The quality of bone in the skeleton depends on the amount of bone, geometry, microarchitecture and material properties, and the molecular and cellular regulation of bone turnover and repair. This study aimed to identify material and structural factors that alter in fragility hip fracture patients treated with antiresorption therapies (FxAr) compared to fragility hip fracture patients not on treatment (Fx).

Bone from the intertrochanteric site, femoral head (FH: FxAr = 5, Fx = 8), compression screw cores and box chisel were obtained from patients undergoing hemi-arthroplasty surgery, FxAr (6f, 2m, mean 79 and range [64–89] years), and Fx (7f, 1m, age 85 [75–93] years). Control bone was obtained at autopsy (9f, 4m, 77 [65–88] years). Treated patients were on various bisphosphonates. Samples were resin-embedded, for quantitative backscattered electron imaging of the degree of mineralisation and assessment of bone architecture. Trabecular bone volume fraction (BV/TV) and architectural parameters were not significantly different between FxAr and Fx groups.

Both groups showed normal distributions of weight (wt) % Ca; however, the FxAr was less mineralised than the Fx and the control group (mean wt % Ca: FxAr = 24.3%, Fx = 24.8%, Control = 24.9%). When comparing the FH specimens only, we found that BV/TV in the FxAr was greater than the Fx group (18% vs 15%). All other parameters were not significantly different. In addition, the mineralisation was greater in the FxAr group compared to the Fx group (25.5 % vs 25.0%) but was not significantly different.

Collectively, these data suggest the effect on bone of antiresorptives may be different for patients on antiresorptive treatment that do not subsequently fracture. Assessment of bone material property data together with other bone quality measures may hold the key to better understanding of antiresorptive treatment efficacy.

Evidence is accumulating for the role of bone in the pathogenesis of osteoarthritis (OA). Previous studies have shown a generalised increase in bone mass and hypo-mineralisation in OA patients. However, the molecular and cellular mechanisms involved in the increased bone mass and matrix compositional profiles in OA, at distal skeletal sites to the articular cartilage, have not yet been well defined. This study examined whether gene expression of bone anabolic factors, trabecular bone architecture and matrix mineralisation are altered in human OA and non-OA hipbone. Intertrochanteric (IT) trabecular bone samples were obtained from 15 primary hip OA patients (mean age 65 [48–85] years) and 13 closely age- and gender-matched autopsy controls (mean age 63 [44–83] years). Semi-quantitative RT-PCR analysis revealed elevated mRNA expression levels of alkaline phosphatase (p < 0.002), osteocalcin (p < 0.0001), osteopontin (p < 0.05), collagen type-I α chains COL1A1 (p < 0.0001) and COL1A2 (p < 0.002), in OA bone compared to control, suggesting possible increases in osteoblastic biosynthetic activity and/or bone turnover at the IT region in OA. Interestingly, the ratio of COL1A1:COL1A2 mRNA was almost 2-fold greater in OA bone compared to control (p < 0.001), suggesting the potential presence of collagen type-I homotrimer at the distal site that may associate with hypomineralisation in OA individuals. Using a quantitative backscatter electron imaging technique, mineralisation profiles of IT trabecular bone indicated decreased mineralisation in the OA group compared to the control group (24.2 weight percent calcium [wt%Ca] versus 25.3 wt%Ca). Bone histomorphometric analysis found OA IT bone had increased surface density of bone and decreased trabecular separation compared to control bone. Taken together with a reported increase in diffuse microdamage in OA IT bone (Fazzalari et al. Bone 31:697–702, 2002), possibly due to hypomineralisation, these results are consistent with the altered bone material properties found in OA individuals. The finding of differential gene expression, altered mineralisation and architectural changes in OA bone, at a skeletal site distal to the active site of joint degeneration, supports the concept of systemic involvement of bone in the pathogenesis of OA.