Objective. To examine the cross-sectional association between use of medications that have a bone antiresorptive effect (estrogen, raloxifene, and alendronate) and both the structural features of knee osteoarthritis (OA), assessed by magnetic resonance imaging (MRI) and radiography, and the symptoms of knee OA in elderly women.Methods. Women in the Health, Aging and Body Composition Study underwent MRI and radiography of the knee if they reported symptoms of knee OA, and women without significant knee symptoms were selected as controls. MR images of the knee were assessed for multiple features of OA using the Whole-Organ MRI scoring method, and radiographs were read for Kellgren and Lawrence grade and individual features of OA. Concurrent medication use and knee symptoms were assessed by interview, and knee pain severity was evaluated using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC).Results. There were 818 postmenopausal women from whom we obtained MR images of the knee and data on medication use. Among these women, 214 (26.2%) were receiving antiresorptive drugs. We found no significant association between overall use of antiresorptive drugs and the presence of knee pain and radiographic changes of OA of the knee. Use of alendronate, but not estrogen, was associated with less severity of knee pain as assessed by WOMAC scores. Both alendronate use and estrogen use were associated with significantly less subchondral bone attrition and bone marrow edema-like abnormalities in the knee as assessed by MRI, as compared with women who had not received these medications.Conclusion. Elderly women being treated with alendronate and estrogen had a significantly decreased prevalence of knee OA-related subchondral bone lesions compared with those reporting no use of these medications. Alendronate use was also associated with a reduction in knee pain according to the WOMAC scores.Osteoarthritis (OA) of the knee is a common condition in the United States and a leading cause of disability in elderly people (1-3). Nonoperative therapies are not curative, and a substantial number of affected people ultimately undergo total knee replacements (4).The cartilage degradation that is central to OA is accompanied by important periarticular bone abnormalities, including subchondral bone thickening, deformation and cysts, and marginal osteophytosis. A higher rate of subchondral bone turnover, as indicated by increased uptake of scintigraphic tracer in subarticular bone, is associated with more rapid progression of knee OA (5).
BMD was examined in users of NSAIDs (by COX selectivity) and aspirin in the Health ABC cohort (n ؍ 2853). Significantly higher BMD was found in users of relative COX-2 selective NSAIDs with aspirin (COX-2/ASA) compared with nonusers. This suggests a role for COX-2/ASA in osteoporosis. Introduction:The purpose of this study was to determine the relationship of nonsteroidal anti-inflammatory drug (NSAID) use, by cyclo-oxygenase selectivity (COX), and aspirin use on bone mineral density (BMD) in participants from the Health, Aging, and Body Composition (Health ABC) population-based cohort. It is known that NSAIDs inhibit the COX enzyme and decrease production of prostaglandins, which are involved in regulation of bone turnover. COX has two isoforms, COX-1 and COX-2. Production of prostaglandins associated with bone loss is primarily mediated through the COX-2 pathway. In addition, aspirin may have effects on bone independent of the prostaglandin pathway. Materials and Methods: NSAID (by COX selectivity) and aspirin use and BMD were assessed in 2853 adults (49.5% women, 50.5% men; 43.1% black, 56.9% white; mean age: 73.6 years) from the Health ABC cohort. For the purposes of this analysis, relative COX-1 selective NSAIDs were defined as having a ratio of COX-1 IC 50 to COX-2 IC 50 of Ͼ1 in whole blood, and relative COX-2 selective NSAIDs were defined as having a ratio of COX-1 IC 50 to COX-2 IC 50 of Ͻ1 in whole blood. Analysis of covariance was used to compare BMD across each NSAID use and aspirin use category adjusting for age, race, gender, weight, height, study site, calcium and vitamin D supplementation, Womac score, history of rheumatoid arthritis, history of arthritis other than rheumatoid, and smoking status. Results: After adjustment for possible confounders, current use of relative COX-2 selective NSAIDs with aspirin was associated with higher BMD at the whole body (4.2%, 1.2-7.3 CI) and total hip (4.6%, 0.5-8.8 CI) by DXA and at both trabecular (34.1%, 15.4 -52.7 CI) and cortical spine (12.8%, 2.3-23.3 CI) by quantitative computed tomography. Conclusions: Our data suggest that the combination of relative COX-2 selective NSAIDs and aspirin is associated with higher BMD at multiple skeletal sites in men and women.
During the past several decades in the United States, there has been a shift in dietary habits, with an increased consumption of processed foods that are high in sodium. It is known that calcium and sodium metabolism are linked and that higher sodium intakes may increase calcium excretion. Epidemiological studies in patients with idiopathic hypercalciuria suggest that hypercalciuria is linked to low bone mass. However, the relationship of sodium intake to bone mineral density (BMD) is controversial in Caucasians and has not been explored in African-Americans. To determine the consequences of sodium intake on bone in African-American and Caucasian postmenopausal women, sodium and calcium excretion and BMD of the total hip were measured in 50 Caucasian and 39 African-American postmenopausal women. After adjustment for race and urine volume, sodium excretion was a significant predictor of calcium excretion (P < 0.01). This relationship was modulated by calcium intake (P < 0.01), but not by race (P = 0.63). There was no significant effect of sodium excretion (P = 0.42) or calcium excretion (P = 0.90) on BMD of the total hip after adjusting for race and urine volume. Sodium excretion is a significant predictor of calcium excretion in both postmenopausal African-American and Caucasian women. The relationship between sodium and calcium excretion is modulated by calcium intake, and the relationship is strongest at low calcium intakes (< or =1000 mg/day). However, sodium excretion in the range of 53.75-283.33 mmole/g/total volume (mmole/g/TV) is not a significant predictor of total hip BMD in elderly African-American and Caucasian postmenopausal women.
Osteoporosis is a serious public health problem, and dietary interventions may potentially be helpful in preventing this disorder. The purpose of this study was to determine the effects of a low sodium diet on bone metabolism in postmenopausal women. This was a longitudinal study to determine the effects of a low sodium (2-g/day) diet on bone. Forty postmenopausal African-American and Caucasian women were enrolled in a 2-g/day sodium diet for 6 months. Sodium and calcium excretion, bone turnover, and calcitropic hormones (intact parathyroid hormone (PTH) and 1,25 dihydroxyvitamin D) were measured before and 6 months after the intervention. In women who had baseline sodium excretions equal to or greater than the average sodium intake in the United States (> or =3.4 g/day), the low sodium diet resulted in significant decreases in sodium excretion (P = 0.01), in calcium excretion (P = 0.01), and in a biomarker of bone turnover, aminoterminal propeptide of type I collagen (P = 0.04). However, there were no significant changes in calcitropic hormones, including intact PTH (P = 0.97) or 1,25 dihydroxyvitamin D (P = 0.49) with the low sodium diet. These findings suggest that in postmenopausal women with sodium intakes > or =3.4 g/day, a low sodium diet may have benefits for skeletal health.
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