Age- and sex-specific 3D bone structure patterns in human radii and tibiae were investigated with respect to individuals osteodensitometric classification to unravel associations with site-specific fracture occurrences and underlying loading patterns. A sample of 385 patients (121 men, 264 women, age: 23-91years) was investigated. The patients were classified according to Dual-X-ray-Absorptiometry T-scores in three groups: control (n=60), osteopenia (n=160), and osteoporosis (n=165). Bone architecture and geometry were assessed by high-resolution peripheral quantitative computed tomography (HR-pQCT) of the cortical and trabecular compartments in distal radii and tibiae. We found site-dependent age- and sex-related trends regarding bone architecture and geometry. Females displayed more pronounced age-related changes than males. Specifically, female radii showed both cortical and trabecular structural deterioration with aging, whereas the tibiae demonstrated exclusively cortical deterioration. The mean cortical perimeter revealed a significant age-related increase even after adjusting for body height and weight, which suggests that periosteal expansion can be observed in both the tibia (males: r=0.295, p=0.001; females: r=0.161, p=0.008) and also in the radius (males: r=0.362, p<0.001; females: r=0.136, p=0.024). Statistically significant inter-group differences (age and sex-adjusted) were found in all of the evaluated structural parameters for both the radius and tibia (except for the trabecular thickness and cortical perimeter). Clearly, osteopenia and osteoporosis cases did not reveal higher cortical perimeters in comparison to controls (p>0.05). The tomographic assessment of bone structure further clarifies the architectural basis for increased bone fragility at distal radii and tibiae with advanced age leading to fracture predilection in females. These findings may represent a morphological link to epidemiological data on age-dependent fracture incidences. Our data supports existence of periosteal apposition at the skeletal sites with different loading magnitudes, but not necessarily as a compensatory mechanism to counterbalance bone loss given the lack of differences in periosteal diameter among control, osteopenia and osteoporosis groups.
Disclosure: The authors declared no competing interests. The work was supported by the Emmy Noether program (Deutsche Forschungsgemeinschaft; grant number BU 2562/2-1), DAAD (Deutscher Akademischer Austauschdienst; grant number A/11/83161), South-Eastern-European-Cooperation of University Medical Center Hamburg-Eppendorf, and Serbian Ministry of Education and Science (grant number III45005).