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- OA, osteoarthritis
- COX, cyclo-oxygenase
- IL, interleukin
- IL1Ra, IL1 receptor antagonist
- MMP, matrix metalloproteinase
- MRI, magnetic resonance imaging
Over the last decade, there have been several interesting advances in the treatment of osteoarthritis (OA). A clearer understanding of the pathophysiology of this disease1 has facilitated the development of new approaches for treatments aimed at specifically and effectively retarding disease progress. New classes of molecules that inhibit one or more OA catabolic processes are under evaluation for their potential to alter the degenerative process.
OA can be described as the degradation and loss of articular cartilage accompanied by subchondral bone remodelling, osteophyte formation, and synovial membrane inflammation. This is clinically reflected by gradual development of fluctuating joint pain, swelling, stiffness, and loss of motion. Pharmacological interventions have focused on treating pain, primarily using non-steroidal anti-inflammatory drugs (NSAIDs), analgesics, and, more recently, specific cyclo-oxygenase-2 (COX-2) inhibitors. The rationale behind this was to inhibit COX, the key enzymes that metabolise arachidonic acid to prostaglandins.
THERAPEUTICS IN OSTEOARTHRITIS
Clinical studies to date have focused on the alleviation of signs and symptoms, for which comparable efficacy has generally been found for NSAIDs and acetaminophen in stable cohorts of patients with mild to moderate OA.2,3 Published data on the use of intra-articular corticosteroids for OA have shown short term (up to four weeks) improvement in signs and symptoms compared with placebo.2,4 The comparative efficacy of these agents in the treatment of episodic crystal induced inflammatory exacerbations superimposed on chronic OA in selected patients,5 for which one might predict the superior efficacy of NSAIDs or corticosteroids over acetaminophen, has not been studied. However, the main objectives in the management of OA are not only to reduce symptoms and minimise functional disability, but also to limit progression of structural changes.
As there are in vitro data to indicate that corticosteroids inhibit synoviocytes and chondrocyte production of interleukin 1 (IL1), COX-2, and tumour necrosis …
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