Читать книгу Bone and Soft Tissue Augmentation in Implantology - Группа авторов - Страница 22

There must be at least one mechanism that controls the resorption of the transplanted bone. One possible explanation could be the function of osteocytes, which are ubiquitously present in the bone, forming a coherent network.¹⁵ Osteocytes can control the formation of boneresorbing cells by expressing RANKL,^89,138,139 a central agonist of osteoclastogenesis.¹¹⁸ In addition, there is increasing evidence from mouse research that dying osteocytes significantly promote osteoclastogenesis.¹²⁰ The resorption of alveolar bone upon tooth extraction, implant placement, and early stages of graft consolidation after bone transplantation may also be associated with osteocytes. In all cases, the bone tissue is separated from the blood vessels, and therefore the oxygen and nutritional supply of the osteocytes by passive diffusion is limited or even impossible. Consequently, osteocytes die, and, by a molecular mechanism, promote the expression of RANKL by the adjacent osteocytes that, in turn, can initiate osteoclastogenesis.^65,66 Molecules released by dying osteocytes can also increase the sensitivity of osteoclast progenitors to RANKL via a C-type lectin receptor. Importantly, unloading-induced bone loss also requires the dying osteocytes to enhance bone resorption via their expression of RANKL.¹⁷ Accordingly, bone resorption, presumably also in dentistry, is bound to dying osteocytes and does not progress uncontrolled. However, it is reasonable to suggest that dying osteocytes can not only transiently push osteoclastogenic resorption, but also the reparation process, through new bone formation as a normal physiologic reaction of remodeling. Thus, the initial boost of bone resorption that occurs at implant sites¹³¹ and upon bone grafting¹⁰⁰ is followed by the attraction of osteogenic progenitor cells that become bone-forming osteoblasts on the surface of the host bone, the autografts, and also on biomaterials, including dental implants.¹³¹

Elegant preclinical studies in mouse models support the hypothesis through experiments in which the apoptosis of the osteocytes were analyzed after the preparation of an implant bed, e.g. drilling tools create a zone of dead and dying osteocytes around the osteotomy²⁹ that is increased as a function of the insertion torque.¹⁹ The pharmacologic suppression of apoptosis can also reduce bone atrophy upon extraction in a rat model.¹⁰⁵ Thus, the strategy exists to develop low-invasive drill designs that initiate low heat and mechanical friction, with the overall goal of preserving osteocyte viability.^1,28 In a bovine femora, test drills can reach 47°C, particularly after repeated use,²⁰ which is similar to experiments performed with polyurethane foam blocks,⁴³ a temperature that causes osteocyte damage and RANKL expression in a rat model.³⁷ Cutting energy is converted into heat.⁸⁰ Bone chips produced by drilling⁸⁰ presumably follow the dying osteocytes – RANKL expression axis and are removed by osteoclasts before the osteoconductive properties come into play. It therefore seems relevant to pay special attention to atraumatic procedures when placing implants, extracting teeth, and probably also removing bone grafts, with the overall aim of maintaining the vitality of osteocytes. For example, at the time of implant insertion in free fibula or iliac crest bone grafts, most of the biopsies showed partial or total necrotic bone.⁵⁸ There is also limited atrophy of free fibular grafts after mandibular reconstruction.^57,110 The question is raised: How much vital bone is necessary for the survival of the graft?