Temporomandibular joint ankylosis caused by chondroid hyperplasia from the callus of condylar neck fracture.

A patient who complained of difficulty in opening his mouth after condylar neck fracture 1 year ago presented typical features of temporomandibular joint ankylosis in clinical and radiologic examinations. To demonstrate a possible pathogenesis of temporomandibular joint ankylosis after condylar neck fracture, the fractured condylar portion removed was examined by histologic and immunohistochemical stainings. Interpositional gap arthroplasty was performed by removing the inferomesially displaced fractured condyle, and reconstruction with subcutaneous dermis to the previous vertical height was performed immediately. The fractured condylar portion was almost intact with slight erosion of the condylar cartilage. In the hematoxylin and eosin and Masson trichrome stainings, an extensive chondroid hyperplasia with abundant hyaline cartilage was shown in the removed condylar portion. There were also hyperplastic features of the synovial membrane, which were abnormally distributed throughout the chondroid tissues. In the immunohistochemical stainings of proliferating cell nuclear antigen (PCNA) and bone morphogenetic protein (BMP)-2 and BMP-4, the chondroid tissues were conspicuously hyperplastic and strongly positive for BMP-4 but sparse for BMP-2. From these results, we think that the hyperplastic chondroid tissue was derived from the callus of the primary fractured site of the condylar neck and propose that the chondroid tissue could proliferate continuously because of synovial tissue support from around the temporomandibular joint, resulting in temporomandibular joint ankylosis. This pathogenesis is quite different from those of other diaphyseal fracture of long bones.