IL-1beta inhibits TGFbeta 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-1beta, IL-6, and TNFalpha, are known to contribute to the development of osteoarthritis, whereas TGFbeta has been associated with articular regeneration. We hypothesized that a balance between IL-1beta and TGFbeta underlies the development of TMJ osteoarthritis, whereby IL-1beta signaling down-regulates TGFbeta expression as part of disease pathology. Our studies in wild-type mice, as well as the Col1-IL1beta(XAT) mouse model of osteoarthritis, demonstrated an inverse correlation between IL-1beta and TGFbeta expression in the TMJ. IL-1beta etiologically correlated with joint pathology, whereas TGFbeta expression associated with IL-1beta 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.
Lim
W H
WH
Department of Orthodontics, School of Dentistry, Dental Research Institute, Seoul National University, Seoul, Korea.
Toothman
J
J
Miller
J H
JH
Tallents
R H
RH
Brouxhon
S M
SM
Olschowka
M E
ME
Kyrkanides
S
S
D000818:Animals; D015536:Down-Regulation; D005260:Female; D053583:Interleukin-1beta / Q000096:biosynthesis / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D008822:Mice, Transgenic; D010003:Osteoarthritis / Q000378:metabolism*; D015398:Signal Transduction; D013704:Temporomandibular Joint / Q000378:metabolism*; D013705:Temporomandibular Joint Disorders / Q000378:metabolism*; D016212:Transforming Growth Factor beta / Q000037:antagonists & inhibitors* / Q000502:physiology
D053583:Interleukin-1beta; D016212:Transforming Growth Factor beta