Condylar hyperplasia  (mandibular hyperplasia) is over-enlargement of the mandible bone in the skull. It was first described by Robert Adams in 1836 who related it to the overdevelopment of mandible. In humans, mandibular bone has two condyles which are known as growth centers of the mandible. When growth at the condyle exceeds its normal time span, it is referred to as condylar hyperplasia. The most common form of condylar hyperplasia is unilateral condylar hyperplasia where one condyle overgrows the other condyle leading to facial asymmetry. Hugo Obwegeser et al. classified condylar hyperplasia into two categories: hemimandibular hyperplasia and hemimandibular elongation. It is estimated that about 30% of people with facial asymmetry express condylar hyperplasia.In 1986, Obwegeser and Makek specifically detailed two hemimandibular anomalies, hemimandibular hyperplasia and hemimandibular elongation. These anomalies can be clinically present in a pure form or in combination. Cause
Condylar hyperplasia has an unknown cause. Several theories exist in literature which related to the cause of condylar hyperplasia. One theory states that an event of a trauma leading to increase in number of repair mechanism and hormones in that area may lead to increase in growth of mandible on that side. Another theory states that an increase in loading of the temporomandibular joint can lead to increase in expression of bone forming molecules. Condylar hyperplasia predominantly affects women with 64% of patients being women. Diagnosis
Diagnosis of asymmetry can be done through many different methods. PA cephalometry, panoramic radiograph, and nuclear imaging are some of the techniques that can be used for diagnosis.
Mutations in the KCNJ5 gene likely result in the production of potassium channels that are less selective, allowing other ions (predominantly sodium) to pass as well. The abnormal ion flow results in the activation of biochemical processes (pathways) that lead to increased aldosterone production, causing the hypertension associated with familial hyperaldosteronism type III.The genetic cause of familial hyperaldosteronism type II is unknown. Diagnosis
Treatment
See also
18-Hydroxycortisol
18-Hydroxycorticosterone

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This article incorporates text from the United States National Library of Medicine ([1]), which is in the public domain.