Change in joint space width: Hyaline articular cartilage loss or alteration in meniscus?

Boston University Clinical Epidemiology Research and Training Unit, Arthritis Center, and Boston Medical Center, Boston, Massachusetts 02118, USA.
Arthritis & Rheumatology (Impact Factor: 7.76). 08/2006; 54(8):2488-95. DOI: 10.1002/art.22016
Source: PubMed

ABSTRACT To explore the relative contribution of hyaline cartilage morphologic features and the meniscus to the radiographic joint space.
The Boston Osteoarthritis of the Knee Study is a natural history study of symptomatic knee osteoarthritis (OA). Baseline and 30-month followup assessments included knee magnetic resonance imaging (MRI) and fluoroscopically positioned weight-bearing knee radiographs. Cartilage and meniscal degeneration were scored on MRI in the medial and lateral tibiofemoral joints using a semiquantitative grading system. Meniscal position was measured to the nearest millimeter. The dependent variable was joint space narrowing (JSN) on the plain radiograph (possible range 0-3). The predictor variables were MRI cartilage score, meniscal degeneration, and meniscal position measures. We first conducted a cross-sectional analysis using multivariate regression to determine the relative contribution of meniscal factors and cartilage morphologic features to JSN, adjusting for body mass index (BMI), age, and sex. The same approach was used for change in JSN and change in predictor variables.
We evaluated 264 study participants with knee OA (mean age 66.7 years, 59% men, mean BMI 31.4 kg/m(2)). The results from the models demonstrated that meniscal position and meniscal degeneration each contributed to prediction of JSN, in addition to the contribution by cartilage morphologic features. For change in medial joint space, both change in meniscal position and change in articular cartilage score contributed substantially to narrowing of the joint space.
The meniscus (both its position and degeneration) accounts for a substantial proportion of the variance explained in JSN, and the change in meniscal position accounts for a substantial proportion of change in JSN.

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Available from: Michael P Lavalley, Sep 23, 2014
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    • "In recent years, there has been a dramatic advance in our understanding of the integral role of the menisci for knee function and the consequences of meniscal abnormality on the development of OA. Studies have found that meniscal degeneration is a general feature of knee OA and contributes to joint space narrowing [1, 2]. Meniscal lesions at baseline were more common in knees that developed OA than in the knees that did not develop OA during a 30-month follow-up period [3]. "
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    ABSTRACT: Phosphocitrate (PC) inhibited meniscal calcification and the development of calcium crystal-associated osteoarthritis (OA) in Hartley guinea pigs. However, the mechanisms remain elusive. This study sought to examine the biological activities of PC in the absence of calcium crystals and test the hypothesis that PC is potentially a meniscal protective agent. We found that PC downregulated the expression of many genes classified in cell proliferation, ossification, prostaglandin metabolic process, and wound healing, including bloom syndrome RecQ helicase-like, cell division cycle 7 homolog, cell division cycle 25 homolog C, ankylosis progressive homolog, prostaglandin-endoperoxide synthases-1/cyclooxygenase-1, and plasminogen activator urokinase receptor. In contrast, PC stimulated the expression of many genes classified in fibroblast growth factor receptor signaling pathway, collagen fibril organization, and extracellular structure organization, including fibroblast growth factor 7, collagen type I, alpha 1, and collagen type XI, alpha 1. Consistent with its effect on the expression of genes classified in cell proliferation, collagen fibril organization, and ossification, PC inhibited the proliferation of OA meniscal cells and meniscal cell-mediated calcification while stimulating the production of collagens. These findings indicate that PC is potentially a meniscal-protective agent and a disease-modifying drug for arthritis associated with severe meniscal degeneration.
    07/2013; 2013(8):726581. DOI:10.1155/2013/726581
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    • "It was previously believed that JSN and its changes reflect only articular cartilage thinning, but several studies have shown that alterations in the meniscus, such as meniscal extrusion or subluxation, also contribute to JSN [1,15,16]. A more recent study, by Hunter and colleagues [1], compared MRI and weight-bearing posteroanterior radiographs to explore the relative contribution of several morphologic features, including cartilage, meniscal damage, and position, to the radiographically detected JSN. "
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    ABSTRACT: Imaging of cartilage has traditionally been achieved indirectly with conventional radiography. Loss of joint space width, or 'joint space narrowing', is considered a surrogate marker for cartilage thinning. However, radiography is severely limited by its inability to visualize cartilage, the difficulty of ascertaining the optimum and reproducible positioning of the joint in serial assessments, and the difficulty of grading joint space narrowing visually. With the availability of advanced magnetic resonance imaging (MRI) scanners, new pulse sequences, and imaging techniques, direct visualization of cartilage has become possible. MRI enables visualization not only of cartilage but also of other important features of osteoarthritis simultaneously. 'Pre-radiographic' cartilage changes depicted by MRI can be measured reliably by a semiquantitative or quantitative approach. MRI enables accurate measurement of longitudinal changes in quantitative cartilage morphology in knee osteoarthritis. Moreover, compositional MRI allows imaging of 'pre-morphologic' changes (that is, visualization of subtle intrasubstance matrix changes before any obvious morphologic alterations occur). Detection of joint space narrowing on radiography seems outdated now that it is possible to directly visualize morphologic and pre-morphologic changes of cartilage by using conventional as well as complex MRI techniques.
    Arthritis research & therapy 11/2011; 13(6):247. DOI:10.1186/ar3488 · 3.75 Impact Factor
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    • "The authors argued that the relatively high SRM of the minimal JSW measured by Lyon Schuss may be due to the fluoroscopic guidance providing optimal alignment of the anterior and posterior tibial rim, and to radiography being performed under weight-bearing conditions where the cartilage tissue is compressed, while MRI is performed in a supine non weight-bearing position. Also, it must be kept in mind that radiographic assessment of JSW depends also on meniscus extrusion, and not only on cartilage thickness [113–115] and that meniscus pathology, in particularly subluxation, can therefore cause changes in JSW over time in the absence of cartilage loss. Duryea et al. recently compared the responsiveness (=sensitivity to change) of radiography with that of MRI in the first release of the OAI cohort (150 subjects) over 12 months [116]. "
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    ABSTRACT: Quantitative measures of cartilage morphology (i.e., thickness) represent potentially powerful surrogate endpoints in osteoarthritis (OA). These can be used to identify risk factors of structural disease progression and can facilitate the clinical efficacy testing of structure modifying drugs in OA. This paper focuses on quantitative imaging of articular cartilage morphology in the knee, and will specifically deal with different cartilage morphology outcome variables and regions of interest, the relative performance and relationship between cartilage morphology measures, reference values for MRI-based knee cartilage morphometry, imaging protocols for measurement of cartilage morphology (including those used in the Osteoarthritis Initiative), sensitivity to change observed in knee OA, spatial patterns of cartilage loss as derived by subregional analysis, comparison of MRI changes with radiographic changes, risk factors of MRI-based cartilage loss in knee OA, the correlation of MRI-based cartilage loss with clinical outcomes, treatment response in knee OA, and future directions of the field.
    01/2011; 2011(2090-1984):475684. DOI:10.1155/2011/475684
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