Apoptosis in temporomandibular joint disc with internal derangement involves mitochondrial-dependent pathways. An in vivo study.

OBJECTIVE

Two main apoptosis pathways have been identified: an extrinsic (or death receptor-mediated) and an intrinsic (or mitochondrial) pathway. Apoptotic cell death through the extrinsic pathway has just been described in temporomandibular joint disc (TMJ) with internal derangement (ID); in contrast, no data are available on the involvement of the intrinsic pathway in this tissue. The aim of this work was to investigate whether the intrinsic pathway participates in apoptosis activation in patients with TMJ ID and anterior disc displacement without reduction.

MATERIALS AND

METHODS

Apoptosis activation was studied in TMJ discs from 15 patients with ID and in six unaffected discs using bcl-2-associated X protein (bax), B-cell lymphoma 2 (bcl-2), cytochrome c and caspase 9 immunohistochemistry. A correlation was sought between immunohistochemical findings and degree of disc damage.

RESULTS

None of the pathological TMJ disc sections were immunopositive for bcl-2; negative bcl-2 immunostaining was detected in affected discs; cytochrome c and caspase 9 immunoreactivity was greater in pathological compared to unaffected discs; the difference was significant and correlated with histopathological degeneration score data (Spearman's rho = 0.617).

CONCLUSION

The present findings suggest that in-human TMJ with ID and anterior disc displacement without reduction of cell apoptosis occurs, at least partly, via the mitochondrial pathway, which contributes to the subsequent disc degeneration. These data may have clinical implications and could help devise improved treatment strategies.