Vitamin D Did Not Reduce Knee OA Pain, Cartilage Loss in RCT

Janis C. Kelly

March 09, 2016

Vitamin D, which can reduce bone turnover and cartilage degradation, did not slow progression of knee osteoarthritis (OA) or reduce knee OA pain when tested in a randomized placebo-controlled trial.

Xingzhong Jin, MD, from the Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia, and colleagues published their findings in the March 8 issue of in JAMA.

The researchers, led by Changhai Ding, MD, PhD, also from the Menzies Institute for Medical Research, enrolled 413 patients with symptomatic knee OA and low 25-hydroxyvitammin C levels (defined as 12.5 - 60 nmol/L) in the multicenter study, which was conducted in Tasmania and Victoria, Australia. The researchers randomly assigned the patients to 2 years of monthly treatment with oral vitamin D3 (50,000 IU, n = 209) or with an identical placebo capsule (n = 204). Three hundred forty (82.3%) of the subjects completed the study.

The primary study outcomes were changes (from baseline to month 24) in functional magnetic resonance imaging tibial cartilage volume and in Western Ontario and McMaster Universities Arthritis Index (WOMAC) pain score. The five prespecified secondary outcomes were cartilage defects, tibial plateau bone area, subchondral bone marrow lesion, meniscal tear and extrusion, and lower limb muscle strength. This report included only data for functional magnetic resonance imaging changes in tibiofemoral cartilage defects and in tibiofemoral bone marrow lesions.

After 24 months of treatment, changes with vitamin D vs placebo were: tibial cartilage volume, −3.4%/year vs −4.2%/year (P = .13); WOMAC pain, −49.9 vs −35.1 (P = .10); cartilage defects, 0.3 vs 0.5 (P = .21); and bone marrow lesions, −0.1 vs 0.3 (P = .06). The authors write, "Results showed that even among study participants with low 25-hydroxyvitamin D, supplementation did not slow cartilage loss or improve WOMAC-assessed pain. These data suggest a lack of evidence to support vitamin D supplementation for slowing disease progression or structural change in knee osteoarthritis."

According to the authors, one strength of the study was that it included only patients with symptomatic knee OA who were vitamin D insufficient and who therefore might be most likely to benefit from vitamin D supplements.

The researchers did not prespecify criteria for clinical outcomes such as visual analogue scale knee pain and WOMAC physical function. Post hoc analysis showed that at 24 months, the mean between-group differences for vitamin D vs placebo were WOMAC total −91.4 (P = .02); WOMAC function, −72.9 (P = .008); and visual analogue scale pain, −5.4 (P = .05).

The authors conclude, "Among patients with symptomatic knee osteoarthritis and low serum 25-hydroxyvitamin D levels, vitamin D supplementation, compared with placebo, did not result in significant differences in change in [magnetic resonance imaging]-measured tibial cartilage volume or WOMAC knee pain score over 2 years. These findings do not support the use of vitamin D supplementation for preventing tibial cartilage loss or improving WOMAC knee pain in patients with knee osteoarthritis."

This study was supported by a grant from the Australian National Health and Medical Research Council. The authors have disclosed no relevant financial relationships.

JAMA. 2016;315:1005-1013. Abstract

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