Delaisse Jean-Marie, Søe Kent, Andersen Thomas Levin, Rojek Aleksandra Maria, Marcussen Niels
Clinical Cell Biology, Department of Pathology, Odense University Hospital, Odense, Denmark.
Clinical Cell Biology, Pathology Research Unit, Department of Clinical Research, University of Southern Denmark, Odense, Denmark.
Front Cell Dev Biol. 2021 Mar 30;9:644503. doi: 10.3389/fcell.2021.644503. eCollection 2021.
The current models of osteoclastic bone resorption focus on immobile osteoclasts sitting on the bone surface and drilling a pit into the bone matrix. It recently appeared that many osteoclasts also enlarge their pit by moving across the bone surface while resorbing. Drilling a pit thus represents only the start of a resorption event of much larger amplitude. This prolonged resorption activity significantly contributes to pathological bone destruction, but the mechanism whereby the osteoclast engages in this process does not have an answer within the standard bone resorption models. Herein, we review observations that lead to envision how prolonged resorption is possible through simultaneous resorption and migration. According to the standard pit model, the "sealing zone" which surrounds the ruffled border (i.e., the actual resorption apparatus), "anchors" the ruffled border against the bone surface to be resorbed. Herein, we highlight that continuation of resorption demands that the sealing zone "glides" inside the cavity. Thereby, the sealing zone emerges as the structure responsible for orienting and displacing the ruffled border, e.g., directing resorption against the cavity wall. Importantly, sealing zone displacement stringently requires thorough collagen removal from the cavity wall - which renders strong cathepsin K collagenolysis indispensable for engagement of osteoclasts in cavity-enlargement. Furthermore, the sealing zone is associated with generation of new ruffled border at the leading edge, thereby allowing the ruffled border to move ahead. The sealing zone and ruffled border displacements are coordinated with the migration of the cell body, shown to be under control of lamellipodia at the leading edge and of the release of resorption products at the rear. We propose that bone resorption demands more attention to osteoclastic models integrating resorption and migration activities into just one cell phenotype.
目前破骨细胞性骨吸收模型聚焦于位于骨表面的静止破骨细胞,它们在骨基质中钻出一个坑。最近发现,许多破骨细胞在吸收过程中也会通过在骨表面移动来扩大其坑。因此,钻孔仅仅代表了幅度大得多的吸收事件的开始。这种延长的吸收活动显著促成了病理性骨破坏,但破骨细胞参与这一过程的机制在标准骨吸收模型中尚无答案。在此,我们回顾了一些观察结果,这些结果使我们能够设想破骨细胞如何通过同时进行吸收和迁移来实现延长的吸收。根据标准坑模型,围绕褶皱边缘(即实际的吸收装置)的“封闭区”将褶皱边缘“锚定”在要吸收的骨表面上。在此,我们强调吸收的持续需要封闭区在腔内“滑动”。因此,封闭区成为负责定向和移动褶皱边缘的结构,例如引导针对腔壁的吸收。重要的是,封闭区的位移严格要求从腔壁彻底去除胶原蛋白——这使得强力组织蛋白酶K介导的胶原蛋白溶解对于破骨细胞参与腔扩大不可或缺。此外,封闭区与前沿新褶皱边缘的产生相关,从而使褶皱边缘能够向前移动。封闭区和褶皱边缘的位移与细胞体的迁移相协调,已表明这受前沿片状伪足和后方吸收产物释放的控制。我们提出,骨吸收需要更多关注将吸收和迁移活动整合到单一细胞表型中的破骨细胞模型。