Beck-Broichsitter Benedicta E, Smeets Ralf, Heiland Max
Department of Oral and Maxillofacial Surgery, University Medical Center Hamburg-Eppendorf, Martinistraße, Hamburg, Germany.
Curr Opin Infect Dis. 2015 Jun;28(3):240-5. doi: 10.1097/QCO.0000000000000155.
The term osteomyelitis covers a wide range of inflammatory bone disorders caused by microbial invasion or due to autoinflammatory processes, but furthermore osteomyelitis also occurs at different ages and at preferred localizations in the human skeleton. This article aims to give an overview of the current literature focussing on pathognomonic aspects of osteomyelitis because of microbial invasion.
Outlining the chronological sequence of osteomyelitis originating from the invasion of microbes finally leading to destruction of bone tissue, the formation and proliferation of biofilm structures play a key role in the development of inflammatory bone disorders. The components of the biofilm on the one hand mediate an immune response leading to an increase of local cytokines and induction of osteoclastogenesis but on the other hand also directly interact with the osteoblasts. As a result, the bone-remodelling process is immensely diminished by induction of proapoptotic pathways, decreased proliferation and differentiation of osteoblasts and an additional promotion of osteoclastogenesis.
Although microbial invasion is responsible to be the cause for inflammatory bone disorders, except for an autoinflammatory origin, the underlying and detailed mechanisms in the pathogenesis of osteomyelitis are not yet fully understood, but represent an absolute precondition for the development of effective causal treatment strategies in the future.
骨髓炎这一术语涵盖了由微生物入侵或自身炎症过程引起的广泛的炎症性骨疾病，而且骨髓炎还发生在不同年龄阶段以及人体骨骼的特定部位。本文旨在概述当前聚焦于因微生物入侵导致的骨髓炎特征方面的文献。
概述骨髓炎从微生物入侵开始，最终导致骨组织破坏的时间顺序，生物膜结构的形成和增殖在炎症性骨疾病的发展中起关键作用。生物膜的成分一方面介导免疫反应，导致局部细胞因子增加并诱导破骨细胞生成，但另一方面也直接与成骨细胞相互作用。结果，通过诱导促凋亡途径、减少成骨细胞的增殖和分化以及进一步促进破骨细胞生成，骨重塑过程大大减少。
尽管微生物入侵是炎症性骨疾病的病因，除了自身炎症起源外，骨髓炎发病机制的潜在和详细机制尚未完全了解，但这是未来开发有效的因果治疗策略的绝对前提。
