Biological Mechanisms of Tooth Movement
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Оглавление
Группа авторов. Biological Mechanisms of Tooth Movement
Table of Contents
List of Tables
List of Illustrations
Guide
Pages
Biological Mechanisms of Tooth Movement
Contributors
Preface to the First Edition
Preface to the Second Edition
Preface to the Third Edition
CHAPTER 1 Biological Basis of Orthodontic Tooth Movement: A Historical Perspective
Summary
Introduction
Orthodontic treatment in the ancient world, the Middle Ages, and through the Renaissance period: Mechanics, but few biological considerations
Orthodontic treatment during the Industrial Revolution: Emergence of identification of biological factors
Orthodontic tooth movement in the twentieth and twenty‐first centuries: From light microscopy to tissue engineering and stem cells. Histological studies of paradental tissues during tooth movement
Histochemical evaluation of the tissue response to applied mechanical loads
The era of cellular and molecular biology as major determinants of orthodontic treatment
Conclusions and the road ahead
References
CHAPTER 2 Biology of Orthodontic Tooth Movement: The Evolution of Hypotheses and Concepts
Summary
Introduction
Hypotheses about the biological nature of OTM: The conceptual evolution
Walkhoff’s hypothesis on the biology of OTM
Oppenheim’s transformation hypothesis
The pressure–tension hypothesis
The fluid dynamic hypothesis
The bone‐bending hypothesis
Bioelectric signals in orthodontic tooth movement
Concluding remarks
References
CHAPTER 3 Cellular and Molecular Biology of Orthodontic Tooth Movement
Summary
Introduction
Entities important for tooth movement – the players in the game. Extracellular matrix
Cells
Biomechanical characteristics of the PDL
General regulatory mechanisms. Cell–cell interactions
Cell–matrix interactions
Effects of orthodontic force application. Phases of OTM
Cell biological processes during initial phase and hyalinization
Cell biological processes during real tooth movement
Cell biological processes during relapse and retention
Conclusions
References
CHAPTER 4 Inflammatory Response in the Periodontal Ligament and Dental Pulp During Orthodontic Tooth Movement
Summary
Introduction
Inflammation during tooth movement
Inflammatory mediators in OTM
DAMPs
Prostaglandins
The second‐messenger system
Cytokines
Interleukins
TNF and the RANK/RANKL/OPG system
The chemokine system
Growth factors
Matrix metalloproteinases (MMPs)
Neuropeptides
Substance P and neurokinin A
Calcitonin gene‐related peptide
Vasoactive intestinal polypeptide
Neuropeptide Y
Neuropeptides and OTM: A synthesis
Activation of inflammation, apoptosis, and cell cycles of PDL in OTM
Response of the dental pulp to mechanical forces
Neuropeptide response in dental pulp to orthodontic force
Vasodilatation and angiogenesis response to orthodontic forces
Pain during OTM
Root resorption and inflammation
Root resorption in the cementum
Conclusions
References
CHAPTER 5 The Effects of Mechanical Loading on Hard and Soft Tissues and Cells
Summary
Introduction
Mechanobiology
Mechanotransduction in bone tissue
Mechanotransduction in periodontal tissues
The role of marginal gingiva in orthodontic tooth movement
Marginal gingiva is the mechanosensor of the periodontium
ATP‐purinoreceptors are mechanosensors in marginal gingiva
Conclusions
Acknowledgement
References
CHAPTER 6 Biological Aspects of Bone Growth and Metabolism in Orthodontics
Summary
Introduction
Basic concepts of bone growth and development
Bone formation
Endochondral bone formation
Intramembranous bone formation
Primary growth centers and sites in facial bones
Bone modeling and remodeling
Genetic mechanisms for environment adaptation
Genetic determinants of overall craniofacial growth
Vascular invasion
Inflammatory response
Cellular agents
Factors influencing bone remodeling and modeling. Coupling of bone formation to resorption in bone remodeling
Metabolic control of bone remodeling
Mechanical control of bone remodeling
Mechanical aspects of bone modeling
Bone modeling/remodeling, tooth movement, and external apical root resorption
Cortical bone remodeling
Trabecular bone remodeling
Growth and development of facial bones
Temporomandibular joint development and mature adaptation
Tooth movement and bone modeling
Dental facial orthopedics and bone modeling
Calcium metabolism and tooth movement
Conclusion
Acknowledgement
References
CHAPTER 7 Mechanical Load, Sex Hormones, and Bone Modeling
Summary
Introduction
Osteoblast/osteocyte differentiation and function. Osteoblast differentiation
Osteoblasts as bone‐forming cells
Osteoblasts as regulators of osteoclast formation
Osteocytes
Osteocytes as bone‐remodeling cells
Osteocytes as mechano‐sensory cells
Osteoclast differentiation and function
Osteoclast differentiation
Osteoclast function
Osteoclast‐dependent factors important for osteoblast stimulation during bone remodeling
Sex hormones and their receptors
Genomic signaling through sex‐hormone receptors in bone
Non‐genomic signaling by sex‐hormone receptors
Osteoblasts and osteocytes respond to load‐induced modeling
Wnt/ β ‐catenin pathway
IGF‐1 pathway
Nitric oxide signaling
Prostaglandin pathway
Loading‐induced anabolic response and vitamin A
Osteoclast response to load‐induced modeling
Role of sex hormones for the osteogenic effect of loading. Male sex hormones and loading
Female sex hormones and loading
Sex hormones and OTM
Acknowledgements
References
CHAPTER 8 Biological Reactions to Temporary Anchorage Devices
Summary
Introduction
Clinical factors in the success of TADs
Age of the patient
Loading time point
Implantation site
Insertion torque
Implant diameter and length
Mobility
Mechanical analysis using finite element models
Cortical bone thickness
Insertion angulations
Thread location, properties, and mechanical anisotropy
Exposed length
Histological reactions
Osseointegration process
Immediate loading of orthodontic miniscrews
Time point of loading
The diameter ratio of pilot hole to miniscrew
Inflammatory reactions
Conclusions
References
CHAPTER 9 Tissue Reaction to Orthodontic Force Systems. Are we in Control?
Summary
Introduction
Pressure–tension theory: Still valid?
The influence of the material properties
The influence of the morphology of the alveolar wall
The influence of force level
The influence of the interaction with occlusion
Conclusions
Where are we now? How should we continue?
References
CHAPTER 10 The Influence of Orthodontic Treatment on Oral Microbiology
Summary
Introduction
Microbiology of periodontal disease
Microbiology of dental caries
Changes in the oral microbiome with removable orthodontic appliances
Periodontal bacteria
Cariogenic bacteria
Fungi
Changes in the oral microbiome with fixed orthodontic appliances
Periodontal bacteria
Cariogenic bacteria
Fungi
Effects of different orthodontic bracket types on oral microbiome. Conventional brackets
Self‐ligating brackets
Lingual brackets
Conventional metallic versus aesthetic brackets (composite or ceramic)
Changes in the oral microbiome with orthodontic retainers. Removable orthodontic retainers. Cariogenic bacteria
Periodontal bacteria
Fungi
Fixed orthodontic retainers. Cariogenic bacteria
Periodontal bacteria
Importance of oral hygiene
Impacted teeth, mini‐implants, orthognathic surgery and changes in oral microbiota. Impacted teeth
Mini‐implants
Orthognathic surgery
Conclusions
References
CHAPTER 11 Markers of Paradental Tissue Remodeling in the Gingival Crevicular Fluid and Saliva of Orthodontic Patients
Summary
Why study oral fluids?
What is known about markers in oral fluids during orthodontic tooth movement?
Saliva studies
GCF studies
What is needed for improved diagnostic trials of markers in oral fluids during orthodontic treatment?
Variables associated with the collection and analysis of GCF. GCF collection during orthodontic therapy
Methods of collection
Quantification of GCF constituents
Outcomes associated with orthodontic treatment
The future
Conclusions
References
CHAPTER 12 Genetic Influences on Orthodontic Tooth Movement
Summary
Introduction
Tissue reactions to application of mechanical forces. Reaction of the periodontal ligament
How do changes in the PDL affect tissues?
Reaction of neural tissues
Reaction of the alveolar bone
Gene expression and osteoclasts
Gene expression and osteoblasts/osteocytes
Bone remodeling
Role of growth factors in bone remodeling
Reaction of the pulp tissues
Genetic influences and translational applications
Complications of OTM and its genetic implications
Eruption failure/primary failure of eruption
Tooth relapse
Root resorption
Conclusions
References
CHAPTER 13 Precision Orthodontics: Limitations and Possibilities in Practice
Summary
Introduction. Definition
Evidence‐based guidelines practice versus precision medicine practice
Progression in DNA analysis technology and its impact on clinical research and practice. The Human Genome Project
Genome‐wide association studies (GWAS)
Next‐generation sequencing
Human phenotype ontology
Application in medical practice
Efficacy of risk prediction of Mendelian (single‐gene) versus complex traits
Precision oral healthcare
From personalized to precision orthodontics
Class III malocclusion
External apical root resorption concurrent with orthodontia
Sagittal facial growth during puberty
Primary failure of eruption
Support of next generation sequencing, other genetic studies, and the utility of their application in orthodontics
Education
Conclusion
References
CHAPTER 14 The Effect of Drugs, Hormones, and Diet on Orthodontic Tooth Movement
Summary
Introduction
Prostaglandins and analogues
Implication
Nonsteroidal anti‐inflammatory drugs
Implication
Antiresorptive agents
Implication
Asthma medications
Implication
Corticosteroids
Implication
Antihistamines
Implication
Statins: cholesterol‐lowering drugs
Implication
Drugs inducing gingival enlargement
Implication
Anticholinergic drugs
Implication
Psychiatric drugs
Implication
Hormonal influences on tooth movement. Thyroid hormones
Implication
Parathyroid hormone and analogues
Implication
Growth hormone
Implication
Estrogen
Implication
Relaxin
Implication
Effects of vitamins, minerals, and diet on tooth movement
Vitamins
Vitamin C
Implication
Vitamin D
Implication
Vitamin A
Implication
Minerals
Implication
Fluoride
Implication
Lipids
Implication
Substance abuse and OTM. Alcohol use
Implication
Nicotine use
Implication
Conclusions
References
CHAPTER 15 Biological Orthodontics: Methods to Accelerate or Decelerate Orthodontic Tooth Movement
Summary
Introduction
Early attempts to accelerate tooth movement
Accelerating tooth movement: pharmacological approaches. Local cytokine delivery
Prostaglandins
RANKL
Hormones promoting tooth movement. Parathyroid hormone
1,25‐Dihydroxycholecalciferol (1,25‐(OH)2D3) (Vitamin D3)
Relaxin
Corticosteroids
Conclusion
Accelerating tooth movement: physical stimuli. Direct electric currents and pulsed electromagnetic fields
Vibratory stimulus
Photobiomodulation
Low‐level laser therapy
Light emitting diode (LED) therapy
Surgical approaches
Methods to decelerate tooth movement. Drugs
Local MMP inhibitors and osteoprotegerin transfer
Estrogen
Conclusions
References
CHAPTER 16 Surgically Assisted Tooth Movement: Biological Application
Summary
Introduction
Surgically assisted tooth movement
Biological principles and biomechanical considerations. The regional acceleratory phenomenon
Finite element analysis of surgically assisted tooth movement
Historical background
A different perspective: six rules for effective alveolar corticotomy
1. Alveolar corticotomy is to facilitate OTM
2. Alveolar corticotomy has a limited effect in time
3. Alveolar corticotomy has limited effects in space
4. Alveolar corticotomy needs a proper surgical protocol
The open flap corticotomy and grafting
The flapless corticotomy
5. Alveolar corticotomy needs correct orthodontic management postsurgery
6. Alveolar corticotomy needs a proper selection of patients
Clinical examples
Patient 1 (Figure 16.22)
Patient 2 (Figure 16.23)
Patient 3 (Figure 16.24)
Patient 4 (Figure 16.25)
Patient 5 (Figure 16.26)
Patient 6 (Figure 16.27)
Patient 7 (Figure 16.28)
Patient 8 (Figure 16.29)
Conclusions
References
CHAPTER 17 Precision Accelerated Orthodontics: How Micro‐osteoperforations and Vibration Trigger Inflammation to Optimize Tooth Movement
Summary
Introduction
Sculpting biphasic theory from the bedrock of data
Saturation of the biological response: more does not mean faster
MOPs: hyperlocalized inflammation for safe, minimally invasive accelerated tooth movement
Clinical considerations for MOPs application
1. Accelerate the movement of target teeth
2. Facilitate the desired type of tooth movement
3. Develop biological anchorage
4. Decrease the possibility of root resorption
5. Moving teeth through atrophic bone
Good vibrations: catabolic response during OTM
Conclusion
References
CHAPTER 18 Mechanical and Biological Determinants of Iatrogenic Injuries in Orthodontics
Summary
Introduction
Intraoral iatrogenic effects
Gingival effects
Clinically visible changes
Histological and microbiologic changes
Periodontal changes and alveolar bone loss
Tooth‐related changes
Enamel decalcification and trauma
Pulpal reactions
Root resorption
Soft tissue irritation
Cytotoxicity and allergic reactions
Extraoral iatrogenic effects. Allergy
Extraoral injuries
Burns
Systemic risks. Cross infection
Pain
Swallowing or inhalation of small parts
Conclusions
References
CHAPTER 19 The Biological Background of Relapse of Orthodontic Tooth Movement
SUMMARY
Introduction
Relapse, physiologic recovery, or aging?
The process of relapse. Amount, rate, and duration
Effect of retention
Histological changes during relapse
Collagen fibers of the periodontium and relapse. Terminology
Collagen fibers and relapse after translational tooth movement
Collagen fibers and relapse after rotational tooth movement
Collagen fibers and relapse after closure of extraction space or midline diastema
Turnover of collagen in the periodontium
Biological techniques affecting orthodontic relapse
Oxytalan fibers
Conclusions
References
CHAPTER 20 Planning and Executing Tooth‐movement Research
Summary
Introduction
The scientific method
Evidence generation
Laboratory studies in orthodontic biologic research – in vitro versus ex vivo studies
Cell culture methods
Media preparation, trypsinization, and cell culturing
Animal models
Studies in humans
Methodologies for tooth‐movement research
Tissue level/cellular level studies. Histological studies
Immunohistochemistry
Immunocytochemistry
Flow cytometry
Techniques for genomic studies
Polymerase chain reaction
RT‐PCR versus qPCR
DNA microarray
ChIP assay
Electrophoretic mobility shift assay (EMSA)
Proteomic analysis/cytoplasm‐level studies. Enzyme‐linked immunosorbent assay (ELISA)
Western‐blot analysis
Protein microarray
Toxicology studies. MTT assay
Micronucleus assay
Single cell gel electrophoresis (comet assay)
DNA laddering
Studying mechanobiology
Atomic force microscopy
Magnetic twisting cytometry
Magnetic pulling cytometry
Micropipette aspiration
Laser‐tracking microrheology
Traction force microscopy
Microfabrication
Microfluidics
Conclusions
References
CHAPTER 21 Controversies and Research Directions in Tooth‐movement Research
Summary
Introduction
The optimal orthodontic force concept
Is tooth movement inflammatory or a mechanotransduction process?
How far are biomarkers useful in validating OTM?
Can we accelerate tooth movement by any means?
Alveolar bone density and shape of the alveolar wall
Gingival recession
Periodontal health
Conclusions
References
Index
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Another outlook on differential orthodontic forces was proposed by Storey (1973). Based upon experiments in rodents, he classified orthodontic forces as being bioelastic, bioplastic, and biodisruptive, moving from light to heavy. He also reported that in all categories, some tissue damage must occur in order to promote a cellular response, and that inflammation starts in paradental tissues right after the application of orthodontic forces.
Continuing the legacy of Sandstedt, Kvam and Rygh studied cellular reactions in the compression side of the PDL. Rygh (1974, 1976) reported on ultrastructural changes in blood vessels in both human and rat material as packing of erythrocytes in dilated blood vessels within 30 minutes, fragmentation of erythrocytes after 2–3 hours, and disintegration of blood vessel walls and extravasation of their contents after 1–7 days. He also observed necrotic changes in PDL fibroblasts, including dilatation of the endoplasmic reticulum and mitochondrial swelling within 30 minutes, followed by rupture of the cell membrane and nuclear fragmentation after 2 hours; cellular and nuclear fragments remained within hyalinized zones for several days. Root resorption associated with the removal of the hyalinized tissue was reported by Kvam and Rygh. This occurrence was confirmed by a scanning electron microscopic study of premolar root surfaces after application of a 50 g force in a lateral direction (Kvam, 1972). Using transmission electron microscopy (TEM), the participation of blood‐borne cells in the remodeling of the mechanically stressed PDL was confirmed by Rygh and Selvig (1973), and Rygh (1974, 1976). In rodents, they detected macrophages at the edge of the hyalinized zone, invading the necrotic PDL, phagocytizing its cellular debris and strained matrix.
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