The association between subchondral bone cysts and tibial cartilage volume and risk of joint replacement in people with knee osteoarthritis: A longitudinal study

Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Alfred Hospital, Commercial Rd, Melbourne 3004, Victoria, Australia.
Arthritis research & therapy (Impact Factor: 3.75). 03/2010; 12(2):R58. DOI: 10.1186/ar2971
Source: PubMed


To examine the natural history of subchondral bone cysts and to determine whether knee cartilage loss and risk of joint replacement is higher in knees with cysts, compared with those with bone marrow lesions (BMLs) only or those with neither BMLs nor cysts.
The symptomatic knee in 132 subjects with knee osteoarthritis (OA) was imaged by using magnetic resonance imaging at baseline and 2 years later. Tibial cartilage volume, subchondral bone cysts, and BMLs were measured by using validated methods. Knee arthroplasty over a 4-year period was ascertained.
Bone cysts were present in 47.7% of subjects, 98.1% of whom also had BMLs. Over a 2-year period, 23.9% of subjects had cysts progress, 13.0% developed new cysts, and 11.4% had cysts regress. Bone cysts at baseline were associated with lower medial and lateral tibial cartilage volume compared with those with BMLs only or those with neither (P for trend 0.004 and <0.001, respectively). Annual medial cartilage volume loss was greatest in those with bone cysts compared with those with BMLs only or those with neither (9.3%, 6.3%, and 2.6%, respectively; P for trend, <0.001). As the severity of bone abnormality in the medial compartment increased from no BMLs or cysts present, to BMLs only, to subchondral bone cysts present, the risk of knee replacement was increased (odds ratio, 1.99; 95% confidence interval (CI), 1.01 to 3.90; P = 0.05).
When cysts are present, cartilage loss and risk of knee replacement are higher than if only BMLs are present, suggesting that cysts identify those most likely to benefit from prevention of disease progression. As cysts can regress, they may also provide therapeutic targets in knee OA.

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    • "BMLs arise in regions of predicted high loading and contain abnormal bone, with areas of osteocyte death, areas of bone sclerosis with reduced mineral density [26]. Longitudinal studies have shown that BMLs occur adjacent to sites of current or future cartilage degeneration and are predictive of structural deterioration in knee OA [26–29] and future joint replacement [30]. "
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    ABSTRACT: There is now general agreement that osteoarthritis (OA) involves all structures in the affected joint, culminating in the degradation of the articular cartilage. It is appropriate to focus particularly on the subchondral bone because characteristic changes occur in this tissue with disease progression, either in parallel, or contributing to, the loss of cartilage volume and quality. Changes in both the articular cartilage and the subchondral bone are mediated by the cells in these two compartments, chondrocytes and cells of the osteoblast lineage, respectively, whose primary roles are to maintain the integrity and function of these tissues. In addition, altered rates of bone remodeling across the disease process are due to increased or decreased osteoclastic bone resorption. In the altered mechanical and biochemical environment of a progressively diseased joint, the cells function differently and show a different profile of gene expression, suggesting direct effects of these external influences. There is also ex vivo and in vitro evidence of chemical crosstalk between the cells in cartilage and subchondral bone, suggesting an interdependence of events in the two compartments and therefore indirect effects of, for example, altered loading of the joint. It is ultimately these cellular changes that explain the altered morphology of the cartilage and subchondral bone. With respect to crosstalk between the cells in cartilage and bone, there is evidence that small molecules can transit between these tissues. For larger molecules, such as inflammatory mediators, this is an intriguing possibility but remains to be demonstrated. The cellular changes during the progression of OA almost certainly need to be considered in a temporal and spatial manner, since it is important when and where observations are made in either human disease or animal models of OA. Until recently, comparisons have been made with the assumption, for example, that the subchondral bone is behaviorally uniform, but this is not the case in OA, where regional differences of the bone are evident using magnetic resonance imaging (MRI). Nevertheless, an appreciation of the altered cell function during the progression of OA will identify new disease modifying targets. If, indeed, the cartilage and subchondral bone behave as an interconnected functional unit, normalization of cell behavior in one compartment may have benefits in both tissues.
    Full-text · Article · Jan 2014 · Current Osteoporosis Reports
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    • "The cavitary lesions in subchondral bone, which are normally referred to as ‘subchondral bone cysts’, are commonly reported in patients with OA [113] (Figure 3A, B). Recent evidence suggests that patients with SBCs had greater disease severity and pain, and a higher risk of joint replacement [113]. "
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    ABSTRACT: Osteoarthritis (OA) is a major cause of disability in the adult population. As a progressive degenerative joint disorder, OA is characterized by cartilage damage, changes in the subchondral bone, osteophyte formation, muscle weakness, and inflammation of the synovium tissue and tendon. Although OA has long been viewed as a primary disorder of articular cartilage, subchondral bone is attracting increasing attention. It is commonly reported to play a vital role in the pathogenesis of OA. Subchondral bone sclerosis, together with progressive cartilage degradation, is widely considered as a hallmark of OA. Despite the increase in bone volume fraction, subchondral bone is hypomineralized, due to abnormal bone remodeling. Some histopathological changes in the subchondral bone have also been detected, including microdamage, bone marrow edema-like lesions and bone cysts. This review summarizes basic features of the osteochondral junction, which comprises subchondral bone and articular cartilage. Importantly, we discuss risk factors influencing subchondral bone integrity. We also focus on the microarchitectural and histopathological changes of subchondral bone in OA, and provide an overview of their potential contribution to the progression of OA. A hypothetical model for the pathogenesis of OA is proposed.
    Full-text · Article · Dec 2013 · Arthritis research & therapy
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    • "If osteoclastic bone resorption reduces bony support for the overlying cartilage, this can facilitate progression of OA [25]. Studies of people with knee OA have observed that cartilage loss and risk of knee replacement are higher if subchondral bone cysts are present than if only bone marrow lesions (BMLs) are present, suggesting that cysts identify those most likely to benefit from prevention of disease progression [36]. These studies support the hypothesis that subchondral bone is important to progression of joint disease, and that factors which result in cartilage destruction may come from subchondral bone [37]. "
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