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Age-related changes in multiple components of the musculoskeletal system may contribute
to the well established link between aging and osteoarthritis (OA). This review focused
on potential mechanisms by which age-related changes in the articular cartilage could
contribute to the development of OA.
The peer-reviewed literature published prior to February 2009 in the PubMed database
was searched using pre-defined search criteria. Articles, selected for their relevance
to aging and articular chondrocytes or cartilage, were summarized.
Articular chondrocytes exhibit an age-related decline in proliferative and synthetic
capacity while maintaining the ability to produce pro-inflammatory mediators and matrix
degrading enzymes. These findings are characteristic of the senescent secretory phenotype
and are most likely a consequence of extrinsic stress-induced senescence driven by
oxidative stress rather than intrinsic replicative senescence. Extracellular matrix
changes with aging also contribute to the propensity to develop OA and include the
accumulation of proteins modified by non-enzymatic glycation.
The effects of aging on chondrocytes and their matrix result in a tissue that is less
able to maintain homeostasis when stressed, resulting in breakdown and loss of the
articular cartilage, a hallmark of OA. A better understanding of the basic mechanisms
underlying senescence and how the process may be modified could provide novel ways
to slow the development of OA.