Abstract
The aim of this study was to evaluate levels of osteocalcin (OC), osteoprotegerin (OPG) and total soluble receptor activator of nuclear factor-κB ligand (RANKL), and bone mineral density (BMD) in patients on long-term acenocoumarol (AC) treatment. The cross-sectional study was carried out in 42 patients treated long-term with AC and 28 control subjects. Serum concentrations of OC, OPG, and sRANKL were measured using enzyme linked immunosorbent assay (ELISA) kits, and BMD at the femoral neck and lumbar spine were assessed by dual energy X-ray absorptiometry. A significantly decreased concentration of OC was found in AC users compared to control subjects (4.94 ± 2.22 vs. 10.68 ± 4.5; p < 0.001). Levels of OPG, sRANKL logarithm (log), sRANKL/OPG log ratio, and BMD were comparable between. In female AC users, positive correlations between OC and RANKL log, and between OC and RANKL/OPG log ratio (p = 0.017; p = 0.005, respectively), and a negative correlation between OC and OPG (p = 0.027) were found. Long-term AC anticoagulation significantly decreases OC concentration, but does not affect other bone metabolism markers or BMD. Our results also suggest the possibility that long-term treatment with AC may alleviate bone resorption in postmenopausal women.
Highlights
Bone metabolism is characterized by two opposite actions: formation of new bone by osteoblasts and degradation of old bone by osteoclasts
No differences in terms of age, gender, body mass index (BMI), time elapsed since menopause, and smoking habits were found between AC users and the control group
Concentration, sRANKL log, sRANKL/OPG log ratio, and bone mineral density (BMD) values were comparable in both groups (Table 1)
Summary
Bone metabolism is characterized by two opposite actions: formation of new bone by osteoblasts and degradation (resorption) of old bone by osteoclasts. Vitamin K antagonists (VKAs), including warfarin and acenocoumarol (AC), affect OC carboxylation through the inhibition of the vitamin K-reductase [6], subsequently leading to the production of the functionally inactive form of OC and disturb bone metabolism [7]. RANKL, produced by the osteoblastic cell line and activated T cells, is the factor that activates the formation process of mature osteoclasts by connecting with the RANK [8,9]. The biological effect of OPG, produced by various cells, including osteoblasts [10,11,12], is oppositional to the effects modulated by RANKL. RANKL is responsible for bone resorption, while OPG stops the entire osteoclast maturation pathway, and inhibits resorption. In the case where RANKL is more prevalent than OPG, the rate of resorption is pathologically increased, whereas in the case of OPG predominance over RANKL, the rate of bone resorption is pathologically reduced [15]
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