Abstract

Introduction Bone metabolic markers informatively reflect the complex balance of bone formation/resorption and are widely used in clinical practice. Genetic predisposition also plays a significant role in the etiopathogenesis of aseptic necrosis of the femoral head (ANFH). We aimed to establish probable associations between a number of biochemical parameters of bone tissue metabolism with clinical ones (sex, age, body mass index (BMI)), disease stage, T and Z criteria) with regard to the leading polymorphisms of the vitamin D3 receptor gene (VDR) in patients with ANFH. Materials and Methods Based on clinical and biochemical examination of 273 patients with ANFH, factor analysis was performed. Results Clinical parameters (age, BMI) correlated most with biochemical parameters. Age showed most association with β-CrossLaps, DPD, osteocalcin, and osteoprotegerin; BMI, in turn, was associated with 1.25(OH)2D, 25(OH)D, Ca, and DPID. Carriers of G/G genotype A-3731G were found to have more than a three-fold increased risk of ANFH compared to healthy controls; carriers of G allele had a 2.5‑fold increased risk. Carriage A/A genotype +283 A > G increases the risk of developing ANFH by 2.4 times. Carriage of the A allele of the same locus is associated with a 1.5-fold increased risk of ANFH. Discussion We determined a reliable association of age with β-CrossLaps, DPD, osteocalcin, osteoprotegerin, and BMI with 1.25(OH)2D, 25(OH)D, Ca, and DPD in patients with ANFH, suggesting significant prospects for using these biochemical parameters to monitor changes in bone tissue remodeling. An increased risk of ANFH was established in the presence of the G/G genotype and the G allele of the A-3731G (Cdx2) locus, the A/A genotype of the +283 A > G (BsmI) locus in the VDR gene. Conclusion Associations of BMI with 1.25(OH)2D, 25(OH)D, Ca, DPD characterize the relationship between resorption and osteogenesis processes and somatic parameters of the examined patients with ANFH. The genotypic variants G/G rs11568820 and A/A rs1544410 in the VDR gene are associated with an increased risk of AFHD.

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