Efnisyfirlit

• Contents
• Contributors
• 1: Tooth Development: Embryology of the Craniofacial Tissues
• 1.1 Embryology of the Craniofacial Tissues
• 1.1.1 Origin of Human Tissue
• 1.1.2 The Neural Crest
• 1.1.3 Head Formation
• 1.2 Enamel Development
• 1.2.1 Histogenesis and Morphogenesis
• 1.2.1.1 Bud Stage
• 1.2.1.2 Cap Stage
• 1.2.1.3 Bell Stage
• 1.2.2 Cytodifferentiation
• 1.2.2.1 Presecretory Stage
• 1.2.2.2 Secretory Stage
• 1.2.2.3 Maturation Stage
• 1.2.3 Microstructure of the Enamel
• 1.2.3.1 Enamel Rod
• 1.2.3.2 Enamel Spindle
• 1.2.3.3 Enamel Lamellae and Cracks
• 1.2.3.4 Enamel Tufts
• 1.2.3.5 Interpit Continuum
• 1.2.3.6 Functional Aspects of Enamel Structure
• 1.2.4 Enamel Matrix Proteins
• 1.2.4.1 Enamelin
• 1.2.4.2 Amelogenin
• 1.2.4.3 Ameloblastin
• 1.2.4.4 Amelotin
• 1.2.4.5 Tuftelin
• 1.2.4.6 Proteolytic Enzymes
• 1.3 Pulpodentin Complex
• 1.3.1 Dentin
• 1.3.1.1 Structure of Dentin
• 1.3.1.2 Types of Dentin
• 1.3.1.3 Mineralization of Dentin
• 1.3.1.4 Dentinal Sclerosis
• 1.3.1.5 Dentin Repair
• 1.3.2 Pulp
• 1.3.2.1 Vascular Tissues
• 1.3.2.2 Nerve Fibers
• 1.3.2.3 Connective Tissue Fibers
• 1.3.2.4 Ground Substance
• 1.3.2.5 Lymphatics
• 1.3.2.6 Accessory Canals
• 1.3.2.7 Morphologic Zones of Pulp
• 1.3.3 Cells in the Dental Pulp
• 1.3.3.1 Odontoblast
• 1.3.3.2 Pulp Fibroblast
• 1.3.3.3 Macrophage
• 1.3.3.4 Dendritic Cell
• 1.3.3.5 Lymphocyte
• 1.3.3.6 Mesenchymal Cell
• 1.3.3.7 Mast Cell
• 1.4 Root Development
• 1.4.1 The Initiation of Tooth Root Development
• 1.4.1.1 Epithelial Cell Rests of Malassez (ERM)
• 1.4.1.2 Induction of Differentiation of Mesenchymal Stem Cells
• 1.4.2 Related Signaling Pathway of Root Morphogenesis
• 1.4.2.1 TGF-β/BMP Signaling
• 1.4.2.2 SHH Signaling
• 1.4.2.3 Wnt Signaling
• 1.4.2.4 Notch Signaling
• 1.4.3 Tooth Eruption
• References
• 2: Biofilm and Dental Caries
• 2.1 Dental Plaque and Microbial Biofilm
• 2.1.1 Bacterial Biofilm: An Advanced Mode of Life
• 2.1.1.1 The Concept and Discovery of Biofilm
• 2.1.1.2 Extracellular Polymeric Substances of Biofilm
• 2.1.1.3 Biofilm Formation
• 2.1.1.4 Survival Advantages of Biofilm
• 2.1.2 Dental Plaque as a Typical Bacterial Biofilm
• 2.1.3 Composition of Dental Plaque
• 2.1.4 Spatiotemporal Development of Oral Biofilms
• 2.2 Microbial Etiology of Dental Caries
• 2.2.1 Oral Microbiology at Early Stage
• 2.2.2 Dental Caries as an Infectious Disease
• 2.2.3 Dental Plaque as the Cause of Dental Caries
• 2.2.4 Association of Streptococcus mutans with Dental Caries
• 2.2.5 Nonspecific or Specific Plaque Hypotheses?
• 2.2.6 Ecological Plaque Hypothesis
• 2.2.6.1 Microbial Ecology in the Oral Cavity
• 2.2.6.2 Genetic and Environmental Factors and Oral Microbial Ecology
• 2.2.6.3 Interspecies Interactions and Dental Caries
• 2.3 Dental Caries-Associated Bacteria
• 2.3.1 Carbohydrate Metabolism and Acidogenic Bacteria
• 2.3.2 Major Acidogenic Bacteria
• 2.3.2.1 Streptococcus mutans
• 2.3.2.2 Lactobacilli
• 2.3.2.3 Actinomyces
• 2.3.3 Acid Tolerance of Acidogenic Bacteria
• 2.3.4 Base Generation and Caries Protection
• 2.3.4.1 Urease
• 2.3.4.2 Arginine Deiminase System (ADS)
• 2.3.4.3 Agmatine Deiminase System (AgDS)
• 2.3.4.4 Alkali Production and Biofilm Ecology
• 2.3.4.5 Clinical Relevance of Alkali Production
• 2.3.5 Other Caries-Associated Bacteria
• 2.4 Antimicrobial Approaches to the Management of Dental Caries
• 2.4.1 Chlorhexidine
• 2.4.2 Fluoride
• 2.4.3 Quaternary Ammonium Compounds
• 2.4.4 Triclosan
• 2.4.5 Xylitol
• 2.4.6 Phenolic Antiseptics
• 2.4.7 Natural Products
• 2.5 Ongoing Direction of Oral Dental Plaque Study
• 2.5.1 Metagenomics and Oral Microbiome
• 2.5.2 Evidence-Based Dental Caries Diagnosis
• 2.5.3 Novel Antimicrobial Therapies
• 2.5.3.1 Probiotics
• 2.5.3.2 Salivary Antimicrobial Substances
• 2.5.3.3 Specifically Targeted Antimicrobial Peptides (STAMPs)
• 2.5.3.4 Light Active Killing
• References
• 3: Saliva and Dental Caries
• 3.1 Salivary Flow and Composition
• 3.1.1 Formation of Saliva-Salivary Glands and Secretion
• 3.1.2 Salivary Composition
• 3.1.3 Salivary Flow Rate and Influence Factors
• 3.2 Salivary Influences on Plaque PH and Oral Microflora
• 3.2.1 Salivary Influences on Plaque PH
• 3.2.2 Salivary Influences on Oral Microflora
• 3.3 Xerostomia and Its Management
• 3.3.1 Etiology of Xerostomia
• 3.3.2 Management of Xerostomia
• 3.4 Saliva and Caries Risk Assessment
• 3.4.1 Caries-Associated Bacteria
• 3.4.2 Chemical and Physical Aspects of Saliva
• References
• 4: Demineralization and Remineralization
• 4.1 Dynamics Process of  De-/Remineralization
• 4.2 Investigations of De-/Remineralization
• 4.2.1 Models
• 4.2.1.1 In Vitro Chemical Model
• 4.2.1.2 In Vitro Biofilm Model
• 4.2.1.3 In Situ Model
• 4.2.1.4 Animal Model
• 4.2.2 Detection and Measurement Methods
• 4.2.2.1 Transversal Microradiography (TMR)
• 4.2.2.2 Indentation Techniques
• 4.2.2.3 Micro-CT
• 4.2.2.4 Confocal Laser Scanning Microscopy
• 4.2.2.5 Quantitative Light-Induced Fluorescence
• 4.2.2.6 Optical Coherence Tomography
• 4.3 Methods to Influence the De-/Remineralization Process
• 4.3.1 Traditional Methods
• 4.3.1.1 Fluoride
• 4.3.1.2 Calcium Phosphate
• 4.3.2 Novel Methods
• 4.3.2.1 CPP–ACP and CPP–ACFP
• 4.3.2.2 Natural Medicine
• 4.3.2.3 Laser
• 4.3.2.4 Nanoparticles
• 4.3.3 Biomineralization
• References
• 5: The Diagnosis for Caries
• 5.1 Conventional Diagnosis Methods
• 5.1.1 Inspection
• 5.1.2 Probing
• 5.1.3 Percussion
• 5.2 Special Diagnostic Methods
• 5.2.1 Radiographic Examination
• 5.2.2 Cold and Hot Irritation Test
• 5.2.3 Dental Floss Examination
• 5.2.4 Diagnostic Cavity Preparation
• 5.3 The New Technology of Caries Diagnosis
• 5.3.1 Fiber-Optic Transillumination, FOTI
• 5.3.2 Electrical Impedance Technology
• 5.3.3 Ultrasonic Technique
• 5.3.4 Elastomeric Separating Modulus Technique
• 5.3.5 Staining Technique
• 5.3.6 Quantitative Laser Fluorescence Technique
• 5.4 The Differential Diagnosis of the Superficial Caries
• 5.4.1 Enamel Hypocalcification
• 5.4.2 Enamel Hypoplasia
• 5.4.3 Dental Fluorosis
• 5.4.4 The Key Points of the Differential Diagnosis for Caries
• References
• 6: Dental Caries: Disease Burden Versus Its Prevention
• 6.1 Global Trends of Caries Burden
• 6.1.1 Oral Diseases: One of the Most Costly Diseases to Treat
• 6.1.2 Uneven Distribution of Oral Disease Burden Around the World
• 6.1.3 Developing Global Policies Highlighting the Importance of Oral Health
• 6.2 Caries Burden in China
• 6.2.1 The First and Second National Epidemiological Investigation of Oral Health in China
• 6.2.2 The Third National Epidemiological Investigation of Oral Health in China
• 6.2.2.1 Caries Status of 5-Year-Olds
• 6.2.2.2 Caries Status of 12-Year-Olds
• 6.2.2.3 Caries Status of 35–44-Year-Olds
• 6.2.2.4 Caries Status of 65–74-Year-Olds
• 6.3 Caries Preventive Strategies
• 6.3.1 Primary Prevention
• 6.3.2 Secondary Prevention
• 6.3.2.1 Conventional Caries Detection Methods
• 6.3.2.2 Fiber-Optic Transillumination (FOTI)
• 6.3.2.3 New Caries Detection Methods
• 6.3.3 Tertiary Prevention
• 6.4 Methods for Caries Prevention
• 6.4.1 Dental Plaque Control
• 6.4.2 Restriction on Sugar Consumption and Use of Sucrose Substitute
• 6.4.3 Reinforce Tooth Resistance to Acid
• 6.4.4 Pit and Fissure Sealing
• 6.4.5 Preventive Resin Restoration
• References
• 7: Clinical Management of Dental Caries
• 7.1 The Development of Caries Treatment Theory
• 7.1.1 G.V. Black and Modern Restorative Dentistry
• 7.1.2 Adhesive Bonding Technique and Dental Restoration
• 7.1.3 The Foundation and Principle of Minimally Invasive Caries Treatment
• 7.2 Current Management of Dental Caries and Its Development
• 7.2.1 Minimally Invasive Treatment Technique
• 7.2.2 Minimally Invasive Cavity Preparation
• 7.2.2.1 Nonmachinery Preparation
• 7.2.2.2 Mechanical Rotary Technique
• 7.2.2.3 Minimal Invasive Prevention Technique
• 7.3 Current Silver Amalgam and Techniques for Direct Restorations [4]
• 7.3.1 The Controversy Over Silver Amalgam
• 7.3.2 Indications and Contraindications
• 7.3.3 Silver Amalgam Restoration Technique
• 7.3.3.1 Cavity Shape Preparation
• 7.3.3.2 Silver Amalgam Filling
• 7.4 Resin Composites and Direct Bonding Restoration Technique
• 7.4.1 Resin Composites
• 7.4.2 Etching Adhesive Systems and Bonding Mechanisms
• 7.4.3 Total-Etch Systems
• 7.4.4 Self-Etch Systems
• 7.4.5 Enamel Bonding
• 7.4.6 Dentin Bonding
• 7.5 Resin Composite Bonding Restoration Technique
• 7.5.1 Indications and Contraindications
• 7.5.2 Requirements for Restoration Design
• 7.5.3 Cavity Preparation
• 7.5.4 The Importance of Postprocessing Decoration
• 7.5.5 Problems of Direct Resin Composite Restoration
• 7.5.5.1 Polymerization Shrinkage
• 7.5.5.2 Technique Sensitivity
• 7.5.5.3 Postoperative Sensitivity
• 7.6 The Prospect of the Treatment of Dental Caries
• 7.6.1 Individualized Ideas of Treatment
• 7.6.2 The Importance of Individualized Treatment of Dental Caries
• 7.6.3 The Risk Evaluation Is the Premise of Individualized Treatment of Dental Caries
• 7.6.4 The Development of Technology and Material Provides a Guarantee for the Individualized T
• 7.7 Biological Treatment Methods
• 7.7.1 Restorative Therapy Based on Tissue Engineering of Tooth Regeneration
• 7.7.2 Restorative Therapy Based on Bionics
• References
• 8: Dental Caries and Systemic Diseases
• 8.1 Dental Caries and Bacteremia
• 8.2 Dental Caries and Head and Neck Cancer
• 8.2.1 Dental Caries and Head and Neck Cancer Treatment
• 8.2.2 Dental Caries and Head and Neck Squamous Cell Carcinoma
• 8.2.3 Tooth Loss and Head and Neck Cancer Risk
• 8.2.4 Cariogenic Bacteria and Oral Cancer
• 8.3 Dental Caries and Children Growth
• 8.4 Dental Caries and Atherosclerosis, Cardiovascular Disease, and Heart Attack
• 8.4.1 Dental Caries and Atherosclerosis and Cardiovascular Disease
• 8.4.2 Root Caries and Cardiac Dysrhythmia and Gerodontology
• 8.4.3 Streptococcus mutans and Atherosclerosis
• 8.4.4 Tooth Loss and Cardiovascular Disease and Stroke
• 8.4.5 Pulpal Periapical Diseases and Coronary Heart Diseases
• 8.4.6 Summary
• 8.5 Dental Caries and Immune System Disease
• 8.5.1 Salivary Immunoglobulin A
• 8.5.2 HIV and Dental Caries
• 8.6 Dental Caries and Kidney Diseases
• 8.7 Dental Caries and Gastrointestinal Diseases
• 8.7.1 Dental Caries and Gastroesophageal Reflux Disease
• 8.7.2 S. mutans and Ulcerative Colitis
• 8.8 Dental Caries and Diabetes Mellitus
• 8.8.1 Epidemiological Studies of Diabetes and Dental Caries
• 8.8.2 Root Caries and Diabetes
• 8.8.3 Tooth Loss and Diabetes
• 8.9 Dental Caries and Respiratory Infections
• References
• 9: Models in Caries Research
• 9.1 In Vitro Models in Caries Research
• 9.1.1 In Vitro Chemical Models
• 9.1.1.1 Demineralization Models
• 9.1.1.2 Remineralization Models
• In pH-Lattice Ion “Drift” Protocol
• Constant Composition Protocols
• “pH Cycling” Protocols
• 9.1.2 In Vitro Microbial Model
• 9.1.2.1 Inoculum
• 9.1.2.2 Closed (Batch) System Microbial Models
• 9.1.2.3 Open (Continuous Culture) System Microbial Models
• Flow Cell Biofilm Model and Modified Robbins Device
• Drip-Fed Biofilm Model
• Perfused Biofilm Fermenters
• Artificial Mouth
• Chemostat
• 9.1.3 Microbial-Based De- and Remineralization Model
• 9.2 In Situ Model in Caries Research
• 9.2.1 Classification of In Situ Models
• 9.2.1.1 Removable Appliances
• 9.2.1.2 Fixed Appliances
• 9.3 Animal Model in Caries Research
• 9.3.1 Study on Etiology of Dental Caries
• 9.3.2 Evaluate Anticaries Agent
• 9.4 The Role of Saliva in Caries Models
• References
• Index