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Management of cleft lip and palate 1. /certified fixed orthodontic courses by Indian dental academy


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Management of cleft lip and palate 1. /certified fixed orthodontic courses by Indian dental academy

  1. 1. MANAGEMENT OF CLEFT LIP AND PALATE INDIAN DENTAL ACADEMY Leader in continuing dental education
  2. 2. Introduction Etiology and Pathogenesis of Clefting Epidemiology of Cleft lip and Palate Classification of Cleft Lip and Palate Prenatal Diagnosis of Cleft Lip and Palate. Neonatal Care and Guidelines for Feeding. Maxillary Orthopedics
  3. 3. Introduction  Clefts of the lip and palate are the most common craniofacial birth defects and are among the most common of all birth defects.  Although the severity of the defect varies, multidisciplinary treatment is often required.  Recognized way back in Ancient China (A.D. 390), where the annals of the Chin dynasty recorded the surgical repair of cleft lip, along with detailed post-operative instructions for optimal results.
  4. 4.  In many countries, craniofacial teams have been established in order to provide comprehensive care to the cleft patient.  The orthodontist is required to work collaboratively with the team in order to determine the appropriate timing and sequencing of treatment, in the context of the patient’s other health care needs.
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  6. 6. Etiology and Pathogenesis of Orofacial clefting I. Genetics:  There is much evidence to support the view that genetic factors are associated with oro-facial clefting.  In twins with cleft lip-palate, concordance is far greater for monozygotic twins (40%) than for dizygotic twins.(4.2%)  In twins with isolated cleft palate, concordance is also higher for MZ twins(355) than for DZ twins (7.8%)  Though clefts occur sporadically, some families have more than one individual affected with clefts.
  7. 7.  A. Single gene etiologies:  There are almost 300 syndromes which have a cleft of the lip and palate as a feature.  Out of these, about 150 syndromes are due to Mendelian inheritance of alleles at a single genetic locus.  Great strides have been made in the past few years in mapping genes for such Mendelian disorders.  About 50% : Autosomal recessive.  40% : Autosomal dominant  10% : X linked inheritance.  Out of 150 Mendelian clefting syndromes, about 30 genes have been cloned.
  8. 8.  GL13  7p13  PAX3  2q35  SIX3  2p21  SOX9  COL2A1 etc……
  9. 9.  B. Chromosomal anomalies:  Orofacial clefting is seen as part of phenotype in wide variety of chromosomal rearrangements, including trisomies, deletions, duplications, microdeletions or cryptic rearrangements.  E.g. deletion of 4p (Wolf-Hirschhorn Syndrome), 4q or 5p (Cri-du Chat syndrome) trisomy of 13 or 18, etc.  Role of small rearrangements such as microdeletions, cryptic rearrangements in cleft etiology is important as they are often transmitted within families.
  10. 10.  Micro-deletion of 2q11.2 is now known to be the common etiology for three different syndromes with cleft of secondary palate as a frequent feature.  DiGeorge Syndrome  Velocardiofacial syndrome  Conotruncal anomaly face syndrome. One reason for mapping and cloning genes for syndromic forms of clefting is to help develop strategies for delineating the etiology of nonsyndromic form of clefting, which is by far much more common.
  11. 11. C. Non-syndromic orofacial clefts:  Early estimates of genetic contribution to non- syndromic orofacial clefts ranged from 12-20%, with remainder attributed to environmental factors.  Recent studies estimate the genetic component to be much higher: 20-50%.  Two general approaches: Large scale family studies and Linkage studies with specific genetic markers have been carried out.
  12. 12.  Though there is consistent evidence from family studies, of inheritance at a single major locus, the hypotheses of multiple interacting loci or genetic hererogeneity cannot be ruled out.  Until recently, non syndromic clefting was thought to follow the Multifactorial threshold model, in which environment played an important role.  Recently, linkage analyses have shown candidate loci on seven chromosomes (1, 2, 4, 6, 14, 17, 19) to have positive linkage with CL/P, CP or both.  In addition, genome-wide scans suggest that 3-14 genetic loci may be involved in non-syndromic clefts of primary and secondary palate.
  13. 13. II. Teratogens:
  14. 14.  Cigarette smoking appears to be correlated with clefting and may act alone or synergistically with TGF-α.  Dietary supplements of folic acid are known to reduce the frequency of neural tube defects; possibly folic acid supplements may also reduce the frequency of orofacial clefting.  Mills et al found that prevalence of mutation of methylene tetrahydrofoliate reductase was higher in cleft populations than in the general population.  Thus, impairment of folate metabolism may play a role in the etiology of orofacial clefting.
  15. 15. III. Embryonic basis of orofacial clefting: Parent sex cells unite Zygote formation 2 weeks of rapid proliferation directed partly by Homeobox genes. Bilaminar disc (2 distinct germ layers) Gastrulation (during 3rd week) Trilaminar disc ( 3 germ layers) Neurulation (during 3rd week). PAX6, SHH, FGF signaling Neural plate is derived from ectoderm and extends along long axis of the disc
  16. 16.  Problems in development at this time may result in midline neurologic and craniofacial malformations such as holoprosencephaly, cycloplegis, neural tube defects, midline orofacial clefts. Neural crest cell formation, migration and differenciation:  The ectodermal-derived cells that are found in the margins of the bilateral neural folds and the transition zone between neuro-ectoderm and epidermis.  They migrate as mesenchyme into the embryonic processes of the developing head and neck region, giving rise to diverse neural, skeletal, connective tissue, dental, cardiac, pigment cells.
  17. 17.  Their migration is predetermined in part by interactions with hindbrain neuromeric segments called rhombomeres and paraxial mesoderm segments called somatomeres.  Timing and extent of NCC migration is dependent on a complex patterning of inductive homeobox gene (HOX, MSX) signaling.  Deficiencies in NCC migration or proliferation produce a variety of craniofacial malformations: von Recklinghausen’s Neurofibromatosis, Hemifacial microsomia, Orofacial Clefts, DiGeorge and Treacher Collins syndromes.
  18. 18. Craniofacial development:  Primitive craniofacial complex forms during week 4 post conception.  A series of inductive events between prosencephalon, mesencephalon, rhombencephalon and migrating NCC’s helps to form the five facial prominences (the frontonasal and bilateral maxillary and mandibular prominences)  Movement and destination of NCCs into facial primordia are controlled by a number of gene familes including HOXa1, HOXa2, HOXb1, HOXb3, HOXb4, SHH gene, OTX gene, GSC, DLX, MSX, LHX, PRRX genes.
  19. 19. Fusion of facial processes
  20. 20.
  21. 21.  Clefting of upper lip and primary palate:  The upper lip is formed mainly by contributions from the medial nasal process and the maxillary processes, and from lateral nasal process during 6th week of development  The lateral nasal processes contribute mainly to the outer parts of the nose.  Fusion of these processes requires critically timed co-ordination of growth between the processes, exact spatial localization, and apoptosis of the epithelium that forms the transient nasal fin.
  22. 22.
  23. 23.
  24. 24.  Since fusion of these processes also creates the area of alveolar ridge containing central and lateral incisors, abnormal development of the nasal fin may be involved with clefts of the primary palate.  Primary palatal clefting occurs most commonly at the incisive fissure that separates the lateral incisors and the canine teeth. They may present with dental displacement or dental agenesis, as well as delayed ossification and decreased volume of premaxilla and anterior basal bone of maxilla.
  25. 25.  Clefting of secondary palate:  The secondary palate is formed by the fusion of the two lateral palatal processes projecting medially from the maxillary processes.  Requires a complex interaction of palatal shelf movements, critically timed growth co-ordination between the processes, and apoptosis of epithelium along the medial margins of the palatal shelves.  Begins at 8 ½ weeks in utero.
  26. 26.
  27. 27.  Defects of the secondary palate are expressed as failures of elevation, failures of contact and adhesion, or failures of fusion resulting in clefts. Factors which may limit shelf contact include:  Delay in shelf movement to horizontal position.  Reduced palatal shelf size  Deficient extracellular matrix accumulation  Delayed achievement of mandibular prominence  Head extension  Abnormal craniofacial morphology
  28. 28.  Abnormal 1st arch development  Tongue obstruction to shelf movement, secondary to mandibular retrognathia  Amniotic sac rupture leading to severely constricted fetal head and body posture.
  29. 29. Epidemiology of Cleft Lip and Palate  CL + P is etiologically distinct from isolated cleft palate, except in cases where genetic isolates are inbred and in syndromes like van der Woude’s syndrome. CL + P prevalence rates vary from population to population.  Indians: 1.25 / 1000.  Manipal: 1.23 / 1000 (Valiathan, Dawoodbhoy I, Oberoi S (JPFA 1996)  White Caucasians: 1/ 1000.  Japanese: 2.1 / 1000  Blacks: 0.3 / 1000 (Lowest)  Afghans: 4.9 / 1000
  30. 30.  CL+ P is more common in males  More severe the defect, greater is the proportion of males affected. (For CL+ P, the M:F ratio is 2:1, while for CL alone the M:F ratio is 1.5:1)  Unilateral cleft lip occurs twice as commonly on the left side than on the right side.  10-30 % of cases 10-30% of cases are associated with skin bridges called Simonart’s bands.  There is a positive family history in 40% of cases.  Also there is an increased prevalence associated with consanguinity and increased maternal age.
  31. 31. Isolated Cleft palate:  This is less common as compared to CL+ P.  Prevalence rate in Blacks as well as Whites is 0.4 / 1000.  In Indians it is 0.46 per 1000 live births.(Valiathan et al, JPFA 1996)  Females are affected twice as commonly as males.  Associated more commonly with congenital malformations.  There is a positive family history in 20% of cases.  Not linked to maternal age.
  32. 32.  Variations such as bifid uvula occur more frequently than isolated CP (1 in 80 White individuals.)  Submucous cleft palate: 1 in 1200 to 1 in 2000 live births.
  33. 33. Classification of Clefts of Lip and Palate 1. Davis and Ritchie (1922): Congenital clefts were divided into 3 groups according to the position of the cleft in relation to the alveolar process. Group I : Pre-alveolar clefts, which could be unilateral, bilateral or median. Group II: Post-alveolar clefts involving the soft palate only, the soft and hard palate, or a submucous cleft. Group III: Alveolar clefts, unilateral, bilateral or median.
  34. 34. 2. Veau’s Classification ( 1931): He suggested a classification divided into 4 groups: Group 1: Cleft of the soft palate only. Group 2: Cleft of hard and soft palate extending no further than the incisive foramen, thus involving the secondary palate alone. Group 3: Complete unilateral cleft of soft and hard palate, alveolar ridge and lip. Group 4: Complete bilateral alveolar cleft , usually associated with bilateral clefts of the lip.
  35. 35.
  36. 36. 3. Kernahan and Stark (1958): They recognized the need for a classification based on embryology rather than morphology. The division between the primary and secondary palates is the incisive foramen. They divided clefts as follows: A. Incomplete cleft of the secondary palate. B. Complete cleft of secondary palate. C. Incomplete cleft of primary and secondary palates. D. Unilateral complete cleft of primary and secondary palates. E. Bilateral complete cleft of the primary and secondary palates.
  37. 37.  Pic of kernahan and stark
  38. 38. 4. Kernahan’s Striped Y Classification: The incisive foramen is the reference point. Stippling of the involved portion of the Y provides rapid graphic representation of the original pathologic condition, and lends itself to computer graphic representation
  39. 39. Blocks 1 and 4: Lip. Blocks 2 and 5: Alveolus. Block 3 and 6: Hard palate anterior to incisive foramen. Block 7 and 8: Hard palate posterior to incisive foramen. Block 9: Soft palate.
  40. 40. 5. Schuchardt and Pfeiffer’s symbolic Classification This classification makes use of a chart made up of a vertical block of three pairs of rectangles with an inverted triangle at the bottom. The inverted triangle represents the soft palate while the rectangles represent the lip, alveolus and the hard palate as we go down. Areas affected by clefts are shaded on the chart.
  41. 41. 6. Lahshal Classification (Okriens, 1987) Lahshal is a paraphrase of the anatomic areas affected by the cleft. Based on the fact that clefts of the lip, alveolus and hard palate can be bilateral, while clefts involving the soft palate are usually unilateral Areas involved in the cleft are denoted by specifically indicating the alphabet standing for it. For example, L - - S - - - stands for cleft of right lip and the soft palate. LA - S - - L stands for cleft of the right lip, alveolus and soft palate together with left cleft lip.
  42. 42. 7. American Cleft Lip and Palate Association Classification (Harkins et al 1982) 1. Clefts of Prepalate: This is further subdivided into clefts of lip, clefts of alveolar process, which may be unilateral, bilateral or median. Includes description of antero-posterior extent of the defect in thirds. 2. Clefts of Palate: Further subdivided into clefts of soft palate, hard palate, and includes description of the extent of the cleft antero posteriorly in thirds, and width in mm. 3. Clefts of prepalate and palate: Any combination of clefts described under clefts of prepalate and clefts of palate.
  43. 43. 8.Tessier’s Classification of Unusual Craniofacial Clefts (1976)  Anatomic and descriptive classification system for more complex orbitofacial clefts.  Numbers are assigned to the site of clefting depending on their relationship to the sagittal midline.  Both soft tissue and bony clefts are described.
  44. 44.
  45. 45.
  46. 46. Diagnosing Cleft Lip and Palate  Cleft lip and palate may be diagnosed by prenatal ultrasound, which has become more common because refinements of the diagnostic tool provide images by which congenital and developmental anomalies may be detected more clearly.  It gives the parents the opportunity to be prepared for the birth of an infant with a facial anomaly.  Prenatal counseling provides patients with a level of awareness and realistic expectations at time of
  47. 47.  With the help of prenatal ultrasonography 2223% of clefting cases can be detected.  Cleft lip is easier to diagnose sonographically than cleft palate.  A recent study showed a 73% detection rate for fetal cleft lip with ultrasonography.  Prenatal detection of cleft palate with this technique is much lower (1.4%)  Detection rate for fetal cleft lip is improved greatly if USG is performed after 20 weeks of gestation.
  48. 48.
  49. 49. Limitations of ultrasound technique for diagnosing orofacial cleft include:  Unfavorable position of fetus  Hand or umbilicus overlying the face  Maternal obesity  Presence of multiple gestation  Reduced amniotic fluid  Prior abdominal surgery  Additional fetal abnormalities
  50. 50.  Three dimensional ultrasonography imaging is a new technique that presents views of the fetal face with greater clarity than conventional 2D imaging.  Its sensitivity in diagnosing cleft lip and palate is considerably greater than 2D imaging. (Johnson et al, Radiology, 2000)
  51. 51. Advantages of Prenatal Cleft Diagnosis:  Psychological preparation of patients  Education of parents on management of cleft  Preparation for neonatal care and feeding.  Opportunity to investigate for other structural or chromosomal abnormalities  Increased choices for patients on whether to continue the pregnancy.  Possibility for fetal surgery  Ability for the plastic surgeon to prepare a plan of management, once the sonologist characterizes the specific type of cleft.
  52. 52.  Disadvantages:  Higher maternal anxiety  Potential for a decision to terminate the pregnancy even in the absence of other malformations.
  53. 53. Fetal surgery and Cleft lip and Palate (From Papadopulos et al, Br J Plastic Surg 2005)  Open fetal surgery has been performed in only a few centers around the world, for life threatening conditions of the fetus which were diagnosed by ultrasound.  Disadvantages include its invasiveness, induction of premature labor and fetal death.  Recent advances in endoscopic surgery may allow keyhole access to the amniotic sac and reduce morbidity of fetal surgery.  As the techniques improve, fetal surgery could also be applied to non life threatening malformations.
  54. 54.  This would be advantageous because wound healing in the fetus takes place without the formation of a scar or callus.  In addition maxillary growth restrictions could be prevented.  In the last 2 decades extensive research has been done on rabbits and sheep, with considerable success in repair of surgically created clefts in the fetus.  However, the authors state that there are still too many unsolved problems with intra-uterine surgery, which make it ethically unjustifiable in humans, at present.
  55. 55. Neonatal Care and Feeding Guidelines  It is important to address parental anxiety and trauma  Early contact and counseling  Explanation of normal and altered anatomy and physiology can guide toward successful feeding.  The normal process of feeding involves sucking and swallowing.  In patients with cleft lip with alveolus, it is not a problem and can be achieved with slight adjustments such as placing a finger over the cleft. This creates negative pressure inside the oral cavity and results in effective swallowing.
  56. 56.  In cleft palate patients this pressure cannot be built up as air is drawn out through the defect to the nose.  A variety of nipples and feeding devices are available which include; Lambs nipple, enlarged cross cut nipple, Mead Johnson Cleft palate nursing bottle. Guidelines during feeding:  The infant is positioned at 45-60 degrees angle to decrease nasal regurgitation.  The nipple is directed to the intact part of the palate.  The child is burped frequently because of excessive air swallow.
  57. 57.  Adjust the flow of milk to the ability of the child to swallow.  Observe the child for choking, cyanosis and abdominal distension.  Use feeding appliances if required. Feeding appliances:  These should be considered if other methods are not successful in the first two weeks. They seal the oro-nasal fistula and enable the child to suck by negative intra-oral pressure.  Can be constructed by an orthodontist, pedodontist or prosthodontist or general dentist.
  58. 58.  Procedure:  Alginate impression: the tray should extend from maxillary frenum at the cleft lip site, posteriorly past the end of the alveolar ridges into the palate, and laterally to include the lateral mucobuccal fold.  In bilateral cleft applainces the finish line is not placed in the anterior area. The bilateral segments are supported uniformly from the lateral position which allows premaxilla to drift posteriorly under lip pressure.  The cleft area and superior aspect of nasal passage should be waxed out during fabrication of the plate.  A small hole should be placed anteriorly in the plate to tie a dental floss to the appliance.
  59. 59.
  60. 60. Other considerations:  Airway assessment  Monitor weight gain  Complete medical and genetic evaluation to identify any syndrome  Audiology and otology evaluation  Plan surgical repair
  61. 61. Maxillary Orthopedics / Naso-alveolar molding.  Cleft lip and palate can present with considerable variation in severity and form.  Generally, the wider more extensive clefts are associated with more significant nasolabial deformity.  These clefts, deficient in hard and soft tissue elements, present a significant surgical challenge to achieve a functional and cosmetic outcome.  From a surgical viewpoint, chances of achieving a finer surgical scar, good nasal tip projection and more symmetrical ,well defined nasolabial complex would be better if the infant presents with a minor cleft deformity.
  62. 62. A fine scar forms when a surgical incision heals under less tension.  Thus, the principal objective of presurgical nasoalveolar molding (NAM) is to reduce the severity of the initial cleft deformity.  This enables the surgeon and the patient to enjoy the benefits associated with the repair of a cleft deformity which is of minimal severity.  Neonatal maxillary orthopedics is usually initiated during the first or second week following birth, in absence of other medical complications, and may be carried out by the orthodontist, the pedodontist, or the prosthodontist.  However, there is still a lack of agreement on early management due to the lack of controlled studies that show better outcome with maxillary orthopedics.
  63. 63. Historical perspective:  Numerous techniques have been documented over the centuries to improve the position of cleft alveolar segments.  In 1686, Hoffman described the use of a head cap with arms extended to the face to retract the premaxilla and narrow the cleft.  The modern concept of an intra-oral device to reposition the cleft alveolar segments was introduced by McNeil (Univ. of Glasgow) in 1950. Through a series of acrylic plates, the segments were actively molded into the desired position
  64. 64.  In 1969, Rosenstein introduced the concept of passive control of cleft segments. Through the use of a passive appliance, the continuous force of the repaired lip could be used over time to attain a more normal arch contour, with the cleft segments coming together to form a butt joint.  In 1975, Georgiade and Latham introduced a pinretained appliance to simultaneously retract the maxilla and expand the posterior segments over a period of days.  Hotz (1987) described the use of a passive orthopedic plate to slowly align the cleft segments without retracting the maxilla. He felt that by the age of 10, the face would grow forward into appropriate balance with the premaxilla.
  65. 65.  During the 1980s, original research for molding cartilage was performed by Matsuo. He recognized that the cartilage in the newborn is soft and lacks elasticity. This was attributed to high level of estrogen at the time of birth, which in turn led to increased hyaluronic acid levels  Hyaluronic acid inhibits the linking of the cartilage intercellular matrix, and may be necessary to relax ligaments, cartilage and connective tissue enabling the fetus to pass through the birth canal.
  66. 66.  The level of estrogen begins to decline immediately after birth.  Matsuo used a stent in the form of silicone tubes to shape the nostrils.  Grayson (1993) adapted the nasal stent to extend from the anterior flange of an intraoral molding plate. Advantages of this method are: Skillful application of force for nasal molding, and no need for intact nasal floor.
  67. 67.  The popularity of maxillary orthopedics was well accepted in the 1960’s and 1970’s, to eliminate the need for subsequent orthodontic treatment.  Later reports suggested that although the initial results of lip repair were easier to attain with cosmetic improvement, there was no long term benefit on the growth of the midface and dento-alveolus.
  68. 68.  Additionally, early or primary bone grafting associated with maxillary orthopedics at time of primary lip repair may have compromised the long-term follow up of treated patients.  Thus, the use of neonatal orthopedics before primary surgical lip repair became a matter of controversy between clinicians.  The current perspective is that neonatal maxillary orthopedics, when provided as an adjunctive procedure to primary definitive lip repair, does have presurgical benefits.
  69. 69.  In general, appliances for use in cleft care can be classified as follows:  Presurgical and Postsurgical  Active and passive.  Extra-oral and intra-oral.  Huebner and Liu( Clinics in Plastic Surgery 1993) advocated the use of passive acrylic appliances to mold the alveoli under pressure from the repaired lip.  In case of unilateral cleft with severely rotated cleft segment and collapse of arch, they use an active appliance with a jackscrew prior to lip closure.
  70. 70.
  71. 71. Grayson’s Technique for Naso-alveolar molding (Clin Plastic Surg 2004) Objectives:  Reduce the severity of initial cleft deformity.  Lip segments almost in contact at rest.  Symmetrical lower lateral alar cartilages.  Adequate nasal mucosal lining.  Uprighting of inclined columella.
  72. 72.  In infants with bilateral clefts of lip, alveolus and palate, aims are non-surgical elongation of the columella, centering of premaxilla, and slow gentle retraction of the premaxilla to achieve continuity with posterior cleft segments.  Additional objectives are reduction in width of nasal tip, alar base.
  73. 73. Procedure:  Heavy bodied silicone impession material is used to take initial impression as soon after birth as possible, when cartilage is plastic and moldable.  Infant is held upside down by surgeon and the impression tray inserted into the oral cavity, seated till impression material just starts to extrude past posterior border.  A stone model is poured, and a molding plate fabricated on it with clear hard acrylic lined with a thin layer of soft denture material.
  74. 74.  Care should be taken to relieve the plate in area of labial frenum and other areas likely to ulcerate.  Parents are instructed to keep the plate in full time and take it out for cleaning once a day.  The appliance is secured extra-orally to the cheeks and bilaterally by surgical tapes, with an orthodontic elastic band at one end.
  75. 75.  The elastics loop over a retention arm extending from the anterior flange of the plate at 45º to the horizontal.  This prevents unseating of the appliance; tapes are changed once a day.  The retention arm is positioned at a point on the labial border of the plate corresponding to the junction of the cleft lip segments, when pulled together. Vertically it should be at junction of upper and lower lips at rest.
  76. 76.  Weekly visits are required to modify the molding plate.  Closure of the alveolar gap brings the lip segments together, reduces the nasal base width, and introduces laxity of the alar rim.  Care should be taken not to add the nasal stent before achieving laxity of the alar rim, else increase in nostril circumference may result.  Elastics attached to the retention arm should exert a force of approximately 2 oz. Retraction of premaxilla as in bilateral clefts requires higher force levels.
  77. 77.  Lip taping: At the 3rd visit, the parents are instructed to place tapes to approximate the cleft lip segments. Tape should be applied at the base of the nose, on the non-cleft side first, then pulled over and adhered to the cleft side.  Philtrum and columella should be brought to the midline.  Note: Taping too low can cause undesirable horizontal lengthening of the lip over time.  Advantage: Lip taping provides some of the benefits of a surgical lip adhesion without the associated surgical morbidity, cost, and scarring.
  78. 78.
  79. 79.  The Nasal Stent: When the cleft alveolus is reduced to 5 mm or less, the nasal stent is added.  The stent is made of 0.036 gauge round stainless steel wire and takes the shape of a swan neck.  It is attached to the base of the retention arm, extends forward and then curves backward entering 3-4 mm past the nasal aperture.
  80. 80.  As the wire extends into the nostril, it is curved back on itself to create a small loop for retention of the intranasal portion of the nasal stent.  This is a hard acrylic kidney shaped component, with an added layer of soft liner
  81. 81.  The upper lobe enters the nose and gently lifts the dome till moderate tissue blanching is seen.  The lower lobe lifts the nostril apex and defines the top of the columella.  In the patient with bilateral clefts, there is a need for two retention arms and two nasal splints.Fabrication steps are same as described for a unilateral cleft.  In addition, a horizontal “prolabial band” of soft denture material is added to join the lower lobes of the two stents, spanning the base of the columella.
  82. 82.
  83. 83. A vertical tape from the prolabial band extends downward to engage the retention arms with elastics. This helps to lengthen the columella nonsurgically.
  84. 84.
  85. 85. Complications associated with Naso-alveolar molding:  Irritation of oral mucosal or gingival tissue.  Heavy application of force by upper lobe of nasal stent, resulting in inflammation of nasal mucosal lining.  Notching of alar rim due to incorrect position or shape of lower lobe of nasal stent.  Irritation of cheeks due to adhesive tape. The tape should be removed slowly or gently, or warm water may be used. Else, a skin barrier can be used as a base for the elastic attachment.  Taping the arms too horizontally or with inadequate activation may lead to posterior dislodgement of the plate.  A 5 mm hole can be placed in the palatal portion of the plate to maintain airflow.
  86. 86. Recent studies on maxillary orthopedics: Long term effects of naso-alveolar molding on three dimensional nasal shape in unilateral clefts (Maull et al Cleft Palate and Craniofacial J Sept 1999) A study done on 10 subjects who underwent presurgical orthopedics till the age of 4 months when primary surgery was done. The authors reported that presurgical naso alveolar molding significantly increase the symmetry of the nose, which is maintained long term into childhood.
  87. 87. A Randomized Prospective Clinical trial of the Effect of Infant Orthopedics in Unilateral Cleft Lip and Palate: Prevention of Collapse of Alveolar segments (Dutchcleft). Prahl et al, Cleft Palate and Craniofacial J 2003.  The authors compared two groups of infants comprising 27 each. One group received infant orthopedics, while the other did not.  From the study it was concluded that infant orthopedics in patients wuth UCLP did not facilitatate contact between maxillary segments, nor did it prevent collapse of alveolar segments.
  88. 88. References:  Marazita M, Mooney M. Current concepts in the Embryology and Genetics of Cleft Lip and Cleft Palate. Clinics in Plastic Surgery 2004; 31(2): 125-140.  Valiathan A, Dawoodbhoy I, Oberoi S. Incidence of cleft lip and palate in Manipal.- A live birth study.Journal of Pierre Fauchard Academy 1996; 10: 15-20.  Huebner and Liu. Maxillary Orthopedics. Clinics in Plastic Surgery 1993: 723-741.  Johnson DD, Pretorius Dh, Budorick NE et al. Fetal lip and primary palate: 3D versus 2D ultrasonography. Radiology 2000;21: 236-250.
  89. 89.  Johnson N, Sandy JR, Prenatal diagnosid of cleft lip and palate. Cleft Palate and Craniofacial J 2003;40: 186-194.  Maull D, Grayson B, Cutting C, Brecht B, Bookstein F. Long term effects of naso-alveolar molding on three dimensional nasal shape in unilateral clefts. Cleft Palate and Craniofacial Journal 1999;36(5): 391-397.  Prahl C, Kuipers Jagtman A, Vanthoff M, Prahl Andersen B. A randomized Prospective Clinical trial of the Effect of Infant Orthopedics in Unilateral Cleft Lip and Palate: Prevention of Collapse of Alveolar segments (Dutchcleft). Cleft Palate and Craniofacial Journal 2003; 40(4): 337342.
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  92. 92. Thank you Leader in continuing dental education