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JOURNAL ARTICLE
RANDOMIZED CONTROLLED TRIAL
Associations Between Knee Effusion-synovitis and Joint Structural Changes in Patients with Knee Osteoarthritis.
Journal of Rheumatology 2017 November
OBJECTIVE: To describe the associations between effusion-synovitis and joint structural abnormalities in patients with knee osteoarthritis (OA) over 24 months.
METHODS: A posthoc analysis using data from a randomized controlled trial in 413 patients with symptomatic OA (aged 63 ± 7 yrs, 208 women). Knee effusion-synovitis volume and score, cartilage defects, cartilage volume, and bone marrow lesions (BML) were assessed using magnetic resonance imaging. Joint space narrowing (JSN) and osteophytes were assessed using radiograph. Least significant change criterion was used to define change in effusion-synovitis volume. Knee symptoms were assessed by Western Ontario and McMaster University OA Index. Multivariable linear/logistic regression and multilevel generalized mixed-effects models were used in longitudinal analyses.
RESULTS: Total effusion-synovitis volume increased modestly from baseline (8.0 ± 8.5 ml) to followup (9.0 ± 10.5 ml). Baseline BML, cartilage defect, JSN, and osteophyte scores were positively associated with change in effusion-synovitis volume (p < 0.05). Baseline cartilage defects and JSN were also associated with change in effusion-synovitis score (p < 0.05). However, neither baseline effusion-synovitis score nor volume consistently predicted change in the above structures except cartilage volume. In the mixed-effects models, knee effusion-synovitis was positively associated with BML (volume: β = 1.19 ml/grade; score: OR = 1.75/grade) and cartilage defects (volume: β = 1.87 ml/grade; score: OR = 2.22/grade), while negatively associated with cartilage volume loss. Change in effusion-synovitis volume was positively correlated with changes in knee pain and stiffness scores (p < 0.05).
CONCLUSION: Knee cartilage and subchondral bone abnormalities predicted change in effusion-synovitis, but effusion-synovitis did not predict knee structural changes. These findings suggest that synovial inflammation is likely the result of joint structural abnormalities in established OA. ClinicalTrials.gov identifier: NCT01176344. Australian New Zealand Clinical Trials Registry: ACTRN12610000495022.
METHODS: A posthoc analysis using data from a randomized controlled trial in 413 patients with symptomatic OA (aged 63 ± 7 yrs, 208 women). Knee effusion-synovitis volume and score, cartilage defects, cartilage volume, and bone marrow lesions (BML) were assessed using magnetic resonance imaging. Joint space narrowing (JSN) and osteophytes were assessed using radiograph. Least significant change criterion was used to define change in effusion-synovitis volume. Knee symptoms were assessed by Western Ontario and McMaster University OA Index. Multivariable linear/logistic regression and multilevel generalized mixed-effects models were used in longitudinal analyses.
RESULTS: Total effusion-synovitis volume increased modestly from baseline (8.0 ± 8.5 ml) to followup (9.0 ± 10.5 ml). Baseline BML, cartilage defect, JSN, and osteophyte scores were positively associated with change in effusion-synovitis volume (p < 0.05). Baseline cartilage defects and JSN were also associated with change in effusion-synovitis score (p < 0.05). However, neither baseline effusion-synovitis score nor volume consistently predicted change in the above structures except cartilage volume. In the mixed-effects models, knee effusion-synovitis was positively associated with BML (volume: β = 1.19 ml/grade; score: OR = 1.75/grade) and cartilage defects (volume: β = 1.87 ml/grade; score: OR = 2.22/grade), while negatively associated with cartilage volume loss. Change in effusion-synovitis volume was positively correlated with changes in knee pain and stiffness scores (p < 0.05).
CONCLUSION: Knee cartilage and subchondral bone abnormalities predicted change in effusion-synovitis, but effusion-synovitis did not predict knee structural changes. These findings suggest that synovial inflammation is likely the result of joint structural abnormalities in established OA. ClinicalTrials.gov identifier: NCT01176344. Australian New Zealand Clinical Trials Registry: ACTRN12610000495022.
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