Cleft/Lip and Palate About: CL results from failure to fuse maxillary processes to nasal elevation (7-8 th week); CPresults

from failed palatine migration occurring 7-12 th week gestation. Causes: There is a family history of facial clefting in 25% of cases, which does not follow either a normal recessive or dominant pattern. The condition appears to be multifactorial. Someinstances of clefting may be because of an overall reduction in the volume of the facialmesenchyme, which leads to clefting by virtue of failure of mesodermal penetration. In some patients, clefting appears to be associated with increased facial width, either alone or inassociation with encephalocele, idiopathic hypertelorism, or the presence of a teratoma. Thecharacteristic U-shaped cleft of the Pierre Robin anomaly is thought to be dependent upon a persistent high position of the tongue, perhaps associated with a failure or delay of neck extension. This prevents descent of the tongue, which in turn prevents elevation and a medialgrowth of the palatal shelves.The production of clefts of the secondary palate in experimental animals has frequently beenaccomplished by drug administration. Agents commonly used are steroids, anticonvulsants,diazepam, and aminopterin. Phenytoin and diazepam may also be causative factors in clefting inhumans. Infections during the first trimester of pregnancy, such as rubella or toxoplasmosis, have been associated with clefting. Pathophysiology : The pathologic sequelae of cleft palate include feeding and nutritionaldifficulties, recurrent ear infections, hearing loss, abnormal speech development, and facialgrowth distortion. The communication between the oral and nasal chamber impairs the normalsucking and swallowing mechanism of the cleft infants. Food particles reflux into the nasalchamber.The abnormal insertion of the tensor veli palati prevents satisfactory emptying of the middle ear.Recurrent ear infections have been implicated in the hearing loss of patients with cleft plate. Thehearing loss may worsen the speech pathology in these patients. Evidence that repair of the cleft palate decreases the incidence of middle ear effusions is inconsistent. However, these problemsare overshadowed by the magnitude of the speech and facial growth problems. Speechabnormalities are intrinsic to the anatomic derangement of cleft palate. The facial growthdistortion appears to be, to a great extent, secondary to surgical interventions. An intactvelopharyngeal mechanism is essential in production of nonnasal sounds and is a modulator of the airflow in the production of other phonemes that require nasal coupling. The complex anddelicate anatomic manipulation of the velopharyngeal mechanism, if not successfully learnedduring early speech development, can permanently impair normal speech acquisition.Multiple studies have demonstrated that the cleft palate maxilla has some intrinsic deficiency of growth potential. This intrinsic growth potential varies from isolated cleft of the palate tocomplete cleft lip and palate. This growth potential is further impaired by surgical repair. Anysurgical intervention performed prior to completion of full facial growth can have significantdeleterious effects on maxillary growth. Disagreement exists as to the appropriate timing of surgery to minimize the harmful effects on facial growth and on what type of surgical intervention is most responsible for growth impairment. The formation of scar and scar contracture in the areas of denuded palatal bones are most frequently blamed for restriction of maxillary expansion.The growth disturbance is exhibited most prominently in the prognathic appearance during thesecond decade of life despite the normal appearance in early childhood. The discrepant occlusionrelationship between the maxilla and the mandible is usually not amenable to nonsurgicalcorrection. Treatment: Cleft lip: o Surgical closure during 1 st weeks of life o

May need revision Cleft palate o Surgical repair between 12-18 mos of age o May require posterior pharyngeal flap or palate bone grafting at a later time Long Term Problems o Extensive orthodontics and prosthodontics needed o Align maxillary segments (birth-18mos) o Repositioning maxillary segment and correct crossbite (2-5yoa) o Correction of faulty occlusion (10-11yoa) o Typical adolescent orthodontia (12-18yoa) o Dental prosthesis o Speech therapy o Recurrent otitis media