Читать книгу Bone and Soft Tissue Augmentation in Implantology - Группа авторов - Страница 11

Regenerative dentistry critically depends on the functional understanding of bone biology – to be precise, bone development, bone modeling and remodeling and bone regeneration – in a physiologic but also in a pathologic and pharmacologic context. Bone biology also describes the cellular and molecular regulation behind Wolff’s law (form follows function), which was later refined by Frost’s Mechanostat theory.⁴⁴ Bone biology is a molecular and cellular system that is essential for mammalian evolution. Besides being a framework connecting to tendons and muscles and for protecting the bone marrow, the skeleton is a storage for calcium and phosphate that is transported via the umbilical vein and later through the mother’s milk into the fetus and newborn. Understanding the delicate interplay of bone-forming cells and bone-resorbing cells – which act in concert with the osteocyte located within the bone matrix, the blood vessels providing support for the respective progenitors, and the cells originally dedicated to the immune system – provides one part of the information necessary for progress in medicine.

The concert has to be orchestrated, which is, in the context of bone biology, the cell-to-cell communication involving the classical path. This path can roughly be divided into local and systemic regulation. Local regulation includes cell communication via cytoplamatic connections or the release of signaling molecules, with particular receptors on the respective target cells. Systemic regulation refers to the endocrine system, whereby hormones or growth factors are released and transported via the bloodstream to target cells elsewhere in the body. It is fascinating to imagine all the different levels – molecular, cellular, tissue, and organ – to be coordinated, with the same aim of homeostasis. In a broader sense, not only does homeostasis maintain the tissue (which would be bone remodeling), it is also the mechanism to regain homeostasis after injury, thus bone regeneration. However, the delicate cellular and molecular mechanisms aiming for homeostasis are sensitive to change; for instance, the drop of steroid hormones during menopause, which causes not only enhanced but also disbalanced bone remodeling and ultimately leads to bone loss and postmenopausal osteoporosis. The mechanical integrity, particularly of the trabecular bone, is rapidly impaired, and fragility fractures of the vertebra and the hip become clinical hallmarks of the disease.¹⁰⁷ Postmenopausal osteoporosis is but one example of how bone homeostasis undergoes a catabolic shift that, together with age-related changes, leads to a progression of bone loss over time.

The main focus of this chapter, however, is to provide an explanation of autograft consolidation, and to discuss the clinical success of this therapy at the molecular and cellular levels. With an emphasis on bone augmentation, the chapter is intended to supplement the essential information on bone regeneration that has been obtained from histologic and biomechanical analyses.

It is a well-accepted fact that osteoblasts form the bone⁴⁰ and osteoclasts resorb it.^12,121 The osteocytes are important in that they are the masters of regulation in bone remodeling.³³ The blood vessels are also important as they serve as a source of renewal and, in particular, as a transport medium for the precursor cells of osteoblasts and osteoclasts;^78,134 they are also key in terms of inflammation, and are therefore relevant in pathologic conditions such as inflammatory osteolysis.^55,84 In this context, classical questions are addressed in the chapter, such as the evidence that autografts are considered “osteoconductive, osteogenic and osteoinductive,”⁹⁸ and the possible mechanisms of graft resorption.