IL-lβ 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-1β, IL-6, and TNF α, are known to contribute to the development of osteoarthritis, whereas TGFβ has been associated with articular regeneration. We hypothesized that a balance between IL-1 β and TGFβ underlies the development of TMJ osteoarthritis, whereby IL-1 β signaling down- regulates TGFβ expression as part of disease pathology. Our studies in wild-type mice, as well as the Col1-IL1β^XAT mouse model of osteoarthritis, demonstrated an inverse correlation between IL-1 β and TGFβ expression in the TMJ. IL-1 β etiologically correlated with joint pathology, whereas TGFβ expression associated with IL-1 β 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.