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Bone remodelling in osteoarthritis

Nature Reviews Rheumatology volume 8, pages 665–673 (2012)Cite this article

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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.

Key Points

  • Subchondral cortical bone and subchondral cancellous bone are architecturally, physiologically and mechanically different, and respond differently in osteoarthritis (OA)

  • The initiation and the progression of OA are distinct pathophysiological processes

  • The early stages of OA are characterized by increased vascularity and reduced bone density

  • Late-stage OA is characterized by decreased bone resorption without a decrease in bone formation, and by the development of subchondral sclerosis

  • Increased bone remodelling is a necessary condition for OA; increased subchondral bone density alone does not lead to OA

  • Antiresorptive agents that suppress bone remodelling during late stages of OA have not proven, and are not likely, to be effective treatments

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Figure 1: Stages of progressive join degradation in OA.
Figure 2: Bone and cartilage density.
Figure 3: Subchondral sclerosis in osteoarthritis.
Figure 4: Changes in bone remodelling in late-stage OA.
Figure 5: Hypothetical model for OA pathogenesis.

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

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D. B. Burr has researched data for the article and wrote the article. Both authors made a substantial contribution to discussion of the content and reviewing and editing of the manuscript before submission.

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D. B. Burr declares that he has received research grants from Amgen and Eli Lilly. He has also been on the advisory panel for Merck and has been a consultant for Wright Medical. M. A. Gallant declares no competing interests.

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Burr, D., Gallant, M. Bone remodelling in osteoarthritis. Nat Rev Rheumatol 8, 665–673 (2012). https://doi.org/10.1038/nrrheum.2012.130

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