Aim: Vitamin D insufficiency is associated with an increase in PTH, which might be critical for an increase in bone fragility. However, the role of endogenous PTH in vitamin D insufficiency-induced increase in fracture risk still remains unclear. The present study was performed to examine the relationships among vitamin D insufficiency, bone fragility, PTH and sclerostin, which is produced by osteocytes and inhibits bone formation by inhibiting the Wnt pathway.
Methods: Subjects were 190 healthy postmenopausal women who had undergone osteoporosis screening. Bone mineral density (BMD) was measured using the DXA method at the lumbar vertebrae and femoral neck (FN). The presence of vertebral fractures was confirmed on X-ray and nonvertebral fractures were assessed by the clinical interview. Serum levels of Ca, P, Cr, C-terminal cross-linked telopeptide of type I collagen (CTX), intact PTH, 25-hydoroxyvitamin D (25(OH)D) and sclerostin were measured.
Results: Mean values of age and BMI were 63±8 years and 22.9±3.1 kg/ m2, respectively. Levels of intact PTH, 25(OH)D, CTX and sclerostin were 46±15 pg/ ml, 16.3±4.4 ng/ ml, 0.4±0.2 ng/ ml and 1.3±0.4 ng/ ml, respectively. The percentages of subjects with 25(OH)D levels below 20 ng/ ml were 80.7%. Serum 25(OH)D levels were negatively related to age, Cr, CTX and PTH, although it was positively related to BMD. Multiple logistic regression analysis showed that lower 25(OH)D levels were significantly related to prevalent fracture risk, when adjusted for age, BMI, Ca, P, Cr, CTX, PTH, FN BMD, and sclerostin. Logistic regression analysis revealed that the group with lower PTH and lower 25(OH)D was a significant risk factor for prevalent fracture (odds ratio, 2.33 (95% CI: 1.045.25), P<0.05) even after adjustments for these indices.
Conclusions: Vitamin D insufficiency was related to prevalent fracture risk. In vitamin D insufficiency, functional hypoparathyroidism rather than functional hyperparathyroidism might be a risk factor for bone fragility.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.