Endocrine Abstracts

Introduction: Some patients develop excessive bone metabolism supression during antiresorptive therapy. Low remodelling rate enables increase in tissue mineralisation density and homogenicity of bone trabeculae. Increase in density makes micro-damage more likely. Increased homogenicity provides less resistance to spread of the micro-cracks and slowed remodelling slows down removal of microdemage. All this leads to increased bone fragility.

Aim: To establish whether excessive suppression of bone resorption and entire remodelling process depends on osteoporosis risk factors.

Materials and methods: Prospective, longitudinal study with 200 female participants with diagnosed osteoporosis of was done. Average age was 62.3±9.74 years. Osteocalcine (OC) and β-crosslps (β-CTx) were determined before therapy and three months after initiation of antiresorptive therapy. Group 1: OC and β-CTx below reference range; Group 2: β-CTx below reference range; Group 3: normal levels of OC and β-CTx; Group 4: increased bone metabolism during therapy. Analysed risk factors were: age, smoking habits, menarche, menopause, labours, lactation, fragile fracture, height reduction, osteoporosis in family.

Results: There were no statistically significant differences between age, menarche, menopause (F=0.794, P=0.623), fragile fracture (F=1.315, P=0.27), height reduction (F=0.408, P=0.751), smoking habits (F=0.1.17, P=0.322), fragile fracture in relatives (F=0.572, P=0.638). There was statistically significant difference among groups: group 2 had longer menopause (F=5.171, P=0.002) and longer duration of lactation (F=2.954, P=0.033). Group 4 had longer generative period (F=2.839, P=0.039) and fewer children (F=2.682, P=0.0)

Discussion and conclusion: Osteoporosis risk factors may have the role in excessive suppression of bone metabolism during antiresorptive therapy. further studies of this problem are needed to enable identification of patients who may develop excessive bone turnover suppression as a potential adverse effect of antiresorptive therapy.