Cleft palate, cleft lip and cheilo-palato-schizis - Pathogenesis and causes

Physiology palate formation.Palate formation starts at the end of week 5 of pregnancy. At this stage the palace consists of two parts, called the palace above (primary) and the palace back (side). Median nasal protrusions form the intermaxillary segment, which includes primary and incisors palace. Extends back to the primary Palace incisive foramen.
Palace side, which consists of lateral palatal processes, starting from incisive foramen and includes a portion of a bone and muscle. Lateral palatine processes occurring in week 6 of pregnancy. Deep portion of the jaws comprise projections forming two structures horizontally, which will derive first brachial arch. They are found on either side of the tongue. As the tongue moves back in week 7, lateral processes grow medially. Hard palate before fusion begins and continue back in week 8 of gestation.
Physiology of upper lip formation.Embryonic development is characterized by fusion of the upper lip projections protruding jaws with lateral and medial nasal. This process begins in week 4 of pregnancy and is completely in week 7. Lack of complete mesenchymal migration to join one or both jaws with prominent median nasal prominence result in unilateral or bilateral cleft lip.
Genetic theory.Cleft palate is the genetic basis of heterogeneous and probably multifactorial. Pathways have been described autosomal recessive, autosomal dominant and X Linc. For all parents misfortune of having a child with velo-palatine defect is 1 in 700. In families in which no first-degree relative is affected, the rate of recurrence of cleft lip or cleft palate in infants is 2. 5%. Is affected when a relative degree, the recurrence rate is 10%. Similar recurrence rates occur in children of parents who were born with clefts. If the cleft is part of an autosomal dominant syndrome, the recurrence rate is 50%.
A cleft is associated with a syndrome in 30% of cases. The most common syndrome associated with cleft lip and palate is Van der Woude. It is an autosomal dominant disease characterized by cleft lip and / or palate, with blind sinuses or depressions of the lower lip.
The theory of externalities.Etiology of cleft palate is not well understood, though there is evidence of involvement of external factors. Quite a few of the factors known teratogenic cause cleft. Alcohol consumption during embryological history is present in many children with clefts. Other Teratogens associated with increased frequency of cleft palate include: phenytoin, retinoids and illegal rogurile-cocaine.