Human joints
One disease modifying strategy is to suppress the progressive degradation of cartilage that occurs in OA. human joints Arthritis in the neck. To accomplish this, the ratio of MMP inhibitors to MMP enzymes must be shifted in favor of the former. This could be accomplished by enhancing articular levels of TIMP by recombinant gene therapy or by administration of exogenous TIMP. Studies of exogenous TIMP administration to animals with OA-like disease have had inconclusive results, however, perhaps due to ineffective penetration of this relatively high molecular weight protein into the cartilage matrix. human joints Arthritis cartoons. An alternate approach , that has progressed more rapidly, is to develop oral inhibitors of MMPs. In fact, several synthetic small molecular weight inhibitors of MMPs have proven efficacious in animal models of arthritis and are entering Phase III clinical trials in humans. The antibiotic, tetracycline, and its semisynthetic derivatives, doxycycline and minocycline, have modest MMP inhibitory properties and have prompted investigations of these agents in the treatment of both OA and RA. human joints Canadian-arthritis-society. Finally, inhibition of IL-1, via administration of a soluble IL-1 receptor or receptor antagonist, represents another rational strategy for suppressing MMP synthesis, and preliminary studies in RA are also promising. Enhancing the repair of damaged cartilage constitutes another rational strategy for the treatment and/or prevention of OA. Administration of exogenous growth factors, such as IGF and bFGF, to stimulate chondrocyte proliferation and/or matrix synthesis has had beneficial effects in animals models of OA, and TGF-? has the added advantage of suppressing MMP synthesis.
Human joints
Severe hip pain || Exercise-arthritis || Rheumatoid-arthritis-caregivers || Human joints