Femoral neck fragility in women has its structural and biomechanical basis established by periosteal modeling during growth and endocortical remodeling during aging.

Abstract

To gain insight into the growth- and age-related origins of bone fragility at the proximal femur, we analyzed structural and biomechanical data of the femoral neck from a study of postmenopausal women with hip fractures and their 47 premenopausal daughters. Results were expressed as standard deviations (SD) or Z-scores (mean +/- SEM) adjusted for age and weight, derived using a normal reference population of 262 premenopausal women and 370 postmenopausal women. Women with hip fractures had increased femoral neck (FN) periosteal and endocortical diameters (1.01 +/- 0.26 SD and 1.18 +/- 0.25 SD, respectively). Cortical thickness was reduced by 0.96 +/- 0.1 SD and volumetric bone mineral density (vBMD) was reduced by 1.2 +/- 0.1 SD). The section modulus was normal while the buckling ratio was increased by 1.59 +/- 0.17 SD). Their daughters had increased FN diameter by about one half that of their mothers (0.48 +/- 0.16 SD), while endocortical diameter was increased by only one third (0.44 +/- 0.13 SD). Cortical thickness and vBMD were not reduced, the section modulus was increased (0.48 +/- 0.13 SD) while the buckling ratio was normal. We infer that the larger femoral neck size in women with hip fractures is growth-related; the wider endocortical cavity and thinner cortex is the result of excessive age-related endocortical bone resorption producing a thin cortex in a larger bone predisposing to structural failure by local buckling. The structural basis of bone fragility has some features originating during growth and others during aging.