IL-1β Inhibits TGFβ in the Temporomandibular Joint

Similarly to humans, healthy, wild-type mice develop osteoarthritis, including of the temporomandibular joint (TMJ), as a result of aging. Pro-inflammatory cytokines, such as IL-1 beta, IL-6, and TNF alpha, are known to contribute to the development of osteoarthritis, whereas TGF beta has been associated with articular regeneration. We hypothesized that a balance between IL-1 beta and TGF beta underlies the development of TMJ osteoarthritis, whereby IL-1 beta signaling down-regulates TGF beta expression as part of disease pathology. Our studies in wild-type mice, as well as the Col1-IL1 beta(XAT) mouse model of osteoarthritis, demonstrated an inverse correlation between IL-1 beta and TGF beta expression in the TMJ. IL-1 beta etiologically correlated with joint pathology, whereas TGF beta expression associated with IL-1 beta down-regulation and improvement of articular pathology. Better understanding of the underlying inflammatory processes during disease will potentially enable us to harness inflammation for orofacial tissue regeneration.