Newswise — Low vitamin D levels may cause greater knee pain and difficulty walking in patients with knee osteoarthritis, according to research presented this week at the American College of Rheumatology Annual Scientific Meeting in Boston, Mass.
Knee osteoarthritis is caused by cartilage breakdown in the knee joint. Factors that increase the risk of knee osteoarthritis include being overweight, age, injury or stress to the joints, and family history can increase the risk of knee osteoarthritis.
Recent studies have shown that vitamin D influences both musculoskeletal and neuromuscular function. Taking a closer look at this, in a two-year trial of vitamin D supplements on knee osteoarthritis progression, researchers tested whether vitamin D deficiency at study entry is associated with pain and physical function in OA patients. Researchers studied 65 women and 35 men in their sixties who showed signs of having knee OA by measuring blood levels of vitamin D, their baseline knee pain, the time needed for arising several times from a chair, and the time needed to walk 20 meters.
Of the 100 participants, 47 percent were vitamin D deficient, with vitamin D levels below 30 ng/ml. This deficiency contributed to increased pain and difficulty walking among the participants. However, the deficiency did not affect time need to stand and sit repeatedly.
Vitamin D promotes the absorption of calcium and phosphorus needed for bone mineralization, growth and repair. Sources of vitamin D are available to a lesser extent from dietary sources typically found in fortified margarine, oily fish, liver, fortified breakfast cereals and dairy products. Sun exposure helps vitamin D to become active.
Absorption of vitamin D from food and conversion of it to the active form is less efficient in elderly persons. For this reason, vitamin D supplements of 400-800 and calcium doses of 1,200 to 1,500 mg a day are recommended to prevent osteoporosis. The results of this study suggest that Vitamin D supplements may also help in arthritis treatment.
"These preliminary results suggest that, among people with knee osteoarthritis, having a low vitamin D level is associated with more knee pan and greater functional limitation," said Tim McAlindon, MD, MPH; associate professor of medicine, division of rheumatology, Tufts New England Medical Center; and an investigator in the study. "Future results from this ongoing randomized, double-blinded, placebo-controlled clinical trial of vitamin D will help determine whether vitamin D is an effective disease-modifying intervention for knee osteoarthritis."
The ACR is an organization of and for physicians, health professionals, and scientists that advances rheumatology through programs of education, research, advocacy and practice support that foster excellence in the care of people with or at risk for arthritis and rheumatic and musculoskeletal diseases. For more information on the ACR's annual meeting, see http://www.rheumatology.org/annual.
Presentation Number: 199
Low Vitamin D Levels are Associated with Greater Pain and Slow Walking Speed in Patients with Knee Osteoarthritis (KOA)
Jun Wang1, Melynn Nuite1, Laura M. Wheeler1, Prutha Badiani1, Johane Joas1, Erica L. McAdams1, Fletcher Jeremiah1, Michael P. Lavalley2, Bess Dawson-Hughes3, Timothy E. McAlindon1. 1Tufts-New England Medical Center, Boston, MA; 2Boston University School of Public Health, Boston, MA; 3Jean Mayer USDA HNRC on Aging, Boston, MA
The clinical status of patients with knee OA is primarily predicated by their level of pain and their muscle function. Recent studies have shown that vitamin D influences both musculoskeletal health and neuromuscular function. Vitamin D deficiency is common among elders and those with comorbidities. This suggests that vitamin D may especially influence the clinical status of patients with knee OA. This study examined whether serum 25-hydroxyvitamin D (25(OH)D) level was associated with pain and physical function in patients with symptomatic knee OA.
Methods: We performed a cross-sectional analysis of baseline data among participants of a clinical trial of knee OA progression. Eligibility criteria included (1) chronic knee symptoms, (2) radiographic tibiofemoral OA [K/L grade >=2], (3) serum 25(OH)D <80 ng/ml. The physical function evaluation comprised the timed chair stand and 20-meter walking tests. Knee pain was evaluated using the WOMAC pain subscale. Serum 25(OH)D level was measured using liquid chromatography tandem mass spectrometry (LC/MS/MS) method. We defined vitamin D deficiency as serum 25(OH)D <30 ng/ml. We used multivariate logistic regression models to analyze the association between vitamin D deficiency with the pain and physical function scores, adjusting for sex, race, age, body mass index (BMI), month of blood draw, and K/L grade. Each outcome was dichotomized at its median (i.e., WOMAC pain subscale, >6/<=6; 20-meter walking test, >20/<=20 sec; chair stand test, >16/<=16 sec).
Results: The analysis included 65 women (mean age 62 yrs, SD, 8) and 35 men (66 yrs; SD, 9), of whom 47% had 25(OH)D <30 ng/ml. Fifty percent of the subjects had a K/L grade>=3. The subjects had a mean BMI of 30.4 (SD, 5.3), mean pain score of 6.7 (SD, 3.8), mean 20-meter walking time of 17.4 sec (SD, 5.2), and mean chair stand test time of 21.4 sec (SD, 7.8). Vitamin D deficiency was associated with greater knee pain (adjusted OR for WOMAC pain score>6, 3.22, 95% CI, 1.08-9.58). Vitamin D deficiency was associated with a slower walking speed (adjusted OR, 3.24, 95% CI, 1.12-9.42). The association with 25(OH)D was slightly reduced by inclusion of knee pain severity in the model (adjusted OR, 2.94, 95% CI, 0.91-9.44). Vitamin D deficiency was not associated with chair stand time (adjusted OR, 0.92, 95% CI, 0.29-2.92).
Conclusion: Among patients with knee OA, a low 25(OH)D level is associated with greater knee pain and slower walking speed. This association will be explored in the longitudinal setting of our randomized, placebo-controlled trial to determine any causal relationship.
Disclosure Block: J. Wang, None; M. Nuite, None; L.M. Wheeler, None; P. Badiani, None; J. Joas, None; E.L. McAdams, None; F. Jeremiah, None; M.P. Lavalley, None; B. Dawson-Hughes, None; T.E. McAlindon, NIH/NIAMS R01 AR051361, 2; NIH M01 RR 00054, 2.
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