Cartilage failure in osteoarthritis: Relevance of normal structure and function. A review
1991; Wiley; Volume: 4; Issue: 3 Linguagem: Inglês
10.1002/ca.980040303
ISSN1098-2353
Autores Tópico(s)Inflammatory mediators and NSAID effects
ResumoAbstract Osteoarthritis is a multifactorial condition of diverse etiology affecting synovial joints, in which the final common pathway is destruction and loss of articular cartilage (and changes in other joint structures), which normally protects the bone against compressive and shearing forces. Known causes of secondary osteoarthritis can be grouped into those that cause abnormal stresses and those that produce an abnormal cartilage. The resulting imbalance between tissue texture and mechanical environment may eventually lead to cartilage destruction. The histopathology of cartilage fibrillation is described and related to its normal structure, particularly collagen fibril orientation. Load carriage in normal cartilage involves an interaction between the fibril mesh, proteoglycan, and water. Possible defects in normal matrix organization may lead to failure of this mechanism and to structural breakdown of the cartilage. Biochemical changes in the matrix in early osteoarthritis, particularly in experimental models, are described. The initial change, before loss of proteoglycan or fibril breakage, is an increased water content. A similar change is seen in normal cartilage after brief exercise. There may be a mechanism common to both the normal reversible change (thus providing a means for adaption to changed stresses) and the pathological prolonged change. Chondrocyte metabolism and its modification in early degenerative change are described. Factors regulating metabolism include nutrition, growth factors and cytokines, ionic constitution of the matrix, and mechanical stimuli. Known causes of secondary osteoarthritis may act via these factors to cause changes in cell metabolism that play a part in the initiation and ongoing pathogenesis of cartilage failure.
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