The impact of chronic obstructive pulmonary disease on bone strength.

Chronic obstructive pulmonary disease (COPD) is a lifestyle-related disease that develops in middle-aged and older adults, often due to smoking habits, and has been noted to cause bone fragility. COPD is a risk factor for osteoporosis and fragility fracture, and a high prevalence of osteoporosis and incidence of vertebral fractures have been shown in patients with COPD. Findings of lung tissue analysis in patients with COPD are primarily emphysema with a loss of alveolar septal walls, and the severity of pulmonary emphysema is negatively correlated with thoracic spine bone mineral density (BMD). On the other hand, epidemiological studies on COPD and fracture risk have reported a BMD-independent increase in fracture risk; however, verification in animal models and human bone biopsy samples has been slow, and the essential pathogenesis has not been elucidated. The detailed pathological/molecular mechanisms of musculoskeletal complications in patients with COPD are unknown, and basic research is needed to elucidate the mechanisms. This paper discusses the impacts of COPD on bone strength, focusing on findings in animal models in terms of bone microstructure, bone metabolic dynamics, and material properties.

Delayed cortical bone healing due to impaired nuclear Nrf2 translocation in COPD mice.

The effect of the pathogenesis of chronic obstructive pulmonary disease (COPD) on bone fracture healing is unknown. Oxidative stress has been implicated in the systemic complications of COPD, and decreased activity of Nrf2 signaling, a central component of the in vivo antioxidant mechanism, has been reported. We investigated the process of cortical bone repair in a mouse model of elastase-induced emphysema by creating a drill hole and focusing on Nrf2 and found that the amount of new bone in the drill hole was reduced and bone formation capacity was decreased in the model mice. Furthermore, nuclear Nrf2 expression in osteoblasts was reduced in model mice. Sulforaphane, an Nrf2 activator, improved delayed cortical bone healing in model mice. This study indicates that bone healing is delayed in COPD mice and that impaired nuclear translocation of Nrf2 is involved in delayed cortical bone healing, suggesting that Nrf2 may be a novel target for bone fracture treatment in COPD patients.

Prediction of fracture lines of the calcaneus using a three-dimensional finite element model.

The various lines of calcaneal fractures indicate their complex nature and make their treatment challenging. There is still much debate regarding the position and direction of these fracture lines, even for the primary fracture line. The computed tomography-based finite element model is known to provide accurate predictions of fracture loads and virtual fracture locations for the femur and distal radius. This study aimed to establish how to predict the calcaneus fracture lines using the computed tomography-based finite element model for patients with contralateral calcaneal fractures and to investigate whether the predicted lines were similar to those of the fractured calcaneus. The calcanei of five men and two women aged 44-77 years (average age, 60 years) with contralateral calcaneal fractures were analyzed. To assess the precision of the predicted fracture lines of the contralateral calcanei, they were compared with the fracture locations found by three-dimensional models of the calcanei. The fracture lines of the finite element model simulated the actual fracture lines and diagnosed joint depression types of fractures (five cases) and tongue types (two cases), but only under certain conditions for each case. This trial simulated calcaneal fractures using a patient-specific computed tomography-based nonlinear finite element model. Therefore, we suggest that it is possible to reproduce calcaneal fractures using the finite element model. It was possible to predict with precision the actual calcaneal fracture for each patient and to reproduce fracture conditions. Therefore, this method is valuable because it can provide an understanding of the pathomechanism of calcaneal fractures. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 37:483-489, 2019.

pH-dependent color change of colloidal dispersions of gold nanoclusters: effect of stabilizer.

Gold nanoclusters protected by 3-mercaptopropionic acid (MPA-Au nanoclusters) were prepared by citrate-reduction of hydrogen tetrachloroaurate(III) in the presence of sodium 3-mercaptopropionate. Color of the dispersions of MPA-Au nanoclusters changed from red to purple by addition of hydrochloric acid and returned from purple to red by addition of an aqueous sodium hydroxide solution. This reversible response can be attributed to synchronized changes between dispersion and ordering of MPA-Au nanoclusters, determined by transmission electron microscopy. Gold nanoclusters protected by poly(acrylic acid) (PAA-Au nanoclusters) were prepared by UV irradiation of an aqueous solution of hydrogen tetrachloroaurate(III) in the presence of poly(sodium acrylate). The pH-dependent spectral change observed for MPA-Au was not observed for PAA-Au. UV-Vis absorption spectra of colloidal dispersions of PAA-Au nanoclusters after addition of hydrochloric acid and an aqueous sodium hydroxide solution were in good agreement with each other, suggesting the stability of PAA-Au nanoclusters to pH change.