surg Clin N Am 14 (2002) 509–523

515

Fig. 10. (A) Frontal view of a 25-year-old woman with bilateral alveolar cleft after premaxillectomy. (B) Intraoral frontal view shows the discontinuity defect in the anterior maxilla. (C,D) Preoperative dental lateral views. (E) Preoperative occlusal view shows the alveolar defect and the oronasal communication.

dental implants, and a natural reconstruction that aids the orthodontist with final tooth movement. Finally, the morbidity is minimal. The disadvantages are few; long treatment requires patient cooperation and close follow-up. Implant placement ideally should happen 6 to 8 months after the initial surgery. A crestal incision is made to expose the newly developed alveolar bone, and a fixture of adequate size and length is inserted. If

further bone augmentation is needed on the buccal side of the alveolus, the bone collected from the suction tramp may be mixed with alloplastic materials and layered over. A collagen membrane also may be used. The alternatives of taking grafts from the chin or tuberosity also may be considered. There is still the chance to augment the soft tissues at the uncovering stage by various surgical techniques to obtain an ideal alveolar ridge.

516

C.A. Guerrero / Oral Maxillofacial Surg Clin N Am 14 (2002) 509–523

Fig. 11. Diagram shows the treatment planning to reconstruct the anterior maxilla by intraoral bone transport.

Fig. 12. (A) A reconstruction plate is countered and fixed to teeth using interdental wires and acrylic to serve as a guide in the bone transport movement reconstructing the maxillar normal shape. (B) A small incision is made and a osteotomy of the transport disk is performed in both sides of the alveolar discontinuity defect. (C) After water-tight closure, the intraoral devices are placed over the reconstruction plate using transmucosal 2-mm screws and interdental wires.

C.A. Guerrero / Oral Maxillofacial Surg Clin N Am 14 (2002) 509–523

517

Fig. 13. (A – C) After the distraction surgery is accomplished, a 7-day latency period follows and the activation period starts at a 1-mm per day rate until the reconstruction of the continuity defect is achieved. (D) Occlusal view in the activation period. Observe that the nasal communication no longer exists.

518

C.A. Guerrero / Oral Maxillofacial Surg Clin N Am 14 (2002) 509–523

Fig. 14. (A – E) Clinical follow-up of the reconstruction process in the right side of the alveolar defect. Preoperative, after distractor removal, implant placement, abutment preparation, and temporary prosthesis views demonstrate the real maxillary reconstruction obtained with this technique.

C.A. Guerrero / Oral Maxillofacial Surg Clin N Am 14 (2002) 509–523

519

Fig. 15. (A – E) Clinical sequence on the left side. Observe the new tissues created for implant placement and further reconstruction with provisional prosthesis over implants.

520

C.A. Guerrero / Oral Maxillofacial Surg Clin N Am 14 (2002) 509–523

Fig. 16. (A,B) Note the important changes in the dental frontal view. The anteroposterior deficiency was corrected with the forward projection of the bone segments.

Fig. 17. (A – D) Occlusal view of the reconstruction stages when using bone transport by distraction osteogenesis.

C.A. Guerrero / Oral Maxillofacial Surg Clin N Am 14 (2002) 509–523

521

Fig. 18. (A – E) To correct the alveolar defect, a transport disk was design bilaterally taking two teeth in either side. A trifocal bone transport was performed to create new bone that would serve as the implant’s host. Observe how the distraction site has ossified.

522

C.A. Guerrero / Oral Maxillofacial Surg Clin N Am 14 (2002) 509–523

Fig. 19. (A,B) Profile views before and after distraction osteogenesis was accomplished.

References [1] Ilizarov GA. The tension-stress effect on the genesis and growth of tissues. In: Ilizarov GA, editor. Transosseous osteosynthesis. Berlin: Springer-Verlag; 1992. p. 137 – 255. [2] Wagner H. Operative lengthening of the femur. Clin Orthop Rel Res 1978;136:125 – 42. [3] Bell WH, Epker BN. Surgical orthodontic expansion of the maxilla. Am J Orthod 1976;70:517 – 8. [4] Guerrero C. Expansio´n mandibular quiru´rgica. Rev Venez Ortod 1990;48:48 – 50. [5] McCarthy JG, Schreiber J, Karp N, Thorne CH, Grayson BH. Lengthening the human mandible by gradual distraction. Plast Reconstr Surg 1992;89:1 – 10. [6] Molina F, Ortiz Monasterio F. Mandibular elongation and remodeling by distraction: a farewell to major osteotomies. Plast Reconstr Surg 1995;96:825 – 40. [7] Wangerin K, Gropp H. Intraoral distraction osteogenesis for lengthening of the horizontal mandibular ramus. International Congress on Cranial and Facial Bone Distraction Processes 1997; paper #36. [8] Diner PA, Kollar EM, Viguier E, Maurin N, Vazquez MP. Intraoral submerged bidirectional device for man-

[9]

[10]

[11]

[12]

[13]

[14]

[15]

dibular distraction. In: Diner PA, Vazquez MP, editors. International Congress on Cranial and Facial Bone Distraction Processes. Paris: Monduzzi; 1997. p. 67 – 74. Walker D, Nish I. Multi-directional buried mandibular distraction osteogenesis appliances and techniques. J Craniofac Surg 1998;26:205. Karaharju-Suvanto T, Peltonen J, Kahri A, et al. Distraction osteogenesis of the mandible: an experimental study on sheep. J Oral Maxillofac Surg 1992;21: 118 – 21. Guerrero CA, Flores A, Bell WH. Intraoral mandibular distraction osteogenesis. J Oral Maxillofac Surg 1994; 52(Suppl):115 – 6. Block MS, Brister GK. Use of distraction osteogenesis for maxillary advancement: preliminary results. J Oral Maxillofac Surg 1992;52:282 – 91. Hoffmeister B, Wangerin K. Callus distraction technique by an intraoral approach: the floating bone concept. Int J Oral Maxillofac Surg 1997;26(Suppl 1):76. Cohen SR, Rutrick RE, Burstein FD. Distraction osteogenesis of the human craniofacial skeleton: initial experience with a new distraction system. J Craniofac Surg 1995;6:368 – 74. Chin M, Toth BA. Distraction osteogenesis in maxil-

C.A. Guerrero / Oral Maxillofacial Surg Clin N Am 14 (2002) 509–523

[16]

[17]

[18]

[19]

[20]

[21]

[22]

[23]

[24]

[25]

lofacial surgery using internal devices: report of five cases. J Oral Maxillofac Surg 1996;54:45 – 53. Samchucov ML, Cherkashin AM, Cope JB. Distraction osteogenesis: history and biologic basis of new bone formation. In: Lynch SE, Genco RJ, Marx RE, editors. Tissue engineering: applications in maxillofacial surgery and periodontics. Quintessence: Carol Springs, IL; 1999;131 – 46. Cope J, Samchukov ML, Cherkashin AM, Wolford LM, Franco PF. Biomechanics of mandibular distractor orientation: an animal model analysis. J Oral Maxillofac Surg 1999;57:952 – 62. Bell WH, Gonzalez M, Samchukov ML, Guerrero CA. Intraoral widening and lengthening of the mandible in baboons by distraction osteogenesis. J Oral Maxillofac Surg 1999;57:548 – 62. Oda T, Sawaki Y, Ueda M. Experimental alveolar ridge augmentation by distraction osteogenesis using a simple device that permits secondary implant placement. Int J Oral Maxillofac Surg 2000;15:95 – 102. Guerrero CA, Bell WH, Meza LS. Intraoral distraction osteogenesis: maxillary and mandibular lengthening. Atlas Oral Maxillofac Surg Clin North Am 1999;7: 111 – 51. Liou EJW, Chen PKT, Huang C, Chen YR. Interdental distraction osteogenesis and rapid orthodontic tooth movement: a novel approach to approximate a wide alveolar cleft or bony defect. Plast Reconstr Surg 2000;4:1262 – 72. Guerrero CA, Contasti GI. Transverse mandibular deficiency. In: Bell WH, editor. Modern practice in orthognathic and reconstructive surgery. Philadelphia: WB Saunders; 1992. p. 2383 – 97. Epker BN. Distraction osteogenesis for mandibular widening. Atlas Oral Maxillofac Surg Clin N Am 1999;7:29 – 39. Perrott DH, Berger R, Vargervik K, Kaban LB. Use of a skeletal distraction device to widen the mandible: a case report. J Oral Maxillofac Surg 1993;51:435 – 8. Guerrero CA, Bell WH. Intraoral distraction. In: McCarthy JG, editor. Distraction of the craniofacial skeleton. New York: Springer-Verlag; 1999. p. 219 – 48.

523

[26] Contasti GI, Rodriguez AM, Guerrero CA. Orthodontics in intraoral mandibular distraction osteogenesis. In: Samchucov ML, Cope JB, Cherkashin AM, editors. Craniofacial distraction osteogenesis. St. Louis: CV Mosby; 2001. p. 149 – 55. [27] Ueda M. Maxillofacial bone distraction processes using osseointegrated implants and an intraoral device. In: Diner PA, Vasquez MP, editors. International Congress on Cranial and Facial Bone Distraction Processes. Paris: Monduzzi; 1997. p. 75 – 84. [28] Guerrero CA, Gonzalez M, Laplana R, Rojas A. Reconstrucß a˜o do rebordo alveolar mediante distracß a˜o ostogeˆnica para implantes osseointegrados. In: Dinato JC, Polido W, editors. Implantes osseeointegrados: cirugia e pro´ tese. Sao Paolo, Brazil: Artes Me` dicas; 2001. p. 423 – 39. [29] Costantino PD, Shybut G, Friedman CD, et al. Segmental mandibular regeneration by distraction osteogenesis: an experimental study. Arch Otolaryngol Head Neck Surg 1990;116:535 – 45. [30] Fedotov SN. Dosed distraction of the mandible fragments by extra-mouth apparatus in patients with bone defect and mandible fractures. In: Diner PA, Vasquez MP, editors. International Congress on Cranial and Facial Bone Distraction Processes. Paris: Monduzzi; 1997. p. 155 – 60. [31] Klein C. Craniofacial distraction osteogenesis using the ‘‘Frankfurt Craniofacial Distraction Systems.’’ In: Diner PA, Vasquez MP, editors. International Congress on Cranial and Facial Bone Distraction Processes. Paris: Monduzzi; 1997. p. 345 – 51. [32] Guerrero CA, Bell WH, Gonzalez M, Figueroa F. Maxillo-mandibular reconstruction by intraoral bone transport. In: Arnaud E, Diner PA, editors. International Congress on Cranial and Facial Bone Distraction Processes. Paris: Monduzzi; 2001. p. 569 – 74. [33] Guerrero C, Bell W, Gonzalez M, Meza L. Intraoral distraction osteogenesis (bone transport). In: Fonseca R, editor. Oral and maxillofacial surgery. Philadelphia: WB Saunders; 2000. p. 343 – 402.

Oral Maxillofacial Surg Clin N Am 14 (2002) 525 – 537

Secondary cleft surgery and speech E´toile M. LeBlanc, MS, CCCa,b,c,d,* a Private Practice, Speech Science Centre, 75 South Broadway, 4th Floor, White Plains, NY 10601, USA Craniofacial Speech Disorders Center, New York Presbyterian Hospital, 3959 Broadway, New York, NY 10032, USA c Babies and Children’s Hospital of New York, USA d Department of Plastic and Reconstructive Surgery, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA

b

The craniofacial-cleft surgeon searches continually for the combination of treatment regimens that secure successful aesthetics, dental-skeletal form, and speech results in patients with cleft lip and palate. Recent developments in innovative surgical procedures, such as osetodistraction, neuroradiographic and video imaging, and robotic and minimally invasive surgical technology [1], have been welcomed additions to the field. We anticipate how they may translate into cleft surgery protocols, yet we are still in pursuit of practices that will enhance speech outcomes after primary and secondary cleft surgery. Many children have successfully developed normal intelligible speech after surgical repair; however, a review of the literature represents not only what we do know but also what must be learned to ensure desired speech outcomes. The reported incidence of speech problems in cleft lip and palate after primary repair ranges from 5% to 89% depending on the criteria applied [2 – 10]. This variability in results leaves levels of confidence of effect and outcome modest at best. The literature also is replete with conflicting reports on which surgical procedures are the most effective in primary palatoplasty [11 – 13], at which age surgery provides the desired speech outcome [14 – 17], what effects maxillary advancement and distraction have on resonance [18 – 25], and which secondary pharyngoplasty procedure provides

* Speech Science Center, 75 South Broadway, 4th Floor, White Plains, NY 10601, USA E-mail address: [email protected] (E.M. LeBlanc).

the best surgical speech outcome [26 – 32]. Divergent results may lead to evolution of the field but also lends to confusion, misdirection and subsequent mismanagement of many patients. The variability in current practices and research has been marred by methodologic flaws (Table 1). In the past 10 years, from 1992 to 2002, only 13 randomized clinical trial studies were performed in clefting disorders worldwide [33]. A retrospect look at the literature reveals that researchers continue to conduct and publish research based on less than optimal scientific design and have yet to harness the multitude of variables that affect speech outcomes in clefting disorders. Acknowledging and understanding the variables that influence speech outcomes and limitations in controlling these variables have a great effect on our ability as surgeons and speech pathologists to provide better management protocols that lead to optimized speech.

Variable I. The speech matrix The processes and mechanisms that function to carry out speech are virtually multifactorial, with numerous variables directly and indirectly affecting its integrity (Table 2). Should any one determinant of the speech matrix become inoperative, other morphologic components (epigenetically determined and nondeterministic processes) have the capacity to compensate and provide obligatory responses temporally and operationally, as the demands require [34]. They can provide an alternative means in an attempt to achieve more or less the same developmental and functional result, al-

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 4 1 - 9

526

E.M. LeBlanc / Oral Maxillofacial Surg Clin N Am 14 (2002) 525–537

Table 1 Methodical flaws in research of speech outcomes in cleft lip and palate Methodologic design

Speech parameters

Surgical parameters

Lack of interexaminer and intraexaminer reliability Small number of subjects lack of randomized sampling Large propensity of retrospective studies Decreased use of matched control group studies Reliance on one-time assessment accepted Lack of consistency in subject pools Uneven subject distribution across independent variables Lack of double blind studies Limited number of randomized clinical trials

Need for operational definitions

Age of surgery

Lack of objective speech data Comparison of speech results across wide age ranges Inconsistent methods of defining VPI Lack of objective measures of velopharyngeal function Lack of consistency in preoperative and postoperative assessment tools Do not operationally define what speech criteria should be accepted Differing criteria on successful speech results

Type of surgery Age at assessment Multiple surgeons Differing surgical modifications in surgical procedure Do not operationally define criteria of acceptability Differing criteria on successful surgical results

though perhaps with some degree of anatomic and physiologic change in function. The capability to speak originates from a genomic makeup, anatomic structure, and internal and external functional demands. Facets that maintain the drive to speak include environmental and communicative needs (ie, communicative intent, social needs, expectations). Conversely, anatomic limitations and environmental facets (ie, educational services, quality of rehabilitative services, poor social esteem, lack of familial support) have the potential to discourage what level of speech integrity is possible in an individual. Speech represents the internal functional demand on the craniofacial scaffold and its soft tissue envelope. If velopharyngeal, laryngeal, palatal, maxillary, or mandibular segments are missing, unstable, or in poor anatomic relationship with one another, as typically presented in clefting, the functions of breathing, swallowing, and speaking can be impaired [35]. Understanding how speech manifests in an individual with a cleft lip and palate requires understanding the dynamic speech matrix. Speech is made up of the systems of resonance, articulation, and voice. The ‘‘potential’’ primary speech disorders associated with cleft lip and palate are hypernasality (resonance disorder), compensatory articulation disorder secondary to velopharyngeal insufficiency (VPI), and obligatory articulation or dental adaptations (articulation disorders). The underlying cause of obligatory articulation errors is related to dental and skeletal anomalies, whereas hypernasality and a compensatory articulation disorder are directly related to dysfunction of the velopharyngeal mechanism.

Each of these systems may interact with one another and many other abnormal speech processes (secondary speech disorders such as developmental articulation errors, neurologically based articulation disorders), which results in greatly compromised speech and a complicated paradigm for the craniofacial-cleft surgeon. Compensatory articulation disorder secondary to VPI is the typical articulation disorder associated with cleft palate. It involves production of sounds in an aberrant location of the vocal tract (posterior oral cavity, hypopharyngeal and supralaryngeal area). Sound production in this disorder reinforces abnormal placement and inappropriate manipulation of airflow and air pressure, which results in less-than-optimal velar and lateral pharyngeal wall movement of the velopharynx. It is possible that VPI is, in part, related and exacerbated by the presence of compensatory articulation disorders. Velopharyngeal insufficiency may be, in part, ‘‘articulatory based.’’ The child ‘‘learns’’ that velopharyngeal movement is not necessary. The use of the velopharyngeal mechanism may be avoided, although closure may be anatomically possible in these patients. The child also may use other anatomic structures to facilitate velopharyngeal closure, such as lingual, pharyngeal muscular, and epiglottic valving [36,37]. These maladaptive gestures directly affect perceived resonance quality. Phoneme-specific VPI is another example in which hypernasality is perceived and velopharyngeal dysfunction is documented; however, it is purely an articulation disorder and, if assessed correctly, can be treated successfully

E.M. LeBlanc / Oral Maxillofacial Surg Clin N Am 14 (2002) 525–537

527

Table 2 Factors affecting speech outcomes in cleft lip and palate Genetic

Anatomy/Physiology

DNA integrity Cleft type Chromosomal Severity and extent of integrity original defect Type of underlying syndrome Cognitive/IQ status Hearing status Language status Psychosocial status Velopharyngeal integrity Size of velopharyngeal gap Movement of velar/ lateral musculature Type of velophryngeal closure Etiology of insufficiency Cranial base angle Adenoid/tonsillar integrity Dental-skeletal integrity Neurologic integrity Presence of other medical issues Growth rates

Environmental

Speech

Surgical

Quality of educational services Cultural diversity Family and peer support Family and peer interaction Cultural origin Quality of rehabilitative services Presence of intermultidisciplinary team care Experience of team members Stimulating environment for development

Appropriate development Timely preventative services Articulation integrity Resonance integrity Type of articulation disorder Type of resonance disorder Neurologic integrity Hearing integrity Feeding/Voice integrity swallowing status Types of objective speech measures Age at time of assessment Quality of management History of therapeutic intervention Amount of therapeutic intervention

Age of surgery Type of procedure Experience of surgeon Integrity of preoperative assessment Presence of fistulas Success in primary palate closure Use of preorthopedic devices Use of nasal molding devices Postoperative healing and scarring Length of time between surgery and speech assessment Amount of short- and long-term follow-up Presence of postoperative complications One-stage versus two-stage procedures Primary or secondary repair Orthodontic treatment Use of nasopharyngoscopy and procedures Multiview videoflouroscopy

by speech therapy only. Marginal or touch closure of the velopharyngeal mechanism is often remediated by nonsurgical, and/or nonprosthetic management. Articulation and velopharyngeal function are inversely related, and a craniofacial speech assessment that includes at least nasopharyngoscopy is imperative to the decisions being made preoperatively and postoperatively. The act of speech requires elements from various dimensions of the matrix. Its dysfunction, compensatory nature, and rehabilitation depend highly on many factors.

Variable II. Isolated versus syndromic clefting Isolated clefting versus syndrome-related clefting is an important variable to take into account when discussing speech and surgical outcomes. The attributes of the speech disorder in isolated cleft lip and palate have the potential to differ significantly as compared to a syndrome-related cleft lip and palate [38 – 40]. The speech matrix changes in the presence of a syndrome, which depends highly on the natural

history, genotypic and phenotypic characteristics of the syndrome. For example, a child with an isolated cleft lip and palate may potentially present with varying degrees of hypernasality, varying types and degrees of severity of compensatory articulation secondary to VPI, obligatory errors, and transient compromised hearing acuity caused by otitis media. A child with Treacher Collins syndrome may potentially present with varying degrees of hyponasality accompanied by possible VPI secondary to asymmetry [31] or cleft palate, varying types and degree of severity of obligatory errors or compensatory articulation secondary to VPI, and hoarseness, pitch, and loudness problems (voice disorders) caused by laryngeal asymmetry [41]. A child diagnosed with 22q11.2 microdeletion syndrome presents with hearing, cognitive, language, and voice problems and increased use of compensatory articulation errors (as compared to isolated cleft palate). A child diagnosed with Trisomy 21 however, presents with mental retardation, upper airway issues, oral structural anomalies that affect speech in a varying manners [38], and VPI related to clefting or neurologic impairment. The surgeon

528

E.M. LeBlanc / Oral Maxillofacial Surg Clin N Am 14 (2002) 525–537

may increase the chances of appropriate speech and surgical outcome after surgery if the child’s speech profile is well delineated in a manner that determines which component of the disordered speech is directly related to the velopharyngeal mechanism, dental skeletal anomalies, neurologic impairment, learned behavior, and other nonstructural speech issues.

Variable III. The preoperative assessment The successful surgeon understands the existence of the speech matrix effect and seeks out the appropriate speech diagnostic assessment. The use of perceptual speech assessment and direct visualization of the velopharyngeal mechanism by means of nasopharyngoscopy and multiview videofluoroscopy increases the frequency of desired speech outcomes and decreases the chance of postoperative complications. Indirect instrumentation, such as nasometry and aerodynamic pressure flow studies, provides objective measures on airflow and pressure; however, on their own they provide minimal utility in diagnostic etiology and determination of abnormal physiology of the velopharyngeal structure and do not provide distinct information on management. Perceptual speech assessment should be conducted by a well-trained craniofacial speech pathologist who is able to decipher the speech matrix and provide the surgeon with vital information in the following areas: 1. The type and severity of the resonance disorder present 2. The type and severity of the articulation disorder 3. Whether therapeutic intervention is needed 4. Whether therapeutic intervention should be conducted before surgery, in combination with surgery, or after surgery 5. The anticipated speech outcome after surgery. Direct visualization of the velopharyngeal mechanism should provide the surgeon with the following information: 1. The cause of insufficiency 2. To what degree structure contributes to closure or dysfunction (ie, adenoids, tonsils, lingual valving) 3. To what degree movement of the velar, lateral pharyngeal walls, posterior pharyngeal wall, and lingual structure is present 4. To what degree the dysfunction noted is related to learned behavior

5. Which surgical procedure is appropriate for the relative dimensions in the velopharynx 6. Delineation of abnormal structure, such as carotid pulsations associated with 22q11.2 microdeletion syndrome 7. Anticipation of the affect of the intended surgical procedure on desired speech outcome. The relationship between the surgeon and the craniofacial speech pathologist is pivotal for success. The surgeon who cultivates this relationship and is willing to take a transdisciplinary role in surgical management undoubtedly increases the results of desired outcome. The craniofacial-cleft palate specialist, whether a surgeon or a speech pathologist, cannot ignore the significance and impact of a comprehensive diagnostic evaluation. Many erroneous assumptions have been made about velopharyngeal structure and function and sound production based on less than adequate diagnostic regimens, often producing less than adequate treatment outcomes. One cannot provide successful management of hypernasality without a comprehensive articulation assessment and a comprehensive assessment of the velopharyngeal mechanism, which involves at least a nasopharyngoscopy or multiview videofluoroscopic study.

Variable IV. The effects of primary palatoplasty Secondary cleft surgery encompasses a category that is wide and varied. It includes procedures to improve the appearance of the lip and nose, move and stabilize the mandible and maxilla, and improve the function of speech (Table 3). The more severe the initial cleft problem, the more likely the need for secondary or revisional surgery. The individual who needs secondary cleft surgery is affected by many more potential variables that affect desired speech outcome than the person who faces initial primary surgery (Table 4). The infant who needs a primary lip or palate repair presents to the surgeon with significantly fewer demands on the surgeon: (1) the type of unrepaired cleft lip and palate (laterality and severity), (2) status of premaxilla and anterior palate and need for presurgical molding devices, (3) possibility of contributing phenotypic characteristics of an underlying syndrome (ie, airway, cardiac, gastrointestinal anomalies), and (4) the possibility of hearing and feeding issues. The individual who faces secondary cleft surgery (1) generally is much older, (2) may present with lessthan-optimal primary surgical repair with scarring and dehiscence, (3) may present at a much later age than

E.M. LeBlanc / Oral Maxillofacial Surg Clin N Am 14 (2002) 525–537

529

Table 3 Potential speech issues after primary cleft surgery Speech symptom Clinical sign

Resonance

Articulation

Voice

Nose Severe septal deviations, Reduced nasal patency

Hyponasal, hypernasal cul de sac resonance

No known effect

No known effect

Perceived hypernasality weak contact caused by

Weak articulatory contact, adaptive changes

No known effect

Hypernasality, nasal rustling, nasal emission, grimacing, nasal regurgitation, nasal emission

Weak articulatory contact, middorsal palatal stops, lingual backing, obligatory errors

No known effect

Lip Tissue deficiency, poor differentiation from maxilla asymmetry, short upper lip, whistle tip deformity Hard palate Fistula repair

Alveolar cleft Velum Velopharyngeal dysfunction Marginal closure Learned VPI

No known effect

Hypernasality, nasal rustling, nasal emission, nasal turbulence Mild hypernasality Hypernasality, nasal rustling, nasal emission, nasal turbulence

surgically desired, (4) presents with dental occlusal and skeletal anomalies, (5) presents with the possibility of learned maladaptive speech behavior, (6) has other speech problems that may interact and influence speech disorders related to the clefting, (7) has a dysfunctional velopharyngeal mechanism or one at high risk for dysfunction, (8) may contribute phenotypic characteristics of an underlying syndrome, (9) possibly may have hearing, language, and cognitive issues, and (10) may have affected social-emotional integrity. The surgeon who performs secondary cleft procedures faces an increased number of concerns that affect surgical outcome.

Secondary procedures of the nasal deformity Primary repair of a complete or incomplete cleft lip with its associated nasal deformity presents with a potential effect on certain aspects of speech. In the unilateral cleft lip, the patency of the nasal cavity may be affected by nasal collapse, broad flaring nostrils, asymmetry, shortened columella, and a concomitant septal deviation. These anomalies affect the patency of the nasal cavity and might affect speech. Nasal

Compensatory articulation Weak articulatory contact Compensatory articulation

Hoarseness, low volume Hoarseness, low volume Hoarseness, low volume

deformities do not affect sound production or voice. Depending on the degree of nasal deformation, however, there could be an effect on resonance. The individual may present with a hyponasal, hypernasal, or cul de sac resonance quality. Nasal tip and nostril revision is possible in early childhood, although septal and bony surgery to straighten the nose totally should be postponed until full or near full growth of the facial features has occurred. Secondary surgery, such as straightening the nasal septum, is expected to have a positive effect on the elimination of hyponasality (if septal deviation and nasal deformities are the primary sources of the hyponasality perceived). Transient resonance issues, such as hyponasality, may be caused by postsurgical edema, which is expected to dissipate during the healing process.

Secondary procedures of lip deformity Major revisional procedures on the lip are not uncommon. With a wide range of procedures, repair may occur at almost any age. Secondary correction of the cleft lip unilaterally or bilaterally has minimal effect on speech sound production. Primary repair of the lip

530

E.M. LeBlanc / Oral Maxillofacial Surg Clin N Am 14 (2002) 525–537

Table 4 Potential speech issues after secondary cleft surgery Speech symptom Clinical sign

Resonance

Articulation

Voice

Lip/nose revisions

No known effect

No known effect

No known effect

Hypernasality, nasal emission, nasal regurgitation, foul odor Nasal regurgitation, foul odor

Middorsal palatal stops

No known effect

Obligatory errors

No known effect

Hypernasality, nasal emission, nasal regurgitation, hyponasality Hypernasality, nasal emission Transient hypernasality No known effect

Compensatory articulation

No known effect

Improved obligatory

No known effect No known effect No known effect

Hard Palate Oronasal fistula repair

Alveolar bone graft

Velum Secondary pharyngoplasty

Le Fort I advancement Maxillary osteodistraction Mandibular osteodistraction

has marginal effects on sound production. Resonance and voice are rarely—if ever—affected directly or indirectly. Clefting of the lip results in tissue deficiency, poor differentiation from the maxilla, asymmetry, and retropositioning of the maxilla from the mandible. Depending on the type of cleft (unilateral versus bilateral), severity of the cleft, surgical procedure used, and experience of the surgeon, surgical repair may result in scarring, infection, and dehiscence. A repaired short upper lip, a whistle tip deformity, lip incompetence, and immobility caused by scarring, small prolabium, and an underlying pseudo Class III malocclusion may affect production of certain sounds [m, p, b, f, v, w] [41,42]. The effect is often a maladaptive change, so the intended sounds actually may be produced with the dental edge and the lower lip, which results in a [p] or [b] being perceived as having weak articulatory contact, or ‘‘sounding soft.’’ Weak articulatory contact limits the amount of increased intraoral air pressure behind the lips because the lips do not achieve a tight seal for the necessary duration of time that allows for air pressure to build behind them, which provides the possible perception of increased nasality. Production of [f, v] may be affected by a shortened upper lip and may affect the phonemes because of difficulty in maintaining the correct placement of the maxillary dentition on the lower lip (labiodental). Production of [w] and some vowels may be affected by a tight or short upper lip. This effect may be marginal to the untrained ear. Growth and secondary lip revisions of adding bulk and length to the upper

No known effect

lip, age of the child, and how habitual the articulatory adaptation becomes may have positive effects on these sound errors. Superior retropositioning of the maxilla and mandibular and maxillary advancements reportedly has an effect of stretching the lip and increasing lip tension. Offering the tissue changes of that nature allows lips to approximate in a more normalized position for sound production [43]. The sound errors found in clefts of the lip are considered to be attempts to balance the relationship between a functional need (sound production) and insufficient soft and bony structure. Often this equalization is maladaptive in nature.

Secondary correction of the palate Oronasal fistula and unrepaired alveolar clefts An oronasal fistula is noted in 5% to 30% of all primary palate repairs [44]. There are differences in incidence depending on the type of palatoplasty performed, the degree of cleft severity, and the surgeon’s experience. In some cases the fistula is left intentionally, which is called initial fistulas (secondary to intravelar pharyngoplasties); in other cases, fistulas develop because of poor healing (recurrent fistulas) [45]. It is critical to delineate between fistulas associated with unrepaired alveolar clefts and oronasal palatal fistulas. The differentiation is important from a speech perspective. Fistulas caused by an unrepaired alveolar cleft rarely have a direct effect on resonance,

E.M. LeBlanc / Oral Maxillofacial Surg Clin N Am 14 (2002) 525–537

articulation, or voice. Conversely, the size and extent of the alveolar cleft may have the potential for indirect speech effects, such as concomitant nasal emission, weak articulatory contact, and nasal regurgitation. Nasal regurgitation, foul odor, and difficulty in eating in public are often noted as secondary effects [46]. Oronasal fistulas have a direct effect on speech. The effects of an oronasal fistula depend on the location, size, and length of time during sound development and length of time in which the fistula was present. Hypernasality, nasal emission, and articulation errors, such as mid-dorsal palatal stops (compensatory articulation disorder secondary to VPI), have been associated with oronasal fistulas [39, 47,48]. Oronasal fistulas are often the site of resistant sound errors, which may have direct and indirect effects on velopharyngeal closure [48 – 50]. Leblanc and Eisig [39] noted that long-standing history of oronasal fistula was found to have a direct effect on the velopharyngeal closure in patients who underwent a Le Fort I advancement. The presence and effect of fistulas on maxillary osteodistraction are currently unknown. Paying attention to the integrity of speech sounds during the elicited speech sample (with the fistula occluded) provides information on the presence of articulation errors and how hypernasality is masking the extent of the sound errors as well as provides information as to the possible contributions of velopharyngeal dysfunction on the hypernasality being heard. Management of fistulas, especially oronasal fistulas, is important to undertake as soon as possible if it has been determined that they have detrimental effects on speech. Management may include temporary occlusion by use of prosthetic obturators [41] and adhesive patches that adhere to the oral mucosa [51]. In the case of a small fistula (no matter how affected the speech may be), surgical management may be delayed until fistula repair can be performed at the same time as other surgical procedures to reduce the number of times one undergoes general anesthesia. Large fistulas that directly contribute to hypernasality, nasal emission, articulation errors, and nasal regurgitation often require immediate surgery. Surgical closure of oronasal fistulas is common, however its success is often tenuous because of the presence of scar tissue, location, and size [44,52]. There have been few systematic investigations into the effects of the following procedures and the desired speech outcomes: local turnover flaps, modifications of the mucoperiosteal palatal flaps, buccal flaps, and tongue flaps, and the use of pharyngeal flap (a secondary pharyngoplasty procedure) in the presence of posteriorly placed oronasal fistulas [26,44,53]. The

531

positive effects of fistula repair on speech far outweigh the negatives. Velopharyngeal insufficiency All too often the first question asked when hypernasality is heard concerns the integrity of the velopharyngeal musculature. For successful management of hypernasality, however, the first question asked should be how much of the nasality heard is related to VPI and how much—if at all—is it related to ‘‘learned maladaptive sound compensations.’’ Many complicating factors contribute to the perception of hypernasality. The surgeon who achieves the desired speech outcome successfully (1) identifies which contributory speech factors exist, (2) provides a comprehensive structural and physiologic assessment, (3) determines when to manage the patient surgically, and (4) develops an ‘‘haute couture’’ surgical plan (surgery specifically designed for the patient based on in-depth preoperative assessment). Management of VPI depends greatly on the transdisciplinary diagnostic assessment. This assessment involves the use of direct visualization techniques, such as nasopharyngoscopy and multiview videofluoroscopy, measurements of airflow and air pressure through the use of aerodynamic studies, and a craniofacial speech assessment. The debates expressed in the literature and during professional forums that revolve around the issue of which secondary surgical procedure provides the most desired outcome are misplaced. Each procedure has the potential to result in positive outcomes. The debate over which procedure is most effective more appropriately revolves around issues of postoperative manifestations of nasal and airway obstruction. To date, the pharyngeal flap presents with a 10% to 13% increased risk of postoperative airway issues as compared to the sphincter pharyngoplasty [29,54]. There have been several reports of airway obstruction and death associated with posterior pharyngeal flap surgery and obstructive sleep apnea after such surgery [55]. Many surgeons who use the pharyngeal flap procedure do not experience these results. Differences in opinion still exist as to whether hyponasality beyond the postoperative healing process is considered to be normal. Hyponasality does not represent normal resonance [5,9,36,56]. The surgical approaches currently available consist of augmentation of the velum (ie, Furlow doublereversing Z-plasty) and altering the structure and physiology of the pharyngeal musculature (ie, superiorly based pharyngeal flaps, sphincter pharyngoplasties, and augmentation pharyngoplasties).

532

E.M. LeBlanc / Oral Maxillofacial Surg Clin N Am 14 (2002) 525–537

Sphincter pharyngoplasty

Secondary correction of the maxilla and mandible

The sphincterplasty acts on the velopharynx by advancing the posterior pharyngeal wall (dissection of the posterior faucial pillars, with insertion into the posterior pharyngeal wall), reducing the lateral pharyngeal wall dimensions (reducing the overall diameter), and providing a dynamic sphincter action (simulating the natural physiologic action of the velopharynx) [29,35,57 – 59]. Riski et al [58] and Witt et al [59] noted that preexisting and persistent compensatory articulation errors, low lateral flap placement, flap dehiscence, and reduced experience of the surgeon accounted for sphincterplasty failures in the patients who did not demonstrate an improvement in their resonance quality. Pensler et al [60] reported a 4% occurrence of sleep apnea. The sphincter pharyngoplasty has gained an ever-increasing attractiveness by its ease of procedure, favored speech outcomes, and significantly reduced postoperative complications.

Secondary alveolar bone graft

Pharyngeal flap The pharyngeal flap as a procedure to eliminate hypernasality has been reported in the literature with the most vigor and frequency because of its long history. It has been in use in one form or another since 1876 [61]. The success of the pharyngeal flap depends on more factors to ensure resonance integrity than that of the sphincterplasty. The pharyngeal flap relies in part on the mesial movement of the lateral pharyngeal walls, the appropriate width of the flap, the superior placement of the flap, insertion of the free flap into the velum, the size of the lateral ports, flap tissue atrophy, and surgeon experience [62]. In addition to concerns of airway obstruction after pharyngeal flap, questionable resonance results have raised concern about transient changes in facial growth patterns in patients who undergo pharyngeal flaps, particularly maxillary arch changes, mandible angle changes, and increased anterior facial height [63]. Furlow double opposing Z-plasty The Furlow-plasty has enjoyed much use and success with submucous and occult submucous cleft palates. It also has become increasingly popular as a secondary surgical procedure in the presence of status postprimary palatal repair and documented VPI. The success depends on the size of the insufficiency, the movement excursion of the lateral pharyngeal walls, and the presence of compensatory articulation errors.

Alveolar bone grafts (primary and secondary) are designed to stabilize the segments of the maxilla and replace missing bone. Alveolar bone grafting typically occurs between 9 and 11 years of age, when the permanent lateral incisor or the canine tooth roots are approximately one-third developed. The presence of appliances (rapid palatal expansion devices) before bone grafting may affect articulation and resonance indirectly because of the obstructive nature of the appliances affecting lingual placement (affecting spatial relationships) and aerodynamics of airflow and pressure for sound production. This is typically a transient effect [64]. Before the bone graft; a child with a cleft lip presents with dental and occlusal anomalies that have the potential to affect speech (obligatory sound errors, weak articulatory contact of sound, possible nasal emission). Maxillary and mandibular osteodistraction Osteodistraction of the mandible has been used for a decade, since it was first introduced in 1992 by McCarthy et al [65]. Osteodistraction is still relatively new to the flora of utility research endeavors, especially when related to speech. To date, few studies have examined the effects of speech after distraction [21,22,66]. The current data indicate that maxillary distraction of no more than 10 to 15 mm resulted in VPI occurring in transient manner with resolution to predistraction status at least 3 to 6 months after surgery [21]. These results are consistent with the reported literature on Le Fort I advancements. Theoretically, the gradual advancement of the maxilla may allow for progressive adaptation in the velopharyngeal mechanism, although this has not been well researched. Of the scant literature and personal communications available on speech outcomes and maxillary distraction, it is believed that an advancement of 10 mm or more may result in increased velopharyngeal function. Satoh et al [22] noted that seven of eight patients who presented with normal velopharyngeal function and normal articulation before distraction were unchanged after distraction. The average advancement ranged from 4.5 to 7.6 mm in 9- to 11-year-old children, with six subjects presenting with hypertrophic adenoidal tissue. The patient who presented with borderline velopharyngeal closure before distraction exhibited increased VPI after distraction. Satoh et al [22] also noted that the ratio of velar length to pharyngeal depth decreased in all eight subjects

E.M. LeBlanc / Oral Maxillofacial Surg Clin N Am 14 (2002) 525–537

(1.06 – 1.76 before distraction and 0.79 – 1.19 after distraction). Guyette [21] reported on the positive change in sound production after distraction. This finding is supported by several studies on the effect of Le Fort I advancement and articulation [24]. Distraction osteogenesis is a term used to denote several different types of surgical and movement techniques for moving hard and soft tissue in varying directions into more normal positions. Because of this, one is cautioned to make assumptions that the effect on speech would be similar to that noted in Le Fort I advancements. One also is reminded that the literature on speech effects after Le Fort I advancements continues to cause debate because of numerous methodologic flaws in the research. The research conducted to date gave minimal rigor to reliably discussing the short- and long-term effects of maxillary distraction on resonance and articulation.

533

disorder secondary to VPI or secondary articulation disorders, such as developmental or phonologic processing feature disorder. Velopharyngeal function Advancement of the maxilla results in threedimensional changes of the velopharynx, nasopharynx, and hypopharynx. Le Fort I advancement has the potential of impacting the integrity of the function of the velopharyngeal mechanism by modifying its kinematic dynamics. One area of relative agreement in the literature is that postoperative hypernasality is likely to occur in patients with maxillary advancements of 10 mm or more. This is a reported finding in one dimension only, however. Adaptive or maladaptive effects or no effects at all on resonance have been reported [20,39,56 – 74]. Schwarz et al [75] summarized the following findings:

Le Fort I advancement Although maxillary distraction has gained increasing popularity as the procedure to be used for maxillary hypoplasia and retrusion, the Le Fort I advancement continues to be used actively in many surgeons’ protocols. The goal of maxillary repositioning with appropriate movement of osteotomized units includes achieving normal occlusion, normal sized and functioning oral and pharyngeal resonance cavities, and improved facial proportions. Orthognathic surgery requires careful coordination among the surgeon, speech pathologist, and orthodontist. Much debate has occurred over the Le Fort I osteotomy’s effect on speech. Articulation Crowding of the maxillary teeth, increased spaces that result from alveolar fistulas, missing incisors, crossbites, and pseudoprognathism in cleft lip may lead to articulation errors (obligatory disorder) known as distortions (frontal and lateral lisping [s, z, sh, ch, j], lingual retraction [t, d, n], and maladaptive production [p, b, f, v]). Dental-skeletal anomalies have greater potential to effect sound production if they exist before or during the period of sound development (9 months to 4 years) [56]. Correction of Class III malocclusion often improves or resolves obligatory sound errors. Published reports on advancing the maxilla forward, with or without simultaneous sagittal split osteotomies, repeatedly have demonstrated that obligatory errors were eliminated if present in most of the reported cases [23,65,67 – 69]. Le Fort I advancements have minimal to no effect (negative or positive) on compensatory articulation

1. No changes in the normal oral-nasal resonance balance 2. Changes from normal resonance to hypernasality 3. Increase in the severity of hypernasality 4. Decrease in the degree of severity of hypernasality 5. Changes from hypernasality to hyponasality 6. Increase in the degree of hyponasality 7. Decrease in the degree of hyponasality 8. Elimination of hyponasality. The following patient profile has been noted to increase the potential for undesirable changes in velopharyngeal function after Le Fort I advancement [17,39]: 1. Status after primary pharyngoplasty 2. Status after secondary pharyngoplasty (based on pharyngeal flap procedure) 3. Presence or history of marginal or touch velopharyngeal closure 4. Status after long-standing history of oronasal palatal fistula 5. Presence of or suspicion of submucous or occult submucous cleft palate 6. Presence of hypertrophic adenoid tissue 7. History of hypernasality after adenoidectomy or tonsillectomy 8. Presence of compensatory articulation disorder secondary to VPI 9. Presence of cranial base anomalies, such as Apert, Crouzon, Pfeiffer, and Treacher Collins syndromes.

534

E.M. LeBlanc / Oral Maxillofacial Surg Clin N Am 14 (2002) 525–537

Little attention has been paid in the literature to the effects of Le Fort I advancement on sphincter pharyngoplasty and furlow pharyngoplasty, the site of placement (inferior versus superior) and width of the pharyngeal flap, or whether there is a concomitant relapse in velopharyngeal function (with or without secondary pharyngoplasty) in patients who demonstrate a dental-skeletal relapse. To date, there has been no attempt to assess all the potential factors and their predictive value in velopharyngeal outcome. One aspect is ensured: extensive preoperative perceptual and direct visualization (via nasopharyngoscopy) is vital to the success of Le Fort I advancement. Documentation of the risk for velopharyngeal dysfunction does not change the potential undesired resonance outcome. It does lend to appropriate expectations of surgical and speech outcomes, however, with the realization that revision or secondary pharyngoplasty is a possibility in 6 to 9 months after advancement. It is important that such patients be closely monitored longitudinally. The most recent study by Sabry et al [76] noted a low risk of velopharyngeal dysfunction in 12 patients who previously underwent a secondary pharyngoplasty. Six of 9 subjects presented with a degree of VPI (‘‘bubbling’’) before advancement. Three subjects reportedly improved velopharyngeal function, whereas 1 presented with increased VPI, as compared to the preoperative state. The researchers failed to comment on the relationship of velopharyngeal function after advancement and type of secondary pharyngoplasty. A small sample and a poorly delineated mix of nonsyndromic and syndromic patients make the results difficult to interpret. Oronasal fistula The presence or long-standing history of palatal oronasal fistula has been noted to have an impact on velopharyngeal function after maxillary advancement. LeBlanc and Eisig [39] and Poole et al [77] noted that patients who presented with velopharyngeal dysfunction after maxillary advancement exhibited the presence or history of fistula. The deleterious effect of the fistula on the kinematics of the velopharyngeal mechanism has been supported by the work of Isberg and Henningsson [34].

Discussion For the surgeon who performs secondary procedures on clefting disorders, there is a need for careful balancing of occlusal, aesthetic, and speech consid-

erations. Historically, we have learned from the growth of our professions and have moved closer to providing optimized surgical and speech outcomes for patients. We have learned that enhancing surgical procedures, technique and the learning curve do not ensure optimized speech outcomes alone. Speech represents a dynamic matrix of elements that interact with each other and the surgical components. Controlling many of the variables to ensure an optimized outcome is the responsibility of the cleft team. The team is ideally made up of cleft-experienced disciplines that work with each other for the benefit of the patient. The American Cleft Palate-Craniofacial Association [78] has established minimal criteria on the parameters of cleft team care. Based on what we do know at the beginning of the twenty-first century, a comprehensive preoperative speech assessment is fundamental to any cleft surgery. Universal standards have been recently proposed for speech assessment in clefting [5,79], including a rigorous perceptual assessment, nasopharyngoscopy, and multiview videofluoroscopy by a trained craniofacial-cleft speech specialist. The type of articulation disorder presented by the patient has a direct effect on velopharyngeal function, the outcome of secondary pharyngoplasties, maxillary distractions, and Le Fort I advancements. Compensatory articulation disorder secondary to VPI—in the sheer nature of the sound disorder—directly affects the kinematics of velar and lateral pharyngeal wall movement, which results in less than optimal mobility. In many cases, optimizing sound production before secondary pharyngeal cleft surgery changes the physiologic mechanism of the velopharynx and necessitates a different surgical approach. If optimal speech is difficult to obtain at the time that surgery is considered, having appropriate expectations of velopharyngeal function and speech postoperatively is imperative. This is especially important because many secondary pharyngoplasties result in concomitant edema, which leads to hyponasality. This may have a false-positive effect, because when the transient edema resolves, one may perceive hypernasality caused by the presence of the type of articulation errors. Postprimary pharyngoplasties have the potential to place the palate and its function at risk for resonance and articulation disorders. Fistulas, regarded by many surgeons as having minimal effect on speech, have the potential to impact articulation, velopharyngeal function, eating, and the outcomes of secondary pharyngoplasties, maxillary advancements via osteodistraction, and Le Fort I osteotomy. Secondary pharyngoplasties are best used when an ‘‘haute couture’’ approach of assessment and surgery

E.M. LeBlanc / Oral Maxillofacial Surg Clin N Am 14 (2002) 525–537

approach is adopted. Surgical proficiency on the furlowplasty, sphincterplasty, and pharyngeal flap is increasing in the team-centered approach. The criteria for the timing and need for surgery require further development. Each procedure has merits, and under the right hands each procedure has proved to achieve the desired outcomes. In other words, one should do what works, as long as one knows when it is not working. Maxillary and mandibular advancements have the potential to affect the function of the velopharyngeal mechanism. We do know that an anteroposterior direction of movement of more than 10 mm increases the occurrence of perceived hypernasality. There is so much more that we do not know, however. What other movement directions affect velopharyngeal function and in what manner? More clinical research is needed in examining the effects of oronasal fistula, the type and presence of articulation disorders, and the incidence of relapse and velopharyngeal dysfunction. What we do know is that any velopharyngeal mechanism in an individual with a palatal cleft or craniofacial syndrome is at risk for compromise and a comprehensive speech assessment is imperative. This assessment includes direct visualization of the velopharyngeal mechanism via nasopharyngoscopy. The more one knows about clefting and its impact on speech production, oropharyngeal anatomy, and physiology and the basic regimens used in dental and surgical management, the greater the contribution to the successful management process. References [1] Mack MJ. Minimally invasive and robotic surgery. JAMA 2001;285:568 – 72. [2] Dalston RM. Timing of cleft lip palate repair: a speech pathologist’s viewpoint. Problems in Plastic Surgery: Cleft Palate Surgery 1992;2:30 – 8. [3] Hall CD, Golding-Kushner KJ. Long-term follow-up of 500 patients after palate repair performed prior to 18 months of age. Presented at the 6th International Congress of Cleft Palate and Related Craniofacial Anomalies. Jerusalem, 1989. [4] Hardin-Jones MA, Brown CK, Van Demark DR, Morris HL. Long-term speech results of cleft palate with primary pharyngoplasties. Cleft Palate J 1993; 30:55 – 63. [5] Kuehn D, Sells DD, Trost-Cardomone J. Issues in universal reporting parameters for speech. Presented at the 59th Annual American Cleft Palate-Craniofacial Association, Seattle, May 2, 2002. [6] Morris HL. Velopharyngeal competence and primary cleft palate surgery, 1960 – 1971: ‘‘a critical review. Cleft Palate J 1993;10:62 – 71.

535

[7] Muliken JB. Final operations for the older child born with a cleft lip/palate. Available at: http:// www.samizdat.com/pp7.html. Accessed March 5, 2002. [8] Paynter ET, Kinard MW. Perceptual preferences between compensatory articulation and nasal escape of air in children with velopharyngeal incompetence. Cleft Palate J 1979;16:262 – 9. [9] Peterson-Falzone SJ. Compensatory articulations in cleft palate speakers: relative incidence by type. Proceedings of the International Congress on Cleft Palate and Related Craniofacial Anomalies. Jerusalem. 1989. [10] Dalston RM. Communication skills of children with cleft lip and palate: a status report. In: Bardach J, Morris HL, editors. Multidisciplinary management of cleft lip and palate. Philadelphia: WB Saunders; 1990. p. 746 – 9. [11] Bardach J. Cleft palate repair: two flap palatoplasty, research philosophy, technique and results. In: Bardach J, Morris HL, editors. Multidisciplinary management of cleft lip and palate. Philadelphia: WB Saunders; 1990. p. 352 – 65. [12] Brothers DB, Dalston RW, Peterson HD, Lawrence WT. Comparison of the Furlow double-reversing zplasty with the Wardill-Killner procedure for isolated clefts of the soft palate. Plast Reconstr Surg 1995; 95:969 – 77. [13] Buchholz R, Chase R, Jobe R, Smith H. The use of the combined palatal pushback and pharyngeal flap operation: a progress report. Plast Reconstr Surg 1967; 39:554 – 61. [14] Blijdorp P, Miller H. The influence of the age at which the palate is closed on speech in the adult cleft palate patient. J Maxillofac Surg 1984;12:239 – 46. [15] Copeland M. The effects of very early palatal repair on speech. Br J Plast Surg 1990;43:676 – 82. [16] Cosman B, Falk AS. Delayed hard palate repair and speech deficiencies: a cautionary report. Cleft Palate J 1980;17:27. [17] Dorf DS, Curtin J. Early cleft repair and speech outcome: a ten-year experience. In: Bardach J, Morris HL, editors. Multidisciplinary management of cleft lip and palate. Philadelphia: WB Saunders; 1990. p. 341 – 8. [18] Bralley RC, Schoeny ZG. Effects of maxillary advancement on the speech of a submucosal patient. Cleft Palate J 1977;14:98 – 101. [19] Cohen SR, Burstein FD, Stewart MG, Rathburn MA. Maxillary mid-face distraction in children with cleft lip and palate: a preliminary report. Plast Reconstr Surg 1997;99:1421 – 8. [20] Dalston RM, Vig PS. Effect of orthognathic surgery on speech: a prospective study. Am J Orthod 1984;86: 291 – 8. [21] Guyette W, Polley JW, Figueroa AA, Cohen MN. Mandibular distraction osteogensis: effects on articulation and velopharyngeal function. J Craniofac Surg 1996;7:186 – 91. [22] Satoh K, Nagata J, Shomura K, Fukuda J, Ryosuke S. Changes in velopharyngeal function following maxillary distraction. Presented at the 59th Annual

536

[23]

[24]

[25]

[26]

[27]

[28]

[29]

[30]

[31]

[32]

[33]

[34] [35] [36]

[37]

[38]

[39]

E.M. LeBlanc / Oral Maxillofacial Surg Clin N Am 14 (2002) 525–537 American Cleft Palate-Craniofacial Association. Seattle, May 2, 2002. Vallino LD. Speech, velopharyngeal function and hearing before and after orthognathic surgery. J Oral Maxillofac Surg 1990;48:1274 – 81. Witzel MA, Ross R, Munro I. Articulation before and after facial osteotomy. J Maxillofac Surg 1980;8: 195 – 200. Vallino LD, Tompson B. Perceptual characteristics of consonant errors associated with malocclusion. J Oral Maxillofac Surg 1993;51:850. Argamaso RV. The tongue flap: Placement and fixation for closure of postpalatoplasty fistulae. Cleft Palate J 1990;27(4):402 – 10. Crockett DM, Bumstead RM, Van Demark DR. Experience with surgical management of velopharyngeal incompetence. Otolaryngol Head Neck Surg 1988;99: 1 – 9. D’Antonio LL. Correction of velopharyngeal insufficiency using the Furlow double opposing Z-plasty. West J Med 1997;102:101 – 2. De Serres LM, Deleyiannis FW, Eblen LE, Gruss JS, Richardson MA, Sie DC. Results with sphincter pharyngoplasty and pharyngeal flap. Int J Pediatr Otorhinolaryngol 1999;48:17 – 25. Furlow LT. Cleft palate repair by double opposing Z-plasty. Available at: http://www.teachsurgery.org/ public/interplastcd/interplast/surgical/cleft palate/furlowpalat/htmp. Accessed December 26, 2001. Shprintzen RJ, Croft C, Berkman M, Rakoff SD. Pharyngeal hypoplasia in Treacher Collins syndrome. Arch Otolaryngol 1979;105:127. Witt PD, D’Antonio LL, Zimmerman GJ, Marsh JL. Sphincter pharyngoplasty: a preoperative and postoperative analysis of perceptual characteristics and endoscopic studies of velopharyngeal function. Plast Reconstr Surg 1994;93:1154 – 68. Leroux B. Strategies for comparison of protocols: methodological considerations. Presented at the 59th Annual American Cleft Palate-Craniofacial Association. Seattle, May 1, 2002. Enlow DH. Handbook of facial growth, 2nd edition. Philadelphia: WB Saunders; 1982. Hynes W. Observations on pharyngoplasty. Br J Plast Surg 1967;20:244 – 56. LeBlanc EM, Shprintzen RJ. Speech and the maxillofacial complex: a structural-functional perspective for diagnosis and management. Oral Maxillofac Surg Clin N Am 1993;6:113 – 20. Witzel MA. Communicative impairment associated with clefting. In: Shprintzen RJ, Bardach J, editors. Cleft palate speech management: a multi-disciplinary approach. St. Louis: CV Mosby; 1990. p. 137 – 66. Kahn A. Craniofacial anomalies: a beginners guide for speech-language pathologists. San Diego: Singular Publishing Group; 2000. LeBlanc EM, Eisig S. Variables affecting speech outcomes in Le Fort I advancement. J Oral Maxillofac Surg, submitted for publication.

[40] Shprintzen RJ. Syndrome identification for speech language pathology: an illustrated pocketguide. San Diego: Singular Publishing Group; 2002. [41] LeBlanc EM. Fundamental principles in speech language management from birth to adolescence. In: Berkowitz S, editor. Cleft palate treatment from birth to adolescence. San Diego: Singular Publishing Group; 1996. p. 75 – 84. [42] Peterson-Falzone SJ. Speech outcomes in adolescents with cleft lip and palate. Cleft Palate Craniofac J 1995;32:125 – 8. [43] Profit WR, Philips C. Adaptations in lip posture and pressure following orthognathic surgery. Am J Orthod Dentofacial Orthop 1988;93:294 – 482. [44] Cohen SR, Kalinowski J, LaRossa D, Randall P. Cleft palate fistulas: a multivariate statistical analysis of prevalence, etiology and surgical management. Plast Reconstr Surg 1991;87:1041 – 7. [45] Folk SN, D’Antonio LL, Hardesty RA. Secondary cleft deformities. Clin Plast Surg 1997;24:599 – 611. [46] Waite PD, Waite DE. Bone grafting for the alveolar cleft defect. Semin Orthod 1996;2:192 – 6. [47] Henningsson G, Isberg A. Velopharyngeal movements in patients altering between oral and glottal articulation: a clinical and cineradiographic study. Cleft Palate J 1986;21:1. [48] Isberg A, Henningsson G. Influence of palatal fistulae on velopharyngeal movement: a cineradiographic study. Plast Reconstr Surg 1987;79:525 – 30. [49] Karling J, Henningsson G, Larson O, Isberg A. Comparison between two types of pharyngeal flap with regard to configuration at rest and function and speech outcome. Cleft Palate Craniofac J 1999;63:154 – 65. [50] Tachimura T, Hara K, Koh H, Wada T. Effect of temporary closure of oronasal fistulae on levator veli palatine muscle activity. Cleft Palate Craniofacial J 1997;34:505 – 11. [51] Reisberg DJ, Gold HO, Dorf DS. A technique for obturating palatal fistulas. Cleft Palate J 1985;22:286 – 9. [52] Witt PD, D’Antonio LL. Velopharyngeal insufficiency and secondary palatal management: a new look at an old problem. Clin Plast Surg 1997;20:707 – 21. [53] Emory RE, Clay RP, Bite U, Jackson IT. Fistula formation and repair after palatal closure: an institutional perspective. Plast Reconstr Surg 1997;99:1535 – 8. [54] Sie DC, Tampakopoulou DA, de Serres LM, Gruss LE, Eblen LE, Tonick T. Sphincter pharyngoplasty: speech outcome and complications. Laryngoscope 1998;108:1211 – 7. [55] Peterson-Falzone SJ, Hardin-Jones MA, Karnell MP. Cleft palate speech. 3rd edition. St. Louis: Mosby; 2001. p. 318 – 9. [56] Kummer AW. Cleft palate and craniofacial anomalies: effects on speech and resonance. San Diego: Singular Publishing Group; 2001. [57] James NK, Twist M, Turner MM, Milward TM. An audit of velopharyngeal incompetence treated by Orticohea pharyngoplasty. Br J Plast Surg 1967;49: 197 – 201.

E.M. LeBlanc / Oral Maxillofacial Surg Clin N Am 14 (2002) 525–537 [58] Riski JE, Ruff GL, Georgiade GS, Barwick WJ, Edwards PD. Evaluation of the sphincter pharyngoscopy. Cleft Palate Craniofac J 1992;29:254 – 61. [59] Witt PD, Marsh JL, Marty-Grames L, Muntz HR, Gay HD. Management of the hypodynamic pharynx. Cleft Palate J 1995;32:179 – 87. [60] Pensler JM, Reich DS. A comparison of speech results after the pharyngeal flap and the dynamic sphincteroplasty procedures. Ann Plast Surg 1991;26:441 – 3. [61] Bernstein L. Treatment of velopharyngeal incompetence. Arch Otolaryngol 1967;85:67 – 74. [62] Argamaso RV. The pharyngeal flap. In: Kernihan DA, Rosenstein EW, editors. Cleft palate: a system of management. Boston: Little Brown and Co; 1989. p. 263 – 9. [63] Ren YF, Isberg A, Henningsson G. Velopharyngeal incompetence and persistent hypernasality in children without palatal defect. Cleft Palate Craniofac J 1995; 32:47. [64] LeBlanc EM, Cisneros GJ. The dynamics of speech and orthodontic management in cleft lip and palate. In: Shprintzen RJ, Bardach J, editors. Cleft palate speech management: a multi-disciplinary approach. St. Louis: CV Mosby; 1995. p. 305 – 25. [65] McCarthy JG, Schreiber J, Karp N, Thorne CH, Grayson BH. Lengthening the human mandible by gradual distraction. Plast Reconstr Surg 1992;89:1 – 8. [66] Guyette TW, Polley JW, Figueroa AA, Smith BE. Changes in the speech following maxillary osteogenesis. Cleft Palate Craniofac J 2001;38:199 – 205. [67] Kummer AW, Strife JL, Graw WH, Creaghead NA, Lee L. The effects of LeFort I osteotomy with maxillary movement on articulation, resonance and velopharyngeal function. Cleft Palate J 1989;26: 193 – 200. [68] Maegawa J, Sells RK, David DJ. Speech changes after maxillary advancement in 40 cleft lip and palate patients. J Craniofac Surg 1998;9:177 – 82. [69] Maegawa J, Sells RK, David DJ. Pharyngoplasty in patients with cleft lip and palate after maxillary advancement. J Craniofac Surg 1998;9:330 – 5.

537

[70] Okazaki K, Satoh K, Kato M, Iwanoria M, Ohakuho F, Kaboyoshi K. Speech and VP function following maxillary advancement in patients with cleft palate. Ann Plast Surg 1993;26:304. [71] Watske I, Turvey TA, Warren DW, Dalston RM. Alternations in velopharyngeal function after maxillary advancement in cleft palate patients. J Oral Maxillofac Surg 1990;48:685 – 9. [72] Witzel MA. The effect of Le Fort I osteotomy with maxillary movement on articulation, resonance, and velopharyngeal function [commentary]. Cleft Palate J 1989;26:199 – 200. [73] LeBlanc EM, Eisig S, Gonzales M, Cisneros G. Variables affecting the success of Le Fort I osteotomies. Presented at the ACPA Annual Meeting. Scottsdale, AZ, April 14 – 18, 2002. [74] Kummer AW, Strife JL, Graw WH, Creaghead NA, Lee L. Effects of LeFort 1 osteotomy with maxillary movement on articulation, resonance and velopharyngeal function. Cleft Palate J 1989;26:193 – 200. [75] Schwarz CK, Gruner E. Logopaedic findings following advancement of the maxilla. J Maxillofac Surg 1976; 4:40. [76] Sabry MZ, Marsh JL, Marty-Grames L. The effect of surgical maxillary advancement on velopharyngeal function in previously managed velopharyngeal dysfunction patients. Presented at the 59th Annual American Cleft Palate-Craniofacial Association. Seattle, May 2, 2002. [77] Poole MD, Robinson S, Nunn M. Maxillary advancements in cleft palate patients. J Maxillofac Surg 1986; 14:123 – 7. [78] American Craniofacial-Cleft Palate Association. Parameters for evaluation and treatment of patients with cleft lip/palate or other craniofacial anomalies. Cleft Palate Craniofac J 1993;30(Suppl):1 – 16. [79] Moon JB. Strategies for comparison of protocols: velopharyngeal function. Presented at the 59th Annual American Cleft Palate-Craniofacial Association. Seattle, May 2, 2002.

Oral Maxillofacial Surg Clin N Am 14 (2002) 539 – 551

Velopharyngeal insufficiency in patients with cleft palate Bernard J. Costello, DMD, MDa,b,c,*, Ramon L. Ruiz, DMD, MDd,e, Timothy A. Turvey, DDSd,e a Departments of Oral and Maxillofacial Surgery, Pediatric Dentistry, and Pediatric Surgery, University of Pittsburgh Medical Center, Magee-Women’s Hospital, and Children’s Hospital of Pittsburgh, Pittsburgh, PA 15213, USA b University of Pittsburgh Cleft Palate-Craniofacial Center, Pittsburgh, PA 15213, USA c University of Pittsburgh School of Dental Medicine, 3471 Fifth Avenue, Suite 1112, Pittsburgh, PA 15213, USA d Department of Oral and Maxillofacial Surgery, University of North Carolina Craniofacial Center, University of North Carolina at Chapel Hill, USA e Pediatric Oral and Maxillofacial Surgery, North Carolina Children’s Hospital, Brauer Hall, CB# 7450, Chapel Hill, NC 27599-7450, USA

Patients born with cleft palate have, by definition, a malformation that involves critical anatomic components of the velopharyngeal mechanism. Normally, the soft palate, or velum, is part of the complex coupling and decoupling of the oral and nasal cavities to produce orally based or nasally based speech sounds. When a cleft of the soft palate is present, abnormal muscle insertions are located at the posterior edge of the hard palate. Surgery must not be aimed simply at closing the physical palatal defect, but rather at the release of abnormal muscle insertions, establishment of muscle continuity, and correct orientation so that the velum may serve as a dynamic sling-like structure. Despite successful closure of the soft and hard palate, the velopharyngeal valving mechanism may not work adequately to allow for appropriate closure of the nasopharynx from the oropharynx. The insufficient mechanism results in difficulty with certain speech sounds, most often manifesting as velopharyngeal insufficiency (VPI). Most commonly, this insufficiency of the velopharyngeal valving mechanism results in hypernasality, the audible nasal emission of air, which also may be associated with abnormal compensatory articulation problems. Although this is * Corresponding author. University of Pittsburgh School of Dental Medicine, 3471 Fifth Avenue, Suite 1112, Pittsburgh, PA 15213, USA. E-mail address: [email protected] (B.J. Costello).

the most common scenario when speech problems occur in patients with cleft palate, a complex spectrum of issues requires careful evaluation and diagnosis. Most children who have cleft palate repairs performed at the appropriate time in a successful manner have speech that is normal or speech that displays minor abnormalities that can be treated successfully with speech therapy. Approximately 20% of children with palates repaired appropriately develop VPI, that may require additional surgical treatment using one of several surgical options [1]. A second clinical situation in which cleft palate patients may develop VPI is after orthognathic surgical procedures. Depending on the degree of skeletal movement, the soft palate structures may be advanced to the point at which adequate velopharyngeal closure is no longer possible. When this occurs, the patient develops VPI during the postoperative period. VPI in cleft palate patients after Le Fort I midfacial advancement usually resolves within 6 months of the procedure, but there is a small subgroup of patients who benefit from an additional surgical procedure to help with adequate closure of the velopharyngeal mechanism. This article presents an overview of current clinical perspectives of the etiology, diagnosis, and treatment of VPI in patients with cleft palate. Management of patients with VPI encountered in early childhood and after maxillary advancement is discussed.

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 4 5 - 6

540

B.J. Costello et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 539–551

Anatomy and physiology of the velopharyngeal apparatus The anatomy of the velopharyngeal valving system is complex (Fig. 1A,B). The palate is made up of the hard bony palate anteriorly and the soft palate, or velum, posteriorly. The velopharyngeal valving system includes the soft palate and the surrounding lateral and posterior pharyngeal walls. In evaluating velopharyngeal function after cleft palate repair, it is important to consider the complex three-dimensional movements of these different muscle groups that work simultaneously. The mechanism is not simply a closed or open system, but rather a continuum of movement that allows sound to be modified through the changing aperture. The musculature is particularly multifaceted, and the function and contribution of each muscle or muscle group are frequently debated (Table 1) [2 – 7]. The workhorse of the velopharyngeal mechanism is considered to be the levator veli palatini because it elevates the palate to the posterior pharynx [4,5,8]. The tensor veli palatini may not affect velopharyngeal closure directly, but is likely important in functional speech because it tents the musculature drape horizontally. The musculus uvulus is believed to help with velar extension during speech [9]. The palato-

pharyngeus and palatoglossus tonsilar pillars probably antagonize the levator and balance the valving mechanism. Passavant’s ridge extends from the posterior wall anteriorly to help close the velopharyngeal sphincter to a variable extent in some patients [10 – 12]. This is believed to be compensatory in some patients who cannot extend the velum posteriorly because of scarring.

Speech abnormalities in the cleft patient Production of speech sounds occurs because of a complex interplay between multiple anatomic structures that act in concert (see box). One of the complexities of the cleft palate malformation is the function of the velopharyngeal sphincter. Under normal circumstances, sealing the nasal cavity from the oral cavity occurs by simultaneous elevation of the soft palate, contraction of the lateral pharyngeal walls, and activation of the associated musculature to produce a sphincter. This effectively separates the nasal and oral cavities. In patients with a repaired cleft palate, the apparatus is altered and the patient has learned to overcome a short or scarred palate that does not move well by recruiting extra efforts from the adjacent structures. Activation of Passa-

Fig. 1. Anatomy of the palate and velopharyngeal mechanism. (A) Normal anatomy. (B) Unilateral cleft of the primary and secondary palate with associated anatomic abnormalities.

B.J. Costello et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 539–551

541

Table 1 Muscles of the velopharyngeal valving mechanism Muscle

Insertion

Origin

Action

Musculus uvulus Tensor veli palatini Salpingopharyngeus Superior constrictor

Mucous membrane of soft palate Soft and hard palate Palatopharyngeal aponeurosis Medial pharyngeal raphe

Palatal aponeurosis Medial pterygoid palate Torus tubularis Velum; medial pterygoid palate

Levator veli palatini Palatopharyngeus

Soft palate Soft plate aponeurosis

Temporal bone Pharyngeal wall

Palatoglossus

Tongue

Soft palate

Velar extension Opens auditory tube Motion of the lateral walls Posterior and lateral wall sphinctering Elevation of velum Adduction of posterior pillars; spinctering of velum Retract tongue; antagonistic to the levator during speech

vant’s ridge (hypertrophy of tissue in the posterior pharyngeal wall) is an example of a compensatory effort that many cleft patients have developed to overcome the insufficiency of velar movement and stretch.

the appropriate sound. If nasal escape occurs because of incomplete velopharyngeal closure or fistula presence, consonants do not sound as they should because of excessive nasal air emission. This problem often occurs with hypernasality, which is a resonance problem associated with vowel production, not consonant production.

Anatomic variables in speech            

Chest wall Diaphragm Abdomen Larynx Oropharynx Nasophayrnx Hard and soft palate Nasal cavity Maxilla and mandible Tongue Teeth Lips

Warren’s aerodynamic demands theory probably best explains the problems with VPI [13]. He states that severe velopharyngeal closure impairments cause the patient to attempt to articulate pressure consonants at the larynx or pharynx level instead of within the oral cavity. This attempt causes abnormal compensatory articulation sounds. The more common types of speech abnormalities found in patients with cleft palate are described later.

Nasal air emission During the production of consonants, the creation of relatively high oral pressure is critical to producing

Resonance Problems with resonance refer to perturbations, such as hypernasality, that happen above the glottis during vowel production. Hypernasal perturbations occur during the production of vowel sounds that require the appropriate closure of the nasal space from the oral space. Of the 20% of patients who have speech disturbances related to cleft palate, most speech issues present as hypernasality [14,15]. Hyponasality is a reduction in nasal resonance that occurs because of abnormal obstruction (a pharyngeal flap that is too wide).

Articulation Articulation problems may be related to difficulties with creating the adequate amount of oral pressure necessary to create fricative, affricative, oral stop, lateral, and glide sounds (/f/,/th/, /v/, /s/, /z/, /sh/, /zh/, /ch/, /j/, /p/, /b/, /d/, /k/, /g/, /t/, /l/, /r/, /y/, and /w/,). When the velopharyngeal mechanism does function appropriately to close off the nasal cavity, airstream escape makes it challenging to produce these sounds. Compensatory articulation occurs when the patient tries to pathologically shape the airstream more posteriorly in the vocal tract rather than at the normal locations of the anterior palate, teeth, and tongue [13].

542

B.J. Costello et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 539–551

B.J. Costello et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 539–551

543

Fig. 2. (A,B) Speech evaluation form used at the University of Pittsburgh Cleft Palate and Craniofacial Center that uses different categories of speech issues, quantifies the abnormality, and helps calculate a weighted speech score. (From McWilliams BJ, Philips BJ. Audio seminars in speech pathology: velopharyngeal incompetence. Philadelphia: WB Saunders; 1979; and McWilliams BJ, Bradley DP. Ratings of velopharyngeal closure during blowing and speech. Cleft Palate J 1965;2:46 – 55; with permission.)

544

B.J. Costello et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 539–551

Speech evaluations The evaluation of patients with cleft palate malformations necessitates careful consideration of the interaction of different mechanisms involved in speech production and requires the expertise of an experienced speech pathologist. VPI is only one element of speech problems that can be seen in patients with cleft palate. A standardized speech assessment should be used at each center that evaluates these patients (Fig. 2A,B). This formal examination allows for consistency in diagnosis and the ability for quality improvement strategies. The same clinical evaluation and measurements should be obtained for each visit and ideally should be performed by the same speech pathologist(s). Specialized testing such as nasometry, videofluoroscopy, and nasopharyngoscopy usually is warranted in addition to standard screening and evaluation tools. Nasometry can be a useful tool for evaluating speech in patients with a nasality and VPI [16,17].

This mechanical device associates the relative difference between nasal and oral cavity acoustical energy as detected by microphones positioned in the nose and mouth. The device objectively documents oral and nasal resonance characteristics. Several studies have suggested that, despite this technique’s ability to evaluate hypernasality accurately, it is not as effective as clinical evaluation [16,17]. The nasometry device can be a useful tool to track an individual’s response over time, but as a diagnostic tool the device lacks predictable sensitivity and specificity. Videofluoroscopy of the airway using oral contrast material can be helpful in evaluating speech by visualizing the different aspects of the dynamic muscular action and other anatomic factors [18,19]. Fistulas and their impact on speech production also may be appraised in this manner. Multiple views are required to assess the entire velopharyngeal mechanism, and an experienced speech pathologist must be present to administer the verbal testing in the radiology suite. This allows for dynamic testing of

Fig. 3. Superiorly based pharyngeal flap. (A) Elevation of myomucosal flap from the prevertebral fascia and division of the soft palate tissues. (B) Dissection of the oral, nasal, and muscle layers for inset of the flap. (C) Insertion of the flap with closure of the oral mucosa over the raw defect to decrease scarring. (D) Sagittal view of the inset flap at the appropriate vertical height.

B.J. Costello et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 539–551

the velopharyngeal mechanism and for review of the test with other clinicians for treatment planning. Digital imaging and audio data can be stored, manipulated, and analyzed with greater ease than videotape. Nasopharyngoscopy with a fiberoptic flexible scope provides a direct view of the velopharyngeal mechanism from the nasopharynx while the patient is verbally tested by an experienced speech pathologist [18]. The technique avoids exposure to radiation, requires the use of topical anesthesia, compliant behavior of the patient, and good technique. Excellent views of the velopharyngeal mechanism in motion may be obtained, including visualization of the soft palate and the lateral pharyngeal walls during phonation. Information can be stored and reviewed later by other clinicians to allow for treatment planning.

545

Management of cleft-related velopharyngeal insufficiency Once the diagnosis of VPI has been made, treatment may consist of nonsurgical speech therapy, obturation with a speech bulb, placement of a palatal lift, or reconstructive surgery of the airway. Mild VPI may be treated successfully with speech therapy alone, but more significant VPI usually requires surgical management of the palate. Patients who exhibit borderline VPI may be treated with speech therapy, palatal lifters, and speech bulb obturators. Surgical management using one of these procedures is usually considered when more conservative initial measures are unsuccessful. Surgical treatment of VPI is indicated when the problem is related to anatomic factors and docu-

Fig. 3 (continued ).

546

B.J. Costello et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 539–551

mented to be consistent. Which specific procedure is best used for a patient with VPI is frequently debated, but the goal of surgery remains the same. By surgically recruiting additional local tissue to decrease the aperture, complete or improved closure of the velopharyngeal sphincter can occur. Once the diagnosis is confirmed, the timing of surgical intervention should be early to prevent long-term speech difficulties and abnormal articulatory compensations that are difficult to correct later in life. A firm diagnosis of VPI may not be possible before age 3 because appropriate testing is difficult in such young children. For most children, reliable testing can be performed somewhere between 3 and 5 years of age. The decision for surgical intervention is based on the individual child’s speech and phonemic age, however, rather than simply chronologic age. Because no convincing data exist to favor one technique over another, the surgeon and speech pathologist must work together to select the procedure that might offer the best outcome based on the specific clinical situation. The superiorly based pharyngeal flap procedure recruits tissue from the posterior wall of the pharynx and inserts it within the musculature of the soft palate (Fig. 3A – D). Schoenborn first described the pharyngeal flap in 1876 [20 – 22]. This flap essentially creates two lateral ports, which usually can be closed under function effectively if lateral wall motion of the pharynx is good. The port size can vary considerably based on suturing techniques and the width of the tissue flap that is elevated from the prevertebral fascia [1,23]. The length of the flap should allow for adequate insertion into the musculature of the palate without excess draping. Flaps that are too long do not function well because of laxity, and flaps that are too short often thin to the point that the lateral ports are much too large, which perpetuates the VPI. When randomly applied to patients with typical VPI problems, pharyngeal flap procedures are generally approximately 80% effective in improving hypernasality [1,24]. Shprintzen has shown that with careful diagnosis and patient selection this procedure is 97% effective in treating VPI [1,24]. Shprintzen has advocated tailoring the pharyngeal flap width and position based on the particular characteristics seen on flexible endoscopy [24,25]. Thin or wide flaps can be tailored based on characteristics of lateral wall motion. Flaps also can be positioned asymmetrically in some patients who present with asymmetric VPI, such as persons with hemifacial microsomia. If a fistula is present within the soft palate or at the junction of the hard and soft palates, then the pharyngeal flap can be used to close the fistula during insertion into the soft palate mus-

culature. Limited flaps are raised within the velum to allow for layered closure. The inferiorly based pharyngeal flap can be useful, but most surgeons have found it to be of limited use because of its tendency to retract and thin after secondary healing and contracture. The result is a limited degree of velopharyngeal sphincter augmentation. Despite these limitations, however, some studies advocate the use of an inferiorly based pharyngeal flap and report similar speech outcomes when compared with superiorly based flaps [26]. Sphincteroplasty operations recruit lateral tissue, usually from the tonsilar pillar region, to allow for easier velopharyngeal closure (Fig. 4A – D). Many techniques are described, but the most common technique sutures these superiorly based lateral flaps to the posterior wall at the level of the palate to decrease effectively the distance from the soft palate to the posterior pharynx [27 – 30]. When the palate moves effectively but lacks length, this can be a good option. Some authors have suggested that these types of pharyngoplasty procedures have less immediate or late airway complications than pharyngeal flap procedures, but this has yet to be confirmed adequately in a large prospective outcome evaluation. Another potential advantage of the pharyngoplasty is fewer problems with posterior nasal mucous retention. Speech bulbs made of acrylic have been used to augment the velopharyngeal sphincter. Most patients initially treated with speech appliances benefit from pharyngeal flap procedures. Although these devices may be as much as 97% effective in alleviating VPI, patient compliance is limited because the devices are uncomfortable to wear. The use of a speech bulb or palatal lift prosthesis is a better alternative in patients who are not good surgical candidates because of comorbid conditions. Various techniques have described augmentation of the posterior pharyngeal wall in an effort to facilitate closure of the nasal airway. Autogenous and alloplastic implants have been used, including local tissue flaps, rib cartilage, synthetic injections of silicone, Silastic, Teflon, Proplast, and collagen [32,33]. Currently, these types of procedures are rarely used. Improvement in speech after augmentation of the posterior pharyngeal wall is unpredictable [1]. Problems with migration or extrusion of the implant material and an increased incidence of infection often add to the morbidity associated with these procedures. They are no longer recommended in most cases. Some surgeons advocate the use of a revisional palatoplasty instead of a pharyngeal flap procedure in the management of patients with VPI after cleft palate

B.J. Costello et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 539–551

547

Fig. 4. Sphincteroplasty. (A) Incision of the posterior pharyngeal wall and the posterior tonsillar pillars. (B) Elevation of the tonsillar pillar myomucosal flaps. (C) Approximation in the central pharyngeal area to customize the central port size. (D) Sutured flaps placed into the posterior pharyngeal walls and posterolateral pharyngeal walls.

548

B.J. Costello et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 539–551

repair in infancy [34 – 36]. Specifically, a double opposing Z-plasty procedure, or furlow palatoplasty, is carried out to lengthen the soft palate and facilitate velopharyngeal closure. Unfortunately, the anticipated benefits of these ‘‘second palatoplasties’’ have never been established. The clinician also must consider the disadvantages of this type of surgical procedure and weigh them against potential benefits. The double-opposing Z-plasty procedure requires a more aggressive dismantling of the palate than what is required during a conventional pharyngeal flap procedure. The result may be a slightly longer palate, but one with more extensive scarring and less physiologic movement. Another consideration is the significantly higher rate of fistula formation associated with this type of repair [31].

Complications of surgery for velopharyngeal insufficiency Surgery that involves airway structures is always associated with the potential for complications related to postoperative hemorrhage and edema. As a result, patients who undergo attachment of a pharyngeal flap require intensive care unit – level hospitalization with continuous airway monitoring during the first 24 hours. This type of setting permits the rapid recognition and prompt management of these complications and the resultant airway compromise. Of all the procedures related to cleft care, the pharyngeal flap and sphincteroplasty operations carry the greatest risk for early airway compromise. Airway loss and compromise are not common but must be dealt with swiftly. Long-term postoperative complications are frequently seen as part of a continuum of pathologic resistance in the airway that may result after pharyngeal flap surgery. Patients who have undergone pharyngeal surgery to decrease the aperture of the sphincter to allow for closure during the formation of certain speech sounds may present with problems related to snoring, upper airway resistance sequence, or obstructive sleep apnea. These pathologic conditions are each a progressive form of increased resistance within the upper airway. Snoring is the audible sound produced when airflow is inefficient through the upper airway. This may not be significant pathophysiologically but may be bothersome to the significant other if the snoring prevents the other’s normal and restful sleep. Upper airway resistance syndrome develops when more significant resistance occurs without clear obstruction and a decrease in effective oxygenation. This is probably clinically

important and may contribute to long-term health problems. Obstructive sleep apnea is the clear cessation of breathing during sleep that causes an arousal from the normal sleep cycle. This condition contributes to daytime hypersomnolence and is associated with increased risks for hypertension, cardiovascular disease, and stroke. Patients who suffer from hypersomnolence should be evaluated by an experienced sleep specialist and undergo formal polysomnography. Many patients who have had pharyngeal flaps in childhood can tolerate surgical division of the flaps to attempt to alleviate obstructive sleep apnea, although they may require further treatment, including mandibular surgery to alter the airway dynamics below the level of the palate. Adjunctive procedures, such as genioglossus advancement, hyoid suspension, tongue base reduction procedures, or intranasal surgery, may be helpful in improving airflow [37]. Clinicians experienced with treating sleep apnea and clefts are ideally suited to approach these problems, because the balance between a functional velopharyngeal mechanism and efficient airflow in a cleft patient is a delicate one. Skeletal reconstruction for maxillary and mandibular deformities may be helpful in alleviating obstructive sleep apnea and should be considered before other maneuvers that directly change the tissues of the velopharyngeal mechanism, such as dividing the flap [38]. Velopharyngeal considerations after maxillary advancement Forward displacement of the maxilla in noncleft patients is always tolerated well because patients have adequate neuromuscular reserve to compensate for the change in position of the soft palate that results. Midfacial advancement in patients with a repaired cleft palate may worsen preexisting VPI or be the cause of new onset VPI [14,39,40]. A minority of cleft patients, with borderline velopharyngeal closure preoperatively, develop hypernasal speech even after relatively small degrees of maxillary displacement. Patients must be counseled appropriately about the potential for a deterioration in velopharyngeal function after orthognathic surgery. A complete speech evaluation by a speech pathologist familiar with cleft palate speech is also recommended before advancement of the maxilla. Almost all cleft patients have some element of hypernasality immediately after surgery. Of the patients who develop significant hypernasality after maxillary advancement, however, the number of them who require surgical correction with a pharyn-

B.J. Costello et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 539–551

geal flap or sphincteroplasty is low [14,39,40]. Fortunately, resolution gradually occurs with time so that for most patients, returning to baseline speech by 6 months after surgery is typical. Delaying subsequent pharyngeal surgery to reduce nasality for at least 6 months after maxillary advancement is advisable. This delay allows natural compensation to occur and permits bone healing to proceed without introducing more scarring, which may contribute to skeletal relapse. Improvement of nasal speech after surgery is an interesting observation in some patients with pharyngeal flaps in place that have some VPI before midface advancement. Although sibilant distortions and articulation errors secondary to malocclusion are expected to improve, reduction of hypernasality after maxillary advancement is paradoxical. The explanation of this observation is the altered dynamics of the sphincter that result after surgery. Stretching the flap and its positional change apparently improves the dynamics of the velopharyngeal mechanism enough so that improved speech results in some patients. This observation is not predictable, and patients must be cautioned appropriately. When a pharyngeal flap is in place and maxillary advancement is undertaken, the flap should be removed only if it does not permit adequate mobilization of the maxilla. When the flap is in place, nasal intubation can be difficult and the anesthesiologist must be prepared to use endoscopic assistance with endotracheal tube insertion (Fig. 5) [14].

549

Patients who develop VPI that is consistent (longer than 6 months and unresolved with speech therapy) and related to an anatomic problem as documented by videofluoroscopy or nasoendoscopy may be considered for placement of a pharyngeal flap or other treatment.

Distraction osteogenesis for maxillary advancement Recently, techniques combining osteotomies and gradual distraction have been applied in the correction of residual skeletal problems encountered in patients with cleft lip and palate [37,41 – 44]. Gradual distraction of the craniofacial skeleton and the surrounding soft tissues has been explored as an alternative method for skeletal reconstruction in an attempt to overcome some of the inherent limitations associated with conventional techniques. Approximately 20% of patients who have maxillary advancements develop VPI after advancement of the maxilla using traditional techniques. Initially it was believed that VPI would not occur as often with maxillary advancement because the velopharyngeal mechanism would be able to adapt more slowly with the gradual advancement. Initial reports have indicated that VPI does occur at similar rates after maxillary advancement with distraction osteogenesis and offers no significant speech advantage over traditional orthognathic surgery [40,45,46].

Fig. 5. (A,B) A catheter, passed nasally through the velopharyngeal ports, serves to guide the nasoendotracheal tube past the pharyngeal flap. (From Turvey TA, Vig KWL, Fonseca RJ. Maxillary advancement and contouring in the presence of cleft lip and palate. In: Facial clefts and craniosynostosis. Philadelphia: WB Saunders; 1996; p. 441 – 503; with permission.)

550

B.J. Costello et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 539–551

Summary Disturbances in speech are among the most debilitating problems that face children born with cleft palate. Initially, patients who have undergone cleft palate repair must be monitored as speech development proceeds during infancy and early childhood, because approximately 20% develop some degree of VPI. Later in life, necessary skeletal movements also may negatively impact velopharyngeal function after orthognathic surgical procedures. Successful treatment often involves surgical reconstruction of the upper airway and is effective in most cases. Successful correction of VPI allows children to communicate effectively and not suffer needlessly with the stigma of speech disorders related to their palatal cleft.

[14]

[15]

[16]

[17]

[18]

References [1] Posnick JC. The staging of cleft lip and palate reconstruction: infancy through adolescence. In: Posnick JC , editor. Craniofacial and maxillofacial surgery in children and young adults. Philadelphia: WB Saunders; 2000. p. 785 – 826. [2] Croft CB, Shprintzen RJ, Rakoff SJ. Patterns of velopharyngeal valving in normal and cleft palate subjects: a multi-view videofluoroscopic and nasendoscopic study. Laryngoscope 1981;91:265 – 71. [3] Croft CB, Shprintzen RJ, Daniller A, Lewin ML. The occult submucous cleft palate and the musculus uvulae. Cleft Palate J 1978;15:150 – 4. [4] Dickson DR. Normal and cleft palate anatomy. Cleft Palate J 1972;9:280 – 93. [5] Dickson DR, Maue-Dickson W. Velopharyngeal anatomy. J Speech Lang Hear Res 1972;15:371 – 81. [6] Lubker JF. An electromyographic-cinefluorographic investigation of velar function during normal speech production. Cleft Palate J 1968;5:1 – 17. [7] Lubker JF. Normal velopharyngeal function in speech. Clin Plast Surg 1975;2:249 – 59. [8] Kuehn DP, Moon JB. Velopharyngeal closure force and levator veli palatine activation levels in varying phonetic contexts. J Speech Lang Hear Res 1998;41: 451 – 61. [9] Azzam NA, Kuehn PD. The morphology of musculus uvulae. Cleft Palate J 1977;14:78 – 87. [10] Glaser ER, Skolnick ML, McWilliams BJ, Shprintzen RJ. The dynamics of Passavant’s ridge in subjects with and without velopharyngeal insufficiency: a multiview videofluoroscopic study. Cleft Palate J 1979; 16:24 – 33. [11] Passavant G. On the closure of the pharynx in speech. Archiv Heilk 1863;3:305. [12] Passavant G. On the closure of pharynx in speech. Virchows Arch 1869;46:1. [13] Warren DW. Compensatory speech behaviors in cleft

[19]

[20] [21] [22] [23]

[24]

[25]

[26]

[27]

[28] [29]

[30]

palate: a regulation/control phenomenon. Cleft Palate J 1986;23:251 – 60. Fonseca RJ, Turvey TA, Wolford LM. Orthognathic surgery in the cleft patient. In: Fonseca RJ, Baker SJ, Wolford LM, editors. Oral and maxillofacial surgery. Philadelphia: WB Saunders; 2000. p. 87 – 146. Hall C, Golding-Kushner KJ. Long-term follow-up of 500 patients after palate repair performed prior to 18 months of age. Presented at the Sixth International Congress on Cleft Palate and Related Craniofacial Anomalies. Jerusalem, June 1989. Dalston RM, Warren DW, Dalston ET. Use of nasometry as a diagnostic tool for identifying patients with velopharyngeal impairment. Cleft Palate Craniofac J 1991;28:184 – 9. Warrren DW, Dalston RM, Trier WC, Holder MB. A pressure-flow technique for quantifying temporal patterns of palatopharyngeal closure. Cleft Palate J 1985; 22:11 – 9. Shprintzen RJ, Golding-Kushner KJ. Evaluation of velopharyngeal insufficiency. Otolaryngol Clin N Am 1989;22:519. Warren DW, Hofmann FA. A cineradiographic study of velopharyngeal closure. Plast Reconstr Surg 1961;28: 656 – 69. Bernstein L. Treatment of velopharyngeal incompetence. Arch Otolaryngol 1967;85:67 – 74. Rosseli S. Divisione palatine 3 sua aura chirurgico. Alu Congr Internaz Stomatal 1935;36:391 – 2. ¨ ber eine neue methode der staphylorSchoenborn D. U raphies. Arch Klin Chir 1876;19:528. Hogan MV. Clarification of the surgical goals in cleft palate speech and the introduction of lateral port control pharyngeal flap. Cleft Palate J 1973;10:331. Shprintzen RJ. The use of multiview videofluoroscopy and flexible fiberoptic nasopharyngoscopy as a predictor of success with pharyngeal flap surgery. In: Ellis F, Flack E, editors. Diagnosis and treatment of palatoglossal malfunction. London: College of Speech Therapists; 1979. p. 6 – 14. Shprintzen RJ, McCall GN, Skolnick ML, Lencione RM. Selective movement of the lateral aspects of the pharyngeal walls during velopharyngeal closure for speech, blowing, and whistling in normals. Cleft Palate J 1975;12:51 – 8. Whitaker L, Randall P, Graham W, Hamilton R, Winchester F. A prospective and randomized series comparing superiorly and inferiorly based posterior pharyngeal flaps. Cleft Palate J 1972;9: 304 – 11. Jackson I, Silverton JS. The sphincter pharyngoplasty as a secondary procedure in cleft palates. Plast Reconstr Surg 1983;71:180. Jackson IT. Sphincter pharyngoplasty. Clin Plast Surg 1985;12:711 – 7. Orticochea M. Physiopathology of the dynamic muscular sphincter of the pharynx. Plast Reconstr Surg 1997;100:1918 – 23. Orticochea M. Constriction of a dynamic muscle

B.J. Costello et al. / Oral Maxillofacial Surg Clin N Am 14 (2002) 539–551

[31]

[32]

[33]

[34]

[35]

[36]

[37]

[38]

[39]

sphincter in cleft palates. Plast Reconstr Surg 1968; 41:323 – 7. Wilhelmi BJ, Appelt EA, Hill L, Blackwell SJ. Palatal fistulas: rare with the two-flap palatoplasty repair. Plast Reconstr Surg 2001;107:315 – 8. Bluestone CD, Musgrave RH, McWilliams BJ. Teflon injection pharyngoplasty: status 1968. Laryngoscope 1968;78:558 – 64. Smith JK, McCabe DF. Teflon injection in the nasopharynx to improve velopharyngeal closure. Ann Otol Rhinol Laryngol 1977;86:559 – 86. Chen PK, Wu JT, Chen YR, Noordhoff MS. Correction of secondary velopharyngeal insufficiency in cleft palate patients with the Furlow palatoplasty. Plast Reconstr Surg 1994;94:933. Chen PK, Wu JT, Hung KF, Chen YR, Noordhoff MS. Surgical correction of submucous cleft palate with furlow palatoplasty. Plast Reconstr Surg 1996;97:1136. Hudson DA, Grobbelaar AO, Fernandes DB, Lentin R. Treatment of velopharyngeal incompetence by the Furlow Z-plasty. Ann Plast Surg 1995;34:23. Hendler BH, Costello BJ, Silverstein KE, Yen D, Goldberg A. An analysis of uvulopalatopharyngoplasty, genioglossus advancement and maxillo-mandibular advancement for the treatment of obstructive sleep apnea. J Oral Maxillofacial Surg 2001;59: 892 – 7. Figueroa AA, Polley JW, Ko EWC. Maxillary distraction for the management of cleft maxillary hypoplasia with a rigid external distraction system. Semin Orthod 1999;5:46 – 51. Posnick JC, Tompson B. Cleft-orthognathic surgery: complications and long-term results. Plast Reconstr Surg 1995;96:255 – 66.

551

[40] Posnick JC, Ruiz RL. Discussion of management of secondary orofacial cleft deformities. In: Goldwyn RM, Cohen MN, editor. The unfavorable result in plastic surgery: avoidance and treatment. 3rd edition. Philadelphia: Lippincott Williams and Wilkins; 2000. [41] Chen PK, Liou EJW, Hung KF, Huang CS, Chen YR. Lengthening of hypoplastic maxilla in cleft patients using interdental distraction osteogenesis and rapid orthodontic tooth movement [abstract]. Presented at the International Society of Craniofacial Surgery 8th International Congress. Taipei, Taiwan, November 1999. [42] Figueroa AA, Polley JW. Management of severe cleft maxillary deficiency with distraction osteogenesis: procedure and results. Am J Orthod Dentofacial Orthop 1999;115:1 – 12. [43] Polley JW, Figueroa AA. Rigid external distraction: its application in cleft maxillary deformities. Plast Reconstr Surg 1998;102:289 – 311. [44] Polley JW, Figueroa AA, Hohlastos MS. Management of secondary orofacial cleft deformities. In: Goldwyn RM, Cohen MN, editor. The unfavorable result in plastic surgery: avoidance and treatment. 3rd edition. Philadelphia: Lippincott Williams and Wilkins; 2000. [45] Hung KF, Chen PKT, Lo LJ, Yun C, Wang R. Alteration of the velopharyngeal function after rigid midface distraction [abstract]. Presented at the International Society of Craniofacial Surgery 8th International Congress. Taipei, Taiwan, November 1999. [46] Polley JW, Figueroa AA, Ko W. Rigid external distraction, long term follow-up [abstract]. International Society of Craniofacial Surgery 8th International Congress. Taipei, Taiwan, November 1999.

Oral Maxillofacial Surg Clin N Am 14 (2002) 553 – 562

The management of oronasal fistulas in the cleft palate patient Orrett E. Ogle, DDS Department of Dentistry, Oral and Maxillofacial Surgery, Room 2B-320, Woodhull Medical and Mental Health Center, 760 Broadway, Brooklyn, NY 11206, USA

An oronasal fistula is an abnormal communication between the oral cavity and the nose that occurs after surgical repair of a cleft palate. After the primary repair of a cleft palate, oronasal fistulas develop in a certain number of patients; this is the most common defect in the hard palate after the primary surgical repair [1]. These fistulas are sometimes located in the soft palate but occur more frequently in the hard palate. They typically occur at the junction of the primary and secondary palate or at the junction of the hard and soft palate. It is difficult to determine the true incidence of fistula formation after primary repair of a cleft palate because the reports in the literature vary widely, and the centers that generate the reports seem to have a significant influence on the rate of fistula development. The severity (width) of the original cleft, however, shows a direct correlation with the risk of fistula formation [2], and the incidence of fistulas is higher after palatoplasty for complete clefts of the primary and secondary palates than after closure of an isolated secondary palatal cleft [3]. The technique used to close the palate and the experience and skill of the surgeon affect the occurrence rate [4]. Reported incidences over the years have ranged from a low of 5% [5] to between 9% and 50% with one-stage closures in a review article by Shultz [6]. In 1960, Musgrave and Bremner [5] reported the incidence of fistula formation in the palate to be 12.5% for bilateral clefts, 7.7% for unilateral clefts, and 4.6% for isolated clefts of the secondary palate. These numbers seem to be low compared to rates published

E-mail address: [email protected].

more recently in which the mean for isolated cleft palate was reported at 15% [6]. Lilja et al [7] reported an 8% fistula formation rate with their older use of the Wardill-Killner technique, and in the author’s experience this technique produces fewer fistulas in the hard palate than other techniques that close the hard and soft palate in a one-stage procedure. The defect (often referred to as a ‘‘fistula’’) in the anterior alveolar palate (Fig. 1) must be considered a residual cleft rather than a fistula, because this area is usually not repaired as a part of the primary closure of the cleft palate defect in cleft lip and cleft palate patients but is intentionally left opened. The management of this defect is presented elsewhere in this issue and is not discussed in this article. Some of the causes of oronasal fistulas include excessive tension on the primary repair site because of inadequate medial mobilization of the flaps, excessive trauma to the margins of the palatal flaps by instruments during surgery, faulty suturing, traumatic disruption of the healing wound, infections, inadequate attachment of the palatal tissue to the nasal mucosa, hematoma formation between the oral and nasal layers, and flap necrosis. The development of the fistula may be noted in the immediate postoperative period or may not become evident for a few weeks. Surgery to close the fistula should not be attempted too early, and the surgeon should wait until the area is fully healed and the inflammation has subsided completely (4 – 6 months). Attempting to close the defect in the presence of inflammation only makes the fistula worse because sutures do not hold in the inflamed palate and ‘‘walk through’’ the tissue in a few days. The presence of excess foreign body material de-

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 5 0 - X

554

O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 553–562

Fig. 1. Unrepaired alveolar cleft.

creases hygiene at the repaired site, further increases the inflammation, and causes more tissue trauma and increased necrosis, with a resultant loss of additional tissue. An inadequate blood supply also negatively affects the healing process. In most attempts at early closure, only a one-layer closure is achieved, and secondary-breakdown is frequent. Adequate healing and subsequent scar contraction lead to a decrease in the size of the fistula and, in some cases, the fistula might even close spontaneously [8] or decrease to a size at which it causes minimal problems because the patient adapts completely to the larger problems that result from the fistula. Poor blood supply is one of the major contributing factors for the failure of fistula closure. Six to 12 months is the average time for the blood supply to reestablish itself satisfactorily after primary repair of the cleft palate. A wait of longer than 6 months is reasonable before closure of a palatal fistula is attempted.

Problems of oronasal fistulas The problems caused by oronasal fistulas depend on the size of the fistulas and a patient’s ability to accommodate the smaller ones. Some of these fistulas are so small that they may not cause any obvious problems and the patient may be unaware of their existence. On the other hand, some children learn to control the problems caused by the fistula as they get older, despite the persistence of a moderately sized defect, and their complaints are minimal. A fistula is often a nuisance that permits liquids and occasionally solid food to go through into the nose. This is true regardless of the size of the hole. Small fistulas can be bothersome to the patient if popcorn kernels, nuts, or grains become lodged in the opening. Removing the particle can be uncomfortable and embarrassing as the patient noisily tries to suck the particle back

into the mouth. Food particles that become impacted into a small fistula or crevice produce malodorous breath. Leakage from the nose also can be problematic and embarrassing. As nasal secretion seeps into the mouth, it produces a bad taste, poor oral hygiene, and bad breath. Larger fistulas permit a free flow of fluid into the nasal cavity in a volume large enough that it may exit through the naris. When attempting to drink, fluid may embarrassingly escape through the nose and run down on the upper lip. Similarly, mucus from the nasal cavity freely enters the mouth. The oronasal communication also may result in air loss through the nose during speech, which distorts articulation and produces hypernasal speech. Henningsson and Isberg [9] found that a palatal fistula as small as 4.5 mm2 can affect speech and resonance and result in hypernasality, audible nasal escape, and weakness of pressure consonants.

Closure of fistula The repair of a palatal fistula in the cleft palate patient is much more difficult than it seems, and most fistulas present a problem in which an extensive operation is needed to resolve a small defect. In some cases the financial cost may be high because a short stay in the hospital may be required for young children (teenagers can be treated on an ambulatory basis), and dietary restrictions are necessary for 7 to 14 days. Because of sometimes limited surgical access and scar tissue from previous surgery, successful closure is not always achieved. Large fistulas that permit the passage of liquid and food particles into the nose or affect speech should be closed as early as possible. When the fistula is small and presents minimal problems to the patient, closure can be delayed for several years. Small fistulas may be left untreated if they present no significant problem. It is the author’s belief, however, that most of these defects should be closed at some point to provide a healthy oral and nasal environment. Most of these openings can be closed by using local tissue from the roof of the mouth without having to resort to distal flaps. The local blood supply is usually good enough to allow safe mobilization of mucoperiosteal flaps from the hard palate despite the presence of scarring. When additional tissue is needed, a flap may be developed from the tongue. In the case of the posterior fistulas addressed in this article, the tongue flap is posteriorly based. Closure of a communication between the oral and nasal cavities should be two layered because it

O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 553–562

provides greater support and stability of the repair and reduces the risk of failure. A two-layered closure can be obtained by turning medial and lateral flaps from the cleft margin (turnover flaps) to form the nasal floor. This area can be covered with a palatal flap based on the greater palatine artery [10]. When a palatal rotational flap is used, the suture line ideally should be over bone. The design of this palatal flap is similar to the one used to close a chronic oro-antral fistula, which results from perforation into the maxillary sinus as a complication of exodontia [11]. When designing the flaps on the palate for closure of the fistula, the flaps must be larger than the actual defect. This rule applies to the turnover flap and the rotation flap. The palatal mucoperiosteum is stiff, particularly when scarred by previous surgery. It does not transpose easily, nor is it elastic enough to stretch. The design also must permit adequate mobilization of the flaps to allow complete coverage of the defect without tension. To avoid failure, the flaps should be freed up sufficiently to allow them to come together in a tension-free manner. Oronasal fistulas in the soft palate do not require early treatment unless speech is affected. If there is adequate movement in the soft palate and speech is grossly unaffected, these fistulas may be closed at the same time that the bone graft for the alveolar cleft is performed [3]. The soft palate fistula can be closed easily by excising the fistula and closing the defect in two layers. Although it is tempting to close a narrow defect that follows the line of the palatal cleft in the hard palate by performing a modified von Langenbeck procedure (advancement flaps) and suturing the edges of the fistula medially in one layer, the surgeon must be aware that this technique has a high failure rate. Closure of the oronasal fistula in patients younger than age 5 is controversial. Before that age the maxilla has not matured adequately, and a secondary surgical intervention would disrupt the overlying periosteum, which further compromises the existing blood supply, increases the scarring with greater scar contraction on the alveolus, and worsens the malocclusion by the time of the full permanent dentition. Multiple procedures to achieve complete palatal closure were believed by some surgeons to cause inhibition in maxillary growth [12], which is still the belief of some cleft surgeons. Disruption of the overlying palatal periosteum at an early age also has been believed to cause midface growth restriction [13]. Contrary to this concept, other authors have stated that no hard evidence supports the theory that delaying surgery improves growth [14,15]. Many surgeons believe, however, that scar tissue produced by leaving

555

denuded area on the palate leads to subsequent dental malocclusion [16]. Because of this, some cleft centers with strong orthodontic input wait until the patient is at least 10 years old before attempting fistula repair. (Readers also should refer to the article by Bishara elsewhere in this issue for further discussion of this topic.) The quality of the speech always should be the guiding factor. For cases in which speech is severely affected, the surgeon, in consultation with the speech pathologist, may consider closing the fistula early. A speech distortion acquired at an early age is not necessarily permanent, however, and may be corrected through vigorous speech therapy after closure of the fistula and orthodontic or orthodontic/surgical treatment is completed [17]. As an alternative to early surgery, an obturator may be used to manage the oronasal fistula. D’Antonio et al [18] found a significant improvement in the perceptual and aerodynamic characteristics of speech with temporary occlusion of hard palate fistulas. Early speech problems may be managed successfully on a temporary basis with a palatal prosthesis if compliance can be maintained [19], although it should be noted that 35% of patients studied were noncompliant with the prostheses. Isberg and Hennigsson [20] reported that obturation of the fistula consistently improved velopharyngeal activity regardless of its size and recommended that preoperative velopharyngeal videofluoroscopy be performed with an obturator in place. A palatal prosthesis, however, never should be considered as definitive treatment, and surgical repair of the defect always should be the final goal. If a palatal prosthesis is used, the child should be monitored carefully by a speech pathologist and surgery should be considered if adequate speech does not develop. Another use of the palatal prosthesis may be diagnostic, because it may be used to cover the defect preoperatively to give the surgeon the ability to predict surgical outcomes before secondary repair if the decision was made to repair the fistula before age 5. A maxillary denture with an attached speech bulb may be used to obturate the fistula in older individuals if requested by the patient (Fig. 2). The palatal prosthesis also can be used to obturate the fistula while the maxillary arch is expanded orthodontically [21].

Surgical techniques Longitudinal fistulas along the line of the palatal cleft If the fistula is long ( > 15 mm) and narrow (3 – 7 mm), closure may be attempted with a modification

556

O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 553–562

Fig. 2. Denture with an attached speech bulb that was used to obturate an oronasal fistula in an elderly edentulous cleft patient.

of the von Langenbeck procedure. With small fistulas it is difficult to obtain adequate closure of the nasal mucosa because of a lack of working access, and often it is not possible to bring the bleeding edges together because they tend to roll upward into the nasal cavity. A secure two-layered closure must be obtained and there should be minimal tension on the closure of the nasal mucosa. The cross-section of the fistula is measured and divided into two. The incision near the edges of the fistula must provide the additional tissue that is needed to bridge the defect. The distance obtained by halving the width of the fistula is noted, and an additional 2 to 4 mm is added, which provides the distance from the edge of the fistula where the medial incisions are placed. An adequate nasal flap is important to provide a tension-free closure. In addition to providing tissue to lengthen the nasal mucosa and bridge the defect, the additional border of oral mucosa is away from the edge of the fistula, which may be inflamed, and is better able to hold sutures. The two medial incisions are placed adjacent to the fistula. The length of these incisions should extend approximately 5 to 7 mm beyond the end of the fistula anteriorly and posteriorly. Lateral releasing incisions are then made. The surgeon is able to see a scar line between where the flap for the primary closure meets with the area that was left denuded to heal by secondary intention. The lateral releasing incisions should be placed on this scar line and should be long, which gives an adequate flap and

good lateral release and maintains the arterial blood supply. The incision is made to bone. Starting at the lateral incisions, a full-thickness mucoperiosteal flap is lifted widely off the bone. The surgeon should be careful to maintain the periosteal elevator on the bone while lifting the entire periosteum. (Fig. 3). The dissection is continued medially to end at the previously made incision at the margins of the fistula. The surgeon should see the periosteal elevator exiting this incision. The lateral flap is mobilized completely. The surgeon should grasp the flap with a 1  2 delicate Adson forcep (12 cm) or any other long, fine tooth forceps and check to see if the flap can be advanced to approximately 3 mm beyond the midline without tension. This test should be conducted at several points. Once the surgeon is certain that the lateral flaps can reach the midline in a tensionfree manner, attention is directed to the nasal mucosa. Using a combination of straight and curved Freer elevators, the mucosa is elevated carefully toward the fistula. Small nicks may have to be placed at the ends of the incision to obtain adequate release to be able to turn over the flap. At the bony margin, the nasal mucosa is freed carefully from the superior aspect of the palatal shelve. The dissection of the nasal mucosa is complete when it is able to reach 2 to 3 mm beyond the midline at least at three points in a tension-free manner. Once the four flaps have been developed and adequately mobilized, they are sutured in the midline.

Fig. 3. Developing an oral mucosal flap for closure of fistula using a modified von Langenbeck technique.

O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 553–562

The nasal mucosa is closed with 4-0 Vicryl on a P3 or RB1 needle. When closing the nasal mucosa, the knots are placed into the nasal cavity so as to minimize dead space between the nasal and oral mucosal layers. The palatal mucosa is advanced and closed in the midline with 4-0 Vicryl (Fig. 4). Mattress sutures are used to evert the wound margin; inversion of the margins of the palatal mucosa would cause a recurrence of the fistula.

Large round fistulas (Fig. 5A) This type of fistula is best closed by using a lining turnover flap hinged on the edge of the defect and a covering flap of palatal tissue mobilized from the side of the cleft. The turnover flaps form the floor of the nose, which permits epithelium to be placed into the nasal cavity and the bleeding side facing toward the mouth. The bleeding tissue is covered by the rotational flap. An incision is placed around the fistula (Fig. 5B,C). The distance of the incision from the edge of the defect is determined as described in the previous section. The flap must be long enough to reach beyond the midline of the defect because the closure must be tension free. The flap is elevated carefully and is turned over 180° to form the lining of the nasal cavity

Fig. 4. Complete closure of the nasal mucosa and partial closure of the oral mucosa using the modifiedvon Langenbeck technique.

557

(Fig. 6A,B). These flaps are closed with 5-0 Vicryl on a RB1 or P3 needle. A template is fabricated from the packaging paper of the surgical glove. The paper is cut to shape to cover the defect completely. Holding the paper over the defect, an ideal base of the rotational flap is determined. A hemostat or blunt periosteal elevator is used to secure the paper template at the proposed base of the rotational flap, and the anterior edge is transposed over the palate to give the length and size of the palatal flap. It is wise to add a few extra millimeters to the tip and to one of the borders to ensure adequate tissue for closure. The palatal flap is outlined and cut (Fig. 7). The flap is mobilized fully all the way to the greater palatine foramen, which is located approximately opposite to the third molar at the junction of the vertical alveolus and the horizontal shelf of the palate. As the surgeon approaches the foramen, a small bony projection is noted. The flap must be mobilized fully and rotated freely. As the flap is rotated medially, some bunching of the tissue is noted at the medial turn. A triangular wedge may be excised to permit the flap to lay flat. The palatal mucoperiosteal flap is rotated and sutured in place with 4-0 Vicryl sutures to cover all cut margins. It is best to place the first suture at the tip of the rotational flap and take it to the deepest portion of the defect left by the turnover flap. Once this is secured, the posterior areas are closed followed by the anterior area closest to the surgeon (Fig. 8A,B). The ‘‘re-mucosalization’’ of the hard palate is by secondary intention. The coverage of the denuded area on the hard palate with new mucosa occurs rapidly, is usually complete by postoperative week 4, and results in a near normal appearing hard palate surface. Because this process takes place over bone, contracture and donor site deformity are minimal if performed in the secondary dentition stage. If done in the primary dentition stage, however, the resulting scar may have an adverse effect on dental development. Postoperative discomfort is minimal. The author does not advise the use of a prefabricated prosthesis to attempt coverage of the donor site defect because the prosthesis may cause pressure on the inflamed flap and compromise its blood supply. An area of dead space between the bone and the rotational flap that results in the anterior portion of the wound, can be obliterated by placing Gelfoam or strips of absorbable collagen hemostatic sponges between the flap and the bone. The surgeon should be sure that hemostasis is complete before discharging the patient from the operating suite. Bleeding points may be controlled with low power electrocautery.

558

O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 553–562

Fig. 5. (A) Large, round oronasal fistula in the posterior portion of the hard palate. (B) Outline of the incision for the turnover flaps for creating the nasal floor. The epithelial portion of the hinged flap is in the nasal passage. (C) One side of the hinged flap developed and being turned into the nasal floor.

Fig. 6. (A,B) Turnover flaps sutured to create the nasal floor.

O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 553–562

559

Soft palate fistulas

Fig. 7. Outline of rotation flap to form the outer layer of the closure.

A #12 or #15 Bard Parker blade is used to split the tissues in the middle of the fistula. Using a combination of the Jeter cleft palate scissors (a pair of angled scissors) and the Dean scissors, the oral mucosa is separated from the underling layer of muscle and nasal mucosa. A fairly wide dissection is made until it is possible to bring both layers to the midline without tension. The tissue should be grasped with fine tooth forceps with minimal force. Care must be taken not to handle the palatal mucosa excessively with these forceps because it traumatizes the wound margin and produces inflammation, which makes it difficult to hold the sutures in the immediate postoperative phase. The layer of muscle and nasal mucosa is closed with 4-0 Vicryl, as is the palatal mucosa. At least two mattress sutures should be placed in the oral mucosa to evert the margins.

Small round/oval fistulas (Fig. 9)

Tongue flap

The technique for closing these smaller fistulas is identical to that described for the large, round fistulas except that only one turnover flap is made (Fig. 10A,B). The turnover flap should be big enough to cover the defect completely. It is sutured beyond the clinical defect. When cutting the rotational flap, it should not be cut exactly at the edge of the defect; rather, a small margin of tissue should be left to hold sutures from the turnover flap. The rotational flap is measured, cut, elevated, and sutured into place with 4-0 Vicryl.

The tongue flap is indicated for closure of a palatal fistula in cleft palate patients with a persistent large palatal defect, in heavily scarred palates, and in cases in which previous attempts at fistula closure have been unsuccessful. It should not be the first method of choice and should be used only when other methods are not feasible. The tongue is undoubtedly the most important organ in the oral cavity with respect to sensation and function. Taking tissue from it may cause some sensory deficits and deformity that may otherwise be avoided by using local flaps to this

Fig. 8. (A,B) Postoperative view of immediate closure.

560

O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 553–562

Fig. 9. Small oval fistula in the middle zone of the hard palate.

more complex technique. It must be noted, however, that no reports have shown that removing sizeable segments from the tongue causes any impairment of speech or movement and that loss of tongue sensation and taste is temporary [22]. The tongue flap offers the advantages of an abundance of tissue for palatal reconstruction, an excellent blood supply, and ease of rotation. The posteriorly based midline tongue flap gives the greatest blood supply [23,24] and, consequently, a high success rate [22]. There is also low donor morbidity with tongue flaps [22,25]. Where possible, a two-layered closure also should be achieved with the tongue flap [26], but because of the cases in which the tongue flap is used for posterior fistulas this is often not possible. The surgery is performed under general anesthesia with a nasotracheal tube. The margins of the fistula

are deepithelialized by beveling the periphery of the defect to increase the area of contact. The bevel is placed away from the defect so as to increase the bleeding surfaces on the palatal mucosa adjacent to the defect. The bevel should be fairly large to expose a widely bleeding surface onto which the tongue flap is sutured. The tongue flap is designed so that the base of the flap lies slightly behind the posterior border of the fistula with the tongue in the neutral position. The width of the flap should be sufficient to fill the crosssectional defect, and the length should be long enough (Fig. 11) to allow for the turnover with some freedom of tongue movement. The creation of a long pedicle permits slack in the flap, which allows greater freedom of movement of the tongue [27]. The base of the flap should be at least half the width of the tongue or two thirds the width of the fistula to ensure a rich blood supply. The base should be as wide as anatomically possible. The tongue is dried and the flap design is marked on the dorsum of the tongue with a surgical marking pen. The flap is raised with either a #15 scalpel blade or electrocautery with an even thickness. The thickness of the flap should be between 7 and 10 mm and includes the underlying muscle, which ensures a rich vascularity. After full mobilization of the flap, complete hemostasis is obtained at the donor site, which is then closed with resorbable sutures. In attaching the tongue flap, 4-0 Vicryl is first placed in the posterior portion of the defect. Approximately six sutures are preplaced. The needles are left attached to the sutures, and they are left long. The

Fig. 10. (A) Outline of incisions for one turnover flap and a rotational flap to close the defect and form the outer layer. (B) Immediate postoperative closure.

O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 553–562

Fig. 11. Posteriorly based tongue flap with long pedicle.

alignment of the tongue flap is determined and the position where each suture will be placed is ascertained. At least three sutures from the margins of the fistula are placed into the tongue flap and left untied originally. The knots may be tied after the third suture is in place. The remaining preplaced sutures are passed through the tongue flap and secured. The remainder of the unclosed margins, which are accessible, is closed completely with interrupted sutures. In most cases the flap is usually left with a raw surface, but it may be tubed. Maxillo-mandibular fixation (MMF) can be used to decrease movement and tension on the sutures and ensure the security of the flap insertion [28,29]. At the end of the procedure the surgeon should evaluate the adequacy of the airway. A bite block may be left in the mouth for the first 12 hours and the patient kept in a beach chair position. Patients who have had previous velopharyngeal flaps should be intubated for 1 or 2 days after tongue flap surgery and MMF should not be performed. After 21 days, the pedicle is divided close to the palate and any defects noted in the anterior are closed. The surgeon should attempt to contour this final inset portion of the tongue flap so that it matches the contour of the palatal vault as much as possible, because protruding tissue from the palate may cause speech defects [30]. Final contouring of the tongue flap on the palate should not be done before 4 to 6 months after the original pedicle has been separated because the blood supply to the graft may not be established fully before 3 months [29]. The remaining portion of the tongue pedicle is reinserted into the donor site of the tongue. Postoperative scars and minor changes in shape are noted on the tongue, but it does not interfere with speech or movement. In badly scarred palates there is always the possibility that a flap may not establish a good blood supply with the surrounding palatal tissue because of the excessive scarring. If necrosis at the margins of

561

the flap is noted after division of the pedicle, it is most likely caused by an inadequate blood supply from the random-pattern flap. Unfortunately, there is no sure way to test for a lack of adequate blood supply before taking the flap down. One method of testing the adequacy of the blood supply to the distal portion of the flap is by cross-clamping the pedicle with a bulldog clamp before dividing it and observing the color of the flap at the transferred end. If the tongue flap does not turn bluish or blanches and then returns to a near pink color, it can be considered to have enough blood supply to be able to divide it from its base. (Placing the bulldog clamp should be done using a small volume of local anesthesia without a vasoconstrictor.) Sometimes, however, the bulldog clamp may not compress the flap adequately to affect the donor blood source. The anesthesia for the takedown of the flap is a hazardous procedure and is usually a challenge to the anesthesiologist. The surgeon and the anesthesiologist may be faced with a child who cannot open his or her mouth widely, and the view and access to the pharyngeal area are obstructed. For general anesthesia, a sedated awake fiberoptic nasotracheal intubation is required, but if the patient is unable or unwilling to cooperate, it is a technically difficult and frustrating experience. The surgeon should seek a pediatric anesthesiologist who is experienced with fiberoptic intubation and has a good disposition. In older children, local anesthesia by infiltration may decrease the challenge, because after the area is numb the flap simply may be separated close to the palate to allow for the intubation. Adequate hemostasis should be obtained by the surgeon before turning the patient over to the anesthesiologist for intubation. Once induced, the surgeon may then perform the procedure under ideal control.

Summary This article presented surgical techniques that may be used to close oronasal fistulas. The author believes that the oral and maxillofacial surgeon can adapt these techniques easily to his or her practice and they are most frequently successful. Although these techniques have been presented to manage defects seen in the cleft palate patient, they are not solely limited to cleft surgery but may be adapted for other fistulas on the palate. A detailed description of the tongue flap was presented because this flap is versatile and may be used for other intraoral reconstructive procedures.

562

O.E. Ogle / Oral Maxillofacial Surg Clin N Am 14 (2002) 553–562

Acknowledgment The author wishes to thank Dr. Hope Wettan for the drawings and Dr. Steven Wettan for technical advice with the illustrations used in this article.

References [1] Stal S, Spira M. Secondary reconstructive procedures for patients with clefts. In: Serafin D, Georgiade NG, editors. Pediatric plastic surgery. St. Louis: CV Mosby Co.; 1984. p. 352. [2] Biavati MJ, Bassichis B. Cleft palate. Available at: http://www.emedicine.com/ent/topic136.htm. Accessed October 18, 2001. [3] Jackson IT, Fasching MC. Secondary deformities of cleft lip, nose and cleft palate. In: McCarthy JG, editor. Plastic surgery. Philadelphia: WB Saunders; 1990. p. 2814. [4] Rintala AE, Haapanen M. The correlation between training and skill of the surgeon and reoperation rate for persistent cleft palate speech. Br J Oral Maxillofac Surg 1995;33:295 – 6. [5] Musgrave RH, Bremner JC. Complications of cleft palate surgery. Plast Reconstr Surg 1960;26:180 – 9. [6] Schultz RC. Management and timing of cleft palate fistula repair. Plast Reconstr Surg 1986;78:739 – 45. [7] Lilja J, Elander A, Lohmander A, et al. Isolated cleft palate and submucous cleft palate. Oral Maxillofac Surg Clin N Am 2000;12:455 – 68. [8] Rintala AE, Ranta R. Spontaneous narrowing of the palatal cleft during the first year of life: a quantitative study. Scand J Plast Reconstr Surg Hand Surg 1987; 21:35 – 8. [9] Henningsson G, Isberg A. Influence of palatal fistula on speech and resonance. Folia Phoniatr 1987;39:183. [10] Bardach J, Slayer KE. Cleft palate repair. In: Bardach J, Slayer KE, editors. Surgical techniques in cleft lip and palate. Chicago: Year Book Medical Publishers; 1987. [11] Baker PR. Closure of oral antral communications and treatment of sinus infections. In: Dym H, Ogle OE, editors. Atlas of minor oral surgery. Philadelphia: WB Saunders; 2001. p. 131 – 2. [12] Chapman JH, Birch DA. An orthodontic and otolaryngological review of thirty four cleft lip and cleft palate patients. Br J Surg 1965;52:646. [13] Millard Jr DR. Wide and or short cleft palate. Plast Reconstr Surg 1962;29:40. [14] Ross RB. Treatment variables affecting facial growth in complete unilateral cleft lip and palate. Part 5: Timing of cleft palate repair. Cleft Palate J 1987;24:54.

[15] Witzel MA, Salyer K, Ross RB. Delayed hard palate closure: the philosophy revisited. Cleft Palate J 1984; 21:263. [16] Ross RB. Facial growth in cleft lip and palate. In: McCarthy JG, editor. Plastic surgery. Philadelphia: WB Saunders; 1990. p. 2437. [17] Peter-Falzone SJ. Speech outcome after closure of oronasal fistulas with bone graft: discussion. J Oral Maxillofac Surg 2001;59:1413 – 4. [18] D’Antonio LL, Barlow SM, Warren DW. Studies of oronasal fistulae: implications of speech motor control. Presented at the Annual Meeting of the AmericanSpeech-Language-Hearing Association. San Antonio, TX, November 20 – 23, 1992. [19] Marsh JL, Wray RC. Speech prosthesis versus pharyngeal flap: a randomized evaluation of the management of velopharyngeal incompetency. Plast Reconstr Surg 1980;65:592 – 4. [20] Isberg A, Hennigsson G. Influence of palatal fistulas on velopharyngeal movements: a cineradiographic study. Plast Reconstr Surg 1987;79:525. [21] Clasper R. A combined obturator and expansion appliance for use in patients with patent oral-nasal fistula. Br J Orthod 1995;22:357. [22] Kim M, Lee J, Choi J, et al. Two stage reconstruction of bilateral alveolar cleft using a Y-shaped anterior based tongue flap and iliac bone graft. Cleft Palate Craniofac J 2001;38:432 – 7. [23] Johnson PA, Banks P, Brown AE. Use of the posteriorly based lateral tongue flap in the repair of palatal fistula. Int J Oral Maxillofac Surg 1992;21:6 – 9. [24] Kinnebrew MC, Malloy RB. Posteriorly based, lateral lingual flaps for alveolar cleft bone graft coverage. J Oral Maxillofac Surg 1983;41:555 – 61. [25] Thind MS, Singh A, Thind RS. Repair of anterior secondary palate fistula using tongue flaps. Acta Chir Plast 1992;34:79 – 91. [26] Jackson IT. Cleft lip and palate. In: Kelly V, editor. Practice of pediatrics. Philadelphia: JB Lippincot Co.; 1985. [27] Carreirao S, Lessa S. Tongue flaps and the closing of large fistulas of the hard palate. Ann Plast Surg 1980; 4:182 – 90. [28] Kim YK, Yeo HH, Kim SG. Use of the tongue flap for intraoral reconstruction: a report of 16 cases. J Oral Maxillofac Surg 1998;56:716 – 9. [29] Steinhauser EW. Experience with dorsal tongue flaps for closure of defects of the hard palate. J Oral Maxillofac Surg 1982;40:787 – 9. [30] Kummer AW, Neal HW. Changes in articulation and resonance after tongue flap closure of palatal fistulas: case reports. Cleft Palate J 1989;26:51 – 5.

Oral Maxillofacial Surg Clin N Am 14 (2002) 563 – 576

Cumulative Index 2002 Volume 14

February May August November

EMERGING BIOMATERIALS, pages 1 – 136 ADVANCED TOPICS IN DENTOALVEOLAR SURGERY, pages 137 – 272 CURRENT MEDICAL AND SURGICAL MANAGEMENT OF SLEEP RELATED BREATHING DISORDERS, pages 273 – 410 SECONDARY CLEFT SURGERY, pages 411 – 576

Note: Page numbers of article titles are in boldface type

A A-2186, in prosthodontic rehabilitation, 78

Alveolus, cleft, facial and dental relationships in, 413 – 414

Abbe´ flap, for cutaneous and vermilion insufficiency, in clefting disorders, 441 – 442, 444 – 445

Amino acid modulators, in pain modulation, 142

Abscess, brain, dentoalveolar surgery and, 237

Anesthesia, in laser therapy, for obstructive sleep apnea syndrome, 321 – 322

Accessory roots, in endodontic treatment, 160 Acetylsalicylic acid, for dentoalveolar surgical pain, 147 – 148 Acrylic resins, in prosthodontic rehabilitation. See Prosthodontic rehabilitation. Adhesive tapes, in wound closure, 100 – 101 Airway compromise, after laser therapy, for obstructive sleep apnea syndrome, 328 Alcohol intake, and sleep-disordered breathing, 298 Alginate carriers, uses of, 35 – 36 AlloDerm as dermal substitute, 65 as oral mucosa substitute, 69 – 71 cosmetic uses of, 57 Allografts as dermal substitutes, 65 cosmetic uses of, 56 Alloplast, cosmetic uses of, 55 Alveolar bone grafts, in orthodontics, for clefting disorders, 472

Anchor sutures, in dentoalveolar surgery, 226

Ankylosis after surgical uprighting, of mesially inclined second molars, 210 – 211 of impacted teeth, 198 Anterior mandibular osteotomy, for obstructive sleep apnea syndrome, 355, 379 – 381 Antibiotics, in dentoalveolar surgery. See Dentoalveolar surgery. Anticoagulants, patients on, and antibiotics, for dentoalveolar surgery, 233 Apical preparation, ultrasonic. See Ultrasonic apical preparation. Apligraf, cosmetic uses of, 56 Apnea-hypopnea index, in patient evaluation, for sleep-disordered breathing, 351 Appetite suppressants, patients on, and antibiotics, for dentoalveolar surgery, 234 – 235 Artecoll, cosmetic uses of, 55

Alveolar clefts, correction of, and speech, 531

Articulation, and speech, in clefting disorders, 541, 544

Alveolar plate molding, in orthodontics, for clefting disorders, 465 – 466

Articulation errors, after surgery, for clefting disorders, 533

1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII: S 1 0 4 2 - 3 6 9 9 ( 0 2 ) 0 0 0 8 4 - 5

564

Cumulative Index 2002 / Oral Maxillofacial Surg Clin N Am 14 (2002) 563–576

Aspirin, for dentoalveolar surgical pain, 147 – 148

Bovine pericardium, in guided bone regeneration, 26

Asplenia, and antibiotics, for dentoalveolar surgery, 237

Brain abscess, dentoalveolar surgery and, 237

Autologous chondrocytes, in cartilage regeneration, 110-112

Buccal finger flap, for alveolar clefts, 482 Butorphanol, for dentoalveolar surgical pain, 146

Autologous fibrin tissue adhesive, in wound closure, 102

C B

Calcium sulfate barrier, in guided bone regeneration, 26

Bacterial endocarditis, antibiotics for, 231 – 233

Calthane, in prosthodontic rehabilitation, 79 – 80

Benzodiazepines, and sleep-disordered breathing, 298 Bilevel positive airway pressure, for sleep-disordered breathing, 301

Capset, in guided bone regeneration, 26

Biodegradable materials, for peripheral nerve injuries. See Peripheral nerve injuries. Bio-Guide, in guided bone regeneration, 25 BioMend Extend, in guided bone regeneration, 25 – 26 Biopsy, in periapical surgery, 184 – 185 Bioresorbable barriers, in guided bone regeneration. See Guided bone regeneration. Bleeding, after laser therapy, for obstructive sleep apnea syndrome, 327 Bone, cosmetic uses of, 57 – 59 Bone grafts for clefting disorders, and speech, 532 for midface deficiency, in clefting disorders, 497, 499 Bone morphogenetic proteins, 3 – 16 after bone injury, 8 – 9 animal studies of, 9 – 10 for craniofacial defects, 9 historical aspects of, 3 – 4 human studies of, 10, 12 signaling mechanisms in, 4 – 8 activity regulation in, 6 family characteristics in, 4 – 6 gene expression in, 7 – 8 serine/threonine kinase activity in, 6 Smads in, 6 – 7 Bone regeneration, guided. See Guided bone regeneration. Bone transport, intraoral. See Intraoral bone transport.

Carbon dioxide laser therapy, for obstructive sleep apnea syndrome, 373 Cardiovascular disease, obstructive sleep apnea syndrome and, 279 Cartilage, cosmetic uses of, 60 Cartilage regeneration, 107 – 118 articular cartilage architecture and, 108 calcification in, 108 – 109 problems with, 107 tissue engineering in, 108 – 115 allografts and ex vivo cartilage, 110 – 112 for full-thickness defects, 109 – 110 for osteochondral defects, 113 – 115 for partial-thickness defects, 109 need for cells in, 109 Catheters, patients with, and antibiotics, for dentoalveolar surgery, 236 Cautery-assisted palatal stiffening surgery, for obstructive sleep apnea syndrome, 389 Cavit, in root end filling, 174 Celebrex, for dentoalveolar surgical pain, 149 Celecoxib, for dentoalveolar surgical pain, 149 Central sensitization, in pain modulation, 140, 142 Cephalometric radiography, in patient evaluation, for sleep-disordered breathing, 353 – 354 Cerebrovascular disease, obstructive sleep apnea syndrome and, 279 Cervical neck wires, for impacted teeth, 193 – 194 Chemical polymerization, of in situ forming biomaterials, 37 Cigarette smoking, and sleep-disordered breathing, 298

Cumulative Index 2002 / Oral Maxillofacial Surg Clin N Am 14 (2002) 563–576

Cleft lip. See Clefting disorders. Cleft palate. See Clefting disorders. Clefting disorders facial and dental relationships in, 411 – 424 clinical studies of, 412 in isolated cleft palate, 414 – 417 in repaired versus unrepaired clefts, 411 – 412 in unilateral cleft lip and alveolus, 413 – 414 in unilateral cleft lip and palate, 417, 419 – 421 lip and palate surgery and, 421 – 422 lip surgery and, 421 pre- and postoperative, 412 – 413 intraoral bone transport in. See Intraoral bone transport. midface deficiency in. See Midface deficiency. orthodontics for. See Orthodontics. prosthodontic rehabilitation for. See Prosthodontic rehabilitation. rhinoplasty for. See Rhinoplasty. scar revision in, 425 – 437 anatomy in, 425 – 426 for lip architecture, 428 – 430, 434 – 435 for lip mobility defects, 428, 434 for lip volume defects, 427 – 428, 430 – 433 for orbicularis oris abnormalities, 428, 433 – 434 patient assessment for, 427 skeletal framework in, 426 – 427 techniques for, 430 – 434 wound management in, 435 – 436 secondary grafts for. See Secondary grafts. secondary surgery for, and speech. See Speech. short upper lip in, 439 – 451 cutaneous and vermilion insufficiency and, 440 – 442, 444 – 445 vermilion insufficiency and, 439 – 440 velopharyngeal insufficiency in. See Velopharyngeal insufficiency.

565

Continuous positive airway pressure for obstructive sleep apnea syndrome, 276, 312 – 313, 385 postoperative, 401 – 402 for sleep-disordered breathing, 299 – 301 Continuous sling, in dentoalveolar surgery, 227 – 228 Continuous sutures, in dentoalveolar surgery, 226 – 227 Coronary heart disease, obstructive sleep apnea syndrome and, 279 Cosmesil, in prosthodontic rehabilitation, 78 Cosmetic materials advances in, 55 – 61 bone, 57 – 59 cartilage, 60 soft tissue, 55 – 57 COX-2 inhibitors, for dentoalveolar surgical pain, 149 CPAP PRO system, for sleep-disordered breathing, 301 – 302 Craniofacial defects, bone morphogenetic proteins for, 9 Crown forms, for impacted teeth, 1912 – 193 Cupid’s bow defects, scar revision in, 435 Cutaneous insufficiency, with vermilion insufficiency, and short upper lip, in clefting disorders, 440 – 442, 444 – 445 Cyanoacrylates, in wound closure, 101 – 102

D Decalcified freeze-dried bone allografts, in guided bone regeneration, 27

Coblation system, for obstructive sleep apnea syndrome, 336, 338 – 341, 343 – 344

Demerol, for dentoalveolar surgical pain, 145 – 146

Codeine, for dentoalveolar surgical pain, 144 – 145

Dentoalveolar surgery analgesia for, 137 – 151 postoperative, 143 – 149 acetylsalicylic acid in, 147 – 148 butorphanol in, 146 celecoxib in, 149 codeine in, 144 – 145 COX-2 inhibitors in, 149 hydrocodone in, 145 ibuprofen in, 148

Collagen, in guided bone regeneration, 25 – 26 Columella, in rhinoplasty, for cleft nose, 456, 458 Composite resin, in root end filling, 174 Computed tomography, in patient evaluation, for sleep-disordered breathing, 354 Connective tissue grafts, oral. See Oral connective tissue grafts.

Dental anatomy, in endodontic treatment, 156 – 160

566

Cumulative Index 2002 / Oral Maxillofacial Surg Clin N Am 14 (2002) 563–576

ketorolac in, 148 – 149 meperidine in, 145 – 146 naproxen in, 148 nonsteroidal anti-inflammatory drugs in, 146 – 149 opioids in, 143 – 144 oxycodone in, 145 pentazocine in, 146 rofecoxib in, 149 pre-emptive, 142 – 143 and risk of brain abscess, 237 antibiotics in, 231 – 240 for bacterial endocarditis, 231 – 233 for immunocompromised patients, 237 – 237 for patients already on antibiotics, 233 for patients on anticoagulants, 233 for patients on appetite suppressants, 234 – 235 for patients with prosthetic joints, 235 – 236 for patients with shunts, catheters, and implants, 236 for unanticipated indications, 234 patterns of use of, 239 routine use of, 237 – 238 when treatment is delayed, 234 coding in, 259 – 267 adjunctive procedures, 266 analgesia, sedation, and general anesthesia, 266 – 267 dentoalveolar infections, 265 – 266 preprosthetic dentoalveolar surgery, 264 – 265 removal of teeth, 261, 264 pain mechanisms in, 137 – 138 modulation of, 138, 140, 142 central sensitization, 140, 142 neuropeptide and amino acid modulators, 142 peripheral sensitization, 138, 140 supraspinal, 142 suturing in, 213 – 229 instruments in, 224 – 225 materials in, 213, 217 bacterial migration in, 221 biologic response to, 218 – 221 choice of, 221 – 223 nonabsorbable versus absorbable, 221 – 223 physical properties of, 217 – 218 needles in, 223 – 224 techniques for, 225 – 228 anchor sutures, 226 continuous sling, 227 – 228 continuous sutures, 226 – 227 figure-eight, 226 horizontal mattress, 226

simple interrupted, 226 sling ligation, 226 vertical mattress, 226 Dermagraft, as dermal substitute, 65 Dermalogen, cosmetic uses of, 56 Diabetes, and antibiotics, for dentoalveolar surgery, 237 Distraction osteogenesis for clefting disorders, 474, 502 and speech, 532 – 533 for velopharyngeal insufficiency, in clefting disorders, 549 – 550 Dressings, in wound closure, 102 – 103 Dura mater, in guided bone regeneration, 26

E Electrical stimulation, for obstructive sleep apnea syndrome, 276 Ellmad system, for obstructive sleep apnea syndrome, 336 – 337 Ellman system, for obstructive sleep apnea syndrome, 336 – 337 Endocarditis, bacterial, antibiotics for, 231 – 233 Endodontic treatment predicting success or failure of, 153 – 165 definitions in, 154 dental anatomy in, 156 – 160 filling materials in, 162 – 163 intraoperative factors in, 154 – 156 jaw anatomy in, 160, 162 preoperative evaluation in, 154 Endoscopic pharyngoscopy, in patient evaluation, for sleep-disordered breathing, 352 – 353 Endosseous implants, 41 – 53 biologic modifications of, 47 – 48 macroretentive features of, 42 microretentive features of, 42 – 47 alterations of surface oxide, 46 – 47 biologic response, 45 – 46 surface roughness, 42 – 44 by blasting or etching, 44 – 45 Engineered tissue, cosmetic uses of, 56 – 57 Envelope technique, for oral connective tissue grafts, 243 Epicel, as dermal substitute, 64

Cumulative Index 2002 / Oral Maxillofacial Surg Clin N Am 14 (2002) 563–576

inferior sagittal osteotomy in, 377 – 379 trephine osteotomy in, 381 – 383 for sleep-disordered breathing, 355

Epithane-3, in prosthodontic rehabilitation, 79 – 80 Esmarch prosthesis, for obstructive sleep apnea syndrome, 311 Extubation, after surgery, for obstructive sleep apnea syndrome, 402

567

Gingival recession, oral connective tissue grafts for, 242 – 243 Gingivectomy, for impacted teeth, 192 Glass ionomer cements, in root end filling, 174

F Fiberoptic examination, after surgery, for obstructive sleep apnea syndrome, 403 Fibrin glue, in wound closure, 102 Figure-eight sutures, in dentoalveolar surgery, 226 Filling materials, in endodontic treatment, 162 – 163 Fistulas, oronasal, and speech, 531, 534 Flap design for impacted teeth, 195 inappropriate, 198 in endodontic treatment, 154 in periapical surgery, 183 in ultrasonic apical preparation, 168 – 169 Flaps for alveolar clefts, 482, 484 for clefting disorders, and speech, 532 for cutaneous and vermilion insufficiency, in clefting disorders, 439 – 442, 444 – 445 for velopharyngeal insufficiency, in clefting disorders, 546

Globus, after laser therapy, for obstructive sleep apnea syndrome, 328 Glossectomy, for obstructive sleep apnea syndrome, 373 – 374 Gore-Tex cosmetic uses of, 55 in guided bone regeneration, 23 – 24 Grafts bone for clefting disorders, and speech, 532 for midface deficiency, in clefting disorders, 497, 499 oral connective tissue. See Oral connective tissue grafts. secondary. See Secondary grafts. Growth factors, in bone healing, 59

Fractures identification of, in endodontic treatment, 155 – 156 of root structures and periapical surgery, 182 – 183 due to ultrasonic apical preparation, 170 – 171

Guided bone regeneration, 17 – 29 biology of, 20 – 21 bioresorbable barriers in, 24 – 27 natural products, 25 – 26 synthetic products, 26 – 27 clinical application of, 27 experimental studies of, 18 – 19 future goals of, 27 – 28 historical aspects of, 17 – 18 membrane design criteria in, 21 – 22 nonresorbable barriers in, 22 – 24 osteopromotion principle in, 19 – 20

Furlow double Z-plasty, for clefting disorders, and speech, 532

Guided tissue regeneration, for gingival recession, 243

G

H

Gastrointestinal effects, of nonsteroidal anti-inflammatory drugs, 147 Genioglossus muscle advancement for obstructive sleep apnea syndrome, 377 – 384, 387 anterior mandibular osteotomy in, 355, 379 – 381 historical aspects of, 377

Hard tissue replacement, in craniofacial reconstruction, 58 Harmonic Scalpel for obstructive sleep apnea syndrome, 344 – 348 results of, 347 – 348 technique for, 345 – 347 Hematomas, in scar revision, for clefting disorders, 436

568

Cumulative Index 2002 / Oral Maxillofacial Surg Clin N Am 14 (2002) 563–576

for velopharyngeal insufficiency, in clefting disorders, 546, 548 patients with, and antibiotics, for dentoalveolar surgery, 236 recession and mucogingival defects around, oral connective tissue grafts for, 243

Herbst oral appliance, for obstructive sleep apnea syndrome, 309 – 310 HIV infections, and antibiotics, for dentoalveolar surgery, 237 Horizontal mattress sutures, in dentoalveolar surgery, 226 Hydrocodone, for dentoalveolar surgical pain, 145 Hyoepiglottoplasty, for obstructive sleep apnea syndrome, 374 Hyoid suspension for obstructive sleep apnea syndrome, 374, 387 for sleep-disordered breathing, 355 Hypernasality after surgery, for velopharyngeal insufficiency, 548 – 549 correction of, and speech, 531 – 534 in clefting disorders, 501 – 502 Hypertension obstructive sleep apnea syndrome and, 279 sleep-disordered breathing and, 298 Hypertrophic scars, of lips, scar revision in, 435 Hypocapnic apneic threshold, in sleep, 287 Hypopharyngeal surgery, for obstructive sleep apnea syndrome. See Soft tissue hypopharyngeal surgery. Hypothyroidism, and sleep-disordered breathing, 298 – 299

I Ibuprofen, for dentoalveolar surgical pain, 148 Immunocompromised patients, and antibiotics, for dentoalveolar surgery, 236 – 237 Impacted teeth etiology of, 188 incidence of, 187 – 188 localization of, 188 – 190 radiographs of, 188 – 189 surgical exposure of, 187 – 199 closed techniques for, 195 – 198 complications of, 198 historical aspects of, 192 – 194 open techniques for, 194 – 195 orthodontics in, 190 – 192 Implant-retained maxillofacial prostheses, studies of, 88 – 90 Implants endosseous. See Endosseous implants.

In situ forming biomaterials, 31 – 40 chemical polymerization of, 37 diffusion of, 34 – 35 enzymatic cross-linking of, 36 – 37 ionic cross-linking of, 35 – 36 pH triggered systems, 34 photopolymerization of, 37 – 38 self-assembling systems, 38 swelling of, 34 thermally triggered systems, 31 – 34 Infections, after laser therapy, for obstructive sleep apnea syndrome, 328 Inferior sagittal osteotomy, for obstructive sleep apnea syndrome, 377 – 379 Integra, as dermal substitute, 65 Intraoral bone transport in clefting disorders, 509 – 523 historical aspects of, 510 – 512 technique for, 512 – 514 Intubation, after surgery, for obstructive sleep apnea syndrome, 402

J Jaw anatomy, in endodontic treatment, 160, 162 Joint arthroplasty, and antibiotics, for dentoalveolar surgery, 235

K Kapetansky-Juri advancement flap, for vermilion insufficiency, in clefting disorders, 439 – 440 Ketorolac, for dentoalveolar surgical pain, 148 – 149 Klearway oral appliance, for obstructive sleep apnea syndrome, 310 – 311

L Lambone, in guided bone regeneration, 26 Laminar bone, in guided bone regeneration, 26

Cumulative Index 2002 / Oral Maxillofacial Surg Clin N Am 14 (2002) 563–576

569

Laser midline glossectomy, for obstructive sleep apnea syndrome, 373

Maxillary advancement, for clefting disorders, and velopharyngeal insufficiency, 548 – 549

Laser therapy for obstructive sleep apnea syndrome, 319 – 331 historical aspects of, 319 – 320 patient evaluation for, 320 – 321 polysomnography before, 320 – 321 uvulopalatopharyngoplasty, 325, 339, 348 clinical studies of, 329 – 330 complications of, 327 – 329 postoperative care for, 326 – 327 uvulopalatoplasty, 321 – 323, 325, 348, 367, 389 anesthesia in, 321 – 322 clinical studies of, 329 – 330 complications of, 327 – 329 postoperative care for, 326 – 327 safety in, 322 technique for, 322 – 323, 325

Maxillary stabilization for clefting disorders, and speech, 532 – 534 for midface deficiency, in clefting disorders, 499 – 500

Lateral sliding flap, for alveolar clefts, 482 Le Fort I advancement, for clefting disorders, and speech, 533 Leucine zipper motif, characteristics of, 38 Lingualplasty, for obstructive sleep apnea syndrome, 373 Lip architecture defects, scar revision in, 428 – 430, 434 – 435 Lip closure, in orthodontics, for clefting disorders, 466 – 468 Lip deformity, correction of, and speech, 530 – 531 Lip mobility defects, scar revision in, 428, 434 Lip volume defects, scar revision in, 427 – 428, 430 – 433 Liposomes, uses of, 33 – 34 Load compensation, loss of, in sleep, 286

M Magnetic resonance imaging, in patient evaluation, for sleep-disordered breathing, 354 – 355 Magnification, in ultrasonic apical preparation, 170 Mandibular repositioners, for obstructive sleep apnea syndrome, 311 Mandibular stabilization, for clefting disorders, and speech, 532 – 534

Maxillomandibular advancement for obstructive sleep apnea syndrome, 387 – 388, 390 – 398 for sleep-disordered breathing, 355 – 356 Medpore, cosmetic uses of, 57 Meperidine, for dentoalveolar surgical pain, 145 – 146 Mesenchymal stem cells, in cartilage regeneration, 112 Mesially inclined second molars etiology of, 202 – 203 incidence of, 202 surgical uprighting of, 201 – 212 and ankylosis, 210 – 211 indications for, 204 options in, 205 risks of, 211 – 212 root development and, 209 – 210 surgical approach to, 204 – 205 technique for, 207 – 209 timing of, 206 treatment time in, 201 Microsurgery, in ultrasonic apical preparation, 170 Midface deficiency in clefting disorders correction of, 491 – 508 bone grafts in, 497, 499 maxillary stabilization in, 499 – 500 preoperative counseling for, 492 – 493 technique for, 493 – 497 timing of, 492 velopharyngeal function in, 500 – 502 Millipore membrane filters, in guided bone regeneration, 24 Mineral trioxide aggregate cement, in root end filling, 174 – 175 Mucogingival defects, oral connective tissue grafts for, 242 – 243 Muller’s maneuver, in patient evaluation, for sleepdisordered breathing, 353 Muscular factors, in sleep, 290 – 291 Myverol, uses of, 32

570

Cumulative Index 2002 / Oral Maxillofacial Surg Clin N Am 14 (2002) 563–576

N Naprosyn, for dentoalveolar surgical pain, 148 Naproxen, for dentoalveolar surgical pain, 148 Nasal air emission, and speech, in clefting disorders, 541 Nasal deformity, correction of, and speech, 529 – 530 Nasal examination, in patient evaluation, for sleepdisordered breathing, 352 Nasal obstruction, radio-ablation of, 341 – 344 Nasal sill, in rhinoplasty, for cleft nose, 456 – 458 Nasal surgery, for obstructive sleep apnea syndrome, 366, 388 Nasometry, of speech, in clefting disorders, 544 Nasopharyngeal surgery, for obstructive sleep apnea syndrome, 388 – 389 Nasopharyngoscopy, of speech, in clefting disorders, 545 Neck wires, cervical, for impacted teeth, 193 – 194 Neuropeptides, in pain modulation, 142 Neutropenia, and antibiotics, for dentoalveolar surgery, 236 – 237 Nonrapid eye movement sleep, in obstructive sleep apnea syndrome, 285 Nonresorbable barriers, in guided bone regeneration, 22 – 24 Nonsteroidal anti-inflammatory drugs, for dentoalveolar surgical pain, 146 – 149

O Obesity and obstructive sleep apnea syndrome, 278 and sleep-disordered breathing, 299 Oblique sliding flap, for alveolar clefts, 482, 484 Obstructive sleep apnea syndrome, 273 – 283. See also Sleep-disordered breathing. after surgery, for velopharyngeal insufficiency, 548 and cardiovascular disease, 279 and cerebovascular disease, 279 and coronary heart disease, 279 and hypertension, 279 and stroke, 279 complications of, 279 epidemiology of, 276 – 279 age in, 277

gender in, 277 – 278 obesity in, 278 race in, 278 future directions in, 279 – 280 historical aspects of, 273 – 275 in 1970s and 1980s, 273 – 275 in pregnancy, 278 laser therapy for. See Laser therapy medical treatment of, 275 – 276 oral appliances for. See Oral appliances. pathophysiology of, 285 – 292, 333 REM sleep in, 287 upper airway obstruction in, 291 upper airway patency in, 290 – 291 sleep physiology in, 285 surgical treatment of, 275, 333 – 350, 365 – 369, 385 – 399 algorithms for, 365 – 366 analgesics in, 402 continuous positive airway pressure in, 276, 401 – 402 discharge criteria in, 403 fiberoptic examination in, 403 genioglossus muscle advancement in. See Genioglossus muscle advancement. Harmonic Scalpel in. See Harmonic scalpel. imaging before, 334 intensive care unit in, 402 intubation/extubation in, 402 maxillomandibular advancement in, 387 – 388, 390 – 398 modalities in, 334 – 335 nasal procedures in, 366, 388 nasopharyngeal and oropharyngeal procedures in, 388 – 389 patient selection for, 333 – 334 postoperative care for, 401 – 404 radiofrequency in. See Radiofrequency. skeletal procedures in, 389 – 391 soft tissue hypopharyngeal procedures in. See Soft tissue hypopharyngeal surgery. Stanford protocol in, 371 – 373, 386 – 387, 401 – 403 tonsillectomy in, 366 tracheostomy in, 385 – 386 tracheotomy in, 402 transpalatal advancement in, 367 uvulopalatopharyngoplasty in, 275, 348, 366 – 367, 386 ventilation in, effects of sleep on, 285 – 287 Obturator prostheses, in prosthodontic rehabilitation. See Prosthodontic rehabilitation. 2-Octylcyanoacrylate, in wound closure, 101 – 102

Cumulative Index 2002 / Oral Maxillofacial Surg Clin N Am 14 (2002) 563–576

Opioids, for dentoalveolar surgical pain, 143 – 144 Oral appliances for obstructive sleep apnea syndrome, 275 – 276, 305 – 317 advances in, 306 – 309 contraindications to, 314 Herbst appliance, 309 – 310 Klearway appliance, 310 – 311 mandibular repositioners, 311 PM Positioner, 311 – 312 protocols for, 306 selection of, 314 Snore Guard, 312 – 313 TheraSnore, 313 tongue retaining device, 313 – 314 for sleep-disordered breathing, 301 – 302 Oral cavity examination, in patient evaluation, for sleep-disordered breathing, 352 Oral connective tissue grafts, 241 – 257 donor factors in, 250 – 253 adequate graft size, 252 adequate graft thickness, 252 – 253 atraumatic harvest, 251 management of epithelial band, 253 optimal selective site, 250 – 251 preservation of periosteal complex, 253 preservation of tissue, 253 tissue quality, 251 – 252 for gingival recession and mucogingival defects around implants, 243 for gingival recession and mucogingival defects around natural teeth, 242 – 243 for papilla reconstruction, 243 – 244 for ridge defects, 244 graft harvest for, 247 – 248 graft insetting in, 248 historical aspects of, 241 host factors in, 248 – 250 compliance and expectations, 250 management of modifiable factors, 250 systemic equilibrium and healing potential, 248 – 250 postoperative care for, 248 preparation for, 244 recipient site factors in, 253 – 255 adequate exposure, 253 – 254 cover-flap integrity, 254 graft insetting and fixation, 254 management of interdental papillae, 254 proper diagnosis, 253 reduced bacterial load, 253 root/implant surface preparation, 254 tension-free closure, 254 – 255

571

tissue bed preparation, 254 vascular potential of recipient bed, 253 recipient site preparation for, 244 – 245, 247 soft-tissue augmentation options in, 241 – 242 Oral mucosa substitutes, 67 – 71 in vitro culture of, 67 – 68 tissue-engineered, 68 – 71 versus skin, structure and function of, 67 Orbicularis oris abnormalities, scar revision in, 428, 433 – 434 Oronasal fistulas, and speech, 531, 534 Oropharyngeal surgery, for obstructive sleep apnea syndrome, 388 – 389 Orthodontic implications of lip and palatal surgery, 422 of unilateral cleft lip and alveolus, 414 Orthodontics for clefting disorders, 463 – 476 appliances in, 472 – 473 goals of, 463, 465 lip closure in, 466 – 468 molding of alveolar plate in, 465 – 466 orthognathic surgery in, 473 – 474 palatal closure in, 468 – 469 presurgical orthopedics in, 465 primary dentition in, 469 – 470 prosthetic issues in, 474 transitional dentition in, 470 – 472 for impacted teeth, 190 – 192 preoperative, in secondary grafts, for alveolar clefts, 480 – 481 Orthognathic surgery, for clefting disorders, 473 – 474 Orthopedics, before orthodontics, for clefting disorders, 465 Osseoquest, in guided bone regeneration, 27 Osteochondral defects, cartilage regeneration in, 113 – 115 Osteogenesis, distraction. See Distraction osteogenesis. Osteopromotion principle, in guided bone regeneration, 19 – 20 Osteotomy for obstructive sleep apnea syndrome. See Genioglossus muscle advancement. for sleep-disordered breathing, 355 Oxycodone, for dentoalveolar surgical pain, 145 Oxygen, for sleep-disordered breathing, 299

572

Cumulative Index 2002 / Oral Maxillofacial Surg Clin N Am 14 (2002) 563–576

P Palamed, in prosthodontic rehabilitation, 80 Palatal augmentation prostheses, indications for, 88 Palatal closure, in orthodontics, for clefting disorders, 468 – 469 Palatal deformity, correction of, and speech, 531 – 532

Pharyngeal flaps for clefting disorders, and speech, 532 for velopharyngeal insufficiency, in clefting disorders, 546 Pharyngeal narrowing, and snoring, 286 – 287 Pharyngoplasty, for clefting disorders, and speech, 532

Palatal flap, for alveolar clefts, 484

Pharyngoscopy, in patient evaluation, for sleep-disordered breathing, 352 – 353

Palatal lift prostheses, indications for, 88

Philtrum, abnormal thickness of, 428

Palatal obstruction, radio-ablation of, 337 – 339

Photopolymerization, of in situ forming biomaterials, 37 – 38

Palatal splint, for alveolar clefts, 484 Palatal stiffening surgery, cautery-assisted, for obstructive sleep apnea syndrome, 389 Palatoplasty for clefting disorders, and speech, 528 – 529 for velopharyngeal insufficiency, in clefting disorders, 548 Papilla reconstruction, oral connective tissue grafts in, 243 – 244 Pentazocine, for dentoalveolar surgical pain, 146 Periapical surgery, 179 – 186 biopsy in, indications for, 184 – 185 cracked or fractured teeth and, 182 – 183 preoperative planning for, 179 – 80 radiographs in, 182 success of, determination of, 180, 182 surgical access in, 183 – 184 with periodontal procedures, 183

Pickwickian syndrome, historical aspects of, 273 Platelet-rich plasma, in secondary grafts, for alveolar clefts, 480 Pluronics, uses of, 32 PM Positioner, for obstructive sleep apnea syndrome, 311 – 312 Poly-l-lactic-co-glycolic acid, uses of, 32, 59 Poly-N-isopropyl acrylamide, uses of, 32 Polyacrylic acid, uses of, 34 Polyethylene glycol photopolymerization of, 37 uses of, 34 Polyethylene oxide, uses of, 32 Polyglactin 910 mesh, in guided bone regeneration, 26

Periodontal procedures, with periapical surgery, 183

Polyglycolic acid, in guided bone regeneration, 26

Peripheral nerve injuries biodegradable materials for, 119 – 134 animal studies of, 120 – 121 future directions in, 131 – 132 postsurgical sensory training in, 123 – 124 presurgical sensory training in, 121 – 122 results of, 124, 126 – 130 morphometric data, 127 – 130 thermal percent maximum possible effect, 124, 126 – 127 statistics on, 124 surgical procedures in, 122 – 123

Polylactic acid, in guided bone regeneration, 26 Polymethacrylic acid, uses of, 34 Polysomnography before laser therapy, for obstructive sleep apnea syndrome, 320 – 321 of sleep-disordered breathing, 295 Polytetrafluoroethylene, in guided bone regeneration, 23 – 24, 27 Polyurethanes, in prosthodontic rehabilitation, 79 – 80

Peripheral sensitization, in pain modulation, 138, 140

Porcine collagen membrane, in guided bone regeneration, 25

Pharyngeal compliance, in sleep, 290

Pregnancy, obstructive sleep apnea syndrome in, 278

Cumulative Index 2002 / Oral Maxillofacial Surg Clin N Am 14 (2002) 563–576

speech aid prostheses in, 88 versus surgery, 76

Primary dentition, in orthodontics, for clefting disorders, 469 – 470 Proptriptyline, for obstructive sleep apnea syndrome, 276 Proroot, in root end filling, 174 – 175 Prosthetic joints, and antibiotics, for dentoalveolar surgery, 235 – 236 Prosthetics, for clefting disorders, 474 Prosthodontic rehabilitation, 75 – 95 acrylic resins in, 80 – 84 coloration of, 80 – 81 extrinsic, 82 intrinsic, 81 – 82 copolymer, 80 emulsions of, 83 – 84 light-cured, 80 methyl methacrylate, 80 processing of, 80 retention of, 82 – 83 adhesives in, 83 pressure-sensitive tape in, 83 silicone adhesives in, 83 constraints in, 75 – 76 economic aspects of, 90 – 91 for clefting disorders, 84 – 86 active appliances in, 85 orthopedic appliances in, 84 – 85 passive appliances in, 85 pin-retained appliances in, 85 presurgical nasoalveloar molding in, 85 – 86 future directions in, 91 implant-retained maxillofacial prostheses in, 88 – 90 extraoral, 89 – 90 intraoral, 88 – 89 obturator prostheses in, 86 – 88 definitive, 86 – 87 interim, 86 studies of, 87 – 88 surgical, 86 palatal augmentation prostheses in, 88 palatal lift prostheses in, 88 polyurethanes in, 79 – 80 silicones in, 76 – 79 foam, 78 HTV silicone, 78 – 79 polymers, 78 room temperature vulcanizing silicones, 77 studies of, 77 – 78 wettability of, 78

573

R Radiofrequency for obstructive sleep apnea syndrome, 335 – 344, 359 – 363, 367 advantages of, 336 Coblation system, 336, 338 – 341, 343 – 344 Ellmad system, 336 – 337 Ellman system, 336 – 337 for nasal obstruction, 341 – 344 for palatal obstruction, 337 – 339, 360 – 361 for tonsillar enlargement, 339 – 341 physics of, 335 – 336, 359 preoperative preparation for, 337 procedures for, 337 Somnoplasty system, 336, 338 – 339, 343 – 344, 389 Surgitron system, 336 – 337 tissue reduction by, 359 – 360 tongue base reduction by, 361 – 362 Radiographs cephalometric, in patient evaluation, for sleepdisordered breathing, 353 – 354 in periapical surgery, 182 of impacted teeth, 188 – 189 Rapid eye movement sleep, in obstructive sleep apnea syndrome, 285, 287 Resolute XT, in guided bone regeneration, 26 – 27 Resonance, and speech, in clefting disorders, 541 Respiratory depression, opioids and, 144 Respiratory disturbance index, in sleep-disordered breathing, 355 Retroglossal obstruction, in obstructive sleep apnea syndrome, 389 Retroplast, in root end filling, 174 Rhinoplasty for bifid nasal tip, 458, 461 for bilateral cleft nose, 457 – 458 columella in, 458 nostril sill in, 458 for clefting disorders, 453 – 462 for nasal tip columella in, 456 nostril sill in, 456 – 457 for nasal tip graft, 456 – 457 for unilateral cleft nose, 453

574

Cumulative Index 2002 / Oral Maxillofacial Surg Clin N Am 14 (2002) 563–576

cartilaginous septum in, 456 pathologic anatomy in, 454 technique for, 454 – 455 timing of, 455 – 456 Ridge defects, oral connective tissue grafts for, 244 Rofecoxib, for dentoalveolar surgical pain, 149 Root end filling, 173 – 177 material for, 174 – 175 Root fractures, identification of, in endodontic treatment, 155 – 156

S Scarring, after laser therapy, for obstructive sleep apnea syndrome, 328 Second molars, mesially inclined. See Mesially inclined second molars. Secondary grafts for alveolar clefts, 477 – 490 goals of, 478 – 479 historical aspects of, 477 incidence and etiology of clefts in, 477 – 478 material and donor sites for, 479 – 480 patient assessment for, 480 presurgical orthodontics for, 480 – 481 technique for, 482, 484, 486 timing of, 479 Semilunar flaps in endodontic treatment, 154 in periapical surgery, 183 Septum, cartilaginous, in rhinoplasty, for cleft nose, 456 b-Sheet structures, characteristics of, 38 Shunts, patients with, and antibiotics, for dentoalveolar surgery, 236 Silastic, in prosthodontic rehabilitation, 78 Silicone prostheses, in prosthodontic rehabilitation. See Prosthodontic rehabilitation. Simple interrupted sutures, in dentoalveolar surgery, 226 Siphenylenes, in prosthodontic rehabilitation, 78 Skeletal surgery, for obstructive sleep apnea syndrome, 389 – 391 Skin grafts, cosmetic uses of, 56 Skin substitutes, 63 – 67 bilayers of epithelium and dermis, 65 – 67

dermis, 64 – 65 epithelium, 64 Sleep-disordered breathing, 293 – 296. See also Obstructive sleep apnea syndrome. apnea frequency in, 295 – 296 diagnosis of, 295 evaluation of, 293 – 294 follow-up of, 296 medical treatment of, 297 – 304 alcohol and, 298 alternative interface systems in, 301 – 302 benzodiazepines and, 298 bilevel positive airway pressure in, 301 continuous positive airway pressure in, 299 – 301 titration of, 301 hypothyroidism and, 298 – 299 oral appliances in, 301 – 302 position restriction in, 299 smoking and, 298 supplemental oxygen in, 299 weight loss in, 299 pattern of apnea in, 293 screening tests for, 294 – 295 upper airway reconstruction for. See Upper airway reconstruction. Sling ligation, in dentoalveolar surgery, 226 Smoking, and sleep-disordered breathing, 298 Snore Guard, for obstructive sleep apnea syndrome, 312 – 313 Soft tissue, cosmetic uses of, 55 – 57 Soft tissue hypopharyngeal surgery for obstructive sleep apnea syndrome, 371 – 376 algorithms for, 371 – 373 glossectomy in, 373 – 374 hyoepiglottoplasty in, 374 hyoid suspension in, 374 laser midline glossectomy in, 373 lingualplasty in, 373 tongue suspension procedures in, 374 Somnoplasty system, for obstructive sleep apnea syndrome, 336, 338 – 339, 343 – 344, 389 Speech secondary cleft surgery and, 525 – 538 for lip deformity, 530 – 531 for maxillary and mandibular deformity, 532 – 534 for nasal deformity, 529 – 530

Cumulative Index 2002 / Oral Maxillofacial Surg Clin N Am 14 (2002) 563–576

for palatal deformity, 531 – 532 isolated versus syndromic clefting in, 527 – 528 preoperative assessment in, 528 primary palatoplasty in, 528 – 529 speech matrix in, 526 – 527 velopharyngeal insufficiency and. See Velopharyngeal insufficiency.

575

Tongue suspension surgery, for obstructive sleep apnea syndrome, 374 Tonsillar enlargement, radio-ablation of, 339 – 341 Tonsillectomy, for obstructive sleep apnea syndrome, 366 Toradol, for dentoalveolar surgical pain, 148 – 149

Speech aid prostheses, indications for, 88

Tracheostomy, for obstructive sleep apnea syndrome, 275, 385 – 386

Speech bulbs, for velopharyngeal insufficiency, in clefting disorders, 546

Tracheotomy, after surgery, for obstructive sleep apnea syndrome, 402

Speech intelligibility, obturator prostheses and, 87

Transitional dentition, in orthodontics, for clefting disorders, 470 – 472

Speech problems, after laser therapy, for obstructive sleep apnea syndrome, 328 Speech therapy, for clefting disorders, 472 Sphincter pharyngoplasty, for clefting disorders, and speech, 532 Sphincteroplasty, for velopharyngeal insufficiency, in clefting disorders, 546

Transmural pressure, of upper airway, in sleep, 290 Transpalatal advancement, for obstructive sleep apnea syndrome, 367 Trephine osteotomy, for obstructive sleep apnea syndrome, 381 – 383 Trismus, and fabrication, of obturator prostheses, 87

Split-night polysomnography, of sleep-disordered breathing, 295 Stadol, for dentoalveolar surgical pain, 146 Stanford protocol, in surgery, for obstructive sleep apnea syndrome, 371 – 373, 386 – 387, 401 – 403 Staples, in wound closure, 100 Stroke, obstructive sleep apnea syndrome and, 279 Supraspinal modulators, in pain modulation, 142 Surgitron system, for obstructive sleep apnea syndrome, 336 – 337 Sutures, in wound closure, 99 – 100

U Ultrasonic apical preparation, 167 – 172 cracks and fractures due to, 170 – 171 errors in, 171 flap design in, 168 – 169 instruments in, 167 – 168 microsurgery and magnification in, 170 technique for, 169 – 170 Ultrasound-assisted uvulopalatopharyngoplasty, for obstructive sleep apnea syndrome. See Harmonic Scalpel. Upper airway caliber, reduced, in sleep, 286 Upper airway dilators, reduced, in sleep, 286

T Talwin, for dentoalveolar surgical pain, 146 TheraSnore, for obstructive sleep apnea syndrome, 313 Thoracic caudal traction, in sleep, 290 Tidal volume, reduced, in sleep, 286 Tissue adhesives, in wound closure, 101 – 102 Tongue base surgery, for obstructive sleep apnea syndrome, 373 – 374 Tongue retaining device, for obstructive sleep apnea syndrome, 313 – 314

Upper airway obstruction, in sleep. See Obstructive sleep apnea syndrome; Sleep-disordered breathing. Upper airway patency, in sleep, 290 – 291 Upper airway reconstruction, for sleep-disordered breathing, 351 – 357 imaging before, 353 – 355 patient evaluation for, 351 – 352 surgical staging in, 355 – 356 upper airway examination in, 352 – 353 Uvulopalatopharyngoplasty for obstructive sleep apnea syndrome, 275, 348, 366 – 367, 386 for sleep-disordered breathing, 355

576

Cumulative Index 2002 / Oral Maxillofacial Surg Clin N Am 14 (2002) 563–576

laser-assisted. See Laser therapy. ultrasound-assisted, for obstructive sleep apnea syndrome. See Harmonic Scalpel.

Videofluoroscopy, of speech, in clefting disorders, 544 – 545 Vioxx, for dentoalveolar surgical pain, 149

Uvulopalatoplasty, laser-assisted. See Laser therapy.

W V Vascular factors, in sleep, 290 – 291 Velopharyngeal function, in clefting disorders, 500 – 502 Velopharyngeal insufficiency after laser therapy, for obstructive sleep apnea syndrome, 327 – 328 in clefting disorders, 539 – 551 anatomy and physiology of, 540 and speech, 540 – 541, 544 and speech evaluation, 544 – 545 surgery for, 545 – 546, 548 and speech, 531 – 534 complications of, 548 – 550 Vermilion insufficiency and short upper lip, in clefting disorders, 439 – 440 scar revision in, 428 with cutaneous insufficiency, and short upper lip, in clefting disorders, 440 – 442, 444 – 445 Vertical mattress sutures, in dentoalveolar surgery, 226 Vicryl, in guided bone regeneration, 26

Weight loss for obstructive sleep apnea syndrome, 275 for sleep-disordered breathing, 299 Wound closure materials, 97 – 106 adhesive tapes, 100 – 101 dressings, 102 – 103 future directions in, 103 – 104 historical aspects of, 97 – 98 patient assessment for, 78 postoperative care and, 103 staples, 100 sutures, 99 – 100 tissue adhesives, 101 – 102 wound anesthesia and, 78 wound assessment for, 78 wound preparation for, 98 – 99 Wound management, in scar revision, for clefting disorders, 435 – 436

Z Zinc oxide – eugenol, in root end filling, 174