Vitamin D does not reduce OA knee pain, progression
Vitamin D supplementation does not slow progression of knee osteoarthritis (OA) or reduce pain associated with the condition, according to a study published January 9 in the Journal of the American Medical Association.
Although some studies have indicated the supplement may offer protection against structural progression, Timothy McAlindon, DM, MPH, of Tufts Medical Center in Boston, Mass. and colleagues found that patients who took vitamin D for 2 years at a dose sufficient to elevate 25-hydroxyvitamin D plasma levels to higher than 36 ng/mL did not experience less knee pain or cartilage volume loss compared with patients who took placebo.
“Knee osteoarthritis is a common age-related musculoskeletal disorder that has significant functional impact and has considerable societal costs through work loss, early retirement, and arthroplasty,” the authors wrote. “Despite its impact, there are no medical treatments established to influence the course of the disease.”
The authors randomized 146 patients aged 45 years and older at Tufts Medical Center between March 2006 and June 2009 with symptomatic knee OA to receive oral cholecalciferol, 2,000 IU/d, with dose escalation to elevate serum levels to more than 36 ng/mL, or placebo. Over the course of the study, patients regularly rated their knee pain on a scale of 0 to 20, with 20 representing extreme pain, and the researchers measured cartilage volume loss using magnetic resonance imaging.
By the end of the study, the researchers noted that 61.3% of the patients in the treatment group and 8.3% in the placebo group had reached the blood level goal of 36 ng/mL; however, there was no significant difference between groups in terms of pain or cartilage loss.
Both groups reported reduced knee pain (treatment group mean: −2.31; 95% CI, −3.24 to −1.38; placebo group mean: −1.46; 95% CI, −2.33 to −0.60). Also, the percentage of cartilage volume decreased similarly in both groups (mean: −4.30; 95% CI, −5.48 to −3.12 vs. mean: −4.25; 95% CI, −6.12 to −2.39; P=.96).
The authors acknowledge that the 2-year duration may have been an insufficient timeframe and that the extent of patient disease may have precluded therapeutic intervention.
