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Journal of Dental Research
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Biological

IL-1β Inhibits TGFβ in the Temporomandibular Joint

W.H. Lim1, J. Toothman2, J.H. Miller2, R.H. Tallents2, S.M. Brouxhon3,5, M.E. Olschowka2 and S. Kyrkanides2,4,*

1 Department of Orthodontics, School of Dentistry, Dental Research Institute, Seoul National University, Seoul, Korea;
2 Division of Orthodontics & TMJ Disorders, Eastman Dental Center, University of Rochester Medical Center, 625 Elmwood Ave, Rochester, NY 14620, USA;
3 Department of Emergency Medicine, School of Medicine, Stony Brook University, Stony Brook, NY 11794, USA; and
4 Departments of Children’s Dentistry and
5 Emergency Medicine, Stony Brook University, Stony Brook, NY 11794-8700, USA

Correspondence: * Kyrkanides{at}gmail.com

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{alpha}, are known to contribute to the development of osteoarthritis, whereas TGFβ has been associated with articular regeneration. We hypothesized that a balance between IL-1β and TGFβ underlies the development of TMJ osteoarthritis, whereby IL-1β signaling down-regulates TGFβ expression as part of disease pathology. Our studies in wild-type mice, as well as the Col1-IL1βXAT mouse model of osteoarthritis, demonstrated an inverse correlation between IL-1β and TGFβ expression in the TMJ. IL-1β etiologically correlated with joint pathology, whereas TGFβ expression associated with IL-1β 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.

Key Words: IL-1β • TMJ pathology • TGFβ

Journal of Dental Research, Vol. 88, No. 6, 557-562 (2009)
DOI: 10.1177/0022034509336823
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