Department of Medicine, McGill University and McGill University Health Centre, Montreal, QC, Canada.
Adv Exp Med Biol. 2019;1164:153-160. doi: 10.1007/978-3-030-22254-3_12.
Skeletal aging begins after peak bone mass is reached; progressive bone loss then occurs. Peak bone mass may occur at different ages in different skeletal sites and varies between sexes. Accelerated loss of bone occurs in the perimenopausal period in women, whereas more gradual but progressive loss of bone occurs in aging men. Changes in bone quality as well as bone quantity occur during growth and subsequent aging. These include changes in bone microarchitecture which may differ between cortical and trabecular compartments and in different sites, and may impact on bone size and geometry. Changes in material properties of bone matrix may also occur with aging. Loss of bone quantity and altered bone quality with aging may weaken bones and culminate in osteoporosis with an increased risk of fractures. Both genetic and epigenetic mechanisms may predispose to osteoporosis. Cellular and molecular events underlie the alterations in bone quantity and quality. Osteoclastic bone resorption and osteoblastic bone formation, tightly regulated by hormones, growth factors, and cytokines, are organized in coordinated activities resulting in remodeling and modeling. Malignancies, and anti-neoplastic therapies, may impact on the cellular and molecular events in the aging skeleton and produce focal or diffuse skeletal lesions and fractures.
骨骼老化始于达到峰值骨量之后；随后会发生进行性骨质流失。峰值骨量可能在不同骨骼部位和性别中出现在不同的年龄。女性在围绝经期会加速骨质流失，而男性则随着年龄的增长逐渐但持续地流失骨质。在生长和随后的衰老过程中，骨量和骨质量都会发生变化。这些变化包括骨微结构的变化，这些变化可能在皮质和小梁骨腔室之间以及不同部位有所不同，并且可能会影响骨的大小和几何形状。骨基质的材料特性也可能随年龄而发生变化。随着年龄的增长，骨量的减少和骨质量的改变可能会使骨骼变弱，最终导致骨质疏松症，增加骨折的风险。遗传和表观遗传机制都可能导致骨质疏松症。细胞和分子事件是骨量和骨质量改变的基础。破骨细胞的骨吸收和成骨细胞的骨形成受激素、生长因子和细胞因子的严格调节，它们以协调的方式组织起来，导致重塑和建模。恶性肿瘤和抗肿瘤治疗可能会影响衰老骨骼中的细胞和分子事件，导致局灶性或弥漫性骨骼病变和骨折。
