PubMed · 1069479
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P D Lewis. 1976. The deviated midline.. https://doi.org/10.1016/0002-9416(76)90223-2
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The cause of hemifacial microsomia (HFM) is currently the subject of much investigation. Despite a large body of clinical and experimental data, little is certain other than the heterogeneity of this malformation complex. Here we suggest that some of the cases previously designated as being multifactorial in origin may be interpreted instead as resulting from a single-gene mutation, by applying a stochastic single-gene model. A variety of models of the pathogenesis of HFM have been described, including the proposal that local embryonic haemorrhage is a causal mechanism. More recently, it has been suggested that an interference in chondrogenesis is primarily responsible for the HFM phenotype. In this paper direct experimental evidence, based on surgical interference of mandibular development in the chick embryo, is applied in favour of the latter concept. In particular, asymmetrical perturbation of Meckel's cartilage has been shown to result in asymmetry of the mandible, and it is proposed that, irrespective of cause, the skeletal pathogenesis of HFM primarily involves the auriculofacial cartilage model.
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Temporomandibular (TM) disorders among children are uncommon. Their many etiologies include interferences with the formative process, malocclusion, and muscle disharmony. Facial pain, earache, headache, difficulty with chewing, and joint noise during mandibular function are symptoms. The two year course of a TM disorder that first became symptomatic in a six month old child is described.