Seref-Ferlengez Zeynep, Kennedy Oran D, Schaffler Mitchell B
Department of Biomedical Engineering, The City College of New York, City University of New York , New York, NY, USA.
Department of Orthopaedic Surgery, Hospital for Joint Diseases, New York University , New York, NY, USA.
Bonekey Rep. 2015 Mar 18;4:644. doi: 10.1038/bonekey.2015.11. eCollection 2015.
Microdamage resulting from fatigue or 'wear and tear' loading contributes to bone fragility; however, the full extent of its influence is not completely understood. Linear microcracks (∼50-100 μm) and diffuse damage (clusters of sublamellar-sized cracks) are the two major bone microdamage types, each with different mechanical and biological consequences. Healthy bone, due to its numerous microstructural interfaces and its ability to affect matrix level repair, deals effectively with microdamage. From a material standpoint, healthy bone behaves much like engineering composites like carbon-fiber reinforced plastics. Both materials allow matrix damage to form during fatigue loading and use microstructural interfaces to dissipate energy and limit microcrack propagation to slow fracture. The terms fracture toughness and 'toughening mechanism', respectively, describe mechanical behavior and microstructural features that prevent crack growth and make it harder to fracture a material. Critically, toughness is independent of strength. In bone, primary toughening features include mineral and collagen interfaces, lamellae and tissue heterogeneity among osteons. The damage tolerance of bone and other composites can be overcome with sustained loading and/or matrix changes such that the microstructure no longer limits microcrack propagation. With reduced remodeling due to aging, disease or remodeling suppression, microdamage accumulation can occur along with loss of tissue heterogeneity. Both contribute additively to reduced fracture toughness. Thus, the answer to the key question for bone fragility of how much microdamage is too much is extremely complex. It ultimately depends on the interplay between matrix damage content, internal repair and effectiveness of matrix-toughening mechanisms.
由疲劳或“磨损”负荷导致的微损伤会促使骨骼变得脆弱；然而，其影响的全部程度尚未完全明晰。线性微裂纹（约50 - 100微米）和弥散性损伤（亚板层尺寸裂纹簇）是两种主要的骨骼微损伤类型，每种类型都有不同的力学和生物学后果。健康的骨骼由于其众多的微观结构界面以及影响基质水平修复的能力，能够有效地应对微损伤。从材料角度来看，健康的骨骼与诸如碳纤维增强塑料之类的工程复合材料非常相似。这两种材料在疲劳加载过程中都会形成基质损伤，并利用微观结构界面来耗散能量，限制微裂纹扩展以延缓断裂。术语断裂韧性和“增韧机制”分别描述了防止裂纹扩展并使材料更难断裂的力学行为和微观结构特征。至关重要的是，韧性与强度无关。在骨骼中，主要的增韧特征包括矿物质与胶原蛋白界面、骨板以及骨单位之间的组织异质性。持续加载和/或基质变化可能会克服骨骼和其他复合材料的损伤耐受性，导致微观结构不再限制微裂纹扩展。随着衰老、疾病或重塑抑制导致的重塑减少，微损伤积累会与组织异质性丧失同时发生。两者都会累加导致断裂韧性降低。因此，关于骨骼脆弱性的关键问题——多少微损伤算过多——的答案极其复杂。这最终取决于基质损伤含量、内部修复以及基质增韧机制有效性之间的相互作用。
