E-Book, Englisch, 472 Seiten
ISBN: 978-1-64724-181-0
Verlag: Quintessence Publishing Co, Inc
Format: EPUB
Kopierschutz: Adobe DRM (»Systemvoraussetzungen)
Autoren/Hrsg.
Weitere Infos & Material
"1. Bone Metabolism Around Dental Implants
2. Vitamin D Deficiency and Early Implant Failure
3. Regenerative Properties of Bone Grafting Materials: A Comparison Between Autografts, Allografts, Xenografts, and Alloplasts
4. Medical Considerations for Dental Implant Placement
5. Media Documentation for Implant Procedures
6. Diagnostic Imaging for Dental Implant Treatment
7. Diagnosis and Treatment Planning for Dental Implant Placement
8. Guided Surgery
9. Socket Preservation and Graftin
10. Use of Platelet-Rich Fibrin in Implant Dentistry
11. A Predictable Method for Dental Implant Placement
12. Immediate Implant Placement
13. Implant Placement in the Esthetic Zone
14. Radiologic Considerations for Maxillary Sinus Floor Bone Augmentation
15. Internal Sinus Elevation
16. Maxillary Sinus Graft Augmentation via Lateral Window
17. Fundamentals of All-on-X Treatment
18. Fully Guided Full-Arch Surgery and Prosthetics
19. Prosthetic Options in Implant Dentistry
20. Considerations for Full-Arch Restorations
21. Abutment Selection and Prosthetic Options for Fixed Restorations
22. Implant Overdentures
23. Achieving Optimal Soft Tissue Outcomes
24. Soft Tissue Grafting: Materials, Techniques, and Timing
25. Partial Extraction Therapy: Single-Tooth and Full-Arch Applications
26. Peri-implantitis
27. Enhancing Peri-implant Emergence Profile and Soft Tissue Contours with GBR
28. Suturing Techniques and Materials for Dental Implant Surgery
29. Guided Bone Regeneration: Principles and Practice
30. Vertical Ridge Augmentation
31. Dental Implant Marketing"
1 Bone Metabolism Around Dental Implants Richard J. Miron Angel Insua Summary Despite the increasing number of studies in the field of implant dentistry investigating novel dental implant surfaces, biomaterials, and growth factors, comparatively very few have studied the biology and metabolism of bone healing and its implication in peri-implant tissue health. The aim of this chapter is to provide a thorough understanding of the biologic properties that impact bone formation and osseointegration, including the coupling mechanisms between immune cells and bone. This chapter focuses on the various bone cells in the body—osteocytes, bone lining cells (BLCs), osteoblasts, and osteoclasts—and their bone remodeling cycle. Furthermore, the importance of immune cells and their impact on biomaterial integration during bone formation and implant osseointegration is also discussed. Finally, the putative effects of cholesterol, hyperlipidemia, and vitamin D deficiency are addressed. Such factors should be monitored during patient care, and ultimately future research should focus on these avenues as well as meticulous maintenance programs to favor both early and long-term maintenance and stability of dental implants. Objectives ? Understand how overall patient health directly affects dental implant osseointegration ? Understand the key cells involved in bone formation, maturation, and maintenance ? Understand the direct role of immune cells on biomaterial and dental implant integration ? Understand the essential role of optimizing the immune system prior to dental implant placement ? Investigate the relationship between vitamin D deficiency and early implant failure and how to avoid such pitfalls Bone regeneration requires bone grafting materials that possess excellent biocompatibility and osteoinductivity without eliciting an antigenic effect. While companies that manufacture replacement biomaterials intended to mimic autogenous bone grafts often report on their osteoconductive, osteoinductive, or osteogenic potential, autogenous bone still favors the greatest bone regeneration compared to allografts, xenografts, and synthetic alternatives because it combines all three of these properties. Thus, despite the increasing number of new bone grafting materials brought to market as substitute replacement grafts, to date there is no true replacement for autogenous bone grafts.1 Autografts carry no risk of immunologic reaction or disease transmission and provide optimal conditions for the penetration of new blood vessels and migration of osteoprogenitor cells. In contrast, many bone grafting substitutes are osteoconductive but have limited osteoinductive potential.2 For bone regeneration to take place, especially with foreign-body biomaterials such as allografts and xenografts or dental implants, there is a great need to better understand the regulatory properties and integration process of these biomaterials. After all, no matter the biomaterial placed, bone formation relies on immune-related factors working at the cellular level. The aim of this chapter is therefore to provide the biologic background on the cells involved in graft consolidation and give a brief overview of fracture healing. This chapter focuses on the bone cells involved in bone formation and dental implant osseointegration, including osteocytes, BLCs, osteoblasts, and osteoclasts, and their bone remodeling cycle. The chapter also addresses the importance of immune cells and their impact on biomaterial integration, as well as the putative effects of cholesterol, hyperlipidemia, and low vitamin D levels. Bone Cells: Osteoclasts, Osteoblasts, and Osteocytes
There are three main cell types in bone tissue involved in the bone remodeling cycle: osteoclasts, osteoblasts, and osteocytes3 (Fig 1-1). Osteoclasts are the bone-resorbing cells that degrade bone tissues. They are derived from hematopoietic stem cells following their differentiation from monocytes in response to two key factors: receptor activator of nuclear factor kappa-B ligand (RANKL)4 and macrophage colony-stimulating factor (M-CSF).5 Osteoclasts can be characterized histologically based on their multinucleated morphology and expression of tartrate-resistant acid phosphatase (TRAP), cathepsin k (CatK), and the calcitonin receptor (CTR). Their formation, activity, and survival are also regulated by various hormones (such as calcitonin and estrogen) that regulate several downstream cytokines and cellular pathways.6 Activated osteoclasts form distinct and unique membrane domains, including the sealing zone, the ruffled border, and the functional secretory domain, which facilitate resorption of bone or bone graft particles.7 Rearrangement of their F-actin fibers from the cytoskeleton forms a ring shape consisting of a dense continuous zone of highly dynamic podosomes.8 These podosomes allow for mineralized bone to be gradually resorbed, creating grooves and tunnels on the bone surface. This process is also quite important for bone remodeling because the resorbed bone liberates calcium phosphates and growth factors contained within the bone matrix that attract bone-forming osteoblasts to the local environment.9 Fig 1-1 The bone remodeling cycle. Osteoclasts—cells that destroy and resorb bone—are present on the bone matrix surface and liberate growth factors and cytokines to the local microenvironment. These growth factors act on mesenchymal stem cells/progenitor cells to rapidly stimulate their proliferation and differentiation toward bone-forming osteoblasts. Osteoblasts lay new bone matrix and, once embedded within the bone matrix, become osteocytes. Osteoblasts perform the opposite role of osteoclasts and are responsible for bone formation (see Fig 1-1). They are derived from cells of the mesenchymal lineage, and their formation and development are controlled locally and systemically by several growth factors, including bone morphogenetic proteins (BMPs).10,11 Osteoblasts secrete a range of molecules including growth factors, cell adhesion proteins, and other extracellular matrix molecules that support new bone formation.6 While osteoblasts are forming bone, they become embedded within bone tissues and transform into osteocytes. Contrary to the short lifespan of osteoblasts and osteoclasts, osteocytes can live for decades within the bone matrix. They no longer produce new bone and instead undergo morphologic changes, losing cytoplasm organelles and acquiring a stellar shape morphology with numerous extensions that connect to other osteocytes through the canalicular network.12 Osteocytes can then transmit signals through this network similar to neuron communication; this communication has a profound impact on neighboring osteoblasts, osteoclasts, and osteocytes. While it was initially believed that osteocytes served only a mechanical transduction function,13 more recently their role has been deemed one of the most important within the bone tissues because they release numerous paracrine signals to their environment, thereby influencing both osteoblasts and osteoclasts.12,14,15 Fracture Healing and Graft Consolidation
Fracture healing is an important process that involves various cell types and a variety of signaling pathways.3,16,17 Unlike other tissues in the body, bone tends to regenerate and repair itself quite rapidly. Natural fracture healing is a four-stage process (Fig 1-2). The first step is hematoma formation. Following injury, a blood clot forms, creating a fibrin matrix with an abundance of infiltrating inflammatory and immune cells that take place with an activation of platelets.16,18 These cells secrete an array of growth factors that initiate the second and third phases of fracture repair.16,18 At the terminal end of the first phase, osteoclast formation occurs from precursor monocytes, and these osteoclasts invade the bone surface, commencing bone resorption.16 Fig 1-2 The fracture healing process is divided into four phases: (1) hematoma formation, (2) fibrocartilage callus formation, (3) bony callus formation, and (4) bone remodeling. The second phase of fracture healing is the repair phase. During this phase, a bone callus is formed. Initially, blood vessels begin to form with infiltration of mesenchymal progenitor cells; this process is responsible for creating a fibrocartilagenous tissue that matures into bone. This woven bone is gradually replaced with dense lamellar bone to form a dense bony callus in phase 3.19 The final phase is the remodeling phase, during which the callus is gradually resorbed. In this stage, the bone is replaced by native bone lacking scar tissue.20 It has been shown that during this phase, resident macrophages play a predominant role in orchestrating host cells.21,22 While these four phases are not described in great detail within the present chapter, it is important to note that graft consolidation is tightly regulated by secretion of growth factors and cytokines (also secreted from autogenous bone particles and blocks). This is all tightly regulated in very distinct cell-to-cell communication events that take place during bone regeneration.3 Role of Osteocytes and Bone Lining Cells in Bone Remodeling
Osteocytes
Osteocytes are the pivotal cells in the regulation of bone...
