Abstract
Background Vascular endothelial growth factor (VEGF) plays an important role in bone angiogenesis, whereas transforming growth factor-β1 (TGF-β1) modulates bone differentiation, matrix formation, and cytokine expression. Aim of the work The aim of the study was to assess the immune expression of VEGF and TGF-β1 in cells lining the bone trabeculae among postmenopausal womεν in relation to bone histomorphometry and their association with osteoporosis. Patients and methods A total of 30 postmenopausal women were recruited for the study. Bone mineral density was measured using DEXA. On the basis of the results of the DEXA scan, they were divided as follows: group I comprised 14 (46.7%) women with normal bone mineral density; group II comprised five (16.7%) women with osteopenia; and group III comprised 11 (36.7%) women with osteoporosis. Iliac crest bone biopsy was taken from each of them. Histomorphometrical study was carried out using H&E stain to evaluate the trabecular microarchitecture in addition to immunohistochemistry for both VEGF and TGF-β1. Results Histomorphometric analysis was statistically and significantly different among the three groups. The area percentage of both TGF-β1 protein and VEGF expression in cells lining the bone trabeculae was statistically and significantly lower in the osteoporotic group compared with the other two groups. A statistically significant negative correlation was found between age and menopause duration and TGF-β1 only. A significant positive correlation was found between trabecular bone thickness and both VEGF (r=0.762, P=0.000) and TGF-β1 (r=0.785, P=0.000). Regression analysis showed only VEGF (t=2.537, P=0.018), and not TGF-β1 (t=0.326, P=0.747), to have independent association with trabecular bone thickness. Conclusion The results of the current study support that VEGF and TGF-β1 may contribute to the pathogenesis of postmenopausal osteoporosis. Further studies on the role of both TGF-β1 and VEGF in postmenopausal osteoporotic patients will be helpful to clarify the etiopathogenesis and treatment of postmenopausal osteoporosis.
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