Original Article
Bone turnover markers may predict the progression of osteonecrosis of the femoral head in aged males
Abstract
Background: Recent studies suggest that the imbalance of bone metabolism is associated with the pathogenesis of osteonecrosis of the femoral head (ONFH). However, limited data exist on the bone turnover markers (BTMs) in these patients compared with the healthy control (HC) comprehensively.
Methods: In total, 196 participants aged 29–83 [53 patients were excluded, 70 nontraumatic ONFH (mean age 57.75±12.61; mean BMI 24.10±3.04) and 73 HC (mean age 54.04±11.12; mean BMI 23.67±3.64)] were recruited in our cross-sectional study. Osteocalcin (OC), t-P1NP (N-terminal procollagen type 1 extension pro-peptide), β-CTx (beta-isomerized type I collagen C-telopeptide breakdown products), 25-hydroxy- cholecalciferol, and parathormone (PTH) were measured using automated analyser.
Results: In comparison to controls, nontraumatic ONFH patients have lower 25(OH)D levels and higher levels of t-P1NP, β-CTx and OC (P<0.01). But there was no significant difference in PTH levels between these two groups. Logistic regression analysis revealed that low 25(OH)D and high t-P1NP were significantly associated with nontraumatic ONFH. ROC curve analysis showed the highest AUC for t-P1NP+25(OH)D model [t-P1NP+25(OH)D: 0.702, 95% CI: 0.620–0.776; t-P1NP: 0.621, 95% CI: 0.536–0.701; 25(OH)D: 0.678, 95% CI: 0.594–0.753]. With regard to the cutoff values calculated from the ROC curves, t-P1NP+25(OH)D model showed 64.29% sensitivity and 73.97% specificity. The deficiency of 25(OH)D occurred at all phases, and other BTMs were in a high rate during different phases according to the ARCO classification.
Conclusions: Both 25(OH)D deficiency and high t-P1NP were independent risk factors for nontraumatic ONFH. Our results suggest that BTMs, t-P1NP+25(OH)D model (t-P1NP ≥54.82 ng/mL and 25(OH)D ≤21.86 ng/mL), may facilitate to diagnose nontraumatic ONFH in aged male patients.
Methods: In total, 196 participants aged 29–83 [53 patients were excluded, 70 nontraumatic ONFH (mean age 57.75±12.61; mean BMI 24.10±3.04) and 73 HC (mean age 54.04±11.12; mean BMI 23.67±3.64)] were recruited in our cross-sectional study. Osteocalcin (OC), t-P1NP (N-terminal procollagen type 1 extension pro-peptide), β-CTx (beta-isomerized type I collagen C-telopeptide breakdown products), 25-hydroxy- cholecalciferol, and parathormone (PTH) were measured using automated analyser.
Results: In comparison to controls, nontraumatic ONFH patients have lower 25(OH)D levels and higher levels of t-P1NP, β-CTx and OC (P<0.01). But there was no significant difference in PTH levels between these two groups. Logistic regression analysis revealed that low 25(OH)D and high t-P1NP were significantly associated with nontraumatic ONFH. ROC curve analysis showed the highest AUC for t-P1NP+25(OH)D model [t-P1NP+25(OH)D: 0.702, 95% CI: 0.620–0.776; t-P1NP: 0.621, 95% CI: 0.536–0.701; 25(OH)D: 0.678, 95% CI: 0.594–0.753]. With regard to the cutoff values calculated from the ROC curves, t-P1NP+25(OH)D model showed 64.29% sensitivity and 73.97% specificity. The deficiency of 25(OH)D occurred at all phases, and other BTMs were in a high rate during different phases according to the ARCO classification.
Conclusions: Both 25(OH)D deficiency and high t-P1NP were independent risk factors for nontraumatic ONFH. Our results suggest that BTMs, t-P1NP+25(OH)D model (t-P1NP ≥54.82 ng/mL and 25(OH)D ≤21.86 ng/mL), may facilitate to diagnose nontraumatic ONFH in aged male patients.
