JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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The value of osteopontin in the assessment of bone mineral density status in postmenopausal women.

BACKGROUND: Osteopontin (OPN) has been implicated in bone remodeling by activating the resorption process. We aimed to study the relationship between OPN, bone mineral density (BMD), bone turnover markers, vitamin D, and osteoporotic vertebral fractures in postmenopausal women.

MATERIALS AND METHODS: Serum levels of OPN, osteocalcin, collagen type 1 cross-linked C-telopeptide (CTX), bone alkaline phosphatase, and vitamin D were assessed in 214 postmenopausal women. Bone mineral density was assessed by dual-energy x-ray absorptiometry in lumbar spine and femoral neck, and osteoporotic vertebral fractures by radiographs.

RESULTS: Osteopontin levels were significantly higher in osteoporosis group versus osteopenic and normal group (all P < 0.05). The cutoff values of OPN for osteoporosis diagnosis were of 9.47 μg/L at the lumbar spine (area under the curve, 0.67; 95% confidence interval, 0.58-0.75; P < 0.001) and 10.15 μg/L at the femoral neck (area under the curve, 0.69; 95% confidence interval, 0.624-0.77; P = 0.0001), respectively. Postmenopausal women with osteoporosis-related vertebral fractures had significantly higher levels of OPN than those without vertebral fractures (15.69 ± 13.26 vs 12.63 ± 12.46 μg/L; P = 0.02). Significant negative correlations were found between OPN and BMD, which persisted after the adjustment for age at the lumbar spine. Osteopontin levels were directly correlated with bone turnover markers (osteocalcin, bone alkaline phosphatase, and CTX). No significant correlation was found between OPN and vitamin D. Multiple regression analysis showed that age, waist circumference, and CTX were independent predictors of serum OPN levels.

CONCLUSIONS: High levels of OPN in postmenopausal women are associated with low BMD, increased levels of bone turnover markers, and osteoporotic vertebral fractures. These findings suggest that OPN might play some role in the pathophysiology of postmenopausal osteoporosis and warrant further clinical investigations.

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