Introductıon: Osteoporosis is a common disease, and several factors contribute to its development.
Recently, there has been increasing evidence that vitamin K (VK) plays a critical role in maintaining
bone strength. Vitamin K serves as a co-factor for the γ-carboxylation of particular proteins to
convert specific glutamic acid residues to γ-carboxyglutamic acid residues. This process involves two
enzymes, γ-glutamyl carboxylase and vitamin K epoxide reductase (VKORC1). The number of studies
investigating the effects of VKORC1 gene mutations on bone mineral density in postmenopausal osteoporosis
patients is limited. The aim of this study was to investigate the relationship between the
VKORC1 -1639G>A polymorphism and osteoporosis in postmenopausal Turkish women.
Methods: The study group consisted of 176 postmenopausal women with osteoporosis and 140 healthy
postmenopausal women. The selection criteria for the healthy controls included non-osteoporotic bone
mineral density (BMD) and similar demographic characteristics to the osteoporosis group. The genotyping
of the VKORC1 -1639G>A polymorphism was conducted using the restriction fragment-length
Results: We found that the genotype frequencies of the GG, GA and AA genotypes were 25.6, 64.2
and 10.2% in the patients and 33.6, 55.8 and 10.7% in the controls, respectively. In the patient and
control groups, the genotype distribution of the studied locus was found to be non-compatible with
Hardy–Weinberg equilibrium. We found a nonsignificant association between the -1639G>A polymorphism
in the VKORC1 gene and osteoporosis in postmenopausal Turkish women.
Conclusion: We have shown that the VKORC1 -1639G>A polymorphism is not a risk factor for postmenopausal