BoneKEy reports最新文献

In this review, I consider the varied mechanisms in cortical bone that help preserve its integrity and how they deteriorate with aging. Aging affects cortical bone in two ways: extrinsically through its effects on the individual that modify its mechanical loading experience and 'milieu interieur'; and intrinsically through the prolonged cycle of remodelling and renewal extending to an estimated 20 years in the proximal femur. Healthy femoral cortex incorporates multiple mechanisms that help prevent fracture. These have been described at multiple length scales from the individual bone mineral crystal to the scale of the femur itself and appear to operate hierarchically. Each cortical bone fracture begins as a sub-microscopic crack that enlarges under mechanical load, for example, that imposed by a fall. In these conditions, a crack will enlarge explosively unless the cortical bone is intrinsically tough (the opposite of brittle). Toughness leads to microscopic crack deflection and bridging and may be increased by adequate regulation of both mineral crystal size and the heterogeneity of mineral and matrix phases. The role of osteocytes in optimising toughness is beginning to be worked out; but many osteocytes die in situ without triggering bone renewal over a 20-year cycle, with potential for increasing brittleness. Furthermore, the superolateral cortex of the proximal femur thins progressively during life, so increasing the risk of buckling during a fall. Besides preserving or increasing hip BMD, pharmaceutical treatments have class-specific effects on the toughness of cortical bone, although dietary and exercise-based interventions show early promise.

Long-term effects of repeated in vivo micro-computed tomography (μCT) scanning at key stages of growth and bone development (ages 2, 4 and 6 months) on trabecular and cortical bone structure, as well as developmental patterns, have not been studied. We determined the effect of repetitive μCT scanning at age 2, 4 and 6 months on tibia bone structure of male and female CD-1 mice and characterized developmental changes. At 2, 4 and 6 months of age, right tibias were scanned using in vivo μCT (Skyscan 1176) at one of three doses of radiation per scan: 222, 261 or 460 mGy. Left tibias of the same mice were scanned only at 6 months to serve as non-irradiated controls to determine whether recurrent radiation exposure alters trabecular and cortical bone structure at the proximal tibia. In males, eccentricity was lower (P<0.05) in irradiated compared with non-irradiated tibias (222 mGy group). Within each sex, all other structural outcomes were similar between irradiated and non-irradiated tibias regardless of dose. Trabecular bone loss occurred in all mice due to age while cortical development continued to age 6 months. In conclusion, repetitive μCT scans at various radiation doses did not damage trabecular or cortical bone structure of proximal tibia in male and female CD-1 mice. Moreover, scanning at 2, 4 and 6 months of age highlight the different developmental time course between trabecular and cortical bone. These scanning protocols can be used to investigate longitudinal responses of bone structures to an intervention.

Periosteum is a smart mechanobiological material that serves as a habitat and delivery vehicle for stem cells as well as biological factors that modulate tissue genesis and healing. Periosteum's remarkable regenerative capacity has been harnessed clinically for over two hundred years. Scientific studies over the past decade have begun to decipher the mechanobiology of periosteum, which has a significant role in its regenerative capacity. This integrative review outlines recent mechanobiological insights that are key to modulating and translating periosteum and its resident stem cells in a regenerative medicine context.

[This corrects the article DOI: 10.1038/bonekey.2014.56.].

The prevalence of obesity and type 2 diabetes mellitus (T2DM) continues to rise, and as a result, research aimed at understanding the molecular basis for the co-morbidities has become an area of much scientific interest. Among the more recently recognized chronic complications of T2DM is the increased risk of fracture, especially hip fracture, that has been reported independent of bone mineral density (BMD). A widely used animal model to study how the development and progression of impaired glucose tolerance affect the skeleton has been the diet-induce obesity (DIO) model. As the name implies, this model employs the use of a version of high-fat diets to induce obesity and the subsequent metabolic perturbations that occur with T2DM. Although the model offers a number of advantages, the literature reveals some inconsistent results. Upon further review, discrepancies in the choice of the experimental high-fat diets and the control diets have become a point of major concern. The variability between diets and study design has made it difficult to compare data and results across studies. Therefore, this review aims to provide guidelines that should be employed when designing studies using DIO models of T2DM.