Читать книгу Bone and Soft Tissue Augmentation in Implantology - Группа авторов - Страница 14

Osteocytes are characterized by a slower metabolism than osteoblasts and present elongations of the cytoplasmic membrane that connect osteocytes to each other and to the surface cells through gap junctions, creating a three-dimensional canalicular network in the mineralized tissue that is particularly impressive in the osteons (Fig 1-3). The diffusion of nutrients and ions, otherwise impossible, is guaranteed by this cell network. A limit in diffusion through the canalicular system exists, which is approximately 100 µm. This is also the mean wall thickness of osteons in the cortical bone and also the packets in trabecular bone. The osteocytes, which control the effector cells (the osteoclasts and osteoblasts),^7,10,33 require a long lifespan because they are embedded in lacunae within the mineralized matrix, and are connected via dendritic processes that run through the canaliculi. The dense, interconnected network that spans the entire skeleton also connects to blood vessels and to the cells on the bone surface, e.g. the lining cells, osteoblasts, and osteoclasts. As recently summarized,¹⁵ 1 mm³ of bone contains about 20,000 to 30,000 osteocytes, each having 100 dendritic processes and a radius of approximately 70 nm. Around 40 billion (10⁹) osteocytes with 20 trillion (10¹²) connections and a total length of dendritic processes of 200,000 km can be calculated for the entire skeleton. The surface area and the volume of the lacuno-canalicular network are around 200 m² and 40 cm³, respectively. Osteocytes are not only interconnected via their dendritic processes but are surrounded by a liquid that connects them to the overall circulation. Osteocytes are obviously predestined to control bone homeostasis at the local and systemic levels. For example, osteocytes are the cells that almost exclusively produce sclerostin, an inhibitor of the Wingless-related integration site (Wnt) signaling pathway.^129,130 The molecular function becomes obvious when one considers bone overgrowth, including the jaw and facial bones of sclerosteosis and van Buchem disease, which are caused by the loss of sclerostin expression and secretion, respectively.^128,130 Mouse models lacking sclerostin also display systemic high bone mass, and increased alveolar bone and cementum.^77,82 Osteocytes are also a main source of RANKL required for physiologic bone remodeling and in pathologic situations, including ovariectomy,^45,94 secondary hyperparathyroidism¹⁴⁰ or glucocorticoid excess.⁹² Mice lacking osteocyte-derived RANKL even resist the bone loss caused by tail suspension.⁹³ Recently, osteocyte-derived RANKL was considered relevant in inflammatory osteolysis⁵¹ and orthodontic tooth movement.¹⁰⁹ Thus, osteocytes control bone formation and bone resorption during good health and during disease, including their expression of sclerostin and RANKL.

Fig 3-1 Osteoclasts (boneresorbing cells), osteoblasts (bone-producing cells), and osteocytes. Osteoclasts are multinucleated cells that are exclusively capable of resorbing bone. In this image, which is a detail taken from Fig 1-7, a group of osteoclasts is resorbing bone next to a seam of osteoblasts, which are producing new bone. An osteoid seam is visible below the osteoblasts. Osteocytes are embedded in the bone. [The image is of pig bone.]