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Abstract Number: 2250

The Effects of Treatment on Disease Symptoms and Progression of Structural Changes in Knee Osteoarthritis Participants from the Osteoarthritis Initiative Progression Cohort

Jean-Pierre Pelletier1, Camille Roubille1, François Abram2, Marc Dorais3, Philippe Delorme1, Jean-Pierre Raynauld1 and Johanne Martel-Pelletier1, 1Osteoarthritis Research Unit, University of Montreal Hospital Research Centre (CRCHUM), Montreal, QC, Canada, 2Medical Imaging Research & Development, ArthroLab Inc., Montreal, QC, Canada, 3StatSciences Inc., Notre-Dame de l’Île-Perrot, QC, Canada

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: chondroitin, DMOAD, Lesions, meniscus and osteoarthritis

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Session Information

Title: Osteoarthritis - Clinical Aspects: Therapeutics

Session Type: Abstract Submissions (ACR)

Background/Purpose: In the perspective of personalized management of osteoarthritis (OA), a clinically relevant concern is the impact of meniscal extrusion on response to treatment. This study evaluated the role of meniscal extrusion on the effects of conventional OA pharmacological treatments and of the combination of glucosamine and chondroitin sulfate (Glu/CS) on knee structural changes.

Methods: Participants (n=600) from the OAI progression cohort were stratified based on whether or not they received conventional OA pharmacological treatment (analgesics/NSAIDs), the presence/absence of medial meniscal extrusion at baseline, and whether or not they received Glu/CS for 24 consecutive months (T24). The main outcomes were knee structural changes including cartilage volume measured by quantitative MRI and loss of joint space width (JSW).

Results: In both – and + analgesics/NSAIDs groups (n=300 each), participants with meniscal extrusion had more severe disease at baseline, more JSW loss (p≤0.0001) and cartilage volume loss in the medial compartment (p=0.003) compared to those without meniscal extrusion. In both analgesics/NSAIDs groups, no significant effect on JSW loss was found at T24 between groups regardless of the presence or absence of meniscal extrusion and of the consumption or not of Glu/CS, whereas significant differences emerged for cartilage volume loss. In the –analgesics/NSAIDs group, at T24, while no difference was found within the participants without meniscal extrusion (mild disease), in participants with meniscal extrusion (more progressive disease), Glu/CS had a protective effect on cartilage volume loss in the medial plateau (p=0.01, univariate analysis; p=0.009, multivariate analysis). In the +analgesics/NSAIDs group, in participants without meniscal extrusion (moderate disease), Glu/CS protected the cartilage volume in the lateral plateau(p=0.007, univariate analysis; p=0.013, multivariate analysis). No effect was found in participants from the +analgesics/NSAIDs group with meniscal extrusion (severe disease).

Conclusion: This study is the first to demonstrate, using qMRI, the response to conventional and Glu/CS treatments in subjects with meniscal extrusion. Data first revealed that Glu/CS prevented cartilage volume loss in patients with mild to moderate disease, i.e., subjects with meniscal extrusion not taking analgesics/NSAIDs and those without meniscal extrusion but taking analgesics/NSAIDs. The non-effect on patients without meniscal extrusion not taking analgesics/NSAIDs, representing very mild disease, probably reflects that the cartilage volume loss was small and unlikely to provide an accurate estimate. Moreover, in subjects with meniscal extrusion who took analgesics/NSAIDs (severe disease), the non-effect observed likely reflects irreversible cartilage damage. The present data argue for MRI based diagnosis of meniscal extrusion in clinical practice to help physicians identify knee OA patients more susceptible to benefit from DMOAD treatment. These data also support the added benefit of using qMRI as an alternative to X-ray for the evaluation of DMOAD agents, especially in patients with less advanced disease.


Disclosure:

J. P. Pelletier,

ArthroLab,

9;

C. Roubille,
None;

F. Abram,

ArthroLab,

3;

M. Dorais,

ArthroLab,

5;

P. Delorme,

ArthroLab,

3;

J. P. Raynauld,

ArthroLab,

5;

J. Martel-Pelletier,

ArthroLab,

9.

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