Fini Milena, Carpi Angelo, Borsari Veronica, Tschon Matilde, Nicolini Andrea, Sartori Maria, Mechanick Jeffrey, Giardino Roberto
Laboratory of Surgical and Preclinical Studies, Rizzoli Orthopaedic Institute, Bologna, Italy.
Front Biosci (Schol Ed). 2010 Jan 1;2(2):468-82. doi: 10.2741/s79.
One of the unfortunate sequelae of increased life expectancy is a growing number of age-related degenerative diseases, a prime example being osteoporosis. This form of metabolic bone disease and related co-morbidities consume tremendous resources and costs from a nation's health care system. Osteoporosis results from genetic, age-related, and hormone-dependent causes as well as a compendium of secondary pathophysiological states. The presence of osteoporosis as a comorbidity confers a significant negative prognostic element following orthopedic procedures. In vitro and in vivo studies of osteoporotic bone implicate microarchitectural bone rarefaction, microenvironmental and functional disturbance of osteoblast-osteoclast coupling, and abnormal tissue and signalling molecule repertoires, each having detrimental effects on the regenerative and osteointegration processes. This review explores the pathophysiology of bone remodeling from a macro- and micro- systems biology standpoint with a focus on cytokine interactions. Furthermore, therapeutic interventions exploiting vulnerable nodes in these physiological networks will be posited. One exciting development in this area is the use of novel biomaterials.
预期寿命增加带来的一个不幸后果是与年龄相关的退行性疾病数量不断增加，骨质疏松症就是一个典型例子。这种代谢性骨病及其相关合并症消耗了国家医疗保健系统的大量资源和成本。骨质疏松症由遗传、年龄相关、激素依赖因素以及一系列继发性病理生理状态引起。作为合并症，骨质疏松症在骨科手术后具有显著的负面预后因素。对骨质疏松性骨的体外和体内研究表明，骨微结构稀疏、成骨细胞-破骨细胞偶联的微环境和功能紊乱以及异常的组织和信号分子组成，每种情况都对再生和骨整合过程产生不利影响。本综述从宏观和微观系统生物学角度探讨骨重塑的病理生理学，重点关注细胞因子相互作用。此外，还将提出利用这些生理网络中脆弱节点的治疗干预措施。该领域一个令人兴奋的进展是新型生物材料的应用。
