Bone Material Properties in Male Idiopathic Osteoporosis.

Abstract

Male idiopathic osteoporosis (MIO), defined as primary osteoporosis with unclear etiology in men, is characterized by low bone mass and increased fracture risk. The underlying pathophysiology remains poorly understood, particularly regarding bone microstructure, turnover, and mineralization. To characterize bone material properties in men with idiopathic osteoporosis using histomorphometry, bone mineralization analysis, and osteocyte lacunae morphology. Transiliac bone biopsies from 20 men with idiopathic osteoporosis (mean age 46.5 ± 12.1 years) were analyzed after exclusion of secondary causes. Undecalcified PMMA-embedded samples were assessed for static and dynamic histomorphometric parameters. Dynamic bone formation was evaluated using tetracycline double labeling. Quantitative backscattered electron imaging determined bone mineralization density distribution in cortical and trabecular compartments and osteocyte lacunae section characteristics. Compared with age-matched reference data, patients exhibited significantly reduced trabecular bone volume fraction (p = 0.007), thickness (p = 0.003), and number (p = 0.03), alongside decreased osteoid thickness (p < 0.001) and osteoblast surface (p = 0.002). Dynamic analysis revealed lower adjusted apposition rate (p = 0.003) and prolonged mineralization lag time (p = 0.007), indicating low bone turnover. Trabecular bone mineralization was reduced, with lower CaMean (p = 0.001), CaPeak (p < 0.001), and CaHigh (p = 0.007), and higher CaLow (p = 0.02). Cortical mineralization remained normal, although cortical width was decreased (p = 0.044). Osteocyte lacunar aspect ratio was significantly reduced in cortical and trabecular bone (both p < 0.001), while lacunar density and area were unchanged. Men with idiopathic osteoporosis present a distinct skeletal phenotype characterized by compromised trabecular microarchitecture, suppressed bone formation, and selective trabecular hypomineralization, despite preserved cortical mineralization. These findings suggest that MIO represents a low-turnover bone disorder with impaired mineralization kinetics.