Difference in subchondral cancellous bone between postmenopausal women with hip osteoarthritis and osteoporotic fracture: Implication for fatigue microdamage, bone microarchitecture, and biomechanical properties

Abstract

Objective. Osteoarthritis (OA) and osteoporosis (OP) of the hip rarely occur in the same patient. The purpose of this study was to determine whether this difference might be attributable to the different quantity and quality of subchondral cancellous bone in the two conditions.Methods. Subchondral cancellous bone from the femoral head was obtained at the time of hip arthroplasty from 60 postmenopausal women, 30 with OA and 30 with OP. In each group, 10 specimens were subjected to compressive fatigue loading and 20 were left nonloaded. Specimens were examined by compressive mechanical testing, micro-computed tomography scanning, fluorescence microscopy, and nanoindentation techniques.Results. Both the ultimate stress and the elastic modulus of cancellous bone from OA patients were significantly higher than those of cancellous bone from OP patients (P < 0.05). Compared to cancellous bone from OP patients, the bone volume fraction and trabecular thickness were significantly increased, but bone matrix mineralization was significantly decreased, in cancellous bone from OA patients (P < 0.05 for each comparison). The microcrack density was significantly higher in OP cancellous bone than in OA cancellous bone (P < 0.001), irrespective of fatigue loading. In addition, fatigue loading resulted in a significant increase in microcrack density in both OA and OP cancellous bone (P < 0.001). There was no significant difference in nanoindentation elastic modulus and hardness between cancellous bone from OA and OP patients, as well as between bones with and without fatigue loading.Conclusion. The difference in mechanical properties between OA and OP cancellous bone is attributed to different bone mass and bone structure. OP cancellous bone is susceptible to fatigue damage due to insufficient structure. However, increased bone volume and platelike structure provide OA cancellous bone a superior capacity to resist fatigue damage.Osteoarthritis (OA) and osteoporosis (OP) are two orthopedic disorders that usually result in high rates of morbidity and disability in people over the age of 50 years, particularly in postmenopausal women (1,2). Although OA and OP commonly occur in the elderly, they rarely coexist in a single patient (1,3). Healey et al (4) reported that only 4% of OP patients had significant osteoarthritis in the hip. It is well known that OP is associated with bone loss and microstructure deterioration, which can reduce bone strength and thereby increase the risk of fragility fracture (5). In contrast, the pathogenesis of OA remains a subject of controversy (6,7). In general, OA initially presents with destruction

Human type H vessels are a sensitive biomarker of bone mass

“…Quantitative measurements revealed that the BV/TV, Tb.Th, Tb.N, and Conn.D values were decreased with BMD (Supplementary Table S1) ( P <0.05), which was consistent with a previous study. 24 The 3D μ CT figures and quantification charts (Figures 3a–i) also showed that microarchitectural changes coincided with BMD. Thus, the patient groups were cross-calibrated by BMD and μ CT; however, significant differences were not observed between the groups according to age ( P =0.065) (Supplementary Figure 3A and Supplementary Table S2).…”

Association between subchondral bone structure and osteoarthritis histopathological grade

“…This finding was expected based on previous morphometric guinea pig model of spontaneous OA 17,18 and human studies. [23][24][25][26][27][28][29] As an adaptation to OA, trabecular bone may increase its stiffness and strength [39][40][41] by changing its structure to resist higher loading due to cartilage loss.…”

Osteoarthritis and bone mineral density: are strong bones bad for joints?

“…In the 1970s, Radin and Rose 63 proposed that increased stiffness of subchondral bone might lead to articular cartilage degeneration through the mechanical effects of increased shear stress. However, subsequent studies using a variety of techniques at different stages of OA progression have revealed complex and opposing changes in apparent density, material density, and stiffness in osteoarthritic subchondral bone, [64][65][66] suggesting that this explanation is too simplistic. 40,67 Thinning of the articular cartilage from below, owing to reactivation of endochondral ossification at the bone-cartilage interface in OA joints resulting in tidemark duplication and advancement, may represent another important mechanism by which increased bone formation could drive the OA process.…”