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Nat Rev Rheumatol. 2012 Nov;8(11):665-73. doi: 10.1038/nrrheum.2012.130. Epub 2012 Aug 7.

Bone remodelling in osteoarthritis.

Author information

1
Department of Anatomy and Cell Biology, MS 5035, Indiana University School of Medicine, Indianapolis, IN 46202, USA. dburr@iupui.edu

Abstract

The classical view of the pathogenesis of osteoarthritis (OA) is that subchondral sclerosis is associated with, and perhaps causes, age-related joint degeneration. Recent observations have demonstrated that OA is associated with early loss of bone owing to increased bone remodelling, followed by slow turnover leading to densification of the subchondral plate and complete loss of cartilage. Subchondral densification is a late event in OA that involves only the subchondral plate and calcified cartilage; the subchondral cancellous bone beneath the subchondral plate may remain osteopenic. In experimental models, inducing subchondral sclerosis without allowing the prior stage of increased bone remodelling to occur does not lead to progressive OA. Therefore, both early-stage increased remodelling and bone loss, and the late-stage slow remodelling and subchondral densification are important components of the pathogenetic process that leads to OA. The apparent paradoxical observations that OA is associated with both increased remodelling and osteopenia, as well as decreased remodelling and sclerosis, are consistent with the spatial and temporal separation of these processes during joint degeneration. This Review provides an overview of current knowledge on OA and discusses the role of subchondral bone in the initiation and progression of OA. A hypothetical model of OA pathogenesis is proposed.

PMID:
22868925
DOI:
10.1038/nrrheum.2012.130
[Indexed for MEDLINE]

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