Osteoarthritis (OA) and osteoporosis (OP) are two skeletal disorders associated with joint structures. Occasionally, OA and OP occur in the same patient. However, the effect of OP changes on OA progression in patients with osteoporotic OA (OP-OA) has not been reported, especially the potential association between subchondral bone and articular cartilage. Thus we investigated the alterations in the microstructure, biomechanical properties, and remodeling of subchondral bone as well as their association with cartilage damage in the hip joint of patients with OP-OA. Thirty-nine femoral head specimens were obtained from patients who underwent total hip arthroplasty (OA group, n = 19; OP-OA group, n = 20), and healthy specimens from cadaver donors were used (control group, n = 10). The microstructure and biomechanical properties of subchondral bone were evaluated by micro–computed tomography and micro–finite-element analysis. Histology, histomorphometric measurements, and immunohistochemistry were used to assess subchondral bone remodeling and cartilage damage. Linear regression analysis was performed to elucidate the relationship between subchondral bone and articular cartilage. In the subchondral bone of the OP-OA group, compared with that of the OA group, aberrant bone remodeling leads to an inferior microstructure and worsening biomechanical properties, potentially affecting transmission of loading stress from the cartilage to the subchondral bone, and then resulting in accelerated OA progression in patients with OP-OA. The results indicate that changes in subchondral bone could affect OA development and the improvement in subchondral bone with bone-metabolism agents may help mitigate OA progression when OP and OA coexist in the same patients. © 2019 American Society for Bone and Mineral Research.

Osteogenesis and angiogenesis are important for bone fracture healing. Irisin is a muscle-derived monokine that is associated with bone formation. To demonstrate the effect of irisin on bone fracture healing, closed mid-diaphyseal femur fractures were produced in 8-week-old C57BL/6 mice. Irisin was administrated intraperitoneally every other day after surgery, fracture healing was assessed by using X-rays. Bone morphometry of the fracture callus were assessed by using micro-computed tomography. Femurs of mice from each group were assessed by the three-point bending testing. Effect of irisin on osteogenic differentiation in mesenchymal stem cells in vitro was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR), alkaline phosphatase staining and alizarin red staining. Angiogenesis of human umbilical vein endothelial cells (HUVECs) were evaluated by qRT-PCR, migration tests, and tube formation assays. Increased callus formation, mineralization and tougher fracture healing were observed in the irisin-treated group than in the control group, indicating the better fracture callus healing due to Irisin treatment. The vessel surface and vessel volume fraction of the callus also increased in the irisin-treated group. The expression of BMP2, CD31, and VEGF in callus were enhanced in the irisin-treated group. In mouse bone mesenchymal stem cells, irisin promoted ALP expression and mineralization, and increased the expression of osteogenic genes, including OSX, Runx2, OPG, ALP, OCN and BMP2. Irisin also promoted HUVEC migration and tube formation. Expression of angiogenic genes, including ANGPT1, ANGPT2, VEGFb, CD31, FGF2, and PDGFRB in HUVECs were increased by irisin. All the results indicate irisin can promote fracture healing through osteogenesis and angiogenesis. These findings help in the understanding of muscle–bone interactions during fracture healing. Irisin was one of the most important monokine secreted by skeletal muscle. Studies have found that irisin have anabolic effect one bone remodeling through affecting osteocyte and osteoblast. Based on our study, irisin could promote bone fracture healing by increasing bone mass and vascularization, which provide a potential usage of irisin to promote fracture healing and improve clinical outcomes.

We evaluated the compensatory change in ankle alignment due to knee malalignment and its relationship with varus knee deformities, as well as sex differences in compensation. From October 2016 to September 2017, 103 patients with end-stage knee osteoarthritis underwent primary total knee arthroplasty (TKA). Ninety-five knees (78 patients) were included. The hip-knee-ankle angle (HKA) and ankle alignment and tilt were evaluated with full-leg standing anteroposterior radiographs. The ankle alignment was estimated according to the tibiotalar angle, tibial anterior surface angle (TAS), and lateral distal tibial angle. The talar tilt angle (TT), anatomical talocrural angle, angle between the tibial plateau and distal tibial plafond, angles between the ground and distal tibial plafond, and angles between the ground and upper talus were measured to evaluate ankle tilt. The patients were separated into two sex-based groups; correlations between the HKA and ankle parameters were estimated. The mean HKA in men and women was 8.16 ± 4.36° and 7.69 ± 5.93°, respectively. The relative tilt of the talus and distal tibia plafond to the ground was increased when varus knee deformities progressed. In women, there was a positive correlation between the knee alignment and TAS (r = − 0.295, p = 0.016). As the knee mechanical axis became more varus, the distal tibia plafond became more valgus. In women, a negative correlation was observed between the HKA and TT (r = − 0.359, p = 0.003). Compensatory changes in the ankle alignment and TT to knee alignment were not observed in men. Compensatory ankle changes should be considered before TKA.

Developmental dysplasia of the hip (DDH) is recognized as a frequent cause of secondary osteoarthritis (OA). The purpose in this study was to compare structural and biomechanical properties of subchondral trabecular bone ​and its relationship with cartilage damage between patients with DDH and patients with primary hip OA. Forty-three femoral head specimens obtained from patients who underwent total hip arthroplasty [DDH, n ​= ​17; primary OA, n ​= ​16; and normal control (NC), n ​= ​10] were scanned by microcomputed tomography and analyzed by individual trabecula segmentation to obtain the microstructural types of subchondral trabecular bone. The biomechanical properties were analyzed by micro-finite element analysis, and cartilage damage was evaluated by histology. The linear regression analysis was used to indicate the association between microstructures, biomechanical property, and articular cartilage. The DDH group showed the lowest total bone volume fractions (BV/TV) and plate BV/TV in the three groups (p ​< ​0.05). There were also different discrepancies between the three groups in plate/rod trabecular number, plate/rod trabecular thickness, trabecular plate surface area/trabecular rod length, and junction density with different modes (plate-plate, rod-rod, and plate-rod junction density). The micro-finite element analysis, histology, and linear regression revealed that the subchondral trabecular bone in the DDH group had inferior biomechanical properties ​and cartilage damage of patients with DDH was more serious with different subchondral trabecular bone microstructures. Our findings detected deteriorating subchondral trabecular bone microstructures in patients with DDH. The mass and type of subchondral trabecular bone play a key role in mechanical properties in DDH, which might be related to cartilage damage. Our findings suggested that changes of subchondral trabecular bone play a critical role ​in DDH progression and that the improvement on subchondral trabecular bone may be a sensitive and promising way in treatment of DDH.