Cleft Palate Essay

SURGICAL MANAGEMENT OF CLEFT LIP/ PALATE

SEMINAR

MAJ SERAT RAHMAN
PG Trainee (Oral & Maxillofacial Surgery)

INTRODUCTION
EMBRYOLOGY
ETIOPATHOGENESIS
FREQUENCY & DISTRIBUTION
CLINICAL CLASSIFICATION
TREATMENT ALGORITHM & OBJECTIVES
SURGERY FOR CLEFT LIP, PALATE, VPI, ALVEOLAR GRAFTING
ORTHOGNATHIC SURGERY, DISTRACTION & ORTHODONTICS
RECENT ADVANCES
INTRODUCTION
Orofacial clefts (ie, cleft lip [CL], cleft lip and palate [CLP], cleft palate [CP] alone, as well as median, lateral [transversal], oblique facial clefts) are among the most common congenital anomalies. Cleft lip and / or palate may be associated with syndromes that include anomalies involving multiple organs. Patients may have impaired facial growth,
In those instances, genetic factors create susceptibility for clefts. When environmental factors (ie, triggers) interact with a genetically susceptible genotype, a cleft develops during an early stage of development. Clefting of the lip and/or palate is associated with more than 150 syndromes. The most commonly recognized syndrome associated with clefts of the lip and palate is Van der Woude syndrome. This syndrome is an autosomal dominant disorder characterized by clefts of the lip and/or palate and blind sinuses, or pits, of the lower lip. Clefts of the secondary palate alone are far more likely to be associated with syndromes than are clefts involving the lip alone or the lip and palate. Most cases of lip clefts are nonsyndromic and believed to be either multifactorial in origin or the result of changes at a major single-gene locus.The overall incidence of associated anomalies (eg, cardiac) is approximately 30% (more common with isolated cleft palate). Environmental causes such as viral infection (eg, rubella) and teratogens (eg, steroids, anticonvulsants like phenytoin, retinoids and illegal drugs (eg, cocaine).) during the first trimester have been linked to facial clefts. The incidence of cleft lip in infants born to mothers who smoke during pregnancy is twice that of those born to nonsmoking mothers. Alcohol consumption
The genetic basis of cleft deformity is most likely heterogeneous and multifactorial. Autosomal recessive, autosomal dominant, and X-linked inheritance patterns have been described. Recent advances in modern molecular biology, new methods of genome manipulation, and availability of complete genome sequences led to an understanding of the roles of particular genes that are associated with embryonic development of the orofacial complex. Genetic mapping of families with inherited forms of cleft palate has resulted in the identification of genes involved in palate development. Associations of specific candidate genes with clefts have not been found consistent across different populations. This may suggest that multiplicative effects of several candidate genes or gene-environmental interactions exist in different populations. Some of these genes include the MSX, LHX, goosecoid, and DLX genes. Additional disturbances in growth factors or their receptors that may be involved in the failure of fusion include fibroblast growth factor, transforming growth factor, platelet-derived growth factor, and epidermal growth factor. The identification of factors that contribute to the etiology is important for prevention, treatment planning, and education. With an increasing number of couples who seek genetic counseling as a part of their family