Geissler Joseph R, Bajaj Devendra, Fritton J Christopher
Department of Orthopaedics, New Jersey Medical School, Rutgers University, 205 S. Orange Avenue, Newark, NJ 07103, USA; Joint Program in Biomedical Engineering, Rutgers Biomedical and Health Sciences, and the New Jersey Institute of Technology, Newark, NJ, USA.
Department of Orthopaedics, New Jersey Medical School, Rutgers University, 205 S. Orange Avenue, Newark, NJ 07103, USA.
J Biomech. 2015 Apr 13;48(6):883-94. doi: 10.1016/j.jbiomech.2015.01.032. Epub 2015 Feb 2.
The biomechanics literature contains many well-understood mechanisms behind typical fracture types that have important roles in treatment planning. The recent association of "atypical" fractures with long-term use of drugs designed to prevent osteoporosis has renewed interest in the effects of agents on bone tissue-level quality. While this class of fracture was recognized prior to the introduction of the anti-resorptive bisphosphonate drugs and recently likened to stress fractures, the mechanism(s) that lead to atypical fractures have not been definitively identified. Thus, a causal relationship between these drugs and atypical fracture has not been established. Physicians, bioengineers and others interested in the biomechanics of bone are working to improve fracture-prevention diagnostics, and the design of treatments to avoid this serious side-effect in the future. This review examines the mechanisms behind the bone tissue damage that may produce the atypical fracture pattern observed increasingly with long-term bisphosphonate use. Our recent findings and those of others reviewed support that the mechanisms behind normal, healthy excavation and tunnel filling by bone remodeling units within cortical tissue strengthen mechanical integrity. The ability of cortical bone to resist the damage induced during cyclic loading may be altered by the reduced remodeling and increased tissue age resulting from long-term bisphosphonate treatment. Development of assessments for such potential fractures would restore confidence in pharmaceutical treatments that have the potential to spare millions in our aging population from the morbidity and death that often follow bone fracture.
生物力学文献中包含许多典型骨折类型背后已被充分理解的机制,这些机制在治疗方案规划中起着重要作用。“非典型”骨折与长期使用预防骨质疏松症药物之间的最新关联,重新引发了人们对药物对骨组织水平质量影响的兴趣。虽然这类骨折在抗吸收双膦酸盐药物引入之前就已被认识到,且最近被认为类似于应力性骨折,但导致非典型骨折的机制尚未得到明确确定。因此,这些药物与非典型骨折之间的因果关系尚未确立。对骨生物力学感兴趣的医生、生物工程师和其他人正在努力改进骨折预防诊断方法以及治疗设计,以避免未来出现这种严重的副作用。本综述探讨了长期使用双膦酸盐后越来越多地观察到的非典型骨折模式背后的骨组织损伤机制。我们最近的发现以及其他被综述的研究结果支持,皮质组织内骨重塑单元进行正常、健康的挖掘和隧道填充背后的机制可增强机械完整性。长期双膦酸盐治疗导致的重塑减少和组织老化增加,可能会改变皮质骨抵抗循环载荷期间诱导损伤的能力。开发针对此类潜在骨折的评估方法,将恢复人们对药物治疗的信心,这类治疗有可能使我们老龄化人口中的数百万人免受骨折后常常伴随的发病和死亡之苦。