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Cleft lip and palate /certified fixed orthodontic courses by Indian dental academy


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Cleft lip and palate /certified fixed orthodontic courses by Indian dental academy

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  2. 2. INDIAN DENTAL ACADEMY Leader in continuing dental education
  4. 4. INTRODUCTION: Orofacial clefts are among the most common congenital anomalies requiring multidisciplinary care. Such anomalies include several handicaps such as impaired suckling, defective speech, deafness, malocclusion, gross facial deformity and severe psychological problems. Cleft of lip and the palate is one such condition, that occurs at such a strategic place in the orofacial region and at such a crucial time that it becomes a complex congenital deformity. Management of CLCP involves a multi disciplinary approach requiring the services of an orthodontist, oral surgeon, prosthodontist, otolaryngologist, audiologist, speech therapist, paediatrician.
  5. 5. EPIDEMIOLOGY: Cleft lip and palate is a global problem.(0.28-3.74/1000 live births globally) Least incidence in negroids(0.4%) and maximum in afghans(4.9%) Among Indians it seen maximum in Agrawal community and Brahmins(1.7%). The incidence of oral clefts is seen more in males than in females. Cleft lip alone- more in males than female Cleft palate- more in females than males
  6. 6. ETIOLOGY: 1.) Heredity: Transmitted through a male as sex linked recessive gene. Predisposition for cleft lip is 40% while only 18-20% for cleft palate. It is transferred as: a) Monogenic/ single gene disorder-conform to mendelian inheritance b) Polygenic/ multifactorial inheritance- show familial tendency but not mendelian inheritance c) Chromosomal abnormalities: - Down’s Syndrome - Edwards Syndrome (trisomy 18) - Trisomy D and E
  7. 7. SYNDROMES WITH CLEFT LIP AND PALATE Van der woude Syndrome Treacher Collins Syndrome Autosomal Dominant Cleidocranial Syndrome Ectodermal Dysplasia Stickler’s Syndrome Roberts Syndrome Appelt Stndrome Christian Syndrome Autosomal Recessive Meckel Syndrome
  8. 8. 2.) Environmental Factors: Usually occurs due to various influences during Ist trimester. • Environmental terratogens: -Ethyl Alcohol- causes FAS (fetal alcohol Syndrome). -Cigarette smoking- 30% increase in cleft lip and palate and 20% increase in cleft palate in smoking during pregnancy. Nicotine acts synergistically with TGF. -Anti seizure diphenyl hydantion and trimethadione.also causes growth retardation, craniofacial dysmorphism, mental deficiency
  9. 9. MALNUTRITION: Hypervitaminosis A: acute maternal exposure to 13-cis retinoic acid during first trimester causes cell death in the pharygeal arch leading to facial clefting. Vit A analogue used as an antiacne drug. Also proved by animal experiments. Folic Acid: Deficiency of folic acid affects virtually every organ system. It affect the neural tube- neural crest cell migration and differentiation. Anaemia and anorexia INFECTION DURING PREGNANCY: Rubella infection during the first 3 months associated with clefting. PARENTAL AGE: Shaw etal presented evidence that women above the age of 35 had a doubled risk of having a child with CLCP.above 39- tripled risk. Consanguineous marriages- increased risk of CLCP in child.
  10. 10.    EMBRYOLOGY The first pharyngeal arch (mandibular arch), develops two prominences: The maxillary prominence The mandibular prominence
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  15. 15.  As the medial nasal prominences merge with the maxillary prominence, they form an intermaxillary segment.
  16. 16. The intermaxillary segment gives rise to :1. philtrum of the upper lip. 2. The premaxillary part of the maxilla 3. The primary palate.
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  18. 18. Mechanism of palatal shelf elevation *Intrinsic Force within the shelf *Accumulation of Glycosaminoglycans *Accumalation and hydration of Hyaluronic acid. *Increase in vascularity *Contraction of elastic fibres or muscle fibres. *Unequal division in the palatal and the oral epithelium *Neurotransmitters like Serotonin *Increase in Vimentin expression *Master controlling gene is FSP-1,ssh,
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  21. 21. Local Factors: •Failure of the head to elevate and become erect at around the 7-9th week •Failure of the tongue to descend downwards, thus causing a mechanical interference to fusion of the palatine shelves. •Deficiency of Oxygen •Shift of Blood Supply of Face-During the 6th week, most of the midface is supplied by the Stapedial artery which is the branch of the Internal Carotid artery. At around the 7th week, stapedial artery severs from the internal carotid and its terminal branches join the external carotid artery. Delay in this vital step can lead to cleft palate.
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  23. 23. DAVIS AND RITCHIE CLASSIFICATION (1922): They classified congenital clefts based on the position of the cleft in relation to the alveolar process. Group I-Pre alveolar clefts Lip clefts only with subdivisions for unilateral, median, bilateral. Group II-Post alveolar clefts degrees of involvement of soft and hard palate to be specified till the alveolar ridge, submucous clefts included. Group III-Alveolar clefts is complete clefts of palate, alveolus ridge and lip with subdivisions for unilateral, median, bilateral.
  24. 24. II VEAU’S CLASSIFICATION (1931):  Group I Cleft of soft palate only  Group II - Cleft of hard and soft palate, extending no further than the incisive foramen thus involving the secondary palate alone.
  25. 25.   Group III - Complete unilateral cleft of soft and hard palate, lip and alveolar ridge Group IV - Complete bilateral cleft of soft and hard palate, lip and alveolar ridge on both sides.
  26. 26. III KERNAHAN’S STRIPED “Y” CLASSIFICATION (1971):   In this classification the incisive foramen is taken as the reference point “Y” logo are each divided into three sections, representing the lip, the alveolus and the hard palate as far back as the incisive foramen. The stem of the “Y” is also divided into three parts, representing varying degrees of clefting of the hard and soft palates.
  27. 27. V MILLARD’S CLASSIFICATION (1977):   A modification of Kernahan’s striped “Y” classification. . The inverted triangles represent the nasal arch the upright triangles represent the nasal floor. LAHSHAL CLASSIFICATION: L- lip A- Alveolus H- hard palate S– soft palate
  28. 28. Treatment of CLCP: A brief Overview
  29. 29. FEEDING TECHNIQUES  When a cleft lip is present, it may be difficult for the baby to make a good seal around the nipple.  Babies with cleft palate usually need special bottles and techniques to feed properly.  There are three types of bottles for feeding babies with clefts –  the Mead-Johnson Cleft Palate Nurser, the Haberman Feeder and the Pigeon Nipple:  
  30. 30. Feeding obturator  The feeding obturator is a prosthetic aid that is designed to obturate the cleft and restore the separation between the oral  and nasal cavities. It creates a rigid platform  The obturator also prevents the tongue from entering the defect and interfering with spontaneous growth of the palatal shelves.  reduces nasal regurgitation,  reduces the incidence of choking,  also helps in the development of the jaws and contributes to speech
  31. 31. INFANT ORTHOPEDICS Infant orthopedics was pioneered by Burstone at Liverpool in 1950s. Two movements were carried out- expansion of the collapsed segments and pressure against premaxilla to reposition it posteriorly to its correct position. Done by placing light elastic strap across the anterior segment that applies a contraction force. In severe cases pin retained appliances may be required. Also consists of a feeder plate with steel wires bent in to hooks incorporated into the acrylic. After active treatment for 3-6weeks,it is used a retainer. Berkowitz reported the present consensus is that these procedures offer less long term benefit than expected. Hence now used in severely displaced premaxilla cases.
  32. 32.  Displacement of segment make lip repair more difficult  Orthopaedic appliances are used to resposition the segment in early infancy, before lip closure  These appliances also act as “feeding plate” for infants Two types of orthopaedic appliances  Active: pin retained,controlled forces  Passive:
  33. 33. Naso Alveolar Moulding Nasoalveolar molding is a nonsurgical method of reshaping the gums, lip and nostrils before cleft lip and palate surgery, reducing the severity of the cleft. Surgery is performed after the molding is complete, approximately three to six months after birth.  PRESURGICAL NASO ALVEOLAR MOLDING (Grayson etal, 1999) Actively mold and reposition the deformed nasal cartilages and alveolar processes and lengthen the deficient collumella.
  34. 34. LIP CLOSURE  Surgical closure of a cleft lip is done as early in infancy as is compatible with a good long-term result.  at 10 to 12 weeks of age. Therefore PNAM should be completed by then. Techniques  Rotation-advancement technique of Millard  Delaire philosophy
  35. 35. PALATE CLOSURE Objective: • Join the cleft palatal edges, • Lengthen the soft palate, The timing of closure is controversial. Can be done early at 824 months or at 9-12year At 18-24 month Development of normal speech  Tendency towards maxillary underdevelopment At 9-12year Normal growth of maxilla with unrepaired cleft  Reduces surgical morbidity and infection Latest suggestion    Closure of soft palate –age of 12 month Help in development of Speech No growth retardation with early soft palate closure Closure of hard –age of 5-6year
  36. 36. Velopharyngeal Insufficiency  Velopharyngeal insufficiency is a disorder resulting in the improper closing of the velopharyngeal sphincter (soft palate muscle in the mouth) during speech, allowing air to escape through the nose instead of the mouth.  During speech, the velopharyngeal sphincter must close off the nose to properly pronounce strong consonants such as "p," "b," "g," "t" and "d."  The two main speech symptoms of velopharyngeal insufficiency are:  hypernasality and nasal air emission. 
  37. 37. VPD is of 3 types: a) Velopharyngeal Mislearning: due to articulation difficulties b) Velopharyngeal Incompetence: Due to functional abnormalities. (paresis, dysarthia) c) Velopharyngeal Insufficiency: Structural problems like cleft or bifid uvula etc Diagnostic Procedures   Measurement of nasal airflow McKay-Krummer instrument Aerophonoscope Fiberoptic naso-endoscopy Videofluoroscopy Voice resonation Evaluation Articualtion assessment Oral motor assessment
  38. 38. Treatment of VPI      Speech Therapy Some speech problems linked with VPI, such as mispronouncing words, can be treated by speech therapy. Treatment focuses on teaching the child the correct manner and place of articulation Sometimes an obturator is recommended to treat VPI. An obturator is like a modified dental retainer with a speech bulb or palatal lift attached to the back. Each obturator is shaped uniquely to fit the patient’s muscle movements. Speech Surgery: Palatoplasty Sphincter pharyngeoplasty
  39. 39. AIM OF TREATMENT IN CLCP PATIENTS:       To get optimum alignment. Harmonize relationship of the dental arches for speech, mastication, oral health and facial appearance. PRIMARY DENTITION STAGE : Treatment priorities is to correct crossbite by using removal plates or lingual arch. To control or eliminate oral habits, functional shift or space loss after premature loss of primary teeth Afetr the first phase, a removable retainer (atleast night time) is worn till the next phase is begun.
  40. 40.  MIXED DENTITION  A tentative decision on extraction of supernumerary teeth and overretained teeth.  Correction of cross bite- jack screw, RME, quad helix, Niti expanders  Maintain space for proper eruption of teeth.  Expand collapsed segment to improve surgical access to the graft site.  Traumatic occlusion is eliminated in preparation of alveolar graft. (By aligning offending tooth) Correction of jaw relationship- Face mask Therapy 
  41. 41.       FACE MASK THERAPY Used in mild maxillary deficient cleft patient Orthopaedic forces for maxillary protraction Orthopaedic force 350-500 gm per side over 10-12 hr / day for an average of 1215 months. Stability…….(Questionable) Because of two reasons  Counter pressure of a tight lip on the maxilla. Which inhibits its growth  Scarring in pterygo maxillary region after extensive tissue mobilization for palatal closure
  42. 42. Rationale for bone grafting  To restore physiologic continuity of arch for esthetic and hygenic replacement  To provide bone for stability of dental arch and the premaxillary segment  Bone is provided into which unerupted teeth may erupt.  At the time of placement of graft, patent oronasal fistulas can be closed  To allow orthodontic alignment of teeth  To provide support for the lip and the alar base and the nasal tip.
  43. 43. Alveolar bone grafting divided in two types: 1) Primary alveolar bone grafting: done at the time of lip closure at around 10-12 weeks. Common in 1950s. Causes hinderance in maxillary growth. 2) Secondary alveolar bone grafting: done after lip closure at later stage. This is can be dived into three: Early (2-5 years): performed in primary dentition. Rationale is to allow eruption of the lateral incisor if present. Can affect growth of midface. Intermediate (6-15years): performed in late mixed dentition time to allow the eruption of the permanent canine in the graft. There is minimal interference in growth. Late secondary alveolar bone grafting (adolescence to adulthood): Aids in replacement of missing teeth with implants.
  44. 44. CURRENT CONTROVERSIES THREE CONTEMPORARY CONTROVERSIES ARE: 1) Timing of grafting 2) The type of bone for alveolar grafting and donor site 3) Sequencing of orthodontic expansion. Favor of 8-10 year of age (when canines about to erupt-one quarter to two thirds of root complete)- Bergland etal  Erupting tooth is a potent stimulus for bone formation.  After tooth eruption is complete, it can be very difficult to induce the formation of new bone.  Prevents eruption into cleft-periodontal defect  If placed after eruption of permanent teeth then chances of damaging roots and resorption
  45. 45. EXPANSION: If Expansion done before grafting, as after the graft mature and sutures fuse it is difficult to expand maxilla later. Also Expanding the arch before grafting increases the size of cleft and thus more area for placement of bone. But increased amount of bone required and requires more soft tissue dissection for closure. Expansion can also be done 6wks after grafting. It has a potential of stimulating immature bone which may enhance graft survival
  46. 46. GRAFTING MATERIAL Autogeous  Iliac crest  Tibia  Rib  Cranial bone Advantages adequate quantity easily condensed & placed little donor site morbidity adequate volume quality similar to iliac crest for infants. inadequate quantity less resorption rapid vascularization predictable quality Allogenic grafts: it acts a scaffold into which new bone develops. Freeze dried bone( increased chances of immune reaction, HIV infection, longer post operative phase) REVASCULARISATION GRAFT IS SLOW.
  47. 47. PERMANENT DENTITION : Clinical feature of this stage :  Medial displacement of the maxillary segment giving buccal cross bite  Relative maxillary retrognathism, giving reversed incisal overjet.  Deficiency of vertical growth of the upper jaw – REDUCED FACIAL HEIGHT  rotation, malposition and hypodontia of teeth.  Supernumerary teeth  Accentuated curve of spee in maxilla  Collapsed arch forms  Poor oral hygiene and caries
  48. 48. ALIGNMENT OF INCISOR TEETH  Incisors usually rotated and in crossbite. Corrected by means of fixed orthodontic appliance. CORRECTION OF LATERAL DIMENSION  Lack of bony union between two sides of the maxilla, correction in lateral dimension is relatively straight forward.  By expansion appliance Quad Helix Rapid Maxillary Expansion (RME) Patients with clcp have class III malocclusion bcoz of maxillary deficiency (A-P and Vertically), coupled with mandibular overclosure. In such cases use of class III elastics after leveling and aligning will result in upper molar extrusion and favorable downward and backward rotation of mandible.
  49. 49. Orthognathic Surgery combined with Orthodontics Due to severe skeletal discrepancy, there is deterioration of esthetics and occlusion, psychological implications leading to low self esteem, defective speech, oronasal fistulas. Such cases require a combined orthodontic and orthognathic approach. Size and position of maxilla is often a problem, thus maxillary advancement and occasional down grafting needs to be performed. To correct the transverse problem multiple segment LeFort I osteotomies may be required. For a bilateral CLCP three-piece maxillary surgery (allows rotation of segments also) required while for unilateral CLCP a two piece is sufficient.(Vlachos 1996)
  50. 50. Decompensation: Usually requires 12 months. Multiple segment maxillary osteotomies requires segmental treatment. The bracket positions are altered for teeth adjacent to the osteotomy site. Dental compensations in the lower arch also should be addressed ie alleviation of crowding and proclination. Gaps present in the arches due to the missing teeth must be either closed- stable result and prevents reopening of oronasal fistula. Proffit recommends overcorrecting the anterior crossbite in excess of positive overjet- compensate for post surgical relapse. In cases with an overjet of more than 8mm mandibular surgery (BSSO) also must be considered. If not then over advancement of maxilla – unstable and speech defects.
  51. 51. Post surgical orthodontics: involves detailing of occlusion, closure of residual spaces and maintenance of transverse dimension (overlay arches). Lasts for 4-6 months. Retention: After removal of appliance retainers should be placed immediately. Temporary vacuum filled retainers to be avoided-transverse control inadequate. Soldered lingual arch preffered.  TIMING  Never indicated in active facial growth  Ideal time : age 18-19
  52. 52. DISTRACTION OSTEOGENESIS 1903 . Dr. Gavril of Russia-Bone lengthening of leg. It is a procedure that moves two segment of bone slowly apart in such a way that new bone fills the gap.  In distraction osteogenesis, a surgeon makes an osteotomy in an bone and attaches a device known as distractor to both sides of osteotomy.  The distractor is gradually adjust over a period of days or week to stretch the osteotomy so new tissue fills it.
  53. 53. Maxillary surgery required in 25-60% of cases with clcp. (Ross and Subtenly) Distraction osteogenesis allows soft tissue adaptation, including scar tissue. Therefore doesn’t cause a problem with vello- pharyngeal insufficiency thus good results. Distraction Of maxilla first proposed by Molina & Oritz-Monasterio(1998) EXTERNAL DISTRACTORS Advantage: •Direction of force is well controlled Dis advantage: •Cranial surgery is required •Esthetics are compromised
  54. 54. INTERNAL DISTRACTORS Advantage: •Esthetics •Psychological relilef Disadvantage: •Difficult to control the direction of force Prosthodontic Treatment: It may be required in cases where replacement of missing teeth is essential. Removable or fixed prosthesis may be given. It allows for improved speech and better esthetics.
  55. 55. CONCLUSION:  Orofacial clefts have been identified to have a multifactorial etiology and therefore require an interdisciplinary treatment approach ,comprising a team effort in which an orthodontist plays a vital role and works hand in hand with various specialists to provide the best possible line of treatment with a single minded approach , that is to minimize if not eliminate the physical, social and the emotional hardship that a person with orofacial cleft presents.
  56. 56. REFERENCES: • CRANIOFACIAL DEVELOPMENT- Sperber •Surgical orthodontic treatment- Proffit and White •Grayson etal, Pre surgical naso alveolar molding, cleftliip- craniofacial journal 1999:35 •Advances in management of cleft palate: Edwards and Watson •Cleft lip and palate, Seminars in Orthodontics •Baik et al. surgical orthodontic treatment in patients with clcp: conventional surgery vs maxillary distraction, world J Orthod;2:331-40
  57. 57. Leader in continuing dental education