Micrognathism is a condition where the jaw is undersized. It is also sometimes called mandibular hypoplasia. It is common in infants, but is usually self-corrected during growth, due to the jaws increasing in size. It may be a cause of abnormal tooth alignment and in severe cases can hamper feeding. It can also, both in adults and children, make intubation difficult, either during anesthesia or in emergency situations. Causes
While not always pathological, it can present as a birth defect in multiple syndromes including:

Catel–Manzke syndrome
Bloom syndrome
Coffin–Lowry syndrome
Congenital rubella syndrome
Cri du chat syndrome
DiGeorge syndrome
Ehlers–Danlos syndrome
Fetal alcohol syndrome
Hallermann–Streiff syndrome
Hemifacial microsomia (as part of Goldenhar syndrome)
Incontinentia pigmenti
Juvenile idiopathic arthritis
Marfan syndrome
Möbius syndrome
Noonan syndrome
Pierre Robin syndrome
Prader–Willi syndrome
Progeria
Silver–Russell syndrome
Seckel syndrome
Smith–Lemli–Opitz syndrome
Stickler syndrome
Treacher Collins syndrome
Trisomy 13 (Patau syndrome)
Trisomy 18 (Edwards syndrome)
Trisomy 21 (Down syndrome)
Wolf–Hirschhorn syndrome
X0 syndrome (Turner syndrome)

Diagnosis
It can be detected by the naked eye as well as dental or skull X-Ray testing. Treatments
Micrognathia can be treated by surgery, orthodontic braces, and modified eating methods. Early detection of the problem and monitoring as the problems grows can help understand it better and find the most effective treatment procedure. See also
Human mandible
Macrognathism
Retrognathism

References
External links

"Micrognathia". Medline Plus. 12 May 2009. Retrieved 21 May 2011.
This accounts for the lack of glucagon stimulation and epinephrine release that would normally stimulate and enhance glucose release and production from the liver, rescuing the diabetic from severe hypoglycemia, coma, and death. Numerous hypotheses have been produced in the search for a cellular mechanism of hypoglycemic unawareness, and a consensus has yet to be reached. The major hypotheses are summarized in the following table:
In addition, autoimmune diabetes is characterized by a loss of islet specific sympathetic innervation. This loss constitutes an 80–90% reduction of islet sympathetic nerve endings, happens early in the progression of the disease, and is persistent though the life of the patient. It is linked to the autoimmune aspect of type 1 diabetics and fails to occur in type 2 diabetics. Early in the autoimmune event, the axon pruning is activated in islet sympathetic nerves. Increased BDNF and ROS that result from insulitis and beta cell death stimulate the p75 neurotrophin receptor (p75NTR), which acts to prune off axons. Axons are normally protected from pruning by activation of tropomyosin receptor kinase A (Trk A) receptors by NGF, which in islets is primarily produced by beta cells. Progressive autoimmune beta cell destruction, therefore, causes both the activation of pruning factors and the loss of protective factors to the islet sympathetic nerves. This unique form of neuropathy is a hallmark of type 1 diabetes, and plays a part in the loss of glucagon rescue of severe hypoglycemia.