• Approximately one in 1000 children is born with a cleft palate, cleft lip,

or with both anomalies.

• Epidemiology differentiates between cleft lip with or with out cleft

palate and isolated cleft palate, the most common form of which is the palate and isolated cleft palate, the most common form of which is the

cleft lip with cleft palate.

• Cleft lip and palate is the second most common congenital

malformation exceeded only by cardiovascular malformations.

• Unilateral clefts occur six times more often than bilateral clefts.

• The rates of oral clefts in Asian populations are high (0.79 to

3.74 per 1000 individuals); intermediate rates for Caucasians

have been reported (0.91 to 2.69 per 1000 individuals); and

Black African populations have a very low rate of cleft

malformation (0.18 to 1.67 per 1000 individuals). In India one child in 714 births one child in 714 births is born with a cleft defect35,000 children 35,000 children are born with such defects in India every

malformation (0.18 to 1.67 per 1000 individuals).

• Males are more often affected with CL/P, whereas females are

more frequently afflicted with cleft palate only and with severe

forms of CL/P.

• Left sided cleft is more common, than the right side.

35,000 children 35,000 children are born with such defects in India every year (Study of Children Born with Cleft Lips And Palates in India - S Shiva Raju et al

December 2000)

• Cleft occurs alone (non-syndromic) or associated with other congenital anomalies.

• Multifactorial etiology

– Chemical exposures, radiation, maternal hypoxia, teratogenic drugs, nutritional deficiencies, physical obstruction,

• Genetic factors

– Recent studies - cleft malformation is associated with polymorphisms in the – Recent studies - cleft malformation is associated with polymorphisms in the gene encoding TGF alpha, an epidermal growth factor receptor (EGFR) ligand made by most epithelia.

– Mutations in other genes, such as cytochrome P-450, the retinoic acid receptor or NADH dehydrogenase, have also been implicated.

• Environmental factors

• Associated with syndromes

Clefts are seen to be associated with more than 250 syndromes

• Some of them are-

• Waardenburg syndrome

• van der Woude’s syndrome

• Orofacial digital syndrome

• Treacher collin syndrome

• Pierre robin syndrome

• Klippel Feil syndrome

• Repair of the lip is generally deferred deferred until an infant weighs approximately 12 to 14 lbs in order to have more tissue with which to work.

• Palate repair is m/c performed b/w 12-24 months of age.• Clefts involving only the soft palate – 6-18 months.

Repair procedures for lip:1. lip adhesion procedure.• for very difficult & wide cleft of the lip.• M/C used in wide cleft of the lip2. Rose thompson operation or straight line repair.2. Rose thompson operation or straight line repair.• Only for the repair of incomp cleft, prenatal scars &revision of a lip scar.3. Tennison – Randall Triangular flap.• Excellent proced, only little tissue is sacrificed.• Require exact measurements & is mathematical 4. Millard Rotation- Advancement Flap• M/C approach to cleft lip repair.• Does not require the mathematics.• Used in incomplete, complete & wide cleft repairs.• Less precise than Tennison randall.

Controversial

• In 1921, Sir Harold Sir Harold GilliesGillies - "Close the lip early and repair the palate prior to speech".

• Most believe - palate should be closed prior to the time that the child begins to speak. child begins to speak.

• Main area of controversy - timing of hard palate hard palate repair

• Early repair results in scar tissue formation and limitation of maxillary growth

• Early soft palate repair preceding hard palate closure is recommended by some.

• But most surgeons close the hard and soft palate as early as 6-9 months of age and almost always before 18 months of age.

I) Primary Veloplsty• Soft palate closure at early age.• Delayed hard palate closure • Currently rarely indicated. Severe speech problems. Requires additional procedure so tech. difficultII)Von Langenbeck’s palatoplasty• Bipedicle mucoperiosteal flap• Effective only for soft palate clefts.• Effective only for soft palate clefts.III) Oxford palatoplasty (V to Y push-back.) (Kilner 1937; Wardill 1937)• Posteriorly & ant based unipedicle mucoperiosteal flaps.• V-Y rerodisplacement advantages Lengthens palate. Better speech than with Von Langenback’s palatoplasty.• V-Y rerodisplacement disadvantages Def. mucosal coverage of nasal surface, leading to scar contracture &

shortened palate. Failure to close alveolar portion of cleft. Fistulas occurs at hard/soft palate junction.

IV) Two flap tech.

• Only for posteriorly based unipedicle flaps.

• Advantages: Closes alveolar cleft.

• Disadvantage: no palatal lengthening.

RECONSTRUCTION OF ALVEOLAR CLEFT:RECONSTRUCTION OF ALVEOLAR CLEFT:

Surgical goals:

• Oronasal fistula closure.• Oronasal fistula closure.

• Improvement of alveolar ridge form.

• Prevention of tooth loss (primarily the cuspid) d/t lack of pdl support.

• provision of nasal alar base support.

Timing of bone grafting:

1. Primary bone grafting Less than age 2

2. Early secondary grafting Ages 2 to 6

3. Secondary grafting Ages 7-12 (before time of cuspid eruption).

4. Late secondary grafting adult

1. Primary bone grafting at less than age 2 was abandoned b/c ofadverse effects noted in facial growth & arch form.

2. Early sec. grafting b/w ages 2 and 6, is done to provide supportfor eruption of lateral incisor.

• If lat. Incisor is present & appears to be anatomically normal,early secondary grafting may be indicated.

• A child at age 5 still has significant transverse & A-P growthremaining in the maxilla, & placement of an alveolar graft at thatage may interfere with midface growth.age may interfere with midface growth.

• Mx is completed by age 8, & bone grafting performed after thatage does not interfere with mx growth in those dimensions.

3. The m/c time for alveolar cleft grafting is b/w 9 & 11, before thetime the permanent cuspid erupts & when half to 2/3rd of theroots has formed.

• At this age, A-P & transverse mx growth is complete & onlyvertical mx growth remains.

• Objectives of alveolar cleft grafting– To fill fill the bony defect the bony defect and to enable spontaneous canine

eruption

– To close close any oronasal fistulas any oronasal fistulas and eliminate mucosal recesses

– To provide bony support bony support for the alar base– To provide bony support bony support for the alar base

– To improveimprove alveolar contouralveolar contour, dental, and facial aesthetics

– To stabilizestabilize the segments

– To provide provide bonebone for osseointegrated implants

– To aim for nonnon--prosthetic rehabilitationprosthetic rehabilitation

– To improve improve the condition of the the condition of the periodontiumperiodontium and soft tissue

• The ideal patient is between the ages of 8 and 12 years with a maxillary canine root that is one-half to two-thirds developed.

Biologic process of new bone formation b/w the surfaces of bone segmentsthat are gradually separated by incremental traction.

Contribution by Russian surgeon Gavrill Ilizarov.

Ilizarov’s protocol:1. Divide 2/3rd of bony cortex with a narrow osteotome (comp. osteotomy

can be done in mandible b/c of good periosteal supply)

2. Place the distraction device.

3. Latency period: 2 days in young pts & 7 days in old pts. (adequateduration of latency period allow development of # callus).

4. Distraction rate: 1mm/day (0.25mm in 4 increments).

• If < 0.5mm/day- premature consolidation

• If > 1.5mm/day- local ischemia & delayed ossification or pseudoartheosismay occur.)

5. Consolidation period: 6 times the days required for distraction.

Sufficient time for consolidation & remodelling of newly formed bone beforefnal load.