Craniofacial cleft
Van der Meulen classification divides different types of clefts based on where the development arrest occurs in the embryogenesis.
A primary cleft can occur in an early stage of the development of the face (17 mm length of the embryo).
The developments arrests can be divided in four different location groups: internasal, nasal, nasalmaxillar and maxillar.
Other theories are that genetics play a part in the development of facial clefts[7] or that they are caused by amniotic bands.
[9] Occurrences of CL/P are most often (around seventy percent of cases) isolated and nonsyndromic, meaning they are not associated with a syndrome or inherited genetic conditions.
[9][10] Around thirty percent occur with other structural variances, and over 500 syndromes have been identified in which clefting is a principal feature.
[9][10] Clefting can result from teratogens, an agent that disrupts embryo development such as, radiation, maternal infection, chemicals, or drugs.
[9][11] Orofacial clefts have great phenotypic diversity, and their associated genetic environments have called for vast research and investigation.
[12][13] Environmental causes have been found to contribute to craniofacial clefting, however, these are still influenced by and supported by genetic factors.
[14] The craniofacial complex begins its progress in the fourth week of development, and results from neural crest cells migrating to form and fuse the facial primordia.
This is supported through cephalometric and anthropometric comparisons of family members including between triplets, twins, siblings, and parents and children.
[15] Genetic factors of craniofacial clefting can be investigated and tracked through several methods including sequencing in humans, Genome-wide association studies (GWAs), fate mapping, expression analysis, and animal studies (knockout experiments or models with clefting from chemical mutagenesis).
[16] Twin studies and familial clustering have also revealed that facial structure and formation are genetically linked.
Several genes have been associated with craniofacial disorders through experimentation, including sequencing Mendelian clefting syndromes.
[12] The transforming growth factor (TGF) family has provided multiple candidate genes linked with craniofacial development and malformation.
[19][20] Nonsyndromic CL/P has been associated with the transcription factor forkhead box protein E1 (FOXE1), as mutations have resulted in cases of CL/P in mice.
It seems that folic acid contributes to lowering the risk of a child being born with a facial cleft.
[22] A disadvantage of early bone reconstruction is the chance to damage the tooth germs, which are located in the maxilla, just under the orbit.
The best aesthetic result is achieved when the incisions are positioned in areas which attract the least attention (they cover up the scars).
If, however, the function of a part of the face isn't damaged, the operation depends on psychological factors and the facial area of reconstruction.
This plan includes every operation needed in the first 18 years of the patients life to reconstruct the face fully.
The treatment of encephalocele is based on surgery to repair the bony gap and provide adequate protection of the underlying brain.
A possible downside of this reconstruction is that once you performed it at a younger age, you can't lengthen the flap at a later stage.
Repair of the ala (wing of the nose) often requires the inset of cartilage graft, commonly taken from the ear.
[27] The treatment of soft tissue parts of midface anomalies is often a reconstruction from a skin flap of the cheek.
The most common method to reconstruct the midface is by using the fracture/ incision lines described by René Le Fort.
When the cleft involves the maxilla, it is likely that the impaired growth will result in a smaller maxillary bone in all 3 dimensions (height, projection, width).
