الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
OA is the most common chronic joint disorder characterized as joint failure due to progressive changes in several components of the musculoskeletal system that include not only the articular cartilage but also other joint structures.
OA result from a failure of chondrocytes within the joint to synthesize a good quality matrix, and to maintain the balance between synthesis and degradation of the ECM, also increasing synthesis of proteinases, and decreased synthesis of natural inhibitors of these proteinases.
Symptoms are often initially insidious and can be highly variable, including pain and Stiffness and Impaired Function. Signs include localized tenderness, crepitus and cracking on motion, mild joint enlargement, gross firm deformity (later).
Optimal management requires early diagnosis (Standard radiographs are the most common investigations) and awareness of the risk factors that can affect the prognosis.
OA represents a major therapeutic challenge. It is related, at least in part, to the lack of effective therapies able to alter the natural history of OA progression. Thus, the future for better effective symptomatic and/or disease-modifying drugs with a better benefit/risk ratio will certainly come from a better understanding of the pathophysiology of the disease to test specific targets involved in pain and in joint degradative processes.
Some agents have slowed structural progression without symptomatic benefit suggesting that simply slowing progression may not be sufficient to lead to symptom improvement. Pain relief remains a primary unmet medical need. Several compounds are focussed on pain, demonstrating the recent advances in the knowledge of pain pathways at the molecular level.