Comparative high-resolution pQCT analysis of femoral neck indicates different bone mass distribution in osteoporosis and osteoarthritis

Abstract

Starting from these differences in the structural descriptors, our study sustains the presence of a compensatory mechanism in osteoarthritis to preserve the mechanical competence of bone structure, despite the loss of trabecular bone, underlying lower fracture risk.

Evidence for Altered Canonical Wnt Signaling in the Trabecular Bone of Elderly Postmenopausal Women with Fragility Femoral Fracture

“…The BMD of vertebrae L1–L4, neck and total femur, 1/3, and UD radius were not statistically different between the two groups. No significant differences were recorded in the levels of PTH, 25(OH)D, Ca 2+ , and creatinine, thus suggesting that the quality of bone architecture and/or other secondary factors is associated with bone fragility, independently of BMD [3]. …”

“…The absence of any significant difference which has been found between bone density and mineral metabolism parameters in F versus OA cohorts is in line with this view and suggests that bone mass distribution could be critical for fracture risk. Our laboratory showed previously that the loading-induced adaptive distribution of residual bone mass, despite age and disease-related bone loss, is preserved in osteoarthritic subjects, accounting for their reduced fracture risk, while it is lacking in osteoporotic patients [3]. …”

“…Indeed, it was shown that there is a different cortical and trabecular bone distribution in the femoral necks of osteoarthritis subjects when compared to the ones of osteoporotic postmenopausal women with femoral fracture [2]. The cortical and trabecular thickness was shown to be higher in osteoarthritis subjects even in the presence of low volumetric bone density [3, 4]. These structural differences, in particular the critical role of residual bone mass distribution, that is, cortical versus trabecular, better discriminate hip fracture likelihood than areal Bone Mineral Density (aBMD) by DXA [5].…”

“…The downstream effector of Wnt activation, the transcriptional regulator β -catenin, plays disparate roles in different phases of bone remodeling and microdamage repair [10, 11] and might be the underlying critical factor determining the different bone mass distribution in osteoarthritis versus osteoporosis. Indeed, it is known that the mechanical adaptation of the skeleton is in part regulated by Wnt (see [12] for review) and that this mechanical adaptation appears to be better preserved in osteoarthritis versus osteoporosis [3]. …”

CORR Insights®: Patients With Hip Osteoarthritis Have a Phenotype With High Bone Mass and Low Lean Body Mass

“…When more reasonable and specific traits of body composition are available, ambiguous traits like BMI should be abandoned. Regarding the bone phenotype, several experimental studies of hip specimen from pertinent patients have shown that both cortical and trabecular bone traits differ from those in osteoporosis [2,5,7], but notably, the bone tissue in hip osteoarthritis is not stiffer than the bone of healthy subjects [5]. Because these traits are beyond the areal bone mineral density (depicts only one bone projection), 3-D imaging of proximal femur structure is needed for appropriate phenotyping of bone.…”