Cellular S-100 protein immunostaining in human dysfunctional temporomandibular joint discs.

S-100 protein was detected immunohistochemically in diseased human temporomandibular joint discs with different degrees of pathology, and the findings compared with those of normal discs. In normal discs, large nerve trunks in the posterior ligament were strongly stained by anti-S-100 antiserum; the very few chondrocyte-like cells sometimes showed faint staining, while no staining was observed in any fibrochondrocyte-like or fibroblast-like cell. In dysfunctional discs, S-100 protein immunostaining seemed to correlate with structural pathological findings. The discs showing an abnormal collagen arrangement or fragmentation of collagen fibres presented overall the same immunolabelling pattern as normal discs. In discs with fibrocartilaginous metaplasia and dystrophic cartilage formation, fibrochondrocyte cells showed a very strong immunoreaction for S-100 protein and fibroblast-like cells in some instances were also positive. These findings suggest that S-100 upregulation in disc cells can be considered an attempt at tissue repair by chondroid metaplasia following an injury in that it enables fibroblast-like cells and fibrochondrocytes to acquire a chondrogenic phenotype.