Disabling interruptions to chewing and malformed facial development may be caused by bony and fibrous ankylosis of the temporomandibular joint (TMJ) as a result of trauma (31-98% of cases), local or systemic infection (10-49%), systemic disease (10%), or neoplasm.
Ankylosis of the TMJ is one of the most serious complications of condylar fracture. In the cases of trauma, it is hypothesized that intra-articular hematoma, with scarring and excessive bone formation, leads to hypomobility.
Infection of the TMJ is most commonly the result of contiguous spread from otitis media or mastoiditis but may also result from hematogenous spread, including tuberculosis, gonorrhea, and scarlet fever. Systemic causes of TMJ ankylosis include ankylosing spondylitis, rheumatoid arthritis, and psoriasis.
Ankylosis can be classified on the basis of degree of limitation (partial or complete), location of the union (intracapsular versus extracapsular) and type of tissue involved (fibrosis, osseous, or fibro-osseous).
The end result is severing limitation in the range of mandibular motion, which may interfere with speech, oral hygiene, and proper preparation of a food bolus for digestion as well as maintenance of nutrition.
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As the mandible develops, three growth centers are able to produce enlargement this complex bony structure, the condyles, the surface of the ramus, and the alveolus.
Initially, it was believed that the mandible was pushed down and forward by growth at the condylar growth center. This concept has not been borne out by clinical research, in that the condylar cartilage in vitro possesses little independent growth potential and produces only a fraction of the growth pressure of epiphyseal cartilage.
° Gholamreza Shirani / Farnoosh Mohammadi / Mahnaz Arshad / Mohsen Shirazi