Читать книгу Bone and Soft Tissue Augmentation in Implantology - Группа авторов - Страница 17

It is known from preclinical histologic investigations in minipig¹³¹ and mandibular canines,⁹ but also by measuring implant stability in a clinical setting,^108,132 that within the first week, resorption of the peri-implant bone dominates the scene, before bone formation takes over (Fig 1-6). This early catabolic process is required for the removal of micro-damaged necrotic bone, which is characterized by dying osteocytes. After around 1 week, the osteoclasts have disappeared, leaving behind an osteophilic surface onto which new bone is deposited (Fig 1-7).^9,131 Small defects, as they occur between the local bone and the threads of the implants, are bridged with new bone. These relatively small distances are known as jumping distances.¹¹ Primary woven bone formation shows a typical picture, with blood vessels in the center of an open ring of new bone (Fig 1-8). This image supports the assumption that the origin of the cells required for bone formation is based on pericytic progenitor cells of sprouting blood vessels.^78,134 This bone is immature (woven bone).⁹ Subsequently, lamellar bone will strengthen the woven bone that later undergoes modeling and remodeling.

Fig 1-7 Dental implant after 10 days of osseointegration in a pig jaw, from a study by Vasak et al.¹³¹ Ten days after implant placement, feeble trabeculae of new bone have already replaced the damaged old bone. New bone continues to grow. Batches of osteoclasts are resorbing the remaining damaged bone.

Modeling refers to the functional adjustments based on the reaction of the bone to biomechanical stimuli according to Wolff’s law and Frost’s Mechanostat theory.⁴⁴ We are beginning to understand today how resident bone cells perceive and translate mechanical energy into biologic signals. These signals transiently uncouple the remodeling equilibrium of osteoblasts and osteoclasts; otherwise, no structural change of bone anatomy is possible.⁹⁶ Remodeling, then, ensures the preservation of bone quality and long-term implant success. According to current hypotheses, the necrotic bone areas created during loading are resorbed by osteoclasts and are immediately replaced by osteoblasts, which was originally postulated by Frost⁴⁴ and has now been proven to involve the apoptotic and necrotic death of osteocytes.^65,66 Osseointegration is therefore not only the transition from mechanical primary instability to biologic secondary stability due to bone regeneration;⁸⁶ it also requires the continual maintenance of bone quality through remodeling. Bone regeneration and bone remodeling are not necessarily subjected to the same regulatory mechanisms; for example, bone formation during early fracture healing can take place without the resorptive activity of osteoclasts,^50,85 while bone remodeling is strictly based on the coupled effect of osteoclasts and osteoblasts.¹¹² What is true for osseointegration is also observed during graft consolidation – the osseointegration of autografts.

Fig 1-8 Dental implant after 10 days of osseointegration in a pig jaw, from a study by Vasak et al.¹³¹ Dynamics of early bone formation in the grooves of an implant. New bone (purple) is growing on the implant surface as well as on fragments of old bone that is not resorbed (light pink). Erythrocytes (dark blue) indicate the presence of blood vessels.