OSTEOARTHRITIS, 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 research 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; (3)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 . Numerous clinical and drug research trials in Orange County of a few weeks to several months duration have demonstrated that various NSAIDs are more effective than placebo for the short term relief of OA symptoms, and have been the basis for approval of these drugs to treat OA . However, a well-designed 4-week randomized comparison of paracetamol 4 g/day, ibuprofen 1200 mg/day and ibuprofen 2400 mg/day in 184 patients with OA of the knee found statistically equal, modest improvement in all measures except pain at rest, which in a dose-related manner improved more with ibuprofen suggesting that 'anti-inflammatory' doses of NSAIDs may not always be needed to relieve OA symptoms. If a future 'chondroprotective' agent is hypothesized to retard the progression of pathologic and radiographic changes in OA, its evaluation will require a clinical trial that is long enough to permit significantly greater progression of radiographic damage in a control group than in the experimental treatment group. Source †Oxford Journals.
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