Vashishth Deepak
Department of Biomedical Engineering, Center for Biotechnology and Interdisciplinary Studies, Rensselaer Polytechnic Institute, 110 8th Street, Troy, NY 12180, USA.
Crit Rev Eukaryot Gene Expr. 2005;15(4):343-58. doi: 10.1615/critreveukargeneexpr.v15.i4.40.
Age-related nontraumatic fractures are a major public health problem. Even though lower bone mass is the most commonly implicated variable for the age-related increase in fracture incidence, studies show that the resistance of bone material against fracture (toughness) diminishes with age. The mechanisms for the age-related loss of toughness are, however, unknown and may involve alterations in the quality of the bone material. The review of literature presented here identifies changes in the quality of bone material at ultrastructural, lamellar, osteonal, and tissue levels as plausible contributors to the biomechanical changes in aging human bone. The changes in bone quality at these multiple levels of organization result in a systematic breakdown of the mechanical and biological mechanisms that provide bone with its resistance against fracture. Animal studies conducted to date suggest that, similar to bone mass, bone quality may be partially regulated by genetics.
年龄相关性非创伤性骨折是一个重大的公共卫生问题。尽管较低的骨量是与年龄相关的骨折发生率增加最常涉及的变量,但研究表明,骨材料抵抗骨折的能力(韧性)会随着年龄的增长而下降。然而,与年龄相关的韧性丧失机制尚不清楚,可能涉及骨材料质量的改变。本文对文献的综述指出,在超微结构、板层、骨单位和组织水平上骨材料质量的变化可能是导致老年人体骨生物力学变化的合理因素。这些多层次组织结构中骨质量的变化导致了为骨骼提供抗骨折能力的机械和生物学机制的系统性破坏。迄今为止进行的动物研究表明,与骨量类似,骨质量可能部分受基因调控。