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IL-1 beta Inhibits TGF beta in the Temporomandibular Joint
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lim, WH | - |
dc.contributor.author | Toothman, J | - |
dc.contributor.author | Miller, JH | - |
dc.contributor.author | Tallents, RH | - |
dc.date.accessioned | 2010-09-09T06:43:06Z | - |
dc.date.available | 2010-09-09T06:43:06Z | - |
dc.date.issued | 2009-06 | - |
dc.identifier.citation | J Dent Res 88:557-562 | en |
dc.identifier.issn | 0022-0345 | - |
dc.identifier.uri | https://hdl.handle.net/10371/69789 | - |
dc.description.abstract | 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 TNFα, 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-IL1β XAT 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. [PUBLICATION ABSTRACT] | en |
dc.description.sponsorship | This work was funded by grants DE017765 and AR055035 from
the National Institutes of Health. | en |
dc.language.iso | en | en |
dc.publisher | American and International Associations for Dental | en |
dc.title | IL-1 beta Inhibits TGF beta in the Temporomandibular Joint | en |
dc.type | Article | en |
dc.identifier.doi | 10.1177/0022034509336823 | - |
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