Over the last 30 years, the development of molecular biology has revolutionized our understanding of the biochemistry underlying biology and medicine. As yet, there is no introductory text that relates this revolution to topics of major interest to dentistry. Because of increasing demands to make biochemistry useful by translating its findings into better treatments for problems in medicine, the dental field needs a similar textbook. The primary aim of this book is to integrate general biochemistry into topics that specifically pertain to dental health and disease. First and second year dental students have completed a general biochemistry course, but have, at best, a sketchy idea of how the material in that course relates to dentistry. In a traditional dental curriculum, the topics of this book are covered in physiology, nutrition, anatomy, histology, microbiology or immunology. This book was written to enable dental students to integrate their general biochemistry within these topics of dental interest. It was considered neither desirable nor practical to fill the text with references, except for the figures and tables.
The formal discipline of dentistry was initially developed in the late 19th century to treat dental caries, but it quickly spread to treat all diseases that affect the oral cavity. Dental treatments have progressed enormously over the last 40 years, as have treatments for many other diseases. The most powerful new dental treatments have come from water fluoridation, better oral hygiene measures, new mechanical or replacement materials, and the adoption of drugs developed for non-dental diseases. Nevertheless, these measures are not universally effective and improvements can be made in many areas.
The most widespread and commonly treated dental diseases, dental caries and periodontal disease, are chronic conditions caused by interactions between the host and oral bacteria that are still only partially understood in detail. A second aim of this book is therefore to point out the current knowledge for a future generation to build upon. While The descriptions of dental caries and fluoride are pretty standard, describing a modern and coherent view of periodontal disease was a problem.
Contents
1 Necessary Basics: Elements, Isotopes, Ions, Chemical Reactions, Energy Metabolism, and Bacterial Structures
1.1.1. Atomic Structure: Elements and Isotopes
1.1.2. Isotopes Date Paleontology Samples Such as Teeth
1.1.3. Isotopes Indicate Ancient Life Forms and Climate Changes
1.1.4. The Elements in Biology
1.1.5. Fluorides
1.2.1. Chemical Bonds
1.2.2. Electrostatic Bonds (Ions)
1.2.3. Covalent Bonds
1.2.4. Polarized Covalent Bonds
1.2.5. Hydrophobic Bonds
1.3.1. Mechanisms of Energy Production: Respiration and Fermentation
1.3.2. The Oral Microbiota, Dental Caries, and Periodontal Disease
1.4.1. Bacterial Cell Structures
1.4.2. Outer Surface of Bacteria
2 Photosynthesis and Sucrose Production
2.1.1. Role of Photosynthesis in Living Organisms
2.1.2. The Light Reaction
2.2.1. The Dark Reaction
2.2.2. Starch and Sucrose Provide the Carbon Skeletons of All Plant Compounds
2.2.3. Plants Are Autotrophs
2.3.1. Sucrose Is the Primary Transport Sugar and Plays a Central Role in Plant Growth and Development
3 The Connective Tissue Extracellular Matrix and Its Major Components
3.1.1. Major Components of the Connective Tissue (Stromal) Matrix
3.1.2. Collagen
3.1.3. Elastic Fiber System
3.1.4. Glycosaminoglycans
3.1.5. Teeth, Alveolar Bone, and Periodontium
3.2.1. Cell Surface Binding: Integrins, Fibronectin, and Collagen
3.2.2. Thrombospondins
3.3.1. Stromal Nutrition
3.3.2. Stromal Turnover, Inflammation, and Bone Loss
4 Fibrillar and Non-fibrillar Collagens and Integrins
4.2.1. Collagen Fiber Formation
4.2.2. Fiber Cross-Linking: Formation of b- and g-Tropocollagen
4.3.1. The Collagen Superfamily
4.3.2. Fiber-Modifying Non-fibrillar Collagens
4.3.3. General Structure of Non-fibrous Collagens
4.3.4. Beaded Collagen Filaments
4.4.1. Integrin Signaling
5 Basal Laminas and Epithelia
5.1.1. Basal Lamina
5.1.2. Hemidesmosomes and Intermediate Filament Proteins
5.1.3. Basal Lamina of the Dental Epithelial Attachment
5.2.1. General Structure of Skin, Oral and Junctional Epithelia
5.2.2. Protein Composition of Desmosomes
5.2.3. Oral and Junctional Epithelium
6 Elastic Fibers and Proteoglycans
6.1.1. Fibrillin
6.2.1. Elastin
6.3.1. Glycosaminoglycans
6.4.1. Proteo-Glycosaminoglycan Core Proteins and Cartilage Collagens
6.5.1. Major Collagen–Glycosaminoglycan Interactions
7 Collagen Synthesis, Genetic Diseases, and Scurvy
7.2.1. Effects of Collagen Polypeptide Mutations
7.2.2. Ehlers-Danlos Syndrome (EDS)
7.3.1. Ascorbate and Antioxidants
8 The Zincins: Collagen Fiber Processing and Degradation
8.1.1. The Zincin Enzyme Family
8.1.2. Catalytic Action of the Metzincin Family
8.1.3. Metzincin Activation
8.2.1. Fibrillar Procollagen Processing
8.3.1. Matrilysins: Degradation of Collagen and Stromal Proteins
8.3.2. Stromelysins
8.3.3. Enamelysin
8.3.4. Collagenases and Gelatinases
9 Biological Mineralization
9.1.1. Fundamental Properties of Calcium Phosphate Precipitation
9.1.2. Nature of the Apatite Precipitate
9.1.3. Apatite Crystal Substitutions Influence Bone Strength and Solubility
9.1.4. Nucleation
9.2.1. The Structures of Bone, Dentin, and Cementum
9.2.2. Two Mechanisms of Mineralization
9.3.1. Secretion of Osteoid Matrix
9.3.2. Osteoclast Transport of Calcium and Phosphate Ions to Matrix Vesicles
9.3.3. Calcium and Phosphate Ions Precipitate and Rupture Secreted Matrix Vesicles
9.3.4. Structure of the Calcium Transporter Proteins in Matrix Vesicles
9.3.5. The Phosphate Transporter Proteins and Pyrophosphate in Matrix Vesicles
9.4.1. SIBLING Proteins, Phex Gene Function, and Hypophosphatemia
9.4.2. Osteocalcin Is Required for Bone Modeling
9.5.1. Enamel Organ and Matrix Development
9.5.2. Proteins Involved in Enamel Synthesis
9.5.3. Proposed Mechanism of Enamel Synthesis
9.6.1. Summary of Ways in Which Enamel and Bone Differ
9.6.2. Summary of the Vitamins for Bone and Enamel Formation
10 Bone Remodeling and Calcium Metabolism
10.1.2. Proteolysis in the Bone Resorbing Compartment
10.1.3. Demineralization and remineralization
10.1.4. Osteoclast Ion and Proton Transport
10.2.1. Osteoclast Differentiation
10.2.2. Osteoclasts and Inflammation
10.2.3. Osteoporosis: Major Causes and Therapies
10.3.1. Calcium Metabolism, Parathyroid Hormone, and Calcitriol
10.4.1. Vitamin D, Calcitriol, and Calbindins
10.4.2. Rickets and Osteomalacia
10.5.1. Actions of Calcitonin
10.5.2. Calcitonin and PTH Therapy for Osteoporosis
11 Blood Coagulation
11.1.1. The Vascular System
11.1.2. Bleeding and Blood Clotting Problems
11.2.1. Blood Vessel Injury, von Willebrand Factor, and Platelets
11.2.2. The Gamma- (g-) Carboxyglutamate (gla) Domain: A Calcium Ion Chelator
11.3.1. The Extrinsic, Intrinsic, and Common Coagulation Pathways
11.3.2. The Extrinsic Pathway
11.3.3. The Intrinsic Pathway
11.3.4. The Common Pathway
11.3.5. The Hemophiliac (Excessive Bleeding Diseases)
11.4.1. The Fibrin Blood Clot: Production and Prevention
11.4.2. Removal of a Blood Clot
11.5.1. Prevention of Unwanted Blood Clotting
11.5.2. Protein S, Factor V and Factor VIII Mutations
11.6.1. Drugs to Remove a Pathogenic Thrombus or Embolus: "Clot Busters"
11.6.2. Drugs That Inhibit Excessive Clot Formation
11.6.3. Drugs That Retard Clot Formation
11.6.4. Drugs That Inhibit Platelet Activation
11.6.5. Drugs That Promote Clotting
11.6.6. Laboratory Tests to Determine the State of the Blood Clotting System
12 Saliva
12.1.1. Cell Biology of Salivary Glands
12.1.2. Whole Saliva: Collection and Composition
12.1.3. Functions of the Salivary Components
12.1.4. Innate and Acquired Immune Proteins in Saliva
12.1.5. Poor Oral Hygiene Adds Bacteria and Host Leukocyte Products to Saliva
12.2.1. Physiology and Biochemistry of Saliva Secretion
12.3.1. Salivary Mucin Composition
12.3.2. Glycan Composition of Salivary Mucins
12.4.1. Mucin Glycans, ABO Antigens, and Forensic Dentistry
12.5.1. Amylase: Substrates, Products, and Mode of Action
12.5.2. Mechanism of Action of Salivary Amylase
12.5.3. Detection of Salivary and Pancreatic Amylase
12.6.1. Proline-Rich Proteins
12.6.2. Salivary Agglutinin
13 Chronic Periodontitis
13.1.1. Detecting Periodontal Disease
13.1.2. Microbiota in Gingivitis and Chronic Periodontitis
13.1.3. Drugs and Tooth Cleaning to Prevent Gingivitis
13.2.1. Mammalian Cells Recognize Prokaryotic Molecules
13.2.2. PAMPs Induce PRRs to Release Cytokines That Attract Leukocytes
13.2.3. IL-1 Induces Gingival Inflammation
13.2.4. Neutrophils Function in Tissue Destruction
13.2.5. Gingivitis is Reversible; Antiinflammatory Cytokines Mediate Repair
13.3.1. Monocytes Are Converted to Macrophages That Over-Activate Collagenase
13.4.1. Apoptosis in Chronic Periodontitis
13.4.2. Intracellular Induction of Apoptosis
13.4.3. Mechanisms of Apoptosis
13.5.1. Eicosanoids and Periodontal Repair
13.5.2. Eicosanoid Structure
13.5.3. Functions of the Proinflammatory Eicosanoids
13.5.4. Lipoxygenase-Mediated Resolution of Inflammation
13.5.5. Antiinflammatory Drugs
14 Aggressive Periodontitis
14.1.1. Generalized Aggressive Periodontitis
14.2.1. Localized Aggressive Periodontitis
14.2.2. Aa Leukotoxin Composition and Properties
14.2.3. Mutations Enhance Aa Ltx and LAP Severity
14.2.4. Cytolethal Distending Toxin (Cdt)
15 Dental Caries
15.1.2. Sugar, Dental Caries, and the Dental Profession
15.1.3. Sucrose and the Appearance of Acid in Dental Biofilms
15.1.4. Cavities in Animals and Streptococcus mutans
15.2.1. How Sucrose Connects S. mutans to the Oral Microbiota and Dental Caries
15.2.2. Sources of Bacterial Lactic Acid in Caries
15.2.3. Dentinal (Advanced) Dental Caries
15.3.1. Variation in Individual Human Caries Experience
15.3.2. Bacterial Causes of the Variation in Caries Susceptibility
15.3.3. Saliva Causes of Caries Susceptibility
15.3.4. Caries Immunity and Susceptibility
16 Fluoride
16.1.1. Properties of Fluorine and Fluoride
16.1.2. How Mottled Enamel Was Related to Fluoride in the Water Supply
16.1.3. Mottled Enamel Is Moderate to Severe Enamel Fluorosis
16.1.4. Identification of 1 ppm Fluoride in the Water as Optimal for Cavity Protection
16.2.1. Mechanisms of Fluoride Protection from Caries
16.2.2. How Fluoride Protects from Caries
16.3.1. Systemic Effects of Fluoride
16.3.2. Fluoride Toxicity
Index
About the Author
- Martin Levine, Department of Biochemistry and Molecular Biology, Colleges of Medicine and Dentistry, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Product Details
- Hardcover: 320 pages
- Publisher: Springer; 1st Edition (2011)
- Language: English
- ISBN-10: 3540881158
- ISBN-13: 978-3540881155
- Product Dimensions: 9.4 x 6.3 x 0.8 inches
List Price: $189.00
