Ludwig Boltzmann Institute of Osteology at Hanusch Hospital of WGKK and AUVA Trauma Center Meidling, 1st Medical Department, Hanusch Hospital, Vienna, Austria.
Calcif Tissue Int. 2012 Mar;90(3):230-8. doi: 10.1007/s00223-011-9568-z. Epub 2012 Jan 24.
During bone remodeling osteoclasts resorb bone, thus removing material, e.g., damaged by microcracks, which arises as a result of physiological loading and could reduce bone strength. Such a process needs targeted bone resorption exactly at damaged sites. Osteocytic signaling plays a key role in this process, but it is not excluded that osteoclasts per se may possess toposensitivity to recognize and resorb damaged bone since it has been shown that resorption spaces are associated with microcracks. To address this question, we used an in vitro setup of a pure osteoclast culture and mineralized substrates with artificially introduced microcracks and microscratches. Histomorphometric analyses and statistical evaluation clearly showed that these defects had no effect on osteoclast resorption behavior. Osteoclasts did not resorb along microcracks, even when resorption started right beside these damages. Furthermore, quantification of resorption on three different mineralized substrates, cortical bone, bleached bone (bone after partial removal of the organic matrix), and dentin, revealed lowest resorption on bone, significantly higher resorption on bleached bone, and highest resorption on dentin. The difference between native and bleached bone may be interpreted as an inhibitory impact of the organic matrix. However, the collagen-based matrix could not be the responsible part as resorption was highest on dentin, which contains collagen. It seems that osteocytic proteins, stored in bone but not present in dentin, affect osteoclastic action. This demonstrates that osteoclasts per se do not possess a toposensitivity to remove microcracks but may be influenced by components of the organic bone matrix.
在骨重建过程中，破骨细胞吸收骨组织，从而去除材料，例如因生理负荷而产生的微裂纹导致的受损材料，这可能会降低骨强度。这个过程需要有针对性地在受损部位进行骨吸收。骨细胞信号在这个过程中起着关键作用，但不能排除破骨细胞本身可能具有拓扑敏感性，以识别和吸收受损的骨组织，因为已经表明吸收腔与微裂纹有关。为了解决这个问题，我们使用了一种体外纯破骨细胞培养和矿化基质的方法，在这些基质中人工引入微裂纹和微划痕。组织形态计量学分析和统计评估清楚地表明，这些缺陷对破骨细胞的吸收行为没有影响。破骨细胞不会沿着微裂纹吸收，即使在这些损伤旁边开始吸收。此外，对三种不同矿化基质（皮质骨、漂白骨（去除有机基质部分后的骨）和牙本质）上的吸收进行定量分析表明，骨组织的吸收最少，漂白骨的吸收明显增加，牙本质的吸收最多。天然骨和漂白骨之间的差异可以解释为有机基质的抑制作用。然而，由于牙本质中含有胶原，胶原基基质不可能是负责的部分，因为牙本质上的吸收最高。似乎是骨细胞蛋白，储存在骨组织中而不在牙本质中，影响破骨细胞的作用。这表明破骨细胞本身不具有去除微裂纹的拓扑敏感性，但可能受到有机骨基质成分的影响。
