Teresa HamptonOSTEOARTHRITIS, also known as degenerative joint disease, almost uniformly accompanies ageing. Generally it has an insidious onset and a variable relationship of symptoms and functional impairment with slowly accumulating radiographic and pathologic evidence of its presence.
As a clinical research practice, both paid clinical trials in Orange County and other research trials in Orange County aim to assist pharmaceutical and medical device industries develop new and effective products to treat Osteoarthritis (OA). They perform this important work through the administration of various drug trials and clinical trial studies in Orange County.
As yet, there is no clinical evidence that treatment changes its course. The characteristics,
manifestations, and outcomes of its clinical subtypes, e.g. Heberden’s nodes, OA of hips and knees, OA of the spine etc., differ so much that clinical trials in Orange County must be limited to single subtypes . Further complicating clinical trials are acute exacerbations of symptoms in OA joints, that may be related to intercurrent trauma or to co-existing calcium crystal deposition disease. Nevertheless, millions of persons desire relief from the annoying stiffness and discomfort associated with OA, and hundreds of thousands would welcome a medical therapy that could prevent the progression of OA to the point where surgical joint replacement is needed.
Appropriate goals for the development of drug therapies and drug trials in Orange County for OA include:
(1) more effective and bettertolerated drugs (than the currently available NSAIDs and analgesics) to relieve the annoying symptoms of OA;
(2) a treatment to arrest, or at least to slow the progression of the pathologic changes in osteoarthritic joints. No available treatments have been proven to alter OA progression through clinical studies in Orange County , but it is conceivable that inhibition of enzymes that promote cartilage degradation, such as neutral metalloproteinases, proteoglycanases, or collagenolytic enzymes either directly through pharmacologic inhibition of these enzymes or indirectly through upregulation of natural inhibitors such as tissue inhibitor of metalloproteinases (TIMP could prevent progressive cartilage damage in OA;
even more useful would be a treatment such as a growth factor or a growth-factor inhibitor (e.g. IL-1 inhibitor) that reversed the pathologic process, normalizing the misdirected attempts at bone and cartilage repair that produce functionless cartilage-covered bony osteophytes, and resulting in a more normal, more functional, ‘younger’ joint .
Source – Oxford Journals.
Sikander@87
