Cleft Palate

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Seminars in Orthodontics
VOL 2, NO 3 SEPTEMBER 1996
Cleft Lip and Palate

Christos C. Vlachos, DDS, DMD, MS Guest Editor CONTENTS Introduction Christos C. Vlachos The Incidence, Classification, Etiology, and Embryology of Oral Clefts John B. Thornton, Sue Nimer, and Paul S. Howard A Comparison of Treatment Results in Complete Bilateral Cleft Lip and Palate Using a Conservative Approach Versus Millard-Latham PSOT Procedure Samuel Berkowitz The Relationship Between Timing of Cleft Palate Surgery and Speech Outcome: What Have We Learned, and Where Do We Stand in the 1990s? Sally J. Peterson-Falzone Bone Grafting for the Alveolar Cleft Defect Peter D. Waite and Daniel E. Waite Orthodontic Treatment for the Cleft Palate Patient Christos C. Vlachos Orthognathic Surgery for the Cleft Lip and Palate Patient Jeffrey C. Posnick Prosthetic Rehabilitation of the Cleft Palate Patient L. Kirk Gardner and Greg R. Parr Velopharyngeal Impairment in the Orthodontic Population Rodger M. Dalston 161
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Future Issues
Vol 2 No 4 (December 1996) TWEED PHILOSOPHY
James L. Vaden, DDS, Guest Editor
Vol 3 No 1 (March 1997) INTERDISCIPLINARY INTERACTION

Vincent G. Kokich, DDS, MSD, Guest Editor
Vol 3 No 2 (June 1997) ORTHODONTICS AND THE LAW

T. Michael Speidel, DDS, Guest Editor
Recent Issues
Vol 1 No 1 (March 1995) BIOMECHANICS AND APPLIANCE DESIGN
Robert]. Isaacson, DMD, Guest Editor Vol 1 No 2 (June 1995) THE RELEVANCE OF FACIAL ESTHETICS TO ORTHODONTICS Sheldon Peck, DDS, MScD, Guest Editor
Vol 1 No 3 (September 1995) EARLY ORTHODONTIC TREATMENT

Gregory}. King, DMD, DMSc, Guest Editor Vol !No4 (December 1995) HMPOROMANDIBULAR JOINT DISORDERS: FACTS OR FALLACIES Daniel M. Laskin, DDS, MS, Guest Editor
Vol 2 No 1 (March 1996) ORTHODONTICS/PERIODONTICS

Bjorn U. Zachrisson, DDS, MSD, PhD, Guest Editor Vol 2 No 2 (June 1996) MANAGEMENT OF COMPLEX ORTHODONTIC PROBLEMS Ravindra Nanda, BDS, MDS, PhD, Guest Editor
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VOL 2, NO 3
SEPTEMBER 1996
Introduction
hildren born with oral clefts require treatment from a number of health care providers during the first two decades of their life. Patients with cleft lip and palate confront a plethora of problems ranging from feeding difficulties as infants to frequent ear infections and hearing problems, compromised speech, aberrant dentofacial development, malocclusion and, last but not least, esthetic impairment with its unfavorable effects on the psychosocial adaptation of the individual. A well-functioning team of experts, as described by many authors in this issue, provides treatment and support for the patient and parents. Numerous specialties should interact in a timely and sequential manner in the management of these patients. There is considerable variation among different teams as to the appropriate treatment sequence for a given cleft lip and palate patient. The preferred approach may differ depending on the specific problem that the patient has. The need for a simple classification system is essential to facilitate communication and interaction among the cleft lip and palate team members. A basic knowledge of the embryology and etiology of the various oral clefts is a prerequisite for a thorough understanding of the classification system. The timing of primary lip closure is controversial. Some professionals advocate repair of the cleft lip between 2 and 3 months of age. In extreme cases of large defects, lip adhesion (a surgical method) may be performed early and the definitive lip repair is postponed for a later time (5 or 6 months of age). Others advocate presurgical orthopedic treatment to be performed initially, followed by lip adhesion at 1- to 2-months of age, and definitive lip surgery at approximately 6 months of age. Considerable controversy exists as to the advantages and benefits of each of these approaches. The timing of palatal closure is still a matter of conjecture. Although the decision concerning
the appropriate age for palatoplasty is made by the plastic surgeon and the speech pathologist, this decision is important for the orthodontist as well, especially when the possible impact of such procedure (s) on subsequent midfacial growth is considered. During the deciduous dentition stage of development, orthodontic treatment may be appropriate in some instances. Extensive orthodontic procedures are not usually done at this stage. During the mixed-dentition stage, secondary alveolar bone grafting procedures are usually performed. It is generally accepted that the graft placement be preceded by a phase of orthodontic treatment involving the maxillary arch. Alveolar cleft closure affords the patient a number of advantages including stabilization (unification) of the maxilla, closure of oronasal communication, provision of an osseous base for the eruption of canines and other teeth, as well as improved esthetics. The dentofacial deformities of skeletally mature cleft lip and palate patients usually require the combined efforts of the orthodontist and maxillofacial surgeon. The concepts and techniques involved in orthognathic surgery are generally similar to those performed in noncleft orthognathic surgery patients with some modifications reflecting the special problems encountered with cleft palate patients. Prosthodontic management is also often required in these patients. This issue of Seminars in Orthodontics is not a substitute for a comprehensive text on the overall management of the cleft lip and palate patient. The issue rather represents an effort of team specialists to provide information that the orthodontist may use in the management of cleft lip and palate patients. Christos C. Vlachos, DMD, DDS, MS Guest Editor
Seminars in Orthodontics, Vol 2, No 3 (September), 1996: p 161
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The Incidence. Classification, Etiology, and Embryology of Oral Clefts

John B. Thornton, Sue Nimer, and Paul S. Howard
There are numerous problems encountered among individuals with a cleft lip and/or cleft palate. Addressing these problems necessitates a multidisciplinary approach, requiring a team of experts to facilitate care for these individuals. Dentists play a vital role on the team. An orthodontist, pediatric dentist, oral maxillofacial surgeon, and prosthodontist usually represent the dental members of the team. The success of this team depends on expertise within each discipline but also depends on each member having a broad base of knowledge in general about oral clefts. An understanding of other disciplines and how they approach the treatment of oral clefts is important for each team member. Also, each team representative should appreciate the need to understand the causes of oral clefts, how clefts develop in utero, how various populations are affected, and how to recognize and classify an oral cleft. It is difficult to communicate effectively within the team if we fail to recognize the importance of expanding our knowledge to include other aspects of oral clefts beyond treatment perspectives. This article provides the orthodontist with basic information as it relates to the etiology of oral clefts (ie, genetics, teratogens, and medical conditions), the demographics and incidence of oral clefts, the embryology and classification of clefts. (Semin Orthod 1996;2:162-168.) Copyright 1996by W.B. Saunders Company
anagement of the cleft lip and/or cleft palate (CL/CP) patient is a process that starts in infancy and continues on into adulthood. Problems encountered in the CL/CP patient are complex and therefore best managed through a team of experts. Feeding difficulties, for example, can interfere with the nutritional status of an infant and must be dealt with early. There are no simple solutions for approaching the myriad of problems associated with a CL/CP patient. There is more than one school of thought concerning how and when to intervene in the correction of a CL/CP, but planning should
From the Department of Pediatric Dentistry, The Department of Surgery, Division of Plastic Surgery, University of Alabama at Birmingham; and the Department of Pediatric Plastic Surgery, The Children's Hospital of Alabama, Birmingham, AL. Address correspondence and reprint requests to John B. Thornton, DMD, MA, Professor and Director of the Postdoctoral Program in Pediatric Dentistry, University of Alabama at Birmingham, 1919 Seventh Avenue South, Birmingham, AL 35294. Copyright 1996by W.B. Saunders Company 1073-8746/96/0203-0008$5.00/0
commence soon after birth because early management is essential. Through the team approach, professionals from various fields convene to assess the needs of the child and to assist the parents in dealing with the situation. The team usually consist of a plastic surgeon, an oral maxillofacial surgeon, an orthodontist, a pediatric dentist, a prosthodontist, a speech therapist, a psychologist, a nutritionist, and in most cases, a social worker to assist in the facilitation of services. Infant feeding must be addressed. Later speech must be dealt with in a timely manner, seeking every opportunity to enhance the development of normal speech. Another major concern is esthetics. As the team begins to plan the course of events for the CL/CP patient, the development of good selfesteem through good esthetic results is a continual factor of great significance. The impact of CL/CP on the self-esteem of a child can be overwhelming. Often, the scars left from surgery and poor speech persist throughout life. Signifi-
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Seminars in Orthodontics, Vol 2, No 3 (September), 1996: pp 162-168
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Etiology and Embryology of Oral Clefts
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cant goals of the team include maximizing esthetic results and also facilitating the development of the orofacial complex. The dentist plays a major role in the care of the CL/CP patient. To be an effective contributor to the team, the clinician needs to have a thorough knowledge of oral clefts (ie, etiology, embryology, classification, incidence, and demographics) . This article provides the clinician with background information related to these areas.
point between the primary and secondary palates is illustrated in Figure 1. In addition, although not shown in the illustration, a patient may also have a bilateral complete cleft of the lip and palate.
Incidence and Etiology of Oral Clefts

When a child is born with an oral cleft, the parents are usually concerned about the cause of the cleft. A range of negative emotional feelings (eg, rejection, guilt, anguish) may be experienced by the parents before accepting the situation and dealing with the child's problems. Parents need support in response to these negative emotions so that they can deal effectively with their own personal feelings and proceed with helping their child. An oral cleft may be either genetic in origin or associated with a teratogen, a drug taken during pregnancy that may cause birth defects, or may be associated with a medical condition. If the cleft is genetic in origin and associated with a syndrome (eg, Van der Woude syndrome, Apert syndrome, Seckel syndrome), the etiology can be easily determined by understanding the genetic transmission of the particular syndrome. In an isolated cleft, the etiology may be more difficult to determine unless there was a specific teratogen involved in the pregnancy or there existed a medical problem during pregnancy. There is general consensus that heredity is the most significant etiology of clefts.3
Incisive foramen Nostril
Classification of Oral Clefts

Several classifications for oral clefts have been introduced over the years. In the United States, Davis and Ritchie presented a classification in 1922,! and Veau in Europe presented his classification in 1931.2 Both of these classifications, however, omitted some of the common variations of oral clefts, and Veau's classification failed to include clefts of the lip or of the lip and alveolus alone.3 These early classifications placed most of their emphasis on the anatomical alveolar ridge as the significant landmark in the division of oral clefts. Others considered that emphasis should be placed on the incisive foramen, an embryological landmark, which marks the boundary between the primary palate and the secondary palate. The area anterior to the incisive foramen makes up the primary palate, which includes the lip and alveolus. The secondary palate is posterior to the incisive foramen and includes the hard and soft palate. Clefting can occur in the primary palate, the secondary palate, or may involve both. Clefting may be complete, incomplete, unilateral, or bilateral. Also, a cleft of the secondary palate may be submucous where the palatine muscle fails to fuse at the midline, but this is not an actual cleft. The embryological approach using the incisive foramen as a landmark was first introduced in 1942 by Fogh-Anderson in Denmark.4 An understanding of the development of the lip and palate makes it easier to appreciate this method of classification. The incisive foramen divides the primary palate from the secondary palate, creating a midpoint reference.4 Kernahan and Stark presented another classification in 1958 based on using the incisive foramen to divide anterior and posterior cleft deformities and is a classification commonly used today.5 An example of a useful classification with the incisive foramen as a dividing
Figure 1. Ventral view of the palate, gum, lip and nose. (A) Normal; (B) unilateral cleft lip extending into the nose; (C) unilateral cleft involving lip and jaw, and extending to incisive foramen; (D) bilateral cleft involving lip and jaw; (E) isolated cleft palate; (F) cleft palate combined with unilateral anterior cleft. (Reprinted with permission from Sadler TW, Langman's Medical Embryology, 5th ed. Copyright 1985. Baltimore: Williams & Wilkens. Lea & Febiger.)
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Thornton, Nimer, and Howard
Clefts of the lip and the palate are the most common of facial, oral, and vocal anomalies.6 Considering all congenital anomalies of all kinds, clefts of the lip or palate are second only to clubfoot. Some clefts are more prevalent than others. The percentage of oral clefts by type from a population sample of 161 children at the Royal Hospital for Sick Children in Edinburg revealed the following: 16% had a cleft lip, 38% had a cleft lip and cleft palate, and 46% had an isolated cleft of the palate.7 Variations have been recognized in the incidence of oral clefts among races, sexes, and geographical areas. Ross and Johnston noted a difference among racial groups from reviewing selected surveys.8 Summarizing the results of their survey, they showed that African-Americans had the lowest incidence with a range of 0.21 to 0.41 per 1,000 live births. Orientals, especially Japanese, who were the most extensively studied among Orientals, had the highest incidence of clefts with a range from 1.14 to 2.13 per 1,000 live births. In the United States and Western Europe whites had an incidence between 0.77 and 1.40 per 1,000 live births. An isolated study in 1963 among Indians in Montana representing 11 tribes revealed an extremely high incidence of clefting in comparison with other populations having one affected child for every 276 births.9 The latter incidence was twice that of the nonIndian population in the state. Sex differences for oral clefts have also been reported. Boys are affected more often than girls, and boys have more severe clefts than girls.10 More girls, however, are affected with isolated cleft palates than are boys. Genetic disorders are classified into the following groups: (1) chromosomal disorders, (2) single-gene disorders, (3) multifactorial disorders, and (4) mitochondrial disorders.11 Oral clefts are primarily considered to be in the class of multifactorial disorders, although there is not a consensus among researchers on this. Most congenital malformations are considered multifactorial. The expression of a multifactorial disorder is thought to be based on a threshold model, whereby those with more of the disease causing genes and environmental factors are more likely to exceed the threshold and express the disorder (Fig 2). Oral clefts appear to fit into an inheritance mode that is typical for multifactorial disorders and which include the following fac-
General Population Third-degree^ Relatives
Liability
Risk of Malformation Threshold
Figure 2. Distribution curves showing liability-threshold concept of multifactorial inheritance. The closer the degree of relatedness (and thus the greater the number of genes in common) to an affected individual, the greater the liability of expressing the trait. (Reprinted with permission from Persaud TVN, Chudley AE, Skalko RG. Basic Concepts in Teratology. Copyright 1985. New York: Alan R. Liss.)
tors: (1) if more than one family member is affected, the risk of recurrence increases; (2) the more severe the cleft (ie, bilateral cleft lip/cleft palate), the greater the recurrence risk for other siblings or relatives; (3) the risk for recurrence is higher if the affected individual is of the less commonly affected sex; (4) the risk for recurrence usually decreases rapidly in more remotely related relations; and (5) consanguinity increases the rate because of the sharing of genes.11 This multifactorial model, however, has not been fully accepted as an explanation for the mode of transmission for oral clefts. Bixler points out that data from various studies do not fully support the multifactorial-threshold trait, but according to Bixler, no single etiologic model would be appropriate for oral clefts.12 Bixler divides oral clefts into three groups which are represented by (1) syndromic, which includes monogenic (single-gene disorders), chromosomal, and environmental etiologies. Syndromic accounts for 1 % of cleft lip or cleft palates and 8% of isolated cleft palates. The next group is (2) familial, which includes those with two or more affected individuals in first, second or third degree relatives. Familial accounts for 25% of cleft lip/cleft palates and 12% of isolated cleft palates; and lastly, (3) isolated or nonfamilial, which includes all kindreds with only the proband (ie, the first person in a pedigree found to have the defect) affected in first, second, and third degree relatives. This group accounts for
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75% of cleft lip/cleft palates and 80% of isolated cleft palate cases. Oral clefts occurring in association with a syndrome where there are other anomalous findings, accounts for somewhere between 3% to 8% of clefts.12'13 Cohen has identified 154 syndromes with oral clefting.14 The modes of genetic transmission for the 154 syndromes include 35 autosomal dominant, 39 autosomal recessive, 5 X-linked, 16 environmentally induced, 29 chromosomal, and 40 unknown genesis. Oral clefts occur in numerous syndromes associated with a chromosomal disorders. Trisomy 13 is an example of one of the trisomy syndromes in which there is a high percentage of individuals born with clefts.15"17 There are many other anomalies found in trisomy 13 and the prognosis for this syndrome is poor. Oral clefts also may occur in other chromosomal disorders, including trisomy 18, Turner syndrome, Down syndrome, Cri-DuChat syndrome, Wolf-Hirschhorn syndrome, and many others.18'21 There also are a large number of monogenic syndromes with oral clefts. Some examples include Meckel syndrome, which is an autosomal recessive disorder and is associated with polydactyly, polycystic kidneys, encephalocele, cardiac anomalies, and other abnormalities.12 Van der Woude syndrome, an autosomal dominant disorder, is notable for the appearance of lip pits along with a cleft lip/cleft palate, which occurs in 80% of those with this syndrome.22 Lip pits, however, may be the only clinical feature in an individual with this syndrome but may be an indicator for the presence of this gene and the occurrence of a cleft lip/cleft palate in future generations. Apert syndrome is another example of an autosomal dominant disorder in which a cleft palate may be seen.12 Craniosynostosis, ocular hypertelorism, midface deficiency, syndactyly of the hands and feet are some of the clinical features of Apert syndrome. Oral-facial-digital syndrome I is an X-linked dominant trait in which a cleft palate may be seen.12 Other features of this syndrome include dystropia canthorum, hypoplastic alar cartilages, bifid tongue, tooth anomalies, brachydactyly, syndactyly, and clinodactyly. The latter syndrome is lethal in male patients. Lastly among monogenic disorders, Treacher Collins syndrome is a common autosomal dominant disorder which may exhibit a cleft palate. Typical features of this syndrome are
low-set ears, malar hypoplasia, down-slanting palpebral fissures, and micrograthia.14 Another syndrome in which there is no single etiology is Pierre Robin syndrome. This syndrome is recognized by specific clinical findings, such as micrognathia, glossoptosis, cleft palate, and heart defects which are found in a small percentage of cases.19 It can be defined as having multiple defects originating from a single known or presumed structural defect (ie, hypoplasia of the mandible which may prevent the tongue from its normal descent between the palatal shelves).19'23 The multiple anomalies found in Pierre Robin's syndrome result from defects in the first branchial arch and is sometimes referred to as the first arch syndrome, which includes Treacher Collins syndrome.24 Pierre Robin syndrome may also be referred to as the Robin complex or anomalad because it was considered to be a specific syndrome occurring as an isolated defect but is now believed to be nonspecific, representing a broader pattern of syndromes which may have oral clefts (eg, Beckwith-Wiedemann syndrome, Stickler syndrome).14-18 Of significant concern in Stickler syndrome, which may be associated with the Robin anomalad, is the early detection of myopia, caused by retinal detachment, which can lead to blindness if not treated.19 Teratogenic substances, such as certain drugs, can cause birth defects. Infections during pregnancy can produce birth defects. These are considered environmentally induced defects. During pregnancy it is important to be cautious about which medications are taken and cautious about being exposed to viral infections, such as the cytomegalovirus or the rubella virus. Even though 600 exogenous agents have been shown to be capable of causing congenital defects in animals, only 25 are human teratogens.25 There are many factors which influence the development of birth defects when exposure to a teratogen occurs. Some of the factors which determine the impact of a teratogen include the genotype of the mother and the child and the timing and the dose of the drugs.26 A drug, for example, cannot affect the development of a cleft lip or palate if it is taken by the mother after the closure of the lip and the palate in utero. Medications taken during pregnancy have been implicated in oral cleft formation. There are only a few drugs that have been implicated
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and uncertainty exists about the role of some of these medications. Diazepam and other benzodiazepines have been shown in some studies to act as a teratogen for oral cleft formation.27'28 However, there are some conflicting data concerning the role or benzodiazepines in oral cleft formation.29'30 Therefore, these medications are considered to be a weak teratogen but may still place a pregnant mother at risk. Steroids have been implicated in producing oral clefts when taken during pregnancy.31 The incidence of cleft formation has been shown from various studies to range from 0.7% to 1.9%.3132 This medication also appears to have a low effect as a teratogen.26 Other drugs and conditions have been linked to oral cleft formation but with the occurrence of other anomalies. Amphetamine, a diet drug, has been shown to cause oral clefts and other anomalous conditions.33 Diabetes, a medical condition during pregnancy, has also been shown to produce oral clefts.34 There are other medications that produce oral clefts but classified as syndromes because of the particular physical characteristics that are found in affected individuals. The anticonvulsant drug, hydantoin, used in pregnant women with epilepsy can produce offspring with an oral cleft and other distinct clinical features.35 These features include a high arched or cleft palate, dental irregularities, low-set ears, V-shaped eyebrows, heart defects, and mental retardation. Trimethadione, another anticonvulsant, can lead to the development of a syndrome with a distinct phenotype, including an oral cleft.36 Fetal alcohol syndrome is a commonly known condition in children whose mother consumed alcohol during pregnancy. The typical facial appearance of a child with fetal alcohol syndrome includes short palpebral fissures, a hypoplastic upper lip with thinned vermilion border, and a diminished or absent philtrum.37 Midfacial growth deficiency is also a finding in these individuals and occasionally oral clefts have been observed. These children are also developmentally delayed in the mild to moderate range.
human development.38'24 Five facial prominences appear around the stomadeum or primitive mouth. These facial prominences are (1) the unpaired frontonasal prominence, (2) paired maxillary prominences, and (3) paired mandibular prominences (Fig 3).38 During this time of development, the two nasal (olfactory) placodes or thickenings begin to develop on both sides of the frontonasal prominence. The nasal placodes invaginate around the fifth week to form the nasal pits. This invagination of the placodes creates a ridge around the pits, referred to as the lateral nasal prominences (outer edges) and the medial nasal prominence (inner edges) (Fig 3B). Over the following 2 weeks the maxillary prominences increase in size causing the medial nasal prominences to move toward the midline. Eventually, the space between the medial and lateral nasal prominences diminishes and the two prominences fuse on both sides forming the upper lip. The lower lip and jaw form when the mandibular prominences merge across the midline. The possibility of a mandibular cleft lip can occur here, and very rarely, a mandibular bony cleft can occur. The maxillary and lateral nasal prominences are separated by a groove called the nasolacrimal groove, which canalizes to become the nasolacrimal duct. Failure of this groove to canalize can lead to a facial cleft leaving the duct exposed to the surface. There are other situations in which incomplete fusion can create facial clefts. Further development of the frontonasal prominence gives rise to the bridge of the nose. The crest and the tip of the nose and the philtrum of
Nasal pit
Mandibular prominence
Embryology of Oral Clefts

To fully understand oral clefts, it is important to know how the face and oral structures develop in utero. The face and facial structures begin to develop around the end of the fourth week of
Figure 3. Frontal aspect of the face: (A) 5 week embryo, (B) 6-week embryo. The nasal prominences are gradually separated from the maxillary prominence by deep furrows. (Reprinted with permission from TW Sadler. Langman's Medical Embryology, 5th ed. Copyright 1985. Baltimore: Williams & WilkensLea&Febiger.)
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the upper lip are formed by merging of the medial nasal prominences. The alae of the nose form from the lateral nasal prominences. The formation of the primary palate occurs as a result of the merging of the maxillary and medial nasal prominences. It is part of the intermaxillary segment, which also consists of the anterior jaw with the four anterior teeth and the philtrum of the upper lip. The secondary palate becomes apparent around the sixth week of human development when two outgrowths appear from the maxillary prominences called the palatine shelves. At the seventh week the palatine shelves, which initially are directed in an oblique and downward position on each side of the tongue, move upward above the tongue and lie horizontal to the tongue. The shelves fuse forming the hard and soft palate which makes up the primary palate. Anteriorly, the primary palate fuses with the secondary palate. The incisive foramen represents the midline landmark between the primary and secondary palates. Oral clefts result from partial or complete lack of fusion of the maxillary prominence with the medial nasal prominence on one or both sides anterior to the incisive foramen and/or result from failure of the palatine shelves to fuse posterior to the incisive foramen. The palate is thought to form strictly by midline fusion of the palatine shelves; however, fusion of the lip can be prevented by a lack of proliferation of mesodermal cells in the area of the lip derived from the ectoderm of neural crest cells.39 Failure of these mesodermal cells to proliferate could prevent the maxillary prominence from merging with the intermaxillary segment formed by the medial nasal prominence. This can create a cleft lip unilaterally or bilaterally.
classification or types of clefts as well as the etiology and embryology of cleft development. The information provided in this article is only an overview of the areas discussed. The reader should be encouraged to seek more in-depth knowledge and appreciate the fact that new ideas and information on oral clefts will continue to emerge as we learn more about clefts. Serving on the team is a privilege and each child born with a cleft lip and/or palate is relying on that team to help them overcome the problems encountered with this defect, thereby enhancing the quality of life for that special person.
References
1. Davis JS, Ritchie HP. Classification of congenital clefts of the lip and palate. JAMA 1922;79:1323-1327. 2. Veau V. Division: Palative, Anatomic, Chirurgie, Phonetique, Paris: Masson, et cie, 1931. 3. Edwards W, Watson ACH. Advances in the Management of Cleft Palate. New York: Churchill Livingston, 1980. 4. Fogh-Anderson P. The Inheritance of Cleft Lip and Cleft Palate. Copenhagen: A Busch, 1942. 5. Kernahan DA, Stark RB. A new classification for cleft lips and palates. Plast Reconst Surg 1958;22:435-441. 6. Cooper HIL Historical perspectives and philosophy of treatment. In: Cooper HK, Harding RL, Krogman WM, et al, editors. Cleft Palate and Cleft Lip: A Team Approach to Clinical Management and Rehabilitation of the Patient. Philadelphia, PA: Saunders, 1979:2-21. 7. Drillan CM, Ingram TTS, Wilkinson EM. The Causes and Natural History of Cleft Lip and Palate. London: E.S. Livingston, 1966. 8. Ross RB, Johnston MC. Cleft Lip and Palate. Baltimore, MD: Williams and Wilkins, 1972. 9. Tretsven VE. Incidence of cleft lip and palate in Montana Indians. J Speech Hear Dis 1963;28:52-57. 10. Oka SW. Epidemiology and genetics of clefting with implications for etiology. In: Cooper NK, Harding RL, Krogman WM, et al, editors. Cleft Palate and Cleft Lip: A Team Approach to Clinical Management and Rehabilitation of the Patient. Philadelphia, PA: Saunders, 1979: 108-143. 11. Jorde LB, Carey JC, White RL. Medical Genetics. St. Louis, MO: Mosby, 1955. 12. Bixler D. Genetics and clefting. Cleft Palate J 1981;18: 10-18. 13. Fraser FC. The genetics of cleft lip and cleft palate. Am J Hum Genet 1970;22:336-352. 14. Cohen MM Jr. Syndromes with cleft lip and cleft palate. Cleft Palate J 1978;15:306-328. 15. Conen PE, Erkman B, Metaxoton C. The "D" syndrome. Am J Dis Child 1966;! 11.236-247. 16. Halbrecht I, Kletzay O, Komlos L, et al Trisomy D in cyclopia. Obstet Gynecol 1971,37:391-393. 17. Fujimoto A, Ebbin AJ, Towner J, et al. Trisomy in two infants with cyclops. J Med Genet 1973;10:294-296. 18. Haddah HM, Wilkins L. Congenital anomalies associated
Conclusion
Management of the cleft lip and/or cleft palate patient is a complex process. It requires the efforts of professionals representing multiple health-related disciplines. A cooperative team approach is the only way to insure the best possible result. All team members need knowledge related to each individual discipline to achieve a successful cooperative effort. It is, therefore, important to take time to learn all aspects associated with oral clefts, including the
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19. 20.
21.
22.
23.
24. 25. 26.
27. 28.
with gonatal aplasia: Review of 55 cases. Pediatrics 1959;23:885-902. Gorlin RJ, PendborgJJ, Cohen MM Jr. Syndromes of the Head and Neck. New York: McGraw-Hill, 1976. Smith DN. Recognizable Patterns of Human Formation: Genetic Embryologic and Clinical Aspects. Philadelphia, PA: Saunders, 1982. Taylor AI, Challacombe DN, Hawlett DM. Short arm deletion, Chromosomes 4(4P-), a syndrome? Ann Hum Genet 1970;34:137-144. Cervenke J, Gorlin R, Anderson V. The syndrome of pits of the lower lip and cleft lip and/or palate: Genetic considerations. AmJ Hum Genet 1967;19:416-432. Spranger JW, Benirschke K, Hall JH, et al. Errors in morphogenesis: Concepts and terms. J Pediatr 1982;100: 160-165. Moore KL. The Developing Human: Clinically Oriented Embryology. Philadelphia, PA: Saunders, 1977. Persaud TVN, Chudley AE, Skalko BG. Basic Concepts in Teratology. New York: Alan R. Liss, 1985. Isreal J, Baum LD. Genetic aspects of cleft palate and cleft lip and palate. In: Pirruccello FW, editor. Cleft Lip and Palate: Plastic Surgery, Genetics and the Team Approach. Springville: Thomas, 1987:17-40. Saxen I. Association between oral clefts and drugs taken during pregnancy. IntJ Epidemiol 1975;4:37-44. Safra M, Oakly S. Association between cleft lip with or
without cleft palate and prenatal exposure to diazepam. Lancet 1975;2:478-480. 29. Shiono PH, Mills JL. Oral clefts and diazepam use during pregnancy. N Engl J Med 1985;311:919-920. 30. Rosenburg L, Mitchell AA, Parsells JL, et al. Lack of relation between oral clefts to diazepam use during pregnancy. N EnglJ Med 1983;309:1282-1285. 31. Bongiovanni AM, McPadden AJ. Steroids during pregnancy and possible fetal consequences. Fertil Steril 1960,11:181-186. 32. Fraser FC. Pregnancy and adrenocortical hormones. Br Med J 1962;2:479. 33. Erikson M, Larsson G, Zetterstrom R. Amphetamine addiction and pregnancy. Acta Obstet Gynecol Scand 1981;60:253-259. 34. Pederson J. The Pregnant Diabetic and her Newborn. Baltimore, MD: Williams and Wilkins, 1977. 35. Hanson JW, Smith DW. The fetal hydantoin syndrome. J Pediatr 1975;87:285-290. 36. Zachai EH, Mellman WJ, Neiderer B. The fetal trimethadione syndrome. J Pediatr 1975;87:280-284. 37. Cherren SK, Smith DW. The fetal alcohol syndrome. N Engl J Med 1978;298:1063-1067. 38. Sadler TW. Langham's Medical Embryology. Baltimore, MD: Williams & Wilkins, 1990. 39. Stark RB. Congenital defects. In: Stark RB, editor. Cleft Palate: A Multi-Discipline Approach. New York, Harper & Row, 1968:45-49.
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A Comparison of Treatment Results in Complete Bilateral Cleft Lip and Palate Using a Conservative Approach Versus Millard-Latham PSOT Procedure
Samuel Berkowitz
Conservative non-presurgical orthopedic treatment in complete bilateral cleft lip and palate (CBCLP) cases were compared with those treated will the Millard-Latham (M-L) method, which involves the presurgical mechanical retraction of the protruding premaxilla using pinned palatal appliances. In conservatively treated cases, a head bonnet with an external elastic is sometimes used before surgical lip closure to ventroflex the premaxilla thereby reducing tension at the surgical sites. The M-L method involves premaxillary bodily retraction followed by a gingivo-periosteoplasty. In both series of cases the palatal cleft (hard and soft) is closed for patients aged 18 to 30 months using a modified von Langenbeck procedure. A secondary alveolar bone graft is only performed in the conservatively treated series for patients aged 7 to 9 years. Although the premaxilla in 2 of 29 conservatively treated cases were retruded and in anterior crossbite by 10 to 12 years of age, all M-L cases were retruded by 9 years of age requiring maxillary protraction. In the M-L cases 90% showed bony bridging of the alveolar cleft with frequent loss of the lateral incisor space; surgical closure of the nasal floor is facilitated, and early aesthetic improvement is followed by midfacial retrusion. (Semin Orthod 1996;2:169-184.) Copyright 1996 by W.B. Saunders Company
ne of the most controversial areas still remaining in the treatment of cleft lip and palate has to do with the use of presurgical orthopedic treatment (PSOT) as a supposedly viable and beneficial concept and whether it is superior to conservative, nonorthopedic treatment. In recent years, serial documentation of the natural evolution of postnatal facial development of complete bilateral cleft lip and palate (CBCLP) has yielded important information. This has improved the surgeon's ability to arrive
From the Department of Pediatrics and Surgery, the University of Miami School of Medicine. Consultant, Plastic Surgery Department, Miami Children's Hospital, South Miami, FL. Supported in part by Health Foundation of South Florida, which financed the geometric palatal growth studies. Address correspondence to Samuel Berkowitz, DDS, MS, FICD, 6601 SW 80th Street, South Miami, FL 33143. Copyright 1996 by W.B. Saunders Company 1073-8746/96/0203-0009$5.00/0
at different diagnoses that lend themselves to conservative treatment planning, with a more predictable, favorable outcome. However, there are still those who do not wish to wait until after the patient reaches puberty to complete surgicalorthodontic procedures. These clinicians favor instead the attainment of improved facial aesthetics and palatal arch alignment soon after birth, by using either the Millard-Latham (M-L) mechanical maxillary orthopedic technique or other early manipulative procedures. In years past, a lack of information on how surgery influenced facial and palatal development was reflected in the static premises that characterized surgical thinking. During the 1920s and 1930s the surgeon's treatment philosophy was to repair the defect by establishing an anatomical continuity, using external compression techniques at the earliest possible date (Fig I).1'3 The first priority of the treatment goals was
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Figure 1. Mechanical presurgical orthopedic premaxillary retraction appliance created by Brophy. (Reprinted from Brophy TW. Cleft Lip and Palate. Philadelphia, PA: Blakiston's Son and Co, 1923:131-132.)
growth studies. Consequently, they lacked an understanding of the importance of the premaxillary vomerine suture in bilateral cleft lip and palate for the attainment of normal facial growth (Fig2).9'n Reflecting a similar flawed philosophy, Latham, a leading advocate of the PSOT school, under Millard's supervision adapted the principal and procedure of early palatal manipulation previously used by Latham and Georgiade.12-13 Treatment goals were limited to the alignment of the alar base, to permit bone migration across the alveolar cleft, and the attainment of early facial aesthetics. The theory was that this procedure was essentially physiological and would allow normal facial growth and development to proceed unabated. A second contrarian school of thought that arose in the 1950s did not favor presurgical orthopedic treatment. Led by Pruzansky,14 this school included Aduss et al,15 Subtelny,16 Berkowitz,17'18 Graber,19'21 Olin and Bishara,22 Narula and Ross,23 Friede and Pruzansky,9 Friede,10'11 Mazahari et al,24 Bergland et al,25 Shaw et al,26 Semb,27 and Vargervik.28 They believed it was best to reestablish lip muscle continuity soon after birth which would allow natural muscle palatal-molding forces to normalize the dis-
improved speech ability, followed by dental function and facial aesthetics.4 Most surgeons at that time, misunderstanding the embryo-pathogenesis of cleft palate development, and lacking the benefit of long-term facial growth records, did not recognize the extent to which time or, more precisely growth, would serve as their ally or enemy. This surgical philosophy and practice involving early palatal manipulation and cleft closure led to disastrous facial results. In reaction to them, there emerged in the 1950s two schools of thought. One was led by McNeil5"7 and Burston8 who decried the inhibiting effect of then current surgical procedures on the growth of the face, and recommended PSOT to align palatal segments and stimulate palatal development while delaying palatal closure until 5 to 9 years of age. In many ways this school of thought was trapped by the same deficiencies in knowledge experienced by the surgeons with whom McNeil and Burston took issue. Their common error stemmed from not having the kind of information provided by longitudinal facial and palatal
Figure 2. Lateral cephalometric tracing of CBCLP showing the protruding premaxilla forward in the profile, e = premaxillary vomerine suture.
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torted oral and pharyngeal skeletal architecture. Palatal cleft closure was to be performed between the second and fourth years of age, which allowed for an increase in palatal size at the expense of the prevailing cleft space. This article compares conservatively treated cases of CBCLP which involved uniting the lip over the protruding premaxilla (with or without the prior use of external elastics) within the first few months and without the use of presurgical orthopedics, to similar cases involving the M-L presurgical orthopedic treatment procedure.29
Materials
The CBCLP cases involving early orthopedic and nonorthopedic treatment were chosen from the files of the ongoing longitudinal facial and palatal growth studies of the South Florida Cleft Palate Clinic, the University of Miami School of Medicine, and Miami Children's Hospital. Lip, nose, and palate surgery was performed by Millard,29 and secondary alveolar bone grafts and maxillary osteotomies were performed by Wolfe. A Millard-Latham Procedure Latham manipulated the palataly pinned presurgical orthopedic appliance so that mechanical expansion of the lateral palatal segments is followed by the retraction of the protruding premaxilla into position within the arch (Fig 3). Afterward, the floor of the nose is surgically closed and a gingivoperiosteoplasty performed to permit the migration of alveolar bone cells to bridge the alveolar gap space. Following the premaxillary retraction, a lip adhesion is performed in patients 1 to 2 months of age and definitive lip surgery with forked flaps at approximately 6 months of age. This technique was first described by Georgiade and Latham.12'13 The appliance currently used consists of a palatal-support section that is pinned to the palatal processes. A premaxillary stainless steel pin 7/10 mm in diameter is inserted through the posterior stem of the premaxilla. An elastic chain (elastics) passes from the pin posteriorly to pulley wheels on the extension appliance. The elastic chain then passes anteriorly to be secured to a button at the front of the expansion appliance, creating a force of 3 oz or
90 g per side. As the premaxilla retracts, the appliance expands simultaneously, widening the anterior lateral palatal segment. Within 8 to 14 days, the premaxilla is positioned within the palatal segments without ventroflexion. The alveolar clefts are then closed with alveoloperiosteoplasty, which creates a tunnel for bone migration from both sides to bridge the cleft space. Millard and Latham3 believe that this procedure will also advance posteriorly positioned cleft palate segments that have lost their growth impetus from being detached from the nasal septum, which they believe is the growth force for the maxillary complex. Millard and Latham3'29 write that premaxillary retraction and gingivoperiosteoplasty might have a negative effect on palatal growth, but nevertheless believe this tradeoff is acceptable to obtain early aesthetics, to close the floor of the nose, and avoid the need for secondary alveolar bone grafting. Case Report ATreated With M-L PSOT Findings. Mechanical premaxillary retraction soon after birth interferes with midfacial growth, perhaps by affecting the integrity of the premaxillary vomerine suture. The gingivoperiosteoplasty as designed by Millard permits bony bridging of the alveolar cleft space in most cases. The only time bridging does not occur is when a large gap space still remains between the premaxilla and the lateral palatal segments. This failure in bridging the cleft space also happens in complete unilateral cleft lip and palate cases when the alveolar cleft space remains large. There is no evidence that pressure stimulation from a functional PSOT appliance increases palatal growth beyond its inherent growth potential. The amount of orthodontics and orthopedics necessary to achieve ideal occlusion is much greater when using the M-L orthopedic technique than we have found in conservatively treated cases (Figs 3-7). Conservatively treated cases. An external elastic from a head bonnet is occasionally used at 3 to 4 weeks of age to ventroflex the premaxilla before one-stage lip adhesion surgery and definitive lip surgery with the banked forked flaps at approximately 6 months of age. Wolfe performed secondary alveolar bone grafts on patients between 7 and 9 years of age using cranial or iliac cancellous bone. In both series of cases the hard and soft palatal clefts were usually closed between 18
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Figure 3. Presurgical orthopedic appliance developed by Latham to reposition the protruding premaxilla in CBCLP while expanding the lateral maxillary segments. An elastic chain develops 90 g of force on each side. After the segments are aligned, mucoperiosteal flaps are used to close the alveolar clefts. (Reprinted with permission from Millard DRJr. Principalization of Plastic Surgery. Boston, MA: Little, Brown, 1986:360).
can be influenced by tension and pressure. The size of the alveolar cleft space at puberty is frequently dependent on the presence or absence of lateral incisors and/or the degree of premaxillary protrusion, as well as the amount of palatal osteogenic deficiency. A combination of osteogenic and mucoperiosteal tissue deficiency adjacent to the cleft in the mixed and permanent dentition, which is insufficient to permit successful secondary alveolar bone grafting, frequently requires that one or both lateral palatal segments be surgically positioned forward to make contact with the premaxilla. This is especially true if the premaxilla is already in a proper overbite/overjet relationship. Various degrees of midfacial skeletal and muscular hypoplasia, with decreased growth potential, can coexist. Improved surgical techniques can prevent damage to facial growth and development, and can even have a beneficial effect by encouraging "catch-up" palatal growth. Overlapping (collapsed) palatal segments are not inhibited per se from reaching their growth potential. In both conservative and PSOT treatment approaches, when palatal segments are expanded to allow premaxillary alignment, the increased arch width in some cases will still need to be physically retained. Premaxillary ventroflexion leading to severe premaxillary overjet and overbite does not interfere with dental function if left uncorrected until a later age. Nasal cartilage is not an important growth force to the maxilla after birth.
and 30 months of age, using a modified von Langenbeck procedure. Maxillary protraction forces were used during the mixed dentition to correct developing midfacial deficiency. Case Report BConservatively Treated Case Findings. In CBCLP the maxilla, as determined by the occlusion, is not retropositioned relative to the mandible before 6 years of age (Figs 8-15). Midfacial recessiveness appears only after the postpubertal growth spurt as a combined result of an increase in forward mandibular growth coupled with that of the anterior cranial base. The united lip seems to exert a posterior directed orthopedic force to the premaxilla, and perhaps to the maxilla as well which reduces its forward growth. The premaxillary vomerine suture is an important growth site that
Discussion
Pathogenesis of Bilateral Cleft Lip and Palate Failure of undifferentiated mesenchymal cells to migrate normally, in a lateral and medial direction, from the neural crest to the regions of the developing primary and secondary palate causes the agenesis of tissue in the vicinity of the cleft.30'31 Coalescence of the facial processes results in the formation of the primary palate which constitutes the initial separation between the oral and nasal cavities, and eventually gives rise to portions of the upper lip and anterior maxilla. The exact mechanism by which the primary palate is formed is not clear. A secondary palatal cleft can be created by one or more of several factors: tongue resistance, ie, delayed elevation of the palatal processes associated with
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Figure 4. TR.BA.64. Serial casts showing the negative effect of M-L PSOT on midfacial growth and development. 0-3: Before PSOT, a severely protruding premaxilla with large anterior and posterior cleft spaces. 0-5: The Premaxilla has been repositioned between the lateral palatal segments; the hard and soft palatal cleft was closed at 32 months. 2-0: The incisors show a developing anterior open bite and crossbite; 2-0 to 6-9: The progressive development of a buccal and anterior crossbite with an open birth is caused by the retardation of midfacial growth in 3 dimensions; 6-9 to 8-2: A Delaire style facial mask is being worn 12 hours a day. Elastics attached to a labile-lingual heavy arch wire, exerting 350 g offeree per side has led to a slight reduction in the anterior crossbite brought on by the improvement in axial inclination of the central incisors.
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to aberrant muscular forces, and decreased shelf forces. Although there are no examples of mutant genes that can cause this last condition, there are many teratogens to which this mechanism has been related.31 Surgical Treatment Goals Kilner,4 a well-respected plastic surgeon who was active in cleft palate care in the 1930s, prioritized cleft lip and palate treatment goals. In order of importance they were: speech, dental function, and facial aesthetics. These objectives led to the adoption of early surgical closure of palatal clefts, because many speech pathologists at that time (as do some even today) believed that good speech could not be obtained with delayed closure. Berkowitz,32 however, stated that speech studies of individuals, or a small sample of subjects, are often sufficient to evaluate solutions of a particular problem being investigated; however, the fact that a correlation exists between two variables, ie, speech proficiency and age, does not indicate or prove causation. While the age at surgery may be the sole variable studied,
Figure 5. Case T.R. BA-64. (A) Delaire style facial mask showing forehead and chin rests. (B) Intraoral elastics running downward and forward superioinferiorly were creating a protrusive force of 350 g per side. Although heavy labile-lingual arches can be used in the deciduous dentition better results are achieved in the mixed and permanent dentition using rectangular arch wires with hooks placed mesial to the cuspids. (Reprinted with permission from Samuel Berkowitz, Cleft Lip and Palate with An Introduction to Other Craniofacial AnomaliesPerspective in Management, Vol. I, Singular Press.)
blockage by the tongue; narrow shelves, which reflect a deficiency of osteogenic and mesodermal tissue in the primary and secondary palate; failure of the palate to fuse, which can be associated with delayed shelf force and thereby be subject
Figure 6. Serial lateral cephalometric tracings from 2-4 to 8-2. The midface is retrusive with an anterior crossbite. The maxillary retrussiveness is becoming progressively worse, however, there is a slight correction in the anterior crossbite brought on by the change in axial inclination of the maxillary incisors.
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Changing Surgical Concepts from the 1920s to 1950s In a number of significant cross-sectional palatal and facial growth studies, Graber19"21 reported that surgery often performed in the 1920s and 1930s had caused severe midfacial deformity. He reported that management of the cleft problem focused primarily on surgery with the surgeons operating without a full understanding of longterm influences of surgery on facial growth and development. Cleft surgical history up to that time was replete with surgical modifications undertaken in an effort to eliminate excessive tension at the site of surgery, and the reopening of palatal clefts. These failures in performing closure of the cleft palate with soft tissue alone led to the mutilating techniques of osteouranoplasty, or bony closure of the palate. Surgeons used various methods to accomplish segmental approximation such as binding the separated
Figure 7. Superimposed polygons. Registered on Sella (S) and superimposed on the anterior cranial base (SN). There is very little change in midfacial retrussiveness, however, the opening of the mandibular plane is caused by the extrusion of the maxillary molars that support the labile-lingual arch to which the elastics are attached. Figures 6 and 7 show a progressive reduction in midfacial growth relative to that of the anterior cranial base and mandible. Only a slight change at A point is noted, yet the anterior crossbite has been slightly reduced. It is anticipated that a more efficient maxillary orthopedic effect will be achieved with tooth-borne appliances. Note that at 8-2 the mandible has rotated posteriorly with the elongation of the midface.
sensory function, genotype, the geometries of the original deformity, the facial growth pattern, and the surgical procedure performed are also factors that influence speech proficiency. It is difficult and perhaps impossible to show the effectiveness of a treatment philosophy in the clinical setting where many variables cannot be identified, controlled, or manipulated. Therefore, conclusions drawn from such investigations should be considered with caution. Long-term serial facial and palatal growth studies by Pruzansky,33 Aduss et al,15 and Berkowitz17 confirm that ideal treatment objectives of good facial and palatal growth need not be compromised to obtain excellent speech.
Figure 8. Case KK.22. Conservative treatment. Excellent palatal and facial growth and development. Composite photographs from birth to 13 years and 11 months of age showing excellent occlusion (A, B)At birth, (C) head bonnet with elastic band positioned over the premaxilla, (D) Lip closure with a forked flap. (E) The lip tissue from the prolabium is positioned within the nostril to be used at a later age to reconstruct the columella. (F-G) Occlusion at 2 years and 5 months. (I) Final occlusion at 14 years. (Reprinted with permission from Singular Press, Berkowitz S. Cleft Lip and Palate with An Introduction to other Craniofacial AnomaliesPerspective in Management, Vol I.)
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Figure 9. Photographs at 1 year and 11 months. (A and B) Facial front and lateral views. (C) Palatal view showing protruding premaxilla with an open palatal cleft. It was closed at 8 years using a modified von Langenbeck procedure.
lateral segments together in the midline. Both extraoral and intraoral appliances were developed to produce a midpalatal bony union as early in life as possible. Brophy1'2 was the foremost proponent of the latter approach and introduced the steel-clamp and silver-wire bony closure technique. Brophy and his many supporters were convinced that aberrant embryonal and fetal influences forced the lateral halves of the maxilla apart, making the intermaxillary width excessive. For Brophy it was only logical that the first step was to restore normal segmental relationships. Whether the surgeon used a von Langenbeck soft tissue procedure alone, or the Brown-Dorrance push-back
vomer flap closure procedure, the end result was the same, severe scarring with midfacial deformity. As the result of Graber's studies,19'21 performed at Northwestern University Cleft Lip and Palate Institute, and Children's Memorial Hospital in Chicago, he recommended that surgery to the palate be delayed. He believed that the safest age to perform surgery was the fifth year. Many surgeons were influenced by Graber's19"21 and Slaughter and Brodie's34 negative reports on surgical procedures performed at an early age. Their reports favored cleft closure after 1 to 2 years of age. "No palatal surgery at an early age" (before 12 months) became the battle cry for the next decade. Consequently, many orthodontists at various cleft palate research-treatment centers searched for the answers to some basic questions relating to the influence of surgery on palatal growth and development: What happens to the tissue that has been manipulated and traumatized? What is the growth potential of fibrous bands of scar tissue? Can a scar influence the normal growth and development of a surrounding soft tissue structures and the bony skeleton? Does the facial growth of a normal child differ from that of a child with a cleft, and if so, how? Answers to such questions require a fundamental knowledge of the dynamic processes of craniofacial growth, development and maturation, which was lacking at that time and is still misunderstood today. Filling the Vacuum It was in this environment that James Scott, an eminent British anatomist, introduced in the 1950s his facial growth theory35'36 which was readily adopted by McNeil5"7 a prosthodontist from Scotland, and his disciple, Burston8'37 an orthodontist from England. Their beliefs involving the use of pediatric functional prostheses were to influence cleft palate treatment for decades to come. With their introduction of an activist-treatment philosophy of using neonatal maxillary orthopedics, which surgeons readily accepted, the treatment pendulum swung from early surgery to the opposite extreme, ie, palatal closure between 5 and 9 years of age. With this presurgical orthopedic treatment, advocates believed that now something good could be done while waiting to close the cleft space.18
Figure 10. Case KK.22. Frontal and lateral facial photographs at 14 years of age showing excellent facial proportions.
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Figure 11. (A, B) Serial dental casts. 6-1: The large protruding premaxilla is well forward of the lateral palatal segments. 0-4 to 2-2: With lip repair the palatal segments come together reducing the anterior and posterior cleft spaces. The buccal occlusion is excellent. 3-10: The palatal cleft is still open, however, the left lateral segment has moved mesially placing the teeth in crossbite. 6-7: The buccal crossbite has been corrected with a fixed expander and maintained with a fixed palatal retainer. The right side is in Class 1, and the left side is in Class 2. 8-3: The palatal cleft space was closed at 8 years with a secondary alveolar cranial bone graft. 13-11: After orthodontics, all incisors are well positioned.
PSOTThe Claimed Biological Basis for Its Use In his thesis on facial growth Scott35'36 wrote that the downward and forward growth of the upper facial skeleton (maxilla and adjacent bones) is determined to a considerable extent by the direction of growth of the nasal septum cartilage. He placed all the facial sutures in the following two sutural systems: (1) The circummaxillary suture system separating the maxilla from the adjacent bones; (2) The craniofacial suture system separating the maxilla (at fronto-maxillary suture) from the bones connecting the anterior cranial segment. Growth at these suture systems thrusts the upper facial skeletal downward and forward. The separating mechanism was the cartilage of the nasal capsule, especially the cartilage of the nasal septum.
In Scott's hypothesis it was assumed that cartilaginous, interstitial growth was the major source of the expansive force that pushes on the subjacent midfacial skeletal structures, causing both vertical and anterior posterior growth. Postnatally an interstitial expansion (pushing) force resides within the nasal sutural connective tissues, presumably substituting for the cartilaginous forces localized anteriorly. A Critique of the Nasal Capsule Theory Moss et al38 suggested a different biomechanical explanation that did not require that the septum play a primary role in normal midfacial growth. His data suggested that the nasal septal cartilage grows as a secondary, compensatory response to the primary growth of related oro-facial matrices, and that midfacial skeletal growth was not
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Samuel Berkowitz
0-0-12
.ft ft A* S* A S*
0-3
1.4
3-0
2-10
3-10
Figure 12. Computer generated tracings of serial casts using an electromechanical digitizer. All tracings are drawn to scale. This series clearly shows: (1) The gradual decrease in cleft space width as the palatal segments increase in size. (2) The geometric changes of the premaxilla relative to the lateral palatal segments. (3) The ideal incorporation of the premaxilla within the palatal arch with orthodontics.
dependent on any prior or primary growth impetus of the nasal septum cartilages. Moss's functional matrix theory states that neither sutural tissues nor the mandibular-condylar cartilage are primary growth centers. Instead, according to Moss, tissue growth observed at both sites
Figure 14. Serial cephalometric tracings from 3 to 20 years and 3 months. Skeletal and soft tissue profile changes show gradual flattening of the angle of facial convexity.
Figure 13. Superimposed computer generated tracings. Superimposed on V (vorner point on P-P line) and registered on the palatal rugae. This method demonstrates that the premaxilla's position within the maxillary arch is almost constant from birth to 17 years in normal, growing faces. Although there is an extensive amount of posterior and transverse growth there is only a slight relative change in the geometric position of the premaxilla. The face grows "to and around" the premaxilla.
is always secondary and complementary to the primary growth of function-related soft-tissue matrices. Each function is performed by a functional cranial component which in turn has two elements. The first is the functional matrix, consisting of all of the tissues and functioning spaces (nasal, oral, and pharyngeal cavities) necessary to perform a given function. Each matrix is protected or supported by related osseous and cartilaginous fibrous tissues collectively termed a skeletal unit. The midfacial skeletal unit is responsive to oro-facial matrix growth. Expansion of the oral cavity volume is responsible primarily for the dimensional and spatial growth of the midfacial skeleton and of the mandible. Moss concludes that the growth of the nasal septum is secondary and complementary to the primary growth of the nasal cavity, and that growth of the midfacial skeleton is independent of nasal septal growth.
PSOT
McNeil5"7 who is recognized as the father of presurgical orthopedics, without having any
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BaH
Go
Figure 15. Superimposed serial lateral cephaloradio graphs using the Coben Basion Horizontal Method. This series clearly shows an excellent facial growth pattern, and the importance of leaving the premaxilla in its original position within the face. The premaxillary ventroflexion does not significantly change the initial midfacial protrusion. The repaired lip appears to retard midfacial growth as the growth at the anterior cranial base and mandible combine to flatten the facial profile.
pedic treatment and with it primary bone grafting (within the first year). They believed the grafting of autogenous bone from the rib or iliac crest to the cleft space would stabilize the manipulated palatal segments and prevent them from collapsing while allowing for normal midfacial growth. McNeil's hypothesized mechanism and treatment benefits were readily accepted without being scrutinized sufficiently or tested either in the laboratory or the clinic. Clinicians who began performing PSOT and recommending its use were cautioned by Pruzansky14 to avoid overly simplistic and insufficiently supported claims, but it was to no avail. When McNeil's followers observed a rapid increase in palatal size soon after birth, they contend that this change was brought about by his growth-stimulating functional appliance.39 Failing to have serial palatal records to support his premise, and although the mechanisms for the increase in palatal size are still not fully understood, nevertheless, McNeil's theory has gone unchallenged by many clinicians up to the present time. Claimed Benefits of PSOT Forshall et al40 a proponent of PSOT, speculated that "it is obvious that a gross distortion to the maxilla at birth will not only lead to a poor facial appearance but also to a mutilated dental arcade producing faulty tongue movements and hence, speech defects. Therefore, early dental facial orthopedics makes its contribution to treatment insofar as it can control and modify the postnatal development of the maxilla." This position was supported by Dreyer41 and Graf-Pinthus and Bettex.42 Dreyer41 also states, again without having any longitudinal records to support his conclusion, that one or more of the palatal segments in crossbite will become progressively more distorted, and therefore early alignment is necessary for better occlusion and function. He claimed that improper arch alignment produced abnormal swallowing patterns that resulted in speech problems. Along with such unproven benefits of PSOT, the use of a primary bone graft to stabilize the manipulated palate arches and close the alveolar cleft space was recommended as a logical supporting procedure and enthusiastically used by many cleft centers.43'44 Pruzansky,14 disturbed by the scientifically un-
supplemental or serial cast records to support his claims, accepted Scott's theory that the nasal septum was the dynamic force which influenced palatal and midfacial growth. The theory, when related to clefts of the lip and palate, suggests that in complete clefts of the lip and palate, the lateral palatal segments being detached from the nasal septum lack the proper growth impetus. Therefore, at birth the palatal segments were presumably, deficient in mass and retropositioned within the face. McNeil5 concluded that a well-constructed functional orthopedic appliance worn by the newborn would stimulate palatal growth, accelerating the cleft closure process. Burs ton, also lacking cephalometric and cast records, misinterpreted clinical findings and erroneously wrote that the premaxilla in CBCLP was not protruding forward in the facial profile, but instead that the lateral palatal segments were retruded within the face and needed to be brought forward by prosthetic functional means.6 Soon most cleft palate centers in Europe and the United States jumped on this philosophical bandwagon, impatient to perform presurgical ortho-
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supported acceptance of PSOT and primary bone grafting, wrote a scathing dissent against both procedures. His objections were based on accepted physiological principals and the results of his longitudinal facial and palatal growth data. He challenged the theoretical premises on which PSOT and primary bone grafting were based. The speculative benefits of PSOT with primary bone grafting were eventually subjected to rigorous scientific testing. As critics anticipated, long-term assessments using serial cephalometric radiographs and palatal casts exposed the resultant deleterious effects on midfacial and palatal growth and development.45 Approximately a decade after its introduction, primary bone grafting, as predicted by Pruzansky14 was found to be deleterious to midfacial growth,46 and its use was discontinued in almost all cleft palate centers that had adopted the practice. In 1978 Berkowitz47 chaired an international committee sponsored by The American Cleft Palate Association to review the literature to determine whether the claims made by those who favored PSOT in the previous decade were verified by long-term clinical studies. The "State of the Art" findings concluded that primary (performed during the first year) bone graftings into the alveolar area indeed had a deleterious effect on midfacial growth. However, Rosenstein44 still defends its use only if performed as he and Kernahan have devised the procedure. The "The State of the Art" report further found that there was no conclusive evidence that PSOT would normalize feeding, tongue posture, or swallowing, or guide the physiological growth of the palate segments. Nor was there any evidence that PSOT reduced middle-ear infections or aided speech development. Georgiade and Latham's Reasons for Using PSOT In an early report by Georgiade and Latham13 listing the physiological basis for performing mechanical retraction of the protruding premaxilla, the authors present biological factors which they contend, support the use of mechanical premaxillary retraction. Well-documented clinical studies since then have shown their reasons for performing orthopedics to be without a physiological basis. Georgiade and Latham's12'13 concepts, which they claim support their theory of retraction of the protruding maxilla, were
reexamined in light of Berkowitz's recent serial facial and palatal growth studies.18 As Pruzansky14 has previously stated, most erroneous premises on which treatment is based can lead to inaccurate conclusions and therapeutic folly. The following dissents refute the reasons advanced for retracting the protruding premaxilla at birth. Reasons. Georgiade and Latham12'13 described the premaxillary vomerine suture to be a tongue and groove joint with the suture seen on the lateral cephalometric tracing as coursing downward and backward. They theorize that, owing to the geometric relationship of the suture to the vomer premaxillary bone, movement with growth is characterized by a sliding of one bone surface with respect to the other. Therefore, their mechanical system has been designed to apply a posterior directed force to the premaxillary bone, to slide it and the premaxillary vomerine suture posteriorly into a more normal and physiological position. Dissent. Premaxillary growth does not occur that way. The design of the suture permits growth to occur in a downward and forward direction, in response to directive forces of tongue function and the dynamics created by the functional matrix. The geometric relationship of the premaxillary vomerine suture histologically and geometrically is similar to that of other sutures of the maxillary complex, which supports downward and forward growth. Reason. When the maxillary structures are brought into more normal relationships, such as when the premaxilla is retracted and placed within the arch, facial growth will subsequently follow a normal growth pattern. Thus the early restoration of normal relationships will provoke normal growth. Dissent Serial growth studies have shown that after premaxillary retraction the midface, which might appear acceptable during the first 4 to 5 years of age, becomes recessive over a longer time. Midfacial abnormalities develop as the facial growth process proceeds. The evidence seems to indicate that there is very little, if any, midfacial growth remaining after mechanical premaxillary setback caused by interferences with tissue integrity at the premaxillary vomerine suture. A deficient midface never shows sufficient growth acceleration to catch up with the growth of the surrounding skeletal structures.
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Reason. Gingivoperiosteoplasty with the use of an appliance will increase the length of the upper anterior arch. Dissent. The facts show that when the premaxillary segment is brought back into alignment, the anterior arch length turns out to be actually less than it would have been if the procedure were performed during the mixed dentition with the insertion of a secondary alveolar bone graft. Placing the premaxilla within the arch makes no allowances for bone deficiency at the alveolar cleft site. The arch length in these cases usually becomes less at least by the width of the lateral incisor, in some cases the deficiency is even greater. The controversy concerning the advisability of performing neonatal arch manipulation has still not been settled. However, the debate has taken on a new focus, not on whether or not the palatal arches can be manipulated, but rather on the supposed psychological benefits to parents who think that something positive is being done to correct the deformity. More recently, KuypersJagtman,48 Prahl-Anderson49 and Hotz et al50 have expressed the opinion that, besides providing psychological support to the parents, aligning the premaxilla relative to the vomer aids lip closure and future palatal development. KuypersJagtman and Prahl-Andersen have begun a clinical trial study to test this hypothesis. The Protruding Premaxilla According to the functional matrix theory, as the midface grows, bone is laid down in the sutures surrounding the maxillary complex. Any damage to one of these sutures can interfere with the direction and the amount of growth. For example, an excessive amount of scarring at the pyerygomaxillary suture, or at the premaxillary vomerine suture (PVS), will interfere with anteroposterior and vertical maxillary and premaxillary growth. Growth movement of the premaxilla is produced by the growth expansion of all the bones behind and above it and by growth in other parts of the maxilla, especially at the premaxillary vomerine suture (PVS). These displacement growth movements are a result of the "carry effect" as Enlow51 calls it, which is produced by the expansion of the soft tissues associated with the bones, not a "pushing effect" of bones against bones. Scarring of the palatal mucoperi-
osteum, therefore, acts to interfere with the "carry effect" thus preventing the changes in position of the maxilla within the face. There exists some controversy as to why the protruding premaxilla is forward in the facial profile. Latham52'53 believes that the condition results from the action of the septomaxillary ligament, which connects the premaxilla to the growing nasal septum. Other than Latham's initial article on the subject, there has not been any substantiation of this effect by other investigators. Pruzansky,33 Aduss et al,15 Berkowitz,1 Friede and Pruzansky,9 Friede,10 and Friede and Morgan54 believe that the protruding premaxilla is forward in the facial profile because of excessive sutural growth in the PVS. The latter is brought about by an increase in tension created by forces of the tongue positioned within the cleft and the cleft orbicularis oris-buccinator-superior constrictor pharyngeous muscle complex. This tension pulls the palatal segments laterally while failing to restrain the growth at the PVS. The depressed alar base region reflects deficiency and displacement in skeletal tissues, and is not a reflection of a retro-positioned maxilla relative to the mandible as Burston8'87 has suggested. The Position of the Maxilla Within the Face In serial cast studies of complete bilateral clefts of the lip and palate, performed by Berkowitz32 in conservatively, nonorthopedically treated cases, although the maxilla and the mandible may be more posteriorly positioned relative to the anterior cranial base, the two jaws are well related to each other as determined by the occlusion at 6 years of age. In 29 cases studied, none had a Class III malocclusion; one or both palatal segments were in either Class I or Class II. This confirms that the palatal processes being detached from the nasal septum are not retro-positioned within the face, as Scott theorized, and therefore that the cleft palatal processes need not be brought forward as Latham recommends.
Conservative Treatmentthe Best Approach

Improvement in surgical or orthodontic treatment methods, coupled with a better understanding of the natural history of cleft palate growth
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and development, have led to different yet frequently successful treatment protocols. To answer the basic question as to why the same surgery performed by the same surgeon on the same type of cleft can yield different results, one must take into account three mutually dependent critical variables: (1) the cleft defect; (2) the facial growth pattern; and (3) the surgical procedure.55 Lip Surgery (Table 1) The basic requirement in all lip surgery is that the full width of the lip be maintained. Reconstruction must preserve and use all available tissue. Millard has stressed that in bilateral clefts of the lip, the prolabium, regardless of its size, should always be positioned to the vermillion border. The usual sequence of treatment is to repair the lip and to delay release of the nasal tip, by reconstruction of the columella, until a later age. Most surgeons recommend surgical repair of the cleft lip between 2 and 3 months of age. The use of a lip adhesion will initiate palatal molding, with a consequent reduction in the anterior and posterior cleft space. In extreme cases of premaxillary protrusion, lip adhesion can be preceded by the use of an elastic strap which is attached to a head bonnet and placed over the prolabium to cause premaxillary ventroflexion with a subsequent reduction of tension at the surgical site. Palatal Cleft Closure. Millard56 has found a modified von Langenbeck palatoplasty to be the treatment of choice to close the hard and soft palate in one stage at between 18 and 30 months of age. This procedure will maintain a normal vault volume. Palatal closure is unique to every individual. No one procedure suffices for all cases and it is not influenced by the use of PSOT. What to do and when to do it are questions that do not have universally accepted answers. In sum, cleft palate surgical history clearly shows that a single mode of surgery for all cases (in terms of type and timing), can result in severe palatal and midfacial deformity, as well as poor speech development. Unfortunately, some negative results will occasionally occur because of various degrees of osteogenic deficiency despite the surgeon's superior skill and experience. Surgical timing should depend on the size of the cleft space when
Table 1. Timing and Sequencing of Conservative Surgical-Orthodontic Treatment

Orthodontics Surgery
After birth CBCLPexternal elastics (off head bonnet) over protruding premaxiliano obturator 3-4 wks 6 mo 18-30 mo
Lip adhesion Millard-Forked Flap von Langenbeck* (simultaneously closure of the hard and soft palate)
4-5 yrs
5-7 yrs 7-8 yrs
9-1 3 yrs
13-1 7 yrs
17-1 8 yrs
Correction of buccal crossbite only using a fixed "W" palatal expander Fixed palatal retention Align anterior teeth before secondary alveolar bone graft (SABG) Full banded treatment with/without maxillary protraction (Delaire facial mask) Full orthodontics. Evaluate need for presurgical orthodontics Postsurgical orthodontics followed by prosthetics
Secondary alveolar bone graft Cranial or iliac bone Nasal tip or lip revision
Maxillo-mandibular surgeryf Nasal-lip revision if necessary Nasal-lip revisions if necessary
fMaxillo-mandibular surgery is usually performed earlier for girls (around 15 to 16 years of age) than boys whose surgery is performed during the summer before the senior high school year. This allows for maximum facial growth changes and leaves enough time to perform postsurgical orthodontics and prosthetic treatment.
related to the size of the adjacent palatal segment or segments, and not on age alone.32 There are instances when the cleft space is so small at 1 year of age that simple mucoperiosteal approximation is possible without the need of lateral releasing incisions. In all instances, the anterior cleft space should be left open until the palatal segments are orthodontically aligned and ready for a secondary alveolar bone graft using either cranial or iliac crest cancellous bone. Only as we come to understand the relationship between palatal growth and surgery shall we be able to prescribe treatment on an individual basis, with greater assurances of success and without falling prey to the fashions of the moment.
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Conclusion
The PSOT cases under investigation need to be followed through adolescence before a definitive irrefutable statement can be made supporting the use of the M-L presurgical orthopedic procedure. In the meantime, early analysis of the palatal and facial growth pattern of these cases strongly suggests that the long-term effects of M-L PSOT are not conducive to normal palatal and facial growth and development. A conservative treatment approach relies more on physiological forces and requires less orthodontics. In short, flattening of the facial profile cannot be hurried. Obviously, the results of this investigation on the use of the M-L procedure will include treatment of complete unilateral clefts of the lip and palate as well.
Acknowledgment
Thanks are extended to Singular Press, San Diego, CA, for giving permission for the use of photographs from Berkowitz S. Cleft Lip and Palate with An Introduction to Other Craniofacial Anomalies. Perspectives In Management, vol. I. Dr. Lin Hu and Lin Ao performed the digitizing of casts, created the palatal growth graphics, and performed the Coben analyses.
References
1. Brophy TW. Cleft Lip and Palate. Philadelphia, PA: Blakiston's Son, 1923:131-132. 2. Brophy TW. The treatment of congenial cleft palate: A plea for operations in early infancy. Med Rec 66:75, 1904 Trans Am Surg Assoc 22:122, 1904, BJ Child Dis 1:476, 1904 3. Millard DRJr, Latham RA. Improved surgical and dental treatment of clefts. Plast Reconstr Surg 1990;86:856-87l. 4. Kilner TP. The management of the patient with cleft lip and/or palate. Am J Surg 1958;93:204. 5. McNeil CK. Congenital oral deformities. Br Dent J 1956;101:191-198. 6. McNeil CK Orthodontic procedures in the treatment of congenital cleft palate. Dent Records 1950;70:126-132. 7. McNeil CK. Oral and Facial Deformity. London: Sir Isaac Pitman & Sons, 1954. 8. Burston WR. The pre-surgical orthopedic correction of the maxillary deformity in clefts of both primary and secondary palate. In: Wallace AB, editor. Trans Internal Soc Plastic Surgeons, Second Congress, London, 1959. Edinburgh and London: E&S Livingston Ltd, 1960:2836. 9. Friede H, Pruzansky S. Longitudinal study of growth in bilateral cleft lip and palate from infancy to adolescence. Plast Reconstr Surg 1972;49:392-403. 10. Friede H. Studies on facial morphology and growth in
bilateral cleft lip and palate. Dept of Orthod University of Goteborg, Sweden, 1977. 11. Friede H. The vomero-premaxillary suturea neglected growth site in mid-facial development of unilateral cleft lip and palate patients. Cleft Palate J 1978; 15:398-404. 12. Georgiade NG, Latham RA. Intraoral traction for positioning the premaxilla in the bilateral cleft lip. In Georgiade NH, Hagerty RD, editors. Symposium on Management of Cleft Lip and Palate and Associated Deformities. St. Louis, MO, Mosby, 1974:123-127. 13. Georgiade NG, Latham RA. Maxillary arch alignment in the bilateral cleft lip and palate infant , using the pinned coaxial screw appliance. J Plast Reconstr Surg 1975;52:5260. 14. Pruzansky S. Pre-surgical orthopaedics and bone grafting for infants with cleft lip and palate: A dissent. Cleft PalateJ 1964;1:154. 15. Aduss H, Friede H, Pruzansky S. Management of the protruding premaxilla, In Georgiade NG, Hagerty RF, editors. Symposium on Management of Cleft Lip and Palate and Associated Deformities. April 12-14, 1973, St. Louis, MO: Mosby, 1974:111-117. 16. Subtelny JD. The significance of early orthodontic in cleft palate habilitative planning. J Speech Hear Dis 1955;20:135. 17. Berkowitz S. Growth of the face with bilateral cleft lip from 1 month to 8 years of age. Master's thesis, University of Illinois Graduate School, Chicago, IL: 1959. 18. Berkowitz S. Complete bilateral cleft lip and palate. In: Berkowitz S editor. Cleft Lip and PalatePerspectives In Management and an Introduction to Other Craniofacial Anomalies. San Diego, CA: Singular Press, 1996 19. Graber TM. Craniofacial morophology in cleft palate and cleft lip deformities. Surg Gynecol Obstet 1949;88: 359-369. 20. Graber TM. Changing philosophies in cleft palate management. J Pediat 1950;37:400-415. 21. Graber TM. The congenital cleft palate deformity. J Am Dent Assoc 1954;48:375-395. 22. Bishara SE, Olin WH. Surgical repositioning of the premaxilla in complete bilateral cleft lip and palate. Angle Orthod 1972,42:139-147. 23. Narula JK, Ross RB. Facial growth in children with complete bilateral cleft lip and palate. Cleft Palate J 1970;7:239-248. 24. Mazaheri M, Harding RL, Cooper JA, et al. Changes in arch form and dimensions of cleft patients. AmJ Orthod 1972;60:19-32. 25. Bergland O, Semb G, Abydholm F, et al. Secondary bone grafting and orthodontic treatment on patients with bilateral complete clefts of the lip and palate. Ann Plast Surgl986;l7:460-47l. 26. Shaw WC, Asher-McDade C, Brattshtrom V, et al. The RPS: A six-centre international study of treatment outcome in patients with clefts of the lip and palate: Part 5. General discussion and conclusions. Cleft Palate Craniofacj 1992b;29:413-418. 27. Semb G. A study of facal growth in patients with bilateral cleft lip and palate treated by the Oslo CLP team. Cleft Palate Craniofac J 1991b;28:22-39. 28. Vargervik K. Growth characteristics of the premaxilla
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and orthodontic treatment principles in bilateral cleft lip and palate. Cleft Palate J 1983;20:289. 29. Millard DR Jr. Principlization of Plastic Surgery. Boston, MA: Little, Brown, 1986:77. 30. Ross RB, Johnson MC. Cleft Lip and Palate. Baltimore, MD: William & Wilkins, 1972:158. 31. Slavkin HC. Developmental Craniofacial Biology. Philadelphia, PA: Lea and Febiger, 1979. 32. Berkowitz S. Timing cleft palate closureage should not be the sole determinant. J Craniofac Gen Dev Biol 1985;l:69-83(suppl). 33. Pruzansky S. The growth of the premaxillary-vomerine complex in complete bilateral cleft lip and palate. Tandlaegebladet. 197l;75:l 157-1169. 34. Slaughter WB, Brodie AG. Facial cleft and their surgical management in view of recent research. Plast Reconstr Surg 1949,4:311-332. 35. Scott JH. The analysis of facial growth. Part I. The anteroposterior and vertical dimensions. Am J Orthod 1956b;44:507-512. 36. Scott JH. The analysis of facial growth. Part II. The horizontal and vertical dimensions. Am J Orthod 1958c; 44:585-589. 37. Burston WR. Treatment of the cleft palate. Ann R Coll Surg 1967;25:225. 38. Moss ML, Bromberg BE, Song 1C, et al. The passive role of naxal septal cartilage in midfacial growth. Plast ReconstrSurg!968;41:536-542. 39. Weil J. Orthopaedic growth guidance and stimulation for patients with cleft lip and palate. Scand J Plast Reconstr Surgl987;21:57-63. 40. Forshall I, Osborne RP, Burston WR. Observations on the early orthopaedie treatment of cleft lip and palate conditions, In: Hotz R editor. Early Treatment of Cleft Lip and Palate. Bern, Huber, 1964:68. 41. Dreyer CJ. Primary orthodontic treatment for the cleft palate patient. J Dent Assoc S. Africa 1962;13:119-123. 42. Graf-Pinthus B, Bettex M. Long-term observation following presurgical orthopedic treatment in complete clefts of the lip and palate. Cleft Palate J 1974; 11:348-357.
43. Cronin TD, Penoff JH. Bilateral clefts of the primary palate. Cleft Palate J 197l;8:349-363. 44. Kernahan DA, Rosenstein SW, editors. Cleft Lip and Palate, A System of Management. Baltimore, MD: Williams & Wilkins, 1990, 120-127. 45. Friede H, Johanson B. A follow-up study of cleft children treated with primary bone grafting. Scand J Plast Reconstr Surg 1974;8:88-103. 46. Friede H, Johanson B. Adolescent facial morphology of early bone grafted cleft lip and palate patients. Scand J Plast Reconstr Surg 1982;16:41-53. 47. Berkowitz S. Section III. Orofacial growth and dentistry. A state of the art report on neonatal maxillary orthopedics. Cleft Palate J 1977;14:288-301. 48. Kuypers-Jagtman AM. Changes in maxillary arch dimensions and occlusion in unilateral cleft lip and palate subjects. Moordwijkerhoot, Studieweek NVDS 1985;9-21. 49. Prahl-Andersen B. Properative Kisferorthopadesche Behandung von Kunderu Mit Totalen Spaltbidungen, ja oder nein. Stomatal. DDR 1979;29:911-919. 50. Hotz M, Gnoinski W, Perko M, editors. The Zurick Approach: in Early Treatment of Cleft Lip and Palate. Toronto, Hans Huber, 1984:1964-1984. 51. Enlow DH. Handbook of Facial Growth. Philadelphia, PA: Saunders, 1982. 52. Latham RA. The septopremaxillary ligament and maxillary development. J Anat 1969; 104:584-586. 53. Latham RA. Development and structure of the premaxillary deformity in bilateral cleft lip and palate. Br J Plast Surgl973;26:l-ll. 54. Friede H, Morgan P. Growth of the vomero-premaxillary suture in children with bilateral cleft lip and palate; a histological and roentgenocephalometric study. Scand J Plast Reconstr Surg 1976; 10:45-55. 55. Berkowitz S. Cleft Lip and Palate. In: Wolfe SA, Berkowitz S, editors. Plastic Surgery of the Facial Skeleton. Boston, MA: Little, Brown 1989:291-411 56. Millard DR Jr. Cleft Craft III: The Evolution of its Surgery, III: Alveolar and Palatal Deformities. Boston, MA: Little, Brown, 1980:240.
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The Relationship Between Timing of Cleft Palate Surgery and Speech Outcome: What Have We Learned, and Where Do We Stand in the 1990s?
Sally J. Peterson-Falzone
The optimum age for surgical closure of cleft palate remains an unresolved question, despite the fact that many clinicians have studied the issue since the 1930s. This article reviews the debate as it has taken shape over the last several decades, with a prospective view toward how standards of practice may evolve in the foreseeable future. (Semin Orthod 1996;2:185-191.) Copyright 1996 by W.B. Saunders Company
he effort to relate speech outcome to the age at which palatal surgery is performed dates back at least as far as the famous French surgeon Victor Veau,1 who in 1933 reported normal speech in 75% of children who underwent surgery before 12 months of age, 60% of those who underwent surgery between 2 and 4 years of age, and 28% of patients who underwent surgery and were older than 9 years of age. More than 60 years later, the inexperienced clinician may be surprised to learn that despite Veau's conclusions and despite multiple studies of the question there is still disagreement about the age at which surgical closure of a palatal cleft should be accomplished in a normally developing child. The research on this question has been problem-ridden primarily because of the large number of variables that are difficult to control in dealing with the physical variability in clefts; variation in the skill of surgeons; lack of standardization of speech evaluations; and all of the complex factors affecting maturation, growth, and development of the child. In addition, this body of literature has been flawed by the effects of careless methodology, including mixing patients with different types and severities of clefts
From the Center for Cmniofacial Anomalies, University of California-San Francisco, CA. Address correspondence to Sally J. Peterson-Falzone, PhD, 747-S Medical Sciences, Box Q442, University of California, San Francisco, CA 94143-0442. Copyright 1996by W.B. Saunders Company 1073-8746/96/0203-0001$5.00/0
(sometimes with the inclusion of syndromic or multi-anomaly patients), inconsistency in surgical procedures, and failure to provide objective speech data. In fact, the beginning clinician should be forewarned that many articles whose titles seem to promise helpful information on the question of the optimal age for palatal surgery, at least in terms of speech results, are so seriously handicapped by methodological flaws that they are inherently misleading. For example, in the Blijdorp and Muller article,2 the ages at surgery (3 years versus 6 years) were far too late to show a differential effect on speech development, and the assessment of speech consisted of the amount of fogging on a mirror held beneath the nose during production of sustained vowels and a sibilant. Other articles are not original investigations but clinical or theoretical reviews of the topic, eg, Kaplan3; KempFincham et al.4 The review by Egyedi5 of clinical results published by other surgeons regarding maxillary growth, orthodontic complications, effects on otologic health, and speech outcome of palatal surgery is flawed by several misinterpretations of the original articles as well as by illogical conclusions. To gain perspective on this topic, we will first review common clinical practices through the 1970s, together with some of the stronger research information that was gathered up to that time and that was beginning to influence management decisions. We will then examine some major changes that took place in the 1980s, and
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conclude wtih a synthesis of current information and viewpoints.
tion found in the literature through the end of the 1970s: 1. There was a general trend of better speech results (higher percentage of children reported to have normal or acceptable speech) with earlier ages at surgery,7-12-14 but what was considered early in some reports was comparable only to the middle or later age range in other reports. Very few reports of this era included children who underwent surgery before 1 year of age.7'8 2. The highest reported percentage of good speech results was that of Jolleys,9 who claimed that approximately 90% of children who underwent surgery before the age of 2 years had good or excellent speech, but offered no objective speech data. 3. Several authors, usually surgeons, concluded their reports with a recommendation for performing palatal surgery in a general age range: between the ages of 6 and 9 months8; before the age of 8 months7; in the 1-year range10; between the ages of 2 and 3 years.14 Despite such recommendations and increased interest in the question, by the end of the 1970s no one had derived an optimal age for surgery in the normally developing, nonsyndromic child with a cleft. Clinicians continued to seek optimal speech results, but many were also concerned about the possible differential effects of early versus later palatal surgery on subsequent midfacial growth.
Common Practices Into the 1970s

Up through the mid-to-late 1970s, textbooks in pediatrics and surgery in the United States generally cited an age range of 18 to 24 months as the appropriate time for surgical repair of the palate. Little information on normal speech and language development was cited or used in support of this recommended age. Indeed, if the authors of these texts had taken such information into consideration, they would have realized the possible peril of delaying palatal surgery until well past the age of development of the child's first meaningful words. The majority, although not all, of the journal articles up to this time focused on surgical techniques. Judgments of outcome focused on postoperative healing (eg, absence of fistulae) and, oddly, adequacy of velopharyngeal closure as judged on the oral examination. (Velopharyngeal closure cannot be seen on the oral examination, because closure occurs between the upper or nasal surface of the velum and the posterior pharyngeal wall or adenoid pad.) Many articles lacked any objective data on speech,6"11 a deficiency also found in the early work of Veau.1 The role of speech-language pathologists in the evaluation of surgical results became increasingly prominent in the 1960s and 1970s, and this was gradually reflected in the literature,7'12'13 although articles written solely by surgeons continued to predominate.8"11'14 Some publications during this time addressed the issue of timing of palatoplasty, but there was troubling variation in what was considered to be an early age for surgery. In addition, some publications compared speech outcomes across very large age ranges, from those who underwent surgery within the first year or two of life, to patients with palatoplasties delayed until the teenage years. Finally, it is well for the reader to keep in mind that in the majority of articles assessment of surgical results was highly confounded by the variables of type of surgery (often not consistent within a single study), age at surgery, age at evaluation, and method of assessment. Notwithstanding the severe limitations of many studies, the following is a summary of informa-
The 1980s
In 1981, Kaplan3 wrote an extensive review of the publications dealing with the optimal-age-forpalatoplasty issue from the viewpoints of speech, midfacial growth, and types of surgical approaches. Unfortunately, many of the studies he reviewed were handicapped, if not completely invalidated, by one or more of the methodological problems discussed previously. Kaplan3 attempted to bring to the attention of fellow surgeons the fact that children show significant development of early prespeech vocalizations and subsequent emergence of meaningful speech far earlier than had been assumed by other investigators. He advocated palatal closure between the age of 3 and 6 months so that there would be adequate time for tissue healing and
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reduction of edema and the palate could be functionally normal by the age of 9 months. However, he provided no data.3 The following year, Dorf and Curtin15 reported startlingly different speech results between a group of 21 children whose clefts were closed before 12 months of age versus a group of 59 children who underwent surgery and were older than 12 months. Speech was assessed only for presence or absence of compensatory articulations, maladaptive patterns that interfere with intelligibility and that are very difficult to eliminate once they develop.16 Only 10% of the children in the first group developed these patterns, compared with 86% in the group that underwent surgery after the age of 12.5 months. In a later follow-up study of an expanded series of patients, the same authors17 reported an even greater discrepancy in speech performance between the "12 months and younger group" and the children operated on over the age of 12 months. In both articles, the authors stressed the importance of the child's stage of phonemic development, or articulation age, as opposed to chronological age, in deciding on the appropriate age of surgery. That is, a child older than 1 year of age showing a mild lag in speech development may not be as vulnerable to the effects of surgery because he or she is not making the same early demands on the oral and velopharyngeal systems. This caveat about the difference between articulation age and chronological age was often ignored in later articles citing the Dorf and Curtin articles.15'17 Articles addressing optimal age for surgery appeared throughout the remainder of the 1980s,18'23 with some surgeons attempting to move the time of surgery into the first few months of life,18'19'21 but often with little information on how speech was assessed. In 1987, Barimo et al21 published one of the few interdisciplinary articles about speech results as related to age of surgery. They reported impressive results in 22 children randomly selected from a larger group of more than 190 whose palates were closed between the ages of 3 and 8 months. These children were followed longitudinally from the toddler age to nearly 9 years of age, and were found to exhibit no glottal stops or pharyngeal fricatives (two of the most common types of compensatory articulations) and no nasal emission. Thus, the early surgery (mean age 6
months), together with parental involvement and speech stimulation, produced virtually normal speech development in all of these 22 children. (It is important to note that the influence of speech therapy in any of the studies cited here is impossible to assess because of the variability in type, intensity, and quality of therapy.) A parallel development in the late 1980s heightened interest in the relationship between age at palatal surgery and subsequent speech development. Before this time, we had had only a modicum of information about the vocalizations produced by babies with clefts before their palatal surgery. Reports by Grunwell and Russell24'25 and by O'Gara and Logemann26'27 provided a framework for understanding how the physical constraints that the cleft imposed on early vocal output could influence what the child was able to do once the cleft was closed. This work continued in the 1990s, as discussed in the following section. By the end of the 1980s, there was a fairly solid movement toward performing palatal surgery before the end of the first year of life if the child appeared to be a nonsyndromic, normally developing infant, but confusion continued to reign in terms of what constituted surgery that was early enough to truly make a difference. The 1982 study by Dorf and Curtin15 did much to stimulate this movement. Unfortunately, later studies as to whether or not 12 months is truly a watershed age for palatal closure failed to yield similar results,28-29 as will be discussed in the next section. However, a multicenter study by Ross in 198730 provided data to allay fears about deleterious effects of early palatal surgery on midfacial growth. In fact, this massive cephalometric study showed slightly better facial growth for children who underwent surgery in the first year of life over those in any of several later age groups of repair. 30
The 1990s
In the early 1990s, our knowledge regarding prespeech vocalizations and early speech development in infants with clefts continued to increase, improving clinicians' ability to advise parents and to design appropriate stimulation programs for children, but also perpetuating interest in earlier palatal surgery. Some of these studies
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indirectly addressed the question of timing of palatal surgery. O'Gara and Logemann26'27 closely monitored the prespeech vocalizations and early speech sound development in 23 babies from the ages of 3 to 36 months. These babies were divided into an "earlier closure-greater tissue" group (mean age at closure 9.3 months) or a later closure-lesser tissue group (mean age at closure 16.1 months). The babies in the earlier repair group showed an earlier decrease in the use of abnormal speech sounds following palatal surgery, but it must be remembered that the babies in the latter group underwent surgery later because their clefts were more severe. Kemp-Fincham et al4 reviewed the literature on the development of speech motor control and phonetic development in infants, and concluded that there is a particularly sensitive period or state of readiness between the ages of 4 and 6 months. They conjectured that, from the standpoint solely of speech development, it may be important to close the palate before or during the 4-to-6 month period to avoid development of maladaptive articulations. Interestingly, in that same year Copeland31 reported speech results in 100 children who underwent surgery in an age bracket somewhat comparable with the sensitive period suggested by Kemp-Fincham et al.4 The children in the Copeland report underwent palatoplasty between the ages of 9 and 25 weeks, with a mean of 16.4 weeks. (The surgeon was Desai and given the similarity in number of children and age at palatal closure, it seems logical to assume that this was a follow-up of the cases first reported in 1983 by Desai.19) Speech was evaluated only once, reportedly "at the time of the 5 year clinical review," but the range of ages was 3.8 to 6.3 years. Unfortunately, the speech results are difficult to interpret: although 87 children were reported to have acceptable speech, a total of 16 had clinical signs of velopharyngeal inadequacy: 12 with moderate to severe hypernasal resonance and/or nasal air escape, and 4 with compensatory articulations. The author reported differential effects of age at palatal surgery as compared across 3 months, 4 months, 5 months, and 6 months. None of the children who underwent surgery at 3 months were exhibiting compensatory articulations, but there was an increasing number of children exhibiting these behaviors as age at palatal closure in-
creased. Such findings would seem to fit well with the theoretical framework offered by KempFincham et al.4 However, because of the uneven numbers across the four groups, the short time separating the ages at surgery, and particularly the nature of the speech data, the results should be considered with caution. Studies by Peterson-Falzone28 and Dalston,29 reporting on an aggregate of 399 children between them, failed to confirm the Dorf and Curtin findings15'17 of 12 months being a watershed age for surgery. The overall prevalence of compensatory articulations in each of the later studies was less than half that by Dorf and Curtin.17 Although the age at surgery was known for only 90 of children in the Peterson-Falzone report,28 the results again were dissimilar from those of Dorf and Curtin: there was only a small difference between the prevalence of compensatory articulations in the "younger than 12 months" group and that in the "older than 12 months" group. The mean age at surgery for the children who developed these patterns was 24.2 months, whereas the mean for those who did not develop them was 21.2 months, far beyond the expected 12 month boundary. In the Dalston study,29 only 13 of the group had been repaired at 12 months or younger, and 5 (38.5%) were exhibiting these behaviors. Of the 146 closed after 12 months, 40 (27.4%) were using compensatory articulations. Although there were limitations in all four studies,15-17'28'29 as suggested by Dalston, "the patient population studied by Dorf and Curtin may have been atypical." Haapanen and Rantala32 reported slightly better speech results in a group of children whose clefts were closed in the 16 to 20 month range as compared with two other groups, one with surgery in the 12 to 15 months range and one in the 21 to 24 month range. The percentage of children in each of the first two groups who developed normal or practically normal speech was essentially the same (73% and 72%) but none of the children in the 16 to 20 month range at surgery developed compensatory articulations. Unfortunately, the number of children in the 16 to 20 month group was less than half the number in the other two groups. The authors32 concluded "... the age of about 18 months seemed optimal for the repair, but the numbers were too small to come to any firm conclusions." This
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conjecture is reminiscent of common clinical practices 30 years before the article, but the authors had no data on children whose surgery was performed within the first year of life. Two studies on early speech development in toddlers and preschoolers with clefts33'34 noted the important role of time as a determinant in what we hear in the speech of these children, and alerted us to the dangers of relying on studies for which results are based only on one-time assessments. Chapman and Hardin33 reported that children with repaired clefts who had shown significant delays in speech development before the age of two years eventually showed "catch-up," although at a later age than typically seen in children without clefts. In a follow-up of the children they first studied in the late 1980s, O'Gara et al34 interpreted their extensive longitudinal data as follows, "For all 23 babies, regardless of the age of palatoplasty intervention, time is an even stronger variable than age of palatoplasty for development of palatal, alveolar and velar place features, oral stops, and oral fricatives." Changes over time in these babies seemed to gradually erase the earlier discrepancy in speech sound development between the earlier and later closure groups. It is important to note that the children in this series of studies had been consistently monitored and treated by a large interdisciplinary craniofacial team, and the treatment included active intervention in the form of parent counseling to increase stimulation in the home. The same was true of the Barimo et al21 report. Interestingly, a 1994 report by Ysunza and colleagues35 may have been a good illustration of the point that O'Gara et al34 were trying to make: Ysunza et al35 reported that a significantly greater percentage of children who underwent surgery at the ages of 24 and 36 months developed compensatory articulations than did children who underwent surgery at the ages of 6, 12, or 18 months, results that would initially seem to indicate an advantage for earlier surgery. However, the overall number of children who developed these maladaptive patterns was very high (23 of 38 60.5%), signaling the need for a greater number of subjects but perhaps more important the need for close longitudinal follow-up of these cases.
Where Are We Now?

Discerning clinicians will draw their own conclusions about the current state of knowledge regarding an optimal age for palatal surgery based on the studies cited here and other data as they become available in future publications. Conclusions may change as new information becomes available. When you are reading a new study and trying to evaluate its worth, remember to check if judgements about speech were made by a speechlanguage pathologist; and if the speech data are longitudinal or based only on a one-time assessment, particularly if that one assessment took place in the toddler or early preschool years. The conclusions that follow are based solely on the author's interpretation of currently available information: 1. The knowledge we have gained in recent years regarding the effects of early structural constraints on later speech development in children with clefts supports efforts toward earlier palatal surgery in otherwise normal children, perhaps within the first few months of life if such procedures can be performed safely. 2. There is conflicting evidence regarding the question of whether the age of 12 months in an otherwise healthy child is in essence a cut-off age for preventing the development of compensatory articulations. The data in the widely cited article of Dorf and Curtin15'17 have come into question by virtue of the fact that they have not proven replicable. The 1992 conclusion of Dalston28 is still valid in 1996: "... there is insufficient support for the notion that palatal closure before the age of 12 months is inherently superior to surgery performed later." However, more treatment centers are currently collecting longitudinal outcome data on babies operated on within the first 4, 6,9, or 12 months of life.21'24'25'29'31'35 If the results from these centers show a consistent advantage in speech outcome, and if their results in terms of midface deformity are no worse than in babies operated on later,30 there is little doubt that early surgery will be a widely accepted norm in the 21st century. 3. Every clinician involved in the effort to find an answer to the question of optimum age for
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palatal surgery must first be certain that the children whose surgical outcomes will become part of the database are children whose development is not affected by associated anomalies, syndromes, or delayed cognitive development. This point often gets lost or completely ignored in clinical reports. Remember that more than 50% of children born with clefts have one or more associated anomalies.36'37 It is very easy for anyone other than an experienced dysmorphologist to miss subtle signs of syndromes, sequences, or associations of congenital defects. Furthermore, it is easy to miss signs of cognitive delays, hearing loss, and other threats to development if a child is not evaluated by an interdisciplinary team. Mixing surgical results from normally developing children with results from syndromic, multiply involved, or cognitively delayed children will only delay us in deriving the collective body of knowledge that we need.
References
1. Veau V, cited in Morley M. Cleft Palate and Speech, 6th ed. Baltimore, MD: Williams and Wilkins, 1966. 2. Blijdorp P, Muller H. The influence of the age at which the palate is closed on speech in the adult cleft patient. J Maxillofac Surg 1984;12:239-246. 3. Kaplan EN. Cleft palate repair at three months? Ann PlastSurgl981;7:l79-190. 4. Kemp-Fincham SI, Kuehn DP, Trost-Cardamone JE. Speech development and the timing of primary palato plasty. In: Bardach J, Morris, HL, editors. Multidisciplinary Management of Cleft Lip and Palate. Philadelphia, PA: Saunders, 1990:736-745. 5. Egyedi P. Timing of palatal closure. J Maxillofac Surg 1985;13:177-182. 6. Battle RJV. Speech results of palate repair when performed before two years of age. Transactions of the Fourth International Congress on Plastic and Reconstructive Surgery. 1967:425-428. 7. Evans D, Renfrew C. The timing of primary cleft palate repair. ScandJ Plast Surg 1974;8:153-155. 8. Holdsworth WG. Early treatment of cleft-lip and cleftpalate. BrMedJ 1954;! .304-308. 9. 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;7:229-241. 10. Lindsay W, LeMesurier A, Farmer A. A study of the speech results of a large series of cleft palate patients. Plast Reconstr Surg 1962;29:273-288. 11. Peet E. The Oxford technique of cleft palate repair. Plast Reconstr Surg 1961;28:282-294.
12. McWilliams BJ. Cleft palate management in England. Speech Pathol Ther 1960;3:3-7. 13. Morris HL. Velopharyngeal competence and the Demjen W/V-Y technique. In: Morris HL, editor. The Bratislava Project: Some Results of Cleft Palate Surgery. Iowa City, IA: The University of Iowa Press, 1978:49-73. 14. Koberg W, Koblin I. Speech development and maxillary growth in relation to technique and timing of palatoplasty. J Maxillofac Surg 1973;1:44-50. 15. Dorf DS, Curtin JW. Early cleft palate repair and speech outcome. Plast Reconstr Surg 1982;70:74-79. 16. Trost JE. Articulatory additions to the classical description of speech in persons with cleft palate. Cleft Palate J 1981;18:193-203. 17. Dorf DS, Curtin JW. Early cleft palate repair and speech outcome: A ten year experience. In: Bardach J, Morris HL, editors. Multidisciplinary Management of Cleft Lip and Palate. Philadelphia, PA: Saunders, 1990:341-348. 18. Randall P, LaRossa DD, Fakhraee SM, et al: Cleft palate closure at 3 to 7 months of age: A preliminary report. Plast Reconstr Surg 1983;7l .624-627. 19. Desai S. Early cleft palate repair completed before the age of 16 weeks: Observations a personal series of 100 children. Br J Plast Surg 1983;36:300-304. 20. Ainoda N, Yamashita Y, Tsukada S. Articulation at age 4 in children with early repair of cleft palate. Ann Plast Surg 1985;15:415-422. 21. Barimo JP, Habal MB, Scheuerle J, et al: Postnatal palatoplasty, implications for normal speech articulationa preliminary report. Scand J Plast Reconstr Surg 1987;21:239-243. 22. Asher-McDade C, Shaw WC. Current cleft lip and palate management in the United Kingdom. Br J Plast Surg 1990,43:318-321. 23. Harding A, Campbell RC. A comparison of the speech results after early and delayed hard palate closure; A preliminary report. Br J Plast Surg 1989;42:187-192. 24. Grunwell P, Russell J. Vocalisations before and after cleft palate surgery: A pilot study. Br J Dis Commun 1987;22:117. 25. Grunwell P, Russell J. Phonological development in children with cleft lip and palate. Clin Linguistics Phonetics 1988;2:75-95. 26. O'Gara MM, Logemann JA. Phonetic analyses of the speech development of babies with cleft palate. Cleft PalateJ1988;25:122-134. 27. O'Gara MM, Logemann JA. Early speech development in cleft palate babies. In: Bardach J, Morris HL, editors. Multidisciplinary Management of Cleft Lip and Palate. Philadelphia, PA: Saunders, 1990:717-721. 28. Peterson-Falzone SJ. A cross-sectional analysis of speech results following palatal closure. In: Bardach J, Morris HL, editors. Multidisciplinary Management of Cleft Lip and Palate. Philadelphia, PA: Saunders, 1990:750-757. 29. Dalston RM. Timing of cleft palate repair: A speech pathologist's viewpoint. Problems in Plastic and Reconstructive Surgery: Cleft Palate Surgery, 1992;2:30-38. 30. Ross RB. Treatment variables affecting facial growth in
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31. 32.
33.
34.
complete unilateral cleft lip and palate. Part 5: Timing of palate repair. Cleft Palate-CraniofacJ 1987;24:54-63. Copeland M. The effects of very early palatal repair on speech. Br J Plast Surg 1990;43:676-682. Haapanen M-L, Rantala S-L. Correlation between the age at repair and speech outcome in patients with isolated cleft palate. Scand J Plast Reconstr Hand Surg 1992;26:7l-78. Chapman KL, Hardin MA. Phonetic and phonologic skills of two-year-olds with cleft palate. Cleft PalateCraniofacJ 1992;29:435-443. O'Gara MM, Logemann JA, Rademaker AW. Phonetic
features by babies with unilateral cleft lip and palate. Cleft Palate-CraniofacJ 1994;31:446-451. 35. Ysunza A, Guerrero M, Pamplona M, et al. Speech outcome of surgical repair of cleft palate: the effect of age at the time of surgery. Presented before the Society for Ear, Nose, and Throat Advances in Children, Sacramento, CA, December 2, 1994. 36. Jones MC. Etiology of facial clefts: Prospective evaluation of 428 patients. Cleft Palate J 1988;25:16-20. 37. Shprintzen RJ, Siegel-Sadewitz VL, Amato J, et al. Anomalies associated with cleft lip, cleft palate, or both. Am J Med Genet 1985;20:585-595.
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Bone Grafting for the Alveolar Cleft Defect

Peter D. Waite and Daniel E. Waite
Seventy-five percent of all cleft lip and palate patients have osseous defects of the alveolus. Bone grafting of this defect normalizes facial and dental function. Failure to reconstruct the osseous deformity may result in oronasal fistula, fluid reflux, speech pathology, anteroposterior deficiency of the maxilla, transverse deficiency of the maxilla, lack of bone support for the incisors and cuspids, dental crowding, and facial asymmetry. Bone grafting unifies the maxilla and is best done after the majority of facial growth is complete and the secondary dentition is erupting. This is known as secondary bone grafting and yields the best results. The dentofacial deformity of cleft lip and palate is best managed by coordination of dental development, surgery and orthodontics. (Semin Orthod 1996;2:192-196.) Copyright 1996 by W.B. Saunders Company
Dental professionals have made significant contributions to the rehabilitation of the cleft lip and palate patient. The multidisciplinary approach, which was in fact first established by an oral surgeon and orthodontist in Bangor, ME, has become a well accepted team approach. The Lancaster Clinic set the standard and format that many cleft lip and palate clinics follow today.1 This multidisciplinary approach is well-recognized and encouraged by the American Cleft Palate-Craniofacial Association. This article on alveolar clefts is a review discussing the incidence, etiology, diagnosis, and treatment of this anatomical discord of the oral cavity.
The Examination
The medical condition of the cleft patient is often complex. There are many related problems involving the ears, speech, learning, nutrition, and personality. The socialization of the
From the Department of Oral and Maxillofacial Surgery, University of Alabama School of Dentistry, Birmingham, AL; Department of Oral and Maxillofacial Surgery, Baylor College of Dentistry, Dallas, TX. Address correspondence to Peter D. Waite, MPH, DDS, MD, Department of Oral and Maxillofacial Surgery, University of Alabama School of Dentistry, 1919 Seventh Avenue South, Birmingham, AL 35294. Copyright 1996 by W.B. Saunders Company 1073-8746/96/0203-0002$5.00/0
patient is complex, because of the family and social history, personal attitude, frequent surgery, and prolonged difficult dental care. The incidence of cleft lip and palate is reported as 1 in 1,000 live births for whites, 1 in 2,500 live births for blacks, and 1.7 in 500 live births for Orientals. There are some interesting sex differences. Cleft lip, with or without cleft palate, is more common in boys but isolated cleft palate is twice as common in girls.1 The etiology relates to several factors. There is a correlation with: geographic location (Orientals), social, (greater in lower economic groups), parental age, certain diseases (ie, measles), and a reported increase in relation to certain drugs taken by the mother. These and other factors lead most investigators to believe clefting is multifactorial.2 The defect may be unilateral or bilateral involving the palate, lip, and alveolus. It is the alveolar cleft that will be discussed in this article (Figs 1 and 2). The defect creates serious disruption of the dentition and collapse of the alveolar segments. An anterior osseous defect is found in 75% of all cleft lip and palate patients. Only 25% of cleft patients are free of alveolar defects. Bony restoration of the alveolar defect provides normal facial and dental function. Failure to unite and restore the maxillary alveolus results in poor function and greatly compromises the rehabilitation process.3 In bilateral clefts, a severe protruding nasola-
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Figure 1. Newborn infant with complete left cleft lip and palate.
bial segment may be present. In unilateral clefts, the lesser segment is usually more medially and distally displaced. The lateral incisor is frequently missing, but supernumerary teeth may be present. Gingival inflammation, hyperplasia, and caries are common additional findings. The cleft defect may be large with several millimeters of space between the segments and a large opening into the nose, or it may be so small that a probe will be necessary to locate the defect. Anteroposterior development of the midface is decreased and the maxilla is frequently narrow
Figure 2. A 10-year-old mixed dentition patient with multiple missing teeth, and severe collapse of the maxillary arch. This results in crossbite, malocclusion, and persistent alveolar cleft producing oral nasal fistula.
and constricted resulting in a midface hypoplasia being associated with cleft lip and palate. Speech and hearing difficulties are often present.4'5 The osseous deformity of the unilateral cleft commonly manifests flaring of the unilateral alar cartilage, oronasal fistula, anteroposterior deficiency of the maxilla, transverse deficiency of the posterior segments of the maxilla, lack of bone support for the incisors and cuspid teeth, and generalized crowding. The bilateral defect is characterized by a very mobile premaxillary segment that is often abnormally displaced, severe posterior transverse deficiency of the maxilla, and a flattened upper lip and philtrum. When the maxillary central incisor erupts, it frequently is diverted into an anterior crossbite which may force the maxilla into a more retrusive position. This abnormal eruption pattern contributes to the skeletal midfacial deficiency and relative forward shifting of the mandible into a false or pseudoprognathism.4'5 The terminology that seems to be most descriptive for the surgical reconstruction of this deformity is primary and secondary bone grafting of the cleft. Primary bone grafting is carried out within the first 2 years of life and is less popular than secondary bone grafting. Primary bone grafting is considered unfavorable and usually results in crossbite, malocclusion and malunion of the maxilla. Early secondary bone grafting is a confusing term that usually denotes bone grafting between 2 to 5 years of age. Early secondary bone grafting results in improved orofacial development but is often not ideal.6'7 The secondary bone graft (late) refers to grafting after the majority of facial growth is complete and when the secondary dentition is erupting, ie, between the llth and 14th years of life. This timing relates to tooth development and will be discussed later in this article. Longterm success of secondary bone grafting is very good. In an evaluation of 45 patients (32 unilateral and 13 bilateral) followed for 10 years, 91% were successful.8 The foundations for a successful bone graft are normal arch form, optimal orthodontic positioning of the cuspid tooth, closure of the oral nasal fistulae, continuity of the osseous alveolar arch, absence of the transverse posterior relapse, and absence of anterior posterior crossbite.8
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Surgical Objectives
Closure of the alveolar cleft provides a host of benefits to the patient. Stabilization of the segments is an especially significant advantage of the surgery, for the maintenance of the dentition and mastication. Improved oral hygiene will result from the closure of the communication between the oral cavity and nasal cavity. Nasal secretions are prevented from draining into the mouth, which is both an esthetic and oral hygiene advantage. The reverse is also true in that there is a tendency for oral fluids and food to escape into the nose causing irritation, inflammation and, embarrassment (Figs 3 and 4). Stabilization of the clefted segments unites the maxilla to better withstand occlusal forces and prevent further collapse. The placement of the bone graft in the cleft area provides a bony base for the eruption of teeth and greatly enhances the follow-up orthodontic treatment. Erupted teeth proximal to the cleft are supported by the graft and this prevents drifting of proximal teeth into the cleft and their premature loss. Flattening and widening of the alar base which is often present is improved by the bone graft. The bone graft also provides support and improves nasal symmetry. An additional objective of bone grafting is to provide the patient with the feeling of normalcy in a very serious oral facial defect. The latter improves function and esthetics, and contributes to personality, confidence, and social acceptance (Figs 5 and 6).
Figure 4. After the bone is placed, the palatal flaps are then released for primary closure. Often a finger flap from the vestibule is rotated over the alveolus.
Orthodontic Management
The planning and sequencing of the surgical and orthodontic treatment in cleft patients requires the cooperation of a number of health disciplines, especially the orthodontist, pedodontist, and oral and maxillofacial surgeon. A full understanding of facial growth and development is especially significant.2 Dental care of the cleft patient is always an ongoing effort. Once the hard palate is closed regular pedodontic or general dental management is most important in preparation for bone grafting of the cleft. Treatment of incipient caries, maintenance of oral hygiene, tracking of eruption of teeth, documentation of missing teeth or supernumerary teeth, and sometimes maintaining space are all part of the routine. The use of presurgical orthodontics is a mutual decision by the oral surgeon and orthodontist. Tooth movement of the teeth proximal to
Figure 3. The alveolar defect is incised and the nasal rnucosa closed. It is pushed upwards and the bony wall exposed. Bone is then packed into the defect.
Figure 5. (A) Preoperative and (B) postoperative occlusal radiographs show condensed bone graft.
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treatment sequence is prosthodontic reconstruction and soft tissue revisions of the lip and nasal deformity.
Surgical Management of the Alveolar Cleft

Our preference in timing of the cleft surgery and placement of the graft is clearly of the secondary type grafting procedure. The ideal time for alveolar bone grafting is generally between 9 and 11 years of age. However, because dental age and chronological age can differ, a useful guide is the development of the maxillary canine tooth. When the canine root is one-third developed, as best seen on a periapical radiograph, grafting should be considered. One exception is, if the lateral incisor tooth is present, then earlier grafting may be considered.9 The best source of bone for grafting for the alveolar cleft defect is the iliac crest. The rib, the cranium, and the mandible have also been used. However, it is our opinion, that obtaining bone from the anterior portion of the iliac crest provides a good quality and quantity of graft with minimal morbidity. There is some debate over the donor site, but it probably is of little significance as long as the bone is autologous cancellous bone. The patient is best managed with nasoendotracheal anesthesia with the tube placed on the noncleft side. Mucoperiosteal flaps are made on the palate and vestibular surfaces of the maxillary segments, exposing the alveolar stumps of the clefted alveolar bone. After closure of the nasal surface, a piece of harvested iliac cancellous bone is pressed into position. Additional bone is placed under the ala and the nose on the cleft side to provide nasal symmetry. The bone is densely compressed into the defect. The covering flaps are then closed. A protective palatal splint or orthodontic arch wire is sometimes used for further stabilization, although most often no additional stabilization will be necessary.3'5'10 A graft, when properly placed between the alveolar stumps, will firmly stabilize the maxillary segments. Eruption of the canine through the graft begins within 4 to 6 weeks and often proceeds normally. However, orthodontic guidance of the tooth after eruption may be necessary. If the lateral incisor is missing, as it most
Figure 6. Four series of occlusal radiographs show the development of bone, eruption of teeth, and orthodontic development.
the cleft must be done with caution to avoid tipping the root into the cleft space. This orthodontic tooth movement also sacrifices the minimal amount of bone on the roots near the cleft, which compromises the proposed bone graft and may lead to external root resorption. As a general rule orthodontic tooth movement can be performed with improved outcomes after the bone graft has been completed. The presence of the grafted bone provides a good matrix for tooth movement and alignment. A periapical radiograph is the best method to determine the quality and quantity of bone around the teeth proximal to the cleft. Alignment of teeth within the individual clefted arch and even expansion of the arch are orthodontic movements to be considered before bone grafting. Approximately 1 to 3 months following bone grafting, it is usually possible to proceed with orthodontic movement of teeth in the grafted area. The long-term treatment plan will need to be coordinated with the patient's growth and the degree of anteroposterior discrepancy. Orthognathic surgery is usually performed between the ages of 14 and 18. The most common procedure will be a Le Fort I advancement and down graft of the maxilla. The final aspect of this
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often is, a decision must be made to either guide the canine into the lateral incisor position or hold the space for later implant placement or the placement of a dental prosthesis.5
Postsurgical Management
The patient should be ambulatory the day after surgery. Slight favoring of the donor limb may be evident and the patient may experience mild discomfort on sneezing and coughing for 3 to 5 days following surgery. After 24 hours, the patient may shower and clean the donor site. Sutures are removed at 7 to 10 days. Care of the oral cavity begins immediately on the first postsurgical day with great attention to scrupulous oral hygiene. Oral rinses with dilute hydrogen peroxide and saline following all eating or drinking is mandatory. Milk or sticky foods should be limited and special cleansing of the intraoral incisions performed two to three times daily. Sutures are most often resorbable but can be removed between 10 and 14 days. Most patients will be discharged from the hospital on the second or third postoperative day. Home care will be similar to that described previously with the emphasis on oral hygiene and oral soft diet. Orthodontic management will depend on individual situations, however, tooth movement is usually started around the second month after surgery.
However, this early diagnosis and treatment is only a part of the management of a very complicated deformity. Speech, hearing, social activities, learning, self-esteem, and parenting are all areas affected by this problem. A team approach is the only way to manage these patients. In addition the burden of the deformity extends well into adult life.
References
1. Fog-Anderson P. Incidence and etiology, In: Edwards M, Watson ACH, editors. Advancement in the Management of Cleft Palate. Edinburgh: Churchill Livingstone, 1980: 43. 2. Malcolm C, Johnston P. Embryogenesis of cleft lip and palate, In: McCartyJG, editor. Plastic Surgery, vol 4. Cleft Lip and Palate and Craniofacial Anomalies. Saunders, Philadelphia, PA, 1990:2532. 3. Boyne PJ, Sands NR. Secondary bone grafting of residual alveolar and palatal defects. J Oral Surg 1972;30:87-92. 4. Bergland D, Semb G, Abyholm FE, et al. Elimination of the residual alveolar cleft by bone graft and subsequent orthodontic treatment. Cleft Palate J 1986;23:175-205. 5. Vig KW, Turvey TA. Orthodontic surgical interaction in the management of cleft lip and palate. Clin Plast Surg 1985;12:735-748. 6. Rehrmann A, Kober WR, Koch HE Late results of cleft palate repair in patients with primary or secondary bone grafting: Ten year follow up. International Congress on Cleft Palate, Houston, TX: 1969. 7. Johanson B, Ohlsson A. Bone grafting and dental orthopedics in primary and secondary cases of cleft lip and palate. ActaChir Scand 1961;122:112. 8. Hogeman KE, Jacobson S, Sranas CN. Secondary bone grafting in the cleft palate: A follow up of 145 patients. Cleft Palate J 1972,9:9-42. 9. El Deeb M, Waite DE. Canine eruption into the grafted bone in maxillary alveolar cleft defects. Cleft Palate J 1982;19:9-16. 10. Axhausen G. Technik, und Ergebnisse der Spalt Plastiken. Hanser, Munchen: 1952.
Conclusion
The diagnosis and planning for the treatment of the alveolar cleft patient has been discussed.
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Orthodontic Treatment for the Cleft Palate Patient

Christos C. Vlachos
This article is an overview of the treatment possibilities and the role of the orthodontist in the management of patients with cleft palate. Orthodontic intervention and treatment may be indicated soon after birth (infant orthopedics), in the deciduous, mixed, and permanent dentitions and also in the adult patient. This article focuses primarily on decision-making and procedural steps performed by the orthodontist during the permanent dentition stage. The need for coordinated interaction with other team members is emphasized. (Semin Orthod 1996;2:197-204.) Copyright 1996 by W.B. Saunders Company
atients with cleft lip and/or palate face a multitude of problems. These patients often present with functional impairment and esthetic compromise. The latter may have psychological and sociological implications. Functions such as suckling and swallowing, speech, and hearing may be impaired while facial disfigurement and malocclusion are usually present. Successful management of patients with cleft lip/palate requires a multidisciplinary approach. Coordinated treatment by the cleft palate team is an essential requirement to obtain optimum treatment results. The literature is replete with information on the need for a team approach in the management of patients with cleft lip and palate. Unfortunately, little consensus exists on the sequence and timing of treatment for these patients. The following factors may account for the apparent variation of opinions relating to the management of cleft patients: 1. Lack of randomized clinical trials comparing the outcomes of various treatment modalities and/or the effects of timing of therapy. 2. Absence of a common classification system limits meaningful comparisons between various studies.
From the Department of Orthodontics, University of Alabama at Birmingham, School of Dentistry, Birmingham, AL. Address correspondence to Christos Vlachos, DMD, DDS, MS, Department of Orthodontics, University of Alabama at Birmingham, School of Dentistry, Box 23, 1919 7th Ave South, Birmingham, AL 35294. Copyright 1996by WB. Saunders Company 1073-8746/96/0204-0003$5.00/0
3. Treatment sequence is not dictated by equitable representation of the opinions of each and every team member. Dominant team members may mandate treatment on the grounds of their individual bias. 4. Treatment sequence and timing is not always problem-specific. For example, a bilateral cleft palate defect extending into the alveolar bone usually requires a different approach than an incomplete cleft affecting only the posterior part of the secondary palate. Orthodontic treatment may be performed at different stages of the patient's development, depending on the particular problem. Patients presenting with a cleft lip only or a soft palate cleft may never require orthodontic treatment.1 Defects in the latter patients most likely will not significantly influence their occlusion and any malocclusion present may be no different than would occur in a noncleft population. Patients with unilateral or bilateral cleft lip, alveolus and palate may require orthodontic treatment during the following four different stages: 1. Neonatal maxillary orthopedics as an infant. 2. Orthodontic-orthopedic treatment during the deciduous dentition. 3. Orthodontic treatment during the mixed dentition. 4. Orthodontic treatment alone or in conjunction with orthognathic surgery in the permanent dentition.
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Christos C. Vlachos
Neonatal Maxillary Orthopedics

Infant orthopedics/presurgical orthopedic intervention is performed on the maxillary arch of a newborn before the surgical repair of the lip. It was introduced in the 1950s and may be used in patients with bilateral or unilateral cleft lip, alveolus, and palate. The rationale behind this method involves orthopedic realignment of the "collapsed" segments using various mechanisms ranging from simple passive appliances2 to more active orthopedic appliances3 to extraorally activated pin-retained appliances.4 Such treatment is usually performed by an orthodontist, whereas a pedodontist or a maxillofacial prosthodontist may be involved in certain teams. Neonatal maxillary orthopedics has generated considerable debate between various authorities and cleft palate teams.
latter is accompanied by the placement of a protraction face mask to modify and redirect growth. The effectiveness of the technique has been shown but lack of longitudinal data has raised questions on the long-term benefits of this approach.
Mixed Dentition
The decision to intervene orthodontically during the mixed dentition stage of development depends on a careful assessment of the problems present and the potential risks and benefits. Such treatment is not offered routinely to all cleft palate patients but it has been more common since the advent of the alveolar bone grafting procedure.7 Patient evaluation includes an appraisal of the soft tissue condition (ie, presence or absence of oronasal communication); the skeletal aspects of malocclusion in all three planes of space; and dental problems, such as missing/malformed teeth, malposed/rotated incisors, anterior and/or posterior crossbites. Timing of treatment is closely related to the age that the secondary alveolar grafting procedure is performed. The latter is a controversial issue. Some authors8 advocate bone grafting at the age of 5 to 6 years to give the lateral incisor the possibility to migrate into and erupt through the bone graft. Others9 raise concerns that such an early intervention may interfere with maxillary growth and recommend that the graft be placed after the 8th or 9th year of age. The development of the unerupted maxillary canine is another useful guide. When radiographic examination shows that the root of the unerupted canine is onethird or one-half developed, the grafting procedure may be considered. Orthodontics, when carried out in conjunction with bonegrafting, is commenced at least 6 months before graft placement and includes fixed appliances in the maxillary arch. The objectives at this stage include expansion of the posterior and anterior maxilla to develop a favorable arch form and partially or completely eliminate the crossbites, alignment, and/or derotation of malpositioned incisors, as well as improvement of dental function and esthetics. The orthodontist should be careful not to move tooth roots into the cleft defect. Pre-angulated brackets, when used, may cause the incisor root to
Orthodontic-Orthopedic Treatment in the Deciduous Dentition

In children with an alveolar cleft defect, a delay in the eruption of deciduous teeth in the vicinity of the alveolar defect may occur. The deciduous lateral incisor may be malformed or congenitally missing. Apart from this, the deciduous dentition develops as in noncleft children. Although the distribution of the adipose tissue and the soft tissue drape of the young child camouflages the developing skeletal deficiency of the midface in children with clefts, the dentition often reflects the underlying skeletal discrepancy. Unilateral or bilateral anterior and/or posterior crossbites may be present. A functional shift (ie, a slide from centric relation to centric occlusion) may be associated with the crossbite. In some cases, removal of the occlusal interference by equilibration may alleviate the problem. In other cases, orthodontic tooth movement may be necessary. Vig and Turvey5 believe that orthodontic treatment in the deciduous dentition, although possible, is contraindicated. Limited patient cooperation may preclude the use of removable appliances at this stage and the likelihood of prolonged treatment contraindicates this approach. Growth modification at this stage has been proposed by Rygh and Tindlund.6 They recommend utilization of a quad-helix appliance soldered to bands on the primary second molar teeth and canines to expand the upper arch. The
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move distally into a cleft with resulting poor prognosis from a periodontal standpoint. It is preferable to keep the incisor roots invested in bone at the pregrafting stage while the correct tooth angulation can be achieved after successful graft placement. Obviously, such precise control of tooth position can only be achieved with fixed appliances. An added advantage of fixed appliances is that they do not rely on the cooperation of the cleft palate patient. Overretained deciduous (lateral) incisors and canines in the cleft site should be extracted before placing the bone graft. The bone grafting procedure provides continuity to the alveolar ridge, bone for the canine to erupt and osseous support for the adjacent teeth to attain near ideal positions. El Deeb et al10 reported that 27% of 46 patients aged 7 to 14 years showed spontaneous eruption of their canines after bone graft placement. The remainder of the canines moved into position following surgical uncovering (17%) or a combination of surgical exposure and orthodontics (56%). Graft placement is not a requirement for canines to erupt. Should they erupt in the cleft, however, their periodontal prognosis is questionable and does not improve significantly in cases of posteruption graft placement. It is clear that the most favorable case scenario includes grafting of the alveolar defect before canine emergence in the oral cavity. The erupting tooth appears to stimulate the formation of alveolar bone.11 It is generally recommended9 that orthodontic movement resumes actively 3 months after the placement of the graft. Others12 advocate that 2 to 3 weeks postsurgery is sufficient time before postgrafting orthodontics can be reactivated.
per se is smaller than anticipated (5% to 10%).13 Other studies14 indicate that as many as 25% of patients with oral clefts require orthognathic surgery. If the treatment plan indicates a need for orthognathic surgery, it is essential that completion of facial growth be ascertained. Handwrist radiographs in conjunction with serial cephalometric radiographs (three consecutive radiographs 6 months apart showing no change in the length of the mandible) can serve this purpose. Because patients with cleft lip/palate usually have a Class III skeletal deformity, the need for evaluation of their physical maturation is even more crucial. Careful evaluation of the Class III relationship must be performed to assess the contributions to the problem of maxillary deficiency and/or mandibular excess. Soft Tissue Problems Isolated palatal clefts not extending into the alveolar bone and lip may not affect facial esthetics to any significant degree. In general, lip contour and thickness in these patients appear normal. On occasion, a slight maxillary hypoplasia may occur, presumably as a result of an extensively scarred palate.15 Presence of a complete unilateral or bilateral cleft palate, however, may be associated with potentially severe maxillary growth deficiency, manifesting itself with straight or concave facial profile, sagittal deficiency of the maxilla, a thin upper lip, protrusive lower lip, and a deformed nasal tip with inadequate horizontal projection.16 Skeletal Problems In general, a patient with an oral cleft may show a wide spectrum of orthodontic problems with the cleft palate-related anomalies superimposed on them. It is common that the maxilla exhibits deficiency in all three dimensions, ie, anteroposteriorly, transversely, and vertically (Fig 1). Posterior crossbites are common even in cases that exhibit only an isolated cleft palate (not extending into the alveolus). Anterior crossbites are also commonly observed at this stage of development, often despite attempts to correct these problems at the mixed dentition phase of treatment. Crossbites may be present for any or a combination of the following: 1. The crossbite was not corrected fully in the mixed dentition phase of treatment.
Permanent Dentition Treatment

When the patient reaches the final stage in the development of his/her dentition, a thorough evaluation including complete orthodontic records is required. Orthodontic appliances may still be present from the previous treatment phase or orthodontic retainers may be in place. The outcome of this comprehensive evaluation should indicate whether the patient requires comprehensive orthodontics alone or orthodontics in conjunction with orthognathic surgery. Although the percentage of cleft palate patients requiring orthognathic surgery is higher than that of the general population, the percentage
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cleft palate patients are no different from those applied in the treatment of noncleft patients. There are certain unique characteristics, however, that the orthodontist needs to be aware of in the management of the cleft palate patient. An attempt will be made to outline the principles involved with both of these treatment options, ie, orthodontics alone and orthodontics in conjunction with orthognathic surgery.
Figure 1. Pretreatment frontal intraoral view of a patient with unilateral cleft lip and palate. Note the maxillary deficiency in all three planes of space (unilateral anterior crossbite, bilateral posterior crossbite and mandibular overclosure due to vertical deficiency of the maxilla).
Treatment by Orthodontics Alone In the absence of severe skeletal discrepancy and major esthetic concerns, orthodontic treatment alone may be sufficient. Goals of such treatment include: 1. Tooth alignment 2. Establishment of a continuous maxillary arch with favorable arch form 3. Correction of anterior and/or posterior crossbites 4. Stability of occlusion in the presence of dental compensations 5. Favorable dentofacial esthetics The problem of missing or peg lateral incisors is an area of concern common in the cleft patient. Should the lateral incisor space be closed orthodontically and the canines recontoured to resemble laterals? Should the space (s) be maintained or increased in anticipation of prosthetic replacement? The answer to these questions depends on the individual situation and should
2. The crossbite was corrected but the patient failed to use his/her retainer(s). 3. Dental relapse because of unfavorable soft tissue effect (eg, scarring of the palatal tissue as a result of repeated surgeries, lip tissue scarring). 4. Continued unfavorable skeletal growth (ie, the mandible continues to grow while the maxilla lags behind). 5. Maxillary deficiency and/or mandibular excess as in a true skeletal Class III malocclusion. Dental Problems Dental problems facing the orthodontist include the following: 1. Absence of teeth adjacent to the cleft, most often the permanent lateral incisors 2. High incidence of missing teeth in other regions, especially missing bicuspids 3. Malformed teeth 4. Supernumerary teeth 5. Ectopically positioned teeth 6. Lack of osseous support for some teeth compromising the possibility to move these teeth to desired positions 7. Accentuated curve of Spee in the maxilla, the mandible, or both 8. Collapsed arch form (Fig 2) 9. Poor oral hygiene, caries, periodontal disease. Orthodontic concepts and techniques used in the treatment of the permanent dentition of
Figure 2. Pre treatment occlusal view of patient shown in Fig 1. Note maxillary arch asymmetry and collapsed arch form.
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relate to the other components of the malocclusion. Patients with cleft lip and palate usually show a tendency toward a Class III malocclusion because of maxillary deficiency both anteroposteriorly and vertically, coupled with mandibular overclosure (autorotation). Utilization of Class III elastics after initial leveling and alignment results in extrusion of the upper molars and a favorable downward and backward rotation of the mandible.13 Such correction results in an increased facial height, which may be esthetically preferable to the appearance of a retruded midface.17 Anterior crossbite correction may occur as a result of using Class III intermaxillary forces. At an earlier stage of treatment however, a 2 X 4 edgewise appliance may be used with compression coil springs to advance the maxillary incisors labially and increase their faciolingual inclination. Alternatively a torquing arch18 may be used for similar results. Occasionally, a removable bite splint may be placed on the lower arch (before edgewise appliance placement) to facilitate the process of "jumping the bite." Two to three weeks of bite splint use is often sufficient. Patients that have a deep overbite in conjunction with the existing negative overjet (ant crossbite) are more likely to be candidates for this method, and the use of bite splint seems to expedite the correction of the crossbite. Correction of posterior crossbites is often difficult to achieve and more difficult to maintain in the long-term. It is likely that most posterior crossbite relapse occurs from resistance of the palatal scar tissue that only very slowly seems to be able to reorganize to a new expanded position.19 In addition, because the midpalatal suture is absent, no compensatory sutural bony deposition is expected to occur to help stabilize the expansion. Fixed palatal expansion devices such as W-arches and Quad-helices may be used in the maxillary arch (they may be soldered on the molar bands, or be inserted into palatal sheaths and be readily removable and adjustable by the orthodontist). Orthodontics Combined With Orthognathic Surgery When the skeletal discrepancy is severe, facial esthetics and occlusion deteriorate.5 The psychological implications may be profound because
many cleft patients already have low self-esteem (ie, soft tissue scars, peer attitude). Speech may be further impaired as the adenoid tissues shrink at puberty. Oronasal fistulas may be present despite previous attempts to achieve closure. The skeletal deformity present is usually due to maxillary hypoplasia in three dimensions. The mandible may be normal but on occasion it may be dysplastic as may occur in noncleft populations. Mandibular prognathism would magnify the skeletal relationships, whereas mandibular retrognathia depending on the degree, could even reverse the skeletal relationships. Anterior open bites may also be present. Combined orthodontic-surgical treatment requires close cooperation between the orthodontist and maxillofacial surgeon. Complete orthodontic records are necessary to formulate a treatment plan. In addition, periapical and possibly maxillary occlusal radiographs allow an assessment of osseous support of teeth adjacent to cleft site(s) as well as root positions. It is strongly recommended that both orthodontist and surgeon meet to evaluate the records before the formulation of a detailed treatment plan. It is the author's opinion that a telephone conversation is no substitute for an arranged personal meeting between the orthodontist and the surgeon. Because the size and position of maxilla is often a problem, maxillary advancement and occasionally down-grafting needs to be performed to address the anteroposterior and vertical deficiency of the maxilla. The transverse problem may be resolved by merely positioning the maxilla forward relative to the mandible. The reason for the latter is that, just as occurs in some noncleft Class III skeletal malocclusions, the posterior crossbite may not reflect a true transverse discrepancy but rather a mesial position of the mandible relative to the maxilla. However, in the majority of cleft palate patients a true transverse discrepancy is present and multiple segment Le Fort I osteotomy procedures need to be performed. Three-piece maxillary surgery is often required for the treatment of a bilateral cleft lip and palate, whereas a two-piece or three-piece maxillary osteotomy serves well in a patient with a unilateral cleft lip and palate. A two-piece maxillary surgical procedure may address the transverse problem in a unilateral cleft lip and palate case but a three-piece option may also allow rotation of the individual segments
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thereby permitting a more favorable occlusal plane thus reducing the amount of postsurgical orthodontic treatment needed. The decision to section the maxilla in more than one piece implies that leveling and alignment of the maxillary dentition will be performed independently for each segment. Bracket placement may require modifications for the teeth adjacent to planned osteotomy sites. If the cut is to be made between the maxillary canine and first premolar, it is required that a nonangulated bracket or a contralateral canine bracket is bonded on the canine to cause divergence of the canine and premolar roots. The latter will decrease the risk for inadvertently sectioning the canine and/or premolar root at the time of surgery. However, if the incision is to be made between the lateral incisor and canine, the lateral incisor should be bonded with a standard, nonangulated bracket or an opposite-side lateral incisor bracket, whereas the canine should have bonded the customary preangulated bracket. Such a bracket placement method may save time compared with the alternative of using secondorder arch wire bends to diverge roots adjacent to the osteotomy site. Obviously, at times variations of bracket placement alone will not suffice and second-order arch wire bends will be required as well to create the needed root divergence. Presurgical orthodontic treatment usually extends for a period of 12 months. Removal of "dental compensation," especially in the lower arch and the alleviation of crowding is one of the objectives during this stage of treatment. The latter is accomplished by leveling and alignment and occasional use of Class II intermaxillary elastics. In some instances extractions of teeth may become necessary to achieve a favorable position of the incisors with adequate periodontal support. Setting up the surgical cast segments before fabrication of the surgical splint requires an early decision as to whether dental gap(s) will be present at the lateral incisor site after the surgical procedure versus the alternative approach of approximating the canine(s) with the central incisor(s). The latter approach may produce a more stable result and prevent reopening of an oronasal fistula, but an ideal occlusion in this situation may not be possible (Figs 3 and 4). Proffit13 recommended overcorrecting the an-
Figure 3. A presurgical cast set-up that would allow for creation of a lateral incisor space to be addressed by prosthodontics at a later time. Three-piece maxillary Le Fort I osteotomy. Although occlusal interdigitation is satisfactory, this approach invites potential risks such as reopening of a fistula, and questionable posterative stability.
terior crossbite and setting the surgical casts in an excess of positive overjet. The latter is performed to compensate for the anticipated postsurgical relapse. Given the significant relapse potential in these circumstances, the method advocated by Profitt13 is appropriate. If the anteroposterior jaw discrepancy exceeds 8 mm, maxillary "over advancement" could lead to a very unstable result, in addition to further compromising speech. In this situation, mandibular surgery should be considered even though the mandible may be of normal size
Figure 4. Alternative surgical cast set-up for the same patient. Right canine approximates the central incisor. The canine will eventually be reshaped to resemble a lateral incisor. Three-piece maxillary Le Fort I osteotomy (left osteotomy site is between canine and first premolar). This approach may be superior in terms of tissue health and postoperative stability. The occlusal relationships, however, are not ideal.
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and position. Mandibular bilateral sagittal split osteotomy is often indicated when there is a severe cant of the occlusal plane and/or when a mandibular asymmetry exists. Postsurgical orthodontics usually extends for a period of approximately 4 to 6 months. Objectives of the postsurgical phase of orthodontic therapy include detailing of the occlusion and closure of any residual spaces while maintaining the transverse correction. Transpalatal arches or "piggy-back overlay"20 arches (0.036 stainless steel arches) inserted in the headgear tubes may serve well to maintain the transverse dimension of the maxilla or even provide expansion in the event that some postoperative relapse has occurred. Intermaxillary, through-the-bite, and/or vertical box elastics may be used as needed.
Figure 5. Postorthodontic intraoral view of patient shown in the previous figures. Composite buildups or laminate veneers in conjunction with crown lengthening procedures may be necessary at a later time to optimize esthetics.
Retention
The importance of orthodontic retention for patients with facial cleft defects cannot be overemphasized. After removal of the fixed orthodontic appliances from the maxillary arch, a retainer should be placed immediately (ie, the same day). If the postorthodontic result includes one or more edentulous areas that need to be managed prosthodontically, a removable Hawley-type retainer with replacement teeth may be used. Patient cooperation is not usually a problem with the latter type of retainer because of the obvious esthetic benefit that the replacement teeth afford. Temporary clear vacuum-formed retainers are not recommended because they may not provide adequate transverse control to prevent posterior crossbite relapse. When the periodontal tissues are healthy and the patient's age permits, the restorative dentist may proceed with the construction and placement of removable or fixed prostheses as needed. Fixed bridges are generally preferable whenever possible. Occasionally, preprosthetic augmentation of the edentulous area may be necessary for cosmetic purposes (ie, pontic esthetics) or before placement of implant(s). If the prosthetic rehabilitation involves the placement of an anterior fixed prosthesis only, it is recommended that a soldered lingual arch attached to plain molar bands be cemented for transverse retention. A conventional Hawley appliance with an acrylic palate is not a dependable form of retention, because it has been our observation that following lengthy
treatments patients may no longer be motivated, and may not wear their removable retainer as instructed. The estimated length of retention with the fixed lingual arch is indefinite. Risk of caries is certainly a possibility, and it is therefore recommended that the appliance be removed at least once a year for inspection. Use of glassionomer cement is also recommended. The lingual arch does not seem to interfere with the occlusion anteriorly or posteriorly in the majority of patients because a dental deep overbite is not very common in these patients (Fig 5). Nevertheless, a modified approach including a transpalatal arch, eliminating the central loop for comfort but placing extension "finger springs" to the premolar-canine area is recom-
Figure 6. Postorthodontic occlusal view of maxillary arch. A soldered lingual arch has been cemented for long-term retention.
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mended when the amount of vertical incisal overlap prevents the placement of a lingual arch in the anterior maxilla. If no dental spaces exist in the postorthodontic occlusion, a cemented lingual arch in the maxilla is recommended for long-term retention as described previously (Fig 6). Retention for the mandibular arch is no different than that for noncleft orthodontically treated patients. It is realistic to accept the fact that many treated patients will show some relapse and that ideal orthodontic results are often not possible to attain. However, the latter should not detract from the clinician's motivation and commitment to achieve as optimal a result as is possible.
References
1. Btow KW. Treatment of Facial Cleft Deformities. An Illustrated Guide. St. Louis, Ishiyaku EujroAmerica, Inc, 1995:69. 2. Rosenstein S. A new concept in the early orthopedic treatment of cleft lip and palate. Am J Orthod 1969;55: 765-775. 3. Robertson N. Recent trends in the early treatment of cleft lip and palate. Dent Pract 1971 ;21.326-333. 4. Georgiade NG, Latham RA. Maxillary arch alignment in the bilateral cleft lip and palate infant using the pinned coaxial screw appliance. Plast Reconstr Surg 1975;56:5259. 5. Vig K, Turvey T. Orthodontic-surgical interaction in the management of cleft lip and palate. Glin Plast Surg 1985;12:735-748. 6. Rygh P, Tindlund R. Orthopedic expansion and protraction of the maxilla in cleft palate patientsa new treatment rationale. Cleft Palate J 1982;19:104-112.
7. Boyne PJ, Sands NR. Secondary bone grafting of residual alveolar and palatal defects. J Oral Surg 1972;30:87-92. 8. Pirruccello FW. Cleft lip and palate: Plastic surgery, genetics and the team approach. Springfield: Thomas, 1987. 9. Bergland O, Semb G, Abyholm FE. Elimination of the residual alveolar cleft by secondary bone grafting and subsequent orthodontic treatment. Cleft Palate J 1986;23: 175-205. 10. El Deeb M, Messer LB, Lehnert MW, et al. Canine eruption into grafted boned in maxillary alveolar cleft defects. Cleft Palate J 1982;79:9. 11. Steedle JR, Proffit WR. The pattern and control of eruptive tooth movements. Am J Orthod 1985;81:56. 12. Turvey TA, Vig K, Moriarty J, et al. Delayed bone grafting in the cleft maxilla and palate: A retrospective multidisciplinary analysis. Am J Orthod 1984;86:244. 13. Proffit WR, White RR Surgical-Orthodontic Treatment. St. Louis, MO: Mosby, 1991. 14. Ross KB. Treatment variables affecting facial growth in complete unilateral cleft lip and palate: 7. An overview of treatment and facial growth. Cleft Palate J 1987;24:7l. 15. Johnston MD. Orthodontic treatment for the cleft palate patient. Am J Orthod 1958;44:750-7673. 16. Hanada K, Krogman W. A longitudinal study of postoperative changes in the soft tissue profile in bilateral cleft lip and palate from birth to six years. Am J Orthod 1975;67:363-376. 17. Vangervik K. Orthodontic management of unilateral cleft lip and palate. Cleft Palate J 1981;18:256-270. 18. Isaacson RJ, Rebellato J. Two-couple orthodontic appliance systems: Torquing arches. Semin Orthod 1995; 1:3136. 19. Cooper HK, Long RE Sr, Long RE Jr. Orthodontics and oral orthopedics. In: Cooper WE, Harding RL, Krugman WH, et al, editors. Cleft Palate and Cleft Lip: A Team Approach to Clinical Management and Rehabilitation of the Patient. Philadelphia, PA: Saunders, 1979. 20. Mulligan TF. Common sense mechanics. Phoenix, AZ: GSM 2122 East Kaler Drive, 1982.
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Orthognathic Surgery for the Cleft Lip and Palate Patient

Jeffrey C. Posnick
A thoughtful staged reconstruction for the cleft lip and palate patient is the preferred approach. The primary lip and palate repair performed during infancy and early childhood provides the foundation for normal speech, occlusion, facial appearance, and self-esteem. A long-term negative effect of these early surgical interventions is a significant incidence of maxillary growth restriction that produces secondary deformities of the jaws and dentition. This article reviews the variations in presentation, surgical and orthodontic techniques, and the results that we have achieved in patients born with a cleft who underwent primary repair in childhood, had a jaw deformity and malocclusion in adolescence, and underwent orthognathic surgery combined with orthodontic treatment for facial reconstruction and dental rehabilitation. (Semin Orthod 1996;2:205-214.) Copyright 1996 by W.B. Saunders Company
he optimal management of patients with cleft lip and palate continues to challenge the health care delivery system. The primary lip and palate repair performed during infancy and early childhood provides the foundation for normal speech, occlusion, facial appearance, and self-esteem. One long-term negative effect of these early surgical interventions is a significant incidence of maxillary growth restriction that produces secondary deformities of the jaws and malocclusion, which also impacts on speech and self-esteem. Ross documented that in approximately 25% of adult males with a repaired unilateral cleft lip and palate, orthognathic surgery is necessary to permit an adequate functional relationship of the jaws and teeth.1 The cephalometric criteria he applied are traditional ones that are likely to underestimate the actual number of adolescents born with a cleft who would benefit from orthognathic surgery.2
From the Department of Surgery, Department of Pediatrics, Department of Otolaryngology/Head and Neck Surgery and Oral and Maxillofacial Surgery, Georgetown University, Washington, DC. Address correspondence toJeffrey C. Posnick, DMD, MD, FRCSc, FACS, Division of Plastic Surgery, Georgetown Craniofacial Center, Georgetown University Medical Center, 3800 Reservoir Rd NW, Washington, DC 20007. Copyright 1996by W.B. Saunders Company 1073-8746/96/0203-0004$5.00/0
The prevalence and extent of residual rnaxillofacial deformities in the adolescent born with a cleft vary widely depending on a team philosophy about the staging of reconstruction and on available technical expertise.3 In addition, despite a center's preferred method of managing cleft deformities during infancy and childhood, there will be a subgroup of patients who, in adolescence, have multiple neglected or residual cleft-related problems. Our philosophy for management of alveolar clefts and residual perialveolar oronasal fistulas is to fill the bony defect with autogenous iliac (hip) bone graft and close all oronasal fistulas at each cleft site and throughout the palate in the mixed dentition before eruption of the permanent canine tooth.4"5 This procedure is followed by orthodontic closure of the cleft-dental gap whenever feasible.6 If this approach is followed successfully, the adolescent with a cleft who has maxillary hypoplasia may undergo a standard Le Fort I osteotomy for correction.7 Unfortunately, there remains a subgroup of adolescents with a cleft-jaw deformity who have a residually clef ted and perforated (oronasal fistula) maxilla. Recognition of the unique circulation requirements of the upper jaw at the time of osteotomy has allowed us to suggest an effective one-stage approach to manage these residual deformi205
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ties.8"10 The modifications are based on the premise that safe flaps can be developed for independent repositioning of the maxillary segments according to residual deformity in the maxilla, cleft type (unilateral cleft lip and palate [UCLP], bilateral cleft lip and palate [BCLP] or isolated cleft palate [ICP]), and individual variation. (Figs 1 and 2) This article reviews the variations in presentation, surgical techniques, and the results that we have achieved in patients born with a cleft who underwent primary repair in childhood, had a jaw deformity and malocclusion in adolescents, and underwent orthognathic surgery.11 Patients and Methods Basic Patient Data Between 1986 and 1992, 116 adolescents (67 males, 49 females; age range, 15 to 25 years; mean age, 18 years) born with either unilateral cleft lip and palate (n = 66), bilateral cleft lip
and palate (n = 33), or isolated cleft palate (n = 17) underwent orthognathic surgery by the author (Posnick) using consistent surgical techniques. (Figs 3-6) The complications and long-term results of this work has been previously reported.11 All but one patient underwent perioperative orthodontic treatment. All were judged to be skeletally mature at the time of jaw surgery, either by serial cephalometric radiographs or by epiphyseal plate closure on hand radiograph. The clinical follow-up ranged from 1 to 7 years (mean, 40 months) at the close of the study. The patients' primary surgeons (earlier in life) varied, as did the previous cleft-related procedures that they performed. All patients had undergone primary lip and palate repair in infancy or childhood. The number and extent of previous revisional soft-tissue lip, nasal, and palatal procedures varied greatly (from 0 to 10 procedures). Most patients had undergone additional attempts to close the residual oronasal
Figure 1. Illustrations of modified Le Fort I osteotomy of a UCLP patient in two segments. (A) Illustration of direct incisions for completion of osteotomies and fistula closure. (B) Frontal view of bony skeleton before and just after fixation of Le Fort I osteotomy in two segments. The inferior turbinates have been reduced, and a submucous resection of the deviated septum has been performed. Iliac, cancellous bone graft has been placed along the nasal floor. A miniplate is placed vertically along each zygomatic buttress and piriform aperture region while a microplate is placed horizontally across the segmental osteotomy site. (C) Lateral view of maxillofacial skeleton before and just after osteotomies and fixation of modified Le Fort I osteotomy. (D) Illustration of downfractured Le Fort I in two segments after submucous resection of septum, reduction of inferior turbinate through the nasal mucosa opening, followed by water-tight nasal side closure. (E) Palatal view of bony segments before and after repositioning. (F) Illustration indicating oral-side wound closure on both labial and palatal aspects after differential segmental repositioning. (Reprinted with permission from Posnick JC. Orthognathic surgery in the cleft patient. In: Russell RC, editor, Instructional Courses, Plastic Surgery Education Foundation, vol 4. St Louis, MO: Mosby, 1991:129-157.)
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Cleft-Orthognathic Surgery
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Figure 2. Illustrations of modified Le Fort I osteotomy of the BCLP patient in two or three segments. (A) Illustration of the BCLP patient before and after lateral segmental osteotomies and repositioning. (B) Illustrations before and after three-part maxillary osteotomies with repositioning of the segments. (C) Illustration of incisions for modified Le Fort I in three segments. (D) Illustration of down-fractured lateral segments showing exposure for nasal side closure of oronasal fistula and additional view of oral mucosa incisions. (E) Illustration of premaxillary osteotomy from palate side using either a chisel, rongeur, or reciprocating saw. (F) Illustration of oral wounds sutured at the end of the procedure. (G) Palatal view of bony segments before and after repositioning for closure of cleft-dental gaps. (Reprinted with permission from PosnickJC. Orthognathic surgery in the cleft patient. In, Russell RC, editor. Instructional Courses, Plastic Surgery Education Foundation, vol 4. St Louis, MO: Mosby, 1991:129-157.)
fistula; 20 patients underwent bone grafting to fill the alveolar cleft. Seven of 66 unilateral cleft lip and palate patients had previously undergone orthognathic surgery by another surgeon. The basic orthognathic procedure performed in each of our patients included a Le Fort I osteotomy (n = 116). Thirty-two of these patients also had undergone simultaneous sagittal split osteotomies of the mandible; 87 underwent a vertical reduction and horizontal advancement genioplasty of varying degrees.
Operative Technique
The operative technique has been outlined previously and illustrated according to cleft type.9-10
For effective management of the unilateral cleft lip and palate and bilateral cleft lip and palate patients' maxilla, the standard Le Fort I osteotomy techniques had to be modified (Figs 1-2) .9"10 The principle modification consisted of placement of soft-tissue incisions that allowed direct exposure for dissection, osteotomies, disimpaction, fistula closure, bone grafting, and application of plate-and-screw fixation that did not risk circulation injury to the dento-osseousmusculo-mucosal flaps. The routine surgical closure of residual cleft-dental gaps through differential maxillary segmental repositioning also was incorporated. For patients with unilateral cleft lip and palate or bilateral cleft lip and palate,
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Figure 3. A 16-year-old girl with unilateral cleft lip and palate who underwent a modified Le Fort I osteotomy in two segments, bilateral sagittal split osteotomies of the mandible and an osteoplastic genioplasty is shown before and 2 years after surgery. (A) Preoperative frontal view in repose. (B) Frontal view in repose 2 years later. (C) Preoperative frontal view with smile. (D) Frontal view with smile 2 years later. (E) Preoperative oblique view. (F) Oblique view 2 years later. (G) Preoperative profile view. (H) Profile view 2 years later. (I) Preoperative occlusal view. (J) Occlusal view 2 years later. (K) Preoperative articulated dental casts. (L) Articulated dental casts after model surgery. (M) Preoperative cephalometric radiograph. (N) Cephalometric radiograph 1 year later. (Reprinted with permission from Posnick JC, Tompson B. Cleft-Orthognathic surgery: Complications and long-term results. Plast Reconstr Surg 1995;96:255.)
approximation of the maxillary segments for closure of the cleft-dental gaps also closed the dead space of the cleft alveolus and approximated the labial and palatal flaps to allow for
straight forward closure of the recalcitrant oronasal fistula without tension, while providing keratinized mucosa to surround the cleft site (s) and adjacent teeth.
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Figure 4. A17-year-old patient with repaired bilateral cleft lip and palate. He initially presented in childhood with an elongated premaxilla, which eventually showed hypoplasia at skeletal maturity. His residual clefting problems were managed through a combined orthodontic and orthognathic approach using a modified Le Fort I osteotomy in two segments. (A) Preoperative frontal view. (B) Postoperative frontal view. (C) Preoperative lateral view. (D) Postoperative lateral view. (E) Preoperative occlusal view at 13 years of age. Note that the premaxilla appears to be long vertically. (F) After preoperative orthodontic treatment in preparation for jaw surgery at 17 years of age. (G) At 18 months after surgery and completion of orthodontics with resin build-ups of anterior teeth. (H) Occlusal view in mixed dentition phase. The cheek rotation flap used for fistula closure has decreased the vestibular depth and placed nonkeratinized mucosa over the tooth-bearing surface. A sliding mucogingival rotation flap would have been preferable. (I) Dental arch form after modified Le Fort I osteotomy with differential repositioning of three segments to close fistulas and cleft-dental gaps in the regions of the congenitally absent lateral incisors. (Reprinted with permission from Posnick JC, Witzel MA, Dagys AP. Management of jaw deformities in the cleft patient. In: Bardach J, Morris HL, editors. Multidisciplinary Management of Cleft Lip and Palate. Philadelphia, PA: Saunders, 1990:538.)
In anticipation of a degree of postoperative skeletal relapse, surgical overcorrection of several millimeters was planned in the horizontal and transverse dimensions. The exact amount varied with the interdigitation of the teeth.12"13 In our study, all but six patients (110 of 116 patients) underwent simultaneous autogenous cortico-cancellous iliac bone grafting. For patients with unilateral cleft lip and palate or bilateral cleft lip and palate, cancellous graft was used to fill all residual palatal, and floor-of-thenose defects.14 After fixation of the maxilla with
four miniplates, additional corticocancellous grafts were wedged between the zygomatic buttress and piriform aperture on each side and secured with microplates and screws. Prefabricated interocclusal splints were used intraoperatively to facilitate correct placement of the jaws; the final splint was wired to the maxillary arch wire. Maxillo-mandibular fixation was generally applied for 2 to 4 weeks. The prefabricated splint remained wired to the maxillary arch wires for a total of 8 weeks to be certain that the relationship of the maxillary teeth to one
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Figure 5. Twenty-three-year-old patient born with isolated cleft palate. She underwent a standard maxillary Le Fort I osteotomy with horizontal advancement and a vertical reduction and horizontal advancement genioplasty. (A) Preoperative frontal view in repose. (B) Postoperative frontal view in repose. (C) Preoperative frontal view with a smile. (D) Postoperative frontal view with a smile. (E) Preoperative profile view. (F) Postoperative profile view. (G) Preoperative occlusal view. (H) Postoperative occlusal view. (I) Preoperative oblique occlusal view. (J) Postoperative oblique occlusal view. (K) Articulated dental casts before surgery. (L) Artiulated dental casts after model surgery. (M) Preoperative lateral cephalometric roentgenogram. (N) Postoperative lateral cephalometric roentgenogram. (Reprinted with permission from Posnick JC, Ewing MR The role of plate and screw fixation in the treatment of cleft lip and palate jaw deformity. In: Gruss JS, Manson PM, Yaremchuk MJ, editors. Rigid Fixation of the Craniomaxillofacial Skeleton; Stoneham, MA, Butterworth, 1992;36:466-485.)
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Figure 6. A 16-year-old patient with repaired bilateral cleft lip and palate presenting with a marked residual oronasal fistula and poor alveolar bone support to the teeth adjacent to each cleft. She underwent a combined orthognathic and orthodontic approach. (A) Preoperative occlusal view before necessary extractions, orthodontic treatment and modified segmental LeFort I osteotomy. (B) Postoperative palatal view after completion of treatment indicating segmental LeFort I to close: oro-nasal fistula; alveolar clefts; and cleft-dental gaps. (Reprinted with permission from Posnick JC. Orthognathic surgery in the cleft patient. In: Russel RC, editor. Instructional Courses, Plastic Surgery Education Foundation St. Louis, MO: Mosby, 1991:4:148.)
another and to the mandibular teeth remained unchanged. The segmental surgical arch wires were then replaced with a continuous arch wire and the orthodontic treatment was resumed. Orthodontic Technique The UCLP and BCLP patient who presented with maxillary hypoplasia and had not been grafted effectively in the mixed dentition would have two (UCLP) or three (BCLP) separate maxillary segments, each with a varied degree of dysplasia in all three planes. Each segment was evaluated and treated individually in anticipation of segmental surgical repositioning. Radiographic assessment is essential before any orthodontic movement of teeth adjacent to the bone deficient cleft site(s). The panorex radiograph is primarily useful for assessing tooth angulation. Maxillary occlusal and periapical radiographs through the cleft site(s) can help assess the amount and height of the alveolar crestal bone of the adjacent teeth. Both the number of permanent incisors and the amount of dentoalveolar bone in the anterior aspects of the maxilla will differ widely. Lateral incisor-like teeth frequently are found along the edges of the cleft site(s) in either the premaxilla (BCLP) or in the lateral segment(s). These generally are rudimentary with limited root support. When a poorly formed lateral incisor is present, it may be prudent to extract it in the interest of long-term function, aesthetics, and dental rehabilitation. Unerupted supernumerary teeth are also extracted either at the time
of bone grafting in the mixed dentition or at the time of orthognathic surgery. The decision to extract fully erupted normally formed teeth within the lateral segment(s) depends on the volume and height of the bone covering the dental roots adjacent to the cleft(s) and the degree of crowding within each segment. Bicuspid extraction (s) are often necessary to ensure that there is adequate bone for the levelling and aligning of all retained teeth without irreversibly weakening the periodontal support of the teeth adjacent to the cleft(s). The final occlusal result after orthodontic alignment and surgical repositioning of the lateral segment (s) will determine whether the maxillary third molars are required for opposing contact with the lower arch. Planning for extractions in the mandibular arch depends on space requirements and on tooth movements needed to position the incisors ideally over basal bone. As may be used in the noncleft patient, an orthodontic trial set-up of the teeth is helpful in establishing the most appropriate extraction pattern. This is especially important when, after surgery, the mandibular arch will occlude with the maxillary arch where cuspids and bicuspids are advanced to the lateral incisor and cuspid positions. The orthodontist must be cognizant that placement of pre-angulated brackets, as is often used in a noncleft patient, or artistic positioning bends can displace the cleft adjacent root apices from their alveolar housing, with rapid loss of crestal bone height. Loss of vertical alveolar
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height along the cuspid tooth will occur with excessive mesial crown tipping. Some patients lack sufficient bone in the premaxillary region to align the incisors preoperatively. For these patients, appliance placement is best delayed until after surgery. A passive sectional archwire is fabricated for the stabilization of surgical splints. Orthodontic movement is safe once the cleft defects are surgically closed and grafted. Incorporation of all erupted long-term teeth in each maxillary segment within the orthodontic mechanics will facilitate arch leveling and development of the desired arch form. A lingual tube on the maxillary molar band allows the use of a trihelix expansion appliance to help correct extreme dentoalveolar collapse before surgery. The use of a lingual arch may stabilize the result. The development of an ideal mandibular arch transversely is critical for effective repositioning of the upper maxillary segments in the most favorable position at the time of orthognathic surgery. The improved maxillary arch form may enhance stability and will improve speech articulation by providing adequate space for the tongue. A prefabricated acrylic occlusal splint is wired to the maxillary orthodontic appliances in the operating room. Intermaxillary elastic fixation is generally applied for 2 to 4 weeks. With release of intermaxillary fixation, the diet is advanced to mechanical soft, but the acrylic splint remains wired to the maxillary brackets for a total of 8 weeks. Ideally, the orthodontist sees the patient on the day of splint removal and replaces the maxillary sectional archwires with a continuous archwire. The teeth are ligated together to maintain the surgical dental-gap closure. Active orthodontic treatment is reinitiated. Close monitoring for skeletal and dental relapse management is essential.
the cleft dental gap(s), presence of keratinized mucosa along the labial surface of cleft-adjacent teeth, and the need for a prosthetic appliance to complete dental rehabilitation; (2) perioperative complications; (3) the long-term maintenance of a positive overjet and overbite, as determined from the late postoperative cephalometric radiographs.11 Overall, 89% of residual fistulas underwent successful closures as part of the orthognathic surgical procedure. Surgical cleft-dental gap closure was achieved and maintained to the extent planned at 92% of the cleft sites. A fixed (prosthetic) bridge was used successfully for dental rehabilitation to close the gap(s) in all other patients in each cleft site (n = 9). All patients with alveolar clefts (n = 99) maintained keratinized mucosa along the labial surface of the cleft-adjacent teeth (n = 264 teeth). Complications were few and generally not serious. There was no segmental bone loss or loss of teeth because of aseptic necrosis, infection or for other reasons.9 Only 5% of cleft adjacent teeth underwent a degree of gingival recession or root exposure as a result of the maxillary osteotomy procedures; all were retained long term. The long-term maintenance of overjet and overbite measured directly from the late (>1 year) postoperative lateral cephalometric radiographs indicated that 97% of patients maintained a positive overjet and that 89% maintained a positive overbite; 5% shifted to a neutral overbite.
Discussion
The described method for managing oronasal fistulas, alveolar defects, and cleft-dental gaps in patients with unilateral cleft lip and palate or bilateral cleft lip and palate is not intended to replace standard techniques and accepted sequencing of treatment.4"5 It does offer an alternative once the opportunity for grafting the alveolus in the mixed dentition before the eruption of the permanent canine tooth is lost.9"10'15"16 A two-stage approach for the adolescent born with a cleft and presenting with: maxillary hypoplasia; residual alveolar clefts; and fistulas is not costeffective, and the potential overall morbidity is increased. It is in these patients with unilateral cleft lip and palate or bilateral cleft lip and palate that the modified Le Fort I osteotomy offers a
Results
Postoperative variables reviewed in our patients related to: (1) the condition of the clefted dento-alveolar region, including the presence of residual oronasal fistula, mobility of the premaxilla (in bilateral cleft lip and palate patients), adequacy of the bone bridge across the alveolus, any increase in gingival recession and root exposure of cleft adjacent teeth, success of closure of
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reasonable opportunity for the resolution of residual problems (ie, alveolar defects, residual fistulas, and cleft-dental gaps).9'11 There is a small subgroup of patients with bilateral cleft lip and palate who, in early childhood, have very large palatal fistulas combined with bilateral peri-alveolar ones. In general, there are only two options for fistula management in these patients. An anteriorly based dorsal tongue flap combined with an autogenous bone graft is a useful approach in the mixed dentition if the surgeon believes it will produce a successful closure with sufficient bone-graft take.17 If the size of the fistula, amount of dead space, and tissue deficit are very large, even a tongue flap may fail. The best option in these unique and difficult cases is to obturate the fistua with a temporary partial denture and maintain a cleftdental gap(s) until early skeletal maturity, when a modified Le Fort I osteotomy is performed to finally resolve these problems.10 (Fig 6) In a patient with UCLP or BCLP, prosthetic options for the management of the cleft-dental gap(s) in the region of the congenitally absent or inadequate lateral incisor(s) exist. From both facial aesthetic and dental health perspectives, the long-term use of a removable partial denture is always a second choice. Fixed bridgework is a reliable alternative but requires the partial destruction of adjacent normal teeth, frequently looks artificial, requires replacement at intervals throughout the patients life, and demands ongoing meticulous oral hygiene. Placement of a single-tooth osseous integrated implant is an attractive alternative, but the implant requires adequate bone height and volume that is not routinely present at the cleft site(s).18 These options are considered and compared with the method of simultaneous surgical cleft dental gap closure when maxillary hypoplasia also exists. Other dental refinements for the cleft patient's dysmorphic, often hypoplastic and decayed anterior maxillary teeth include porcelainveneer build-ups, composite bonding, sculpting teeth, and bleaching techniques. Each of these refinements may improve the patient's dental aesthetics, smile, and self-esteem and should be considered as part of an interdisciplinary team approach. Uncertainties about velopharyngeal function and management of an in-placed pharyngeal flap should no longer be limiting factors when
orthognathic surgery is necessary in a patient with a cleft.19 Awake nasoendoscopy performed in combination with clinical examination by a speech pathologist and surgeon familiar with cleft patients' speech, can reliably predict current and expected velopharyngeal function in patients scheduled for a Le Fort I osteotomy.20 When significant postoperative velopharyngeal deteriation is anticipated, the patient and family should be educated about the sequencing of treatment, and alternatives should be discussed.
Conclusions
The methods described to manage jaw deformities, malocclusion, residual oronasal fistulas, and bony defects in adolescents born with a cleft are safe and reliable when these methods are performed by an experienced cleft surgeon and team. They enhance the patients quality of life and well-being. They also provide a stable foundation in which final soft-tissue lip and nose revisions may be carried out.
References
1. Ross RB. Treatment variables affecting facial growth in complete unilateral cleft lip and palate: 7. An overview of treatment and facial growth. Cleft Palate J 1987;24:71. 2. Posnick JC. Discussion: Orthognathic surgery in cleft patients treated by early bone grafting. Plast Reconstr Surgl991;87:840. 3. PosnickJC. Orthognathic surgery in the cleft patient. In: Russell RC, editor. Instructional Courses, Plastic Surgery Education Foundation, vol 4. St Louis, MO: Mosby, 1991:129-157. 4. Abyholm FE, Bergland O, Semb G. Secondary bone grafting of alveolar clefts. Scand J Plast Reconstr Surg 1981;15:127. 5. Hall HD, Posnick JC. Early results of secondary bone grafts in 106 alveolar clefts. J Oral Maxillofac Surg 1983;41:289. 6. Proffitt WR. Orthodontic treatment of clefts: Yesterday, Today and Tomorrow. Proceedings of the 48th Annual Meeting, American Cleft Palate-Craniofacial Association, Hilton Head, SC, March 1991:32. 7. Bell WH. Le Fort I osteotomy for correction of maxillary deformities. J Oral Surg 1975;33:412. 8. Posnick JC, Dagys AP. Bilateral cleft Deformity: An integrated surgical and orthodontic approach. Oral Maxillofac Surg Clin North Am 1991;3:693. 9. Posnick JC, Tompson B. Modification of the maxillary Le Fort I osteotomy in cleft-orthognathic surgery. The unilateral cleft lip and palate deformity. J Oral Maxillofac Surg 1992,50:666. 10. Posnick JC, Tompson B. Modification of the maxillary Le
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11.
12.
13.
14. 15.
Fort I osteotomy in cleft-orthognathic surgery. The bilateral cleft lip and palate deformity. J Oral Maxillofac Surgl993;51:2. Posnick JC, Tompson B. Cleft-Orthognathic surgery: Complications and a long-term results. Plast Reconstr Surg 1995;96:255. Posnick JC, Taylor M. Skeletal stability and relapse patterns after Le Fort I osteotomy using miniplate fixation in patients with isolated cleft palate. Plast Reconstr Surg 1994;94:51. Posnick JC, Dagys AR Skeletal stability and relapse patterns after Le Fort I maxillary osteotomy fixed with miniplates: The unilateral cleft lip and palate deformity. Plast Reconstr Surg 1994;94:924. Tessier P, Tulasne JF. Secondary repair of cleft lip deformity. Clin Plast Surg 1984; 11:747. Posnick JC, Witzel MA, Dagys AR Management of jaw deformities in the cleft patient. In: Bardach J, Morris HL,
16.
17.
18.
19.
20.
editors. Multidisciplinary Management of the Cleft Lip and Palate. Philadelphia, PA: Saunders, 1990:530-543. Posnick JC, Ewing MR The role of plate and screw fixation in the treatment of cleft lip and palate jaw deformities. In: Gruss JS, Manson PM, Yaremchuk MJ, editors. Rigid Fixation of the Craniomaxillofaial Skeleton. Butterworth, Stoneham, MA: 1992;36:466-485. Posnick JC, Getz SB Jr. Surgical closure of end-stage palatal fistulas using anteriorly based dorsal flaps. J Oral Maxillofac Surg 1987;45:907. Parel SM, Branemark PI, Jansson T. Osseointegration in maxillofacial prosthetics: I. Intraoral applications. J Prosthet Dent 1986;55:490. Witzel MA, Vallino L. Speech problems in patients with dentofacial deformities. In: Bell WH, editor. Modern Practices in Orthognathic and Reconstructive Surgery, vol 3. Philadelphia, PA: Saunders, 1992:1686. Witzel MA, Munro IR. Velopharyngeal insufficiency after maxillary advancement. Cleft Palate J 1977;14:176.
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Prosthetic Rehabilitation of the Cleft Palate Patient

L. Kirk Gardner and Greg R. Parr
This article is a brief overview of prosthodontic and restorative methods used in the treatment of unilateral and bilateral cleft palate patients. Some past, present, and future methods of rehabilitation are discussed. (Semin Orthod 1996;2:215-219.) Copyright 1996 by W.B. Saunders Company
prosthesis to obturate the cleft of either the hard or soft palate was first attempted by Ambrose Pare in 1565.1 From that time on, techniques and ideas have evolved from those first attempts using sponges, wax, and silver to more modern materials and techniques advocated and used today. With the advanced surgical orthodontic and orthopedic intervention during and after the first year following birth, prosthodontic replacement materials have become less often needed. The management of a patient with cleft lip and palate cannot be adequately accomplished by a single clinician.2 A team of specialists including audiologist, otologist, speech pathologist, social worker, psychologist, pediatrician, oral maxillofacial surgeon, plastic surgeon, orthodontist, pedodontist, and maxillofacial prosthodontist is required to plan and perform treatment for these patients. Growth and development potential of the child can be harnessed in a way as to enable great improvement in the maxillary arch in both unilateral and bilateral cleft lip and palate infants.
The Latham Appliance

The Latham appliance3 was developed by Dr. Ralph Latham, and there are two distinct appliFrom the Departments of Restorative Dentistry and Maxillofacial Prosthetics, University of Alabama at Birmingham School of Dentistry, Birmingham, AL; and the Departments of Oral Rehabilitation and Maxillofacial Prosthetics, Medical College of Georgia School of Dentistry, Augusta, GA. Address correspondence to L. Kirk Gardner, DDS, Associate Professor, Department of Restorative Dentistry, University of Alabama at Birmingham, School of Dentistry, Birmingham, AL 35294. Copyright 1996 by W.B. Saunders Company
ance types. One is used for unilateral cleft palate/cleft lip and the second type for bilateral cleft palate/cleft lip. The appliances are referred to as orthopedic appliances because they primarily move bony segments. The unilateral cleft palate/cleft lip appliance, also called the Dento-Maxillary Advancement Appliance (DMA; Cleft Palate Appliances, West London, Ontario, Canada) (Fig 1) is an appliance which is pinned into place using four surgical steel pins that are placed 4 mm inferiorly to the eruption lines of the alveolus at a 23 to 24 angle, two for each segment. The larger segment and smaller segment are attached together by way of a bar with two hinged riveted bars that are attached to the alveolar segments by way of two acrylic base plates. A screw is attached to the smaller segment and the top of the screw is placed in a cup on the posterior palatal aspect of the larger alveolar segment. The screw is turned clockwise once a day after the appliance has been placed. This rotates the two segments together to reduce the space between the alveolar segments to less than 1 mm. This also reduces the space between the two lip segments. After 4 weeks, the surgeon removes the appliance, closes the lip, and closes the space between the two alveolar segments with a periosteal gingiplasty to allow bone to grow between the two segments and restore growth potential to the maxillary arches. Six months after this closure has been accomplished, the hard and soft palate are closed. At this time, the child has oralpharyngeal competence.
The Bilateral Latham Appliance

The bilateral Latham appliance (Elastic Chain Premaxillary Repositioning Appliance [ECPR]
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orly until the three segments are close together. This movement allows for closure of the lip and the ridges in one surgery, and 6 months later the closure of the palatal defect is performed. This repositioning and realigning at an early age allows for restoration of arch position and allows for future alignment of the dentition by the orthodontist. This allows for simple replacement of the lateral incisor in the unilateral patient, or the incisors for a bilateral patient.
Speech Aids
The speech aid4 replaces hard and soft tissue of the hard and soft palate and obturates the congenital defect for elimination of velopharyhngeal insufficiency. These aids are held in position by a correctly designed removable partial denture framework. However, in the child with a growing maxillary arch, a transitional appliance is often made using wrought wire retentive arms, ball clasps, and orthodontic resin to reduce cost. Tooth retention may also be enhanced by making retentive supra bulge, infra bulge areas on the deciduous and permanent teeth. Acid etch composite buildup of these areas on inappropriately contoured or partially erupted teeth will greatly improve the retention and stability of the partial denture base. The speech aid is then molded physiologically by the prosthodontist and the patient. Dental compound is added and built so that it may coexist with the lateral and posterior pharynx to allow closure of that area while not interfering with the tongue during swallowing. For molding of the impression, the head and neck are rotated side-to-side, the chin moved toward the chest, and the head extended backward as far as the patient can reach. The molding compound is then reduced and a low fusing wax is used to achieve the definitive impression of the pharyngeal area extending backward in the palatal plane to the pharyngeal tubercle of the posterior pharyngeal wall. Once a silicone cast is fabricated, the compound and impression are removed from the acrylic base. The framework is then positioned on the silicone cast and orthodontic acrylic is sprinkled onto the cast in the area of the speech aid to fabricate the finished prosthesis (Fig3). 5
Figure 1. Latham dento-maxillary advancement appliances. Cleft Palate Appliances) (Fig 2) is completely different in design and function. The bilateral appliance widens the two posterior segments and an elastic chain pulls the anterior segment posteri-
Figure 2. Latham elastic chain premaxillary repositioning appliance.
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Restorative Treatment Options in the Permanent Dentition

The Over-partial Denture In the past one of the most popular methods of treatment for both unilateral or bilateral cleft palate patients was the use of the over-partial denture.7 A large number of older cleft palate patients have had soft tissue grafted between the bony segments which eventually contracted and pulled the segments together. Because the segments did not have bony union, they grew separately thereby possibly decreasing the growth potential of the arch. The result was a normalsized mandible and a small maxilla. This has been referred to as a pseudo Class III interarach relationship. Prosthodontic restoration of patients with this type of maxilla uses the over-partial denture to restore both lip support and occlusion. The maxillary arch and remaining teeth are usually in a crossbite relationship with the mandibular arch. The over-partial denture uses a framework that attaches to the remaining teeth by way of a major connector with retentive arms on the teeth. The framework also has a retentive mesh buccally and labially to retain the anterior and posterior denture teeth. Using this type of prosthesis is a prosthetic solution for the pseudo Class III relationship and enables teeth to be placed for esthetics, phonetics, and occlusion. (Figs 4 and 5)
Figure 3. Speech aid prosthesis.
Contraindications of a Speech Aid Prosthesis

1. Feasibility of surgical repairs by way of a pharyngeal flap surgical repair. When surgical repair can be accomplished, it is the method of choice.6 2. Mental retardation. A retarded patient may not be a compliant patient. Compliance is essential for proper care and use of the speech aid appliance. 3. Uncooperative patients and parents. Again, compliance and cooperation by the patient and parents is essential for proper rehabilitation with the prosthesis. 4. A patient with uncontrolled dental caries. A prosthesis could complicate home care. 5. Lack of a trained prosthodontist to construct the speech aid. The construction of a speech aid is a sophisticated process that requires careful attention. The decrease in use of a speech aid prosthesis for cleft patients is the result of pharyngeal flap surgical procedures which eliminates oral-pharyngeal inadequacy. The goal of the maxillofacial prosthodontist is to have cleft palate patients who will eventually only require minimal fixed or removable prosthodontic intervention to restore the cleft patient to optimal function.
Figure 4. Pseudo Class III patient without maxillary overpartial denture.
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three-unit bridge is the preferred treatment in these situations. Implant Prosthodontics A bone graft and implant replacement is an alternative option. However, cleft patients have often had many surgical procedures and they sometimes prefer a three-unit fixed partial denture to any further surgical rehabilitation. When the patient does select the implant restorative implant option, a surgical stent is constructed by the restorative dentist for optimal implant placement. The central incisor and cuspid teeth may still require reshaping by means of porcelain fused to metal crowns, porcelain veneers or composite resin reshaping of the distal aspect of the central incisor and mesial aspect of the cuspid teeth. The implant used in the replacement should be a hex-lock type to prevent rotation of the replacement crown placed on the implant. The soft tissue over the implant area must often be thinned so that esthetic abutments may be used. Many of the implants, have been designed for esthetic anterior abutments, that create ideal tissue emergence profiles for implant restorative prosthetics. Implants may be a preferred method for the patients who wish to be restored to an optimal level of function. Restoration Examples Figure 6 shows a repaired young adult unilateral cleft patient who has had surgical repair and
Figure 5. Pseudo Class III patient with maxillary overpartial denture.
Fixed Prosthodontic Rehabilitation of the Cleft Palate Patient Advancements in surgical, orthopedic, and orthodontic treatments of the maxillary arch has reduced the need for restorative procedures previously required for unilateral and the bilateral cleft palate patients to a more conventional prosthodontic approach. The unilateral cleft palate patient often has a missing lateral incisor tooth and the bilateral patient often has missing maxillary lateral incisor teeth bilaterally. After orthodontic treatment, the resultant lateral incisor space that remains is usually slightly larger than the size of a normal lateral incisor tooth. A three-unit fixed partial denture is preferable as a replacement in these patients because a more optimal shape and form can be restored to the abutment teeth, which are sometimes mottled and discolored, at the same time as replacing the missing lateral incisor tooth. In addition, by increasing the abutment tooth size mesiodistally, the lateral incisor replacement pontic may be decreased in size. Furthermore, occlusion may be optimally restored when using the three-unit fixed partial denture by allowing for appropriate overbite and overjet relationships. Acid-etch resin bonded replacement of the lateral incisor does not allow the restorative options that a fixed partial denture allows. The acid-etch bonded replacement does not permit reshaping of the abutments nor optimal occlusal changes that may be indicated. For these reasons, the fused
Figure 6. Fixed partial denture unilateral.
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four incisor teeth. A definitive removable partial denture would ultimately be fabricated. The female cleft lip and palate patient may have a slight depression in the upper lip area that can be hidden with the use of camouflage cosmetics.7 The scar can be hidden by camouflage cream, proper use of lip liner, and by applying contour shadow along the sides of the nose, and blending those together. For these purposes, a cosmetologist is most useful in order to achieve an optimal result.
Conclusion
In the future, with surgical, orthodontic, and prosthodontic advancements, the cleft palate/ cleft lip patient will no longer be treated as a complex prosthodontic patient, but rather as a conventional fixed partial denture, single tooth implant, or removable partial denture patient. With early intervention by the cleft palate team and with appropriate education of the public, patients can be restored to optimal esthetics and function.
Figure 7. Bilateral transitional removable partial denture.
orthodontic treatment. The definitive prosthodontic treatment of a three-unit fixed partial denture was chosen to redistribute tooth size as well as repair a misshapen left central incisor tooth. Gingival porcelain was also used to reshape a gingival groove in the alveolus for esthetics. The finished fixed prosthesis restores optimal function and esthetics. Figure 7 illustrates a 16-year-old patient who has undergone surgical repair of lip, alveolus, and palate for a bilateral cleft lip and palate and who also had had a pharyngeal flap in addition to orthodontic correction of her permanent dentition. She had some remaining small fistulae in the palate and alveolus which were sealed by conventional palatal coverage using a removable partial denture framework. A transitional partial denture was constructed with ball clasp retention which served as both a retainer following removal of the orthodontic bands and as replacement for the
References
1. Harkins CS. Principles of Cleft Palate Prosthetic. Philadelphia, PA: Temple University Publications by Columbia University Press, 1960:5. 2. Kaepp-Baka H. Cleft Lip and Palate. In: Graff WC, Rosenstein SW, Bzoch KR, editors. Boston: Little Brown, 1971:110. 3. Latham RA. Orthopedic Advancement of a Cleft Maxillary Segment: A Preliminary Report. Cleft Palate J 1980;17:122130. 4. Beumer J III, Curtis TA, Firtell DN. Maxillofacial Rehabilitation Prosthodontic and Surgical Considerations. St. Louis, MO: Mosby, 1979:276-286. 5. Gardner LK, Rahn AO, Parr GR. Using Vinyl Polysiloxane in the Altered Cast Procedure for Speech Aid Prosthesis. J Prosthet Dent 1990;63:62-64. 6. Mazaheri M. Prosthodontics in Cleft Palate Treatment and Research. Report read before the American Prosthodontics Society. Atlantic City, NJ, October, 1963. 7. Makeover MM. Miracles: A Before and After Guide to Corrective Makeup, Cosmetic Surgery and Anti-Aging Strategies. New York: Crown Publishers, 1994:64.

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Vol 3 No 1 (March 1997) INTERDISCIPLINARY INTERACTION

Vol 3 No 2 (June 1997) ORTHODONTICS AND THE LAW

Vol 1 No 3 (September 1995) EARLY ORTHODONTIC TREATMENT

Vol 2 No 1 (March 1996) ORTHODONTICS/PERIODONTICS

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Seminars in Orthodontics, Vol 2, No 3 (September), 1996: p 161

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The Incidence. Classification, Etiology, and Embryology of Oral Clefts

Seminars in Orthodontics, Vol 2, No 3 (September), 1996: pp 162-168

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Incidence and Etiology of Oral Clefts

Classification of Oral Clefts

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Thornton, Nimer, and Howard

General Population Third-degree^ Relatives

Risk of Malformation Threshold

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Embryology of Oral Clefts

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Thornton, Nimer, and Howard

24. 25. 26.

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Seminars in Orthodontics, Vol 2, No 3 (September), 1996: pp 169-184

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A Comparison of Treatment Results

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A Comparison of Treatment Results

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A Comparison of Treatment Results

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