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Abstract
Osteoarthritis (OA) is the most common form of arthritis in the world and is characterized by pain, various disabilities and loss of quality of life. Chondroitin sulfate (CS) is recommended as first-line therapy. CS of non-animal origin is of great interest for safety and sustainability reasons. This study aims to investigate the anti-inflammatory effects, anti-pain and ability-enhancement of a short-term supplementation with non-animal CS in overweight subjects with OA. In a randomized, double-blind, placebo-controlled pilot study, 60 overweight adults with symptomatic OA were allocated to consume 600 mg of non-animal CS (n = 30) or a placebo (n = 30) daily for 12 consecutive weeks. The assessment of knee-pain, quality of life, related inflammation markers and body composition was performed at 0, 4 and 12 weeks. The Tegner Lysholm Knee Scoring (TLKS) scale of the experimental group showed a statistically significant increase (+10.64 points; confidence interval (95% confidence interval (CI) 5.57; 15.70; p < 0.01), while the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) score decreased (−12.24 points; CI 95% −16.01; −8.38; p < 0.01). The results also showed a decrease in the C-reactive protein (CRP) level (−0.14 mg/dL, CI 95% −0.26; −0.04; p < 0.01) and erythrocyte sedimentation rate (ESR) level (−5.01 mm/h, CI 95% −9.18; −0.84, p < 0.01) as well as the visual analogue scale (VAS) score in both knees. In conclusion, this pilot study demonstrates the effectiveness of non-animal CS supplementation in overweight subjects with knee OA in improving knee function, pain and inflammation markers.
Highlights
Knee osteoarthritis (OA) is predicted to become the fourth leading cause of disability worldwide by 2020 [1] and is estimated to affect more than 40 million people in Europe [2] and 4 million people in Italy [3]
Knee OA is associated with joint stiffness, pain, and impairment in joint functions and its prevalence increases with age
Disease progression is associated with cartilage degradation, joint stiffness, joint space narrowing, pain and motility impairment
Summary
Knee osteoarthritis (OA) is predicted to become the fourth leading cause of disability worldwide by 2020 [1] and is estimated to affect more than 40 million people in Europe [2] and 4 million people in Italy [3]. OA has multifactorial etiology, and obesity is one of the most important risk factors for knee OA [4,5,6], together with a sedentary lifestyle. Knee OA is associated with joint stiffness, pain, and impairment in joint functions and its prevalence increases with age. Disease progression is associated with cartilage degradation, joint stiffness, joint space narrowing, pain and motility impairment. OA is further related to local and systemic inflammation. Inflammatory mediators are produced by articular tissues and are involved in disease pathogenesis
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