Background: Temporomandibular joint osteoarthritis (TMJ-OA) is a degenerative disease
that involves changes in subchondral bone and progressive degradation of cartilage. Currently,
rebamipide, a gastroprotective drug, is administered to protect gastric mucosa and accelerate ulcer
Objectives: Recent studies have shown that rebamipide also attenuates cartilage degeneration by
suppressing oxidative damage and inducing homeostasis of the extracellular matrix of articular
chondrocytes. Regarding the latter, reduced expression of cathepsin K, NFATc1, c-Src, and integrin
β3, and increased expression of nuclear factor-kappa B, have been found to be mediated by the transcription
factor, receptor activator of nuclear factor kappa-B ligand (RANKL).
Methods: Treatment with rebamipide was also found to activate, mitogen-activated protein kinases
such as p38, ERK, and JNK to reduce osteoclast differentiation. Taken together, these results
strongly indicate that rebamipide mediates inhibitory effects on cartilage degradation and osteoclastogenesis
Results and Conclusion: Here, we highlight recent evidence regarding the potential for rebamipide
to affect osteoclast differentiation and TMJ-OA pathogenesis. We also discuss the potential role of
rebamipide to serve as a new strategy for the treatment of TMJ-OA.