Laboratory of Regenerative Morphology and Bioartificial Structures (Re.Mo.Bio.S.), Department of Medicine and Surgery - DIMEC, Unit of Biomedical, Biotechnological and Translational Sciences (S.BI.BI.T.), Museum and Historical Library of Biomedicine - BIOMED, University of Parma, Parma, Italy.
OSTEONET-CMG Unit (Osteoporosis, Nutrition, Endocrinology, and Innovative Therapies) at the Medical Center Galliera (CMG), San Venanzio, Italy.
Front Immunol. 2020 Sep 2;11:1737. doi: 10.3389/fimmu.2020.01737. eCollection 2020.
Osteoporosis stems from an unbalance between bone mineral resorption and deposition. Among the numerous cellular players responsible for this unbalance bone marrow (BM) monocytes/macrophages, mast cells, T and B lymphocytes, and dendritic cells play a key role in regulating osteoclasts, osteoblasts, and their progenitor cells through interactions occurring in the context of the different bone compartments (cancellous and cortical). Therefore, the microtopography of immune cells inside trabecular and compact bone is expected to play a relevant role in setting initial sites of osteoporotic lesion. Indeed, in physiological conditions, each immune cell type preferentially occupies either endosteal, subendosteal, central, and/or perisinusoidal regions of the BM. However, in the presence of an activation, immune cells recirculate throughout these different microanatomical areas giving rise to a specific distribution. As a result, the trabeculae of the cancellous bone and endosteal free edge of the diaphyseal case emerge as the primary anatomical targets of their osteoporotic action. Immune cells may also transit from the BM to the depth of the compact bone, thanks to the efferent venous capillaries coursing in the Haversian and Volkmann canals. Consistently, the innermost parts of the osteons and the periosteum are later involved by their immunomodulatory action, becoming another site of mineral reabsorption in the course of an osteoporotic insult. The novelty of our updating is to highlight the microtopography of bone immune cells in the cancellous and cortical compartments in relation to the most consistent data on their action in bone remodeling, to offer a mechanist perspective useful to dissect their role in the osteoporotic process, including bone damage derived from the immunomodulatory effects of endocrine disrupting chemicals.
骨质疏松症源于骨矿物质吸收和沉积之间的失衡。在众多负责这种失衡的细胞中，骨髓 (BM) 中的单核细胞/巨噬细胞、肥大细胞、T 和 B 淋巴细胞以及树突状细胞通过发生在不同骨腔室（松质骨和皮质骨）背景下的相互作用，在调节破骨细胞、成骨细胞及其祖细胞方面发挥着关键作用。因此，免疫细胞在小梁和密质骨内的微地形预计将在确定骨质疏松病变的初始部位方面发挥相关作用。事实上，在生理条件下，每种免疫细胞类型都优先占据 BM 的骨内膜、骨内膜下、中央和/或窦周区域。然而，在存在激活的情况下，免疫细胞会在这些不同的微解剖区域中再循环，从而产生特定的分布。因此，松质骨的小梁和骨干的骨内膜游离缘成为其骨质疏松作用的主要解剖靶标。免疫细胞也可以通过在哈弗氏管和沃尔曼氏管中流动的流出静脉毛细血管从 BM 转移到密质骨的深处。一致地，骨单位的最内部和骨膜后来被它们的免疫调节作用所涉及，成为骨质疏松损伤过程中矿物质再吸收的另一个部位。我们更新的新颖之处在于强调松质骨和皮质骨腔室中骨免疫细胞的微地形与它们在骨重塑中作用的最一致数据有关，提供一个有助于剖析它们在骨质疏松过程中的作用的机制观点，包括源自内分泌干扰化学物质的免疫调节作用的骨损伤。
