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2015 ; 27
(3
): 289-94
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Biologic basis of osteoarthritis: state of the evidence
#MMPMID25784380
Malemud CJ
Curr Opin Rheumatol
2015[May]; 27
(3
): 289-94
PMID25784380
show ga
PURPOSE OF REVIEW: Evidence accumulated since 2010 indicates that human
osteoarthritis should now be reclassified as a systemic musculoskeletal disease
rather than a focal disorder of synovial joints. RECENT FINDINGS: Inflammation
was seen as the key component promoting synovitis as well as progression of
cartilage and bone destruction in osteoarthritis. Thus, metabolic-triggered
inflammation involving cytokines, adipokines, abnormal metabolites, acute phase
reactants and even complement, all appear to play major roles in osteoarthritis
pathophysiology. Immune-mediated inflammation involving T cells and B cells as
well as macrophages is now considered a common finding in osteoarthritis synovial
tissue. Many experimental and clinical analyses showed that the proinflammatory
cytokines, which stimulate matrix metalloproteinase and a disintegrin and
metalloproteinase with thrombospondin motif gene transcription in normal and
osteoarthritis human chondrocyte cultures, are also present at significantly
elevated levels in the synovial fluid of osteoarthritis patients compared with
nonarthritic synovial fluids. SUMMARY: Human osteoarthritis is a systemic
musculoskeletal disorder involving activation of innate and adaptive immune
systems accompanied by inflammation exemplified by the elevated production of
proinflammatory cytokines, which play a significant role in the progression of
the disease. The future of novel therapies for osteoarthritis should consider
developing drug development strategies designed to inhibit proinflammatory
cytokine-induced signal transduction. These strategies have been successful in
the development of drugs for the treatment of rheumatoid arthritis.