IL-1beta inhibits TGFbeta in the temporomandibular joint.
J Dent Res
; 88(6): 557-62, 2009 Jun.
Article
en En
| MEDLINE
| ID: mdl-19587162
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.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Osteoartritis
/
Articulación Temporomandibular
/
Trastornos de la Articulación Temporomandibular
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Factor de Crecimiento Transformador beta
/
Interleucina-1beta
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
J Dent Res
Año:
2009
Tipo del documento:
Article
Pais de publicación:
Estados Unidos