TY - JOUR
T1 - IL-lβ inhibits TGFβ in the temporomandibular joint
AU - Lim, W. H.
AU - Toothman, J.
AU - Miller, J. H.
AU - Tallents, R. H.
AU - Brouxhon, S. M.
AU - Olschowka, M. E.
AU - Kyrkanides, S.
PY - 2009/6/1
Y1 - 2009/6/1
N2 - 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-IL1βXAT 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.
AB - 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-IL1βXAT 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.
KW - Il-1β
KW - Tgfβ
KW - Tmj pathology
UR - http://www.scopus.com/inward/record.url?scp=67650721756&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=67650721756&partnerID=8YFLogxK
U2 - 10.1177/0022034509336823
DO - 10.1177/0022034509336823
M3 - Article
C2 - 19587162
AN - SCOPUS:67650721756
SN - 0022-0345
VL - 88
SP - 557
EP - 562
JO - Journal of Dental Research
JF - Journal of Dental Research
IS - 6
ER -