دانلود کتاب Oral Submucous Fibrosis: A Guide to Diagnosis and Management (Textbooks in Contemporary Dentistry)

فهرست مطالب :

Foreword
Preface
Contents
Contributors
Abbreviations
I: Introduction to Oral Submucous Fibrosis
1: Oral Submucous Fibrosis: A Historical Perspective
1.1 Introduction
1.2 A Sweep Across Time
1.3 Other Relevant Ayurvedic Literature
1.4 Studies on OSF During the Past Century
1.4.1 Studies from South and SE Asia
1.4.1.1 India
1.4.1.2 Sri Lanka
1.4.1.3 Taiwan
1.4.1.4 China
1.4.1.5 Burma
1.4.1.6 Nepal
1.4.1.7 Malaysia
1.4.1.8 Papua New Guinea
1.4.1.9 South Africa
1.5 Summary of Recent History
Summary
References
2: Epidemiology of Oral Submucous Fibrosis: Prevalence and Trends
2.1 Introduction
2.2 Epidemiology of OSF
2.3 Prevalence Data from the Indian Subcontinent
2.4 Prevalence Data from Other Countries in the South Asian Region
2.5 International Prevalence Studies
2.5.1 Western Countries
2.5.2 South Africa
2.6 Gender
2.7 Age
2.7.1 Prevalence of OSF Among Children and Adolescents
2.8 Trends in Etiology
2.9 Discussion
2.10 Conclusion
Summary
References
3: Clinical Features: Oral Submucous Fibrosis
3.1 Introduction
3.2 Brief Review of the Literature
3.3 General Aspects: Age and Sex
3.4 Signs and Symptoms
3.5 Burning Sensation
3.6 Blanching of the Mucosa
3.7 Depigmentation
3.8 Leathery Mucosa
3.9 Marble-Like Appearance
3.10 Depapillation of Tongue
3.11 Vesicles
3.12 Petechia
3.13 Ulceration and Stomatitis
3.14 Fibrous Bands
3.15 Distorted Uvula
3.16 Limited Mobility of Tongue
3.17 Limited Mouth Opening
3.18 Other Associated Clinical Conditions
3.19 Mastication and Deglutition
3.20 Extraoral
Summary
References
4: Associated Conditions of Oral Submucous Fibrosis
4.1 Introduction
4.2 Conditions Affecting the Dental Hard Tissues and Periodontium
4.3 Conditions Affecting the Soft-Tissue Lining of the Oral Cavity
4.3.1 Quid Stain on Oral Mucosa
4.3.2 Chewer’s Mucosa
4.3.3 Oral Candidiasis
4.3.4 Oral Lichenoid Contact Reactions to Betel Quid
4.3.5 Oral Lichen Planus (OLP)
4.3.6 Oral Leukoplakia
4.3.7 Proliferative Verrucous Leukoplakia (PVL)
4.3.8 Erythroplakia
4.3.9 Verrucopapillary Lesions
4.3.9.1 Oral Squamous Papilloma
4.3.9.2 Exophytic Verrucous Hyperplasia (EVH) (Oral Verrucous Hyperplasia—OVH)
4.3.9.3 Oral Verruciform Xanthoma (VX)
4.3.9.4 Oral Verrucous Carcinoma (VC)
4.3.9.5 Oral Squamous Cell Carcinoma (OSCC)
Summary
References
5: Oral Submucous Fibrosis in Childhood
5.1 Introduction
5.2 Epidemiology
5.3 Aetiology
5.4 Vulnerability Factors for Areca Nut Chewing Habits and Developing OSF
5.5 Clinical Features
5.6 Diagnosis
5.7 Management
5.8 Prevention
5.9 Malignant Transformation and Associated Risk Factors of Malignant Transformation
Summary
References
6: Classification Systems for Oral Submucous Fibrosis
6.1 Introduction
6.2 Oral Submucous Fibrosis (OSF): Classification Systems
6.2.1 Desa (1957)
6.2.2 Pindborg and Sirsat (1966)
6.2.3 Wahi and Kapur et al. (1966)
6.2.4 Ahuja and Agarwal (1971)
6.2.5 Bhatt and Dholakia (1977)
6.2.6 Gupta and Golhar (1980)
6.2.7 Warnakulasuriya (1987)
6.2.8 Pindborg (1989)
6.2.9 Katharia et al. (1992)
6.2.10 Bailoor (1993)
6.2.11 Racher (1993)
6.2.12 Khanna and Andrade (1995)
6.2.13 Lai et al. (1995)
6.2.14 Maher et al. (1996)
6.2.15 Haider et al. (2000)
6.2.16 Ranganathan et al. (2001)
6.2.17 Rajendran (2003)
6.2.18 Utsonumiya et al. (2005)
6.2.19 Bose and Balan (2007)
6.2.20 Kumar et al. (2007)
6.2.21 Mehrotra et al. (2009)
6.2.22 More et al. (2011)
6.2.23 Kerr et al. (2011)
6.2.24 Patil and Maheshwari (2014)
6.2.25 Arakeri et al. (2018)
Summary
6.3 Conclusion and Recommendations
References
7: Malignant Transformation of Oral Submucous Fibrosis
7.1 Introduction
7.2 Insight into the Literature
7.3 Malignant Transformation Rate among OSF Patients
7.4 Epithelial Dysplasia and OSF
7.5 Potential Risk Factors of Malignant Transformation among OSF Patients
7.5.1 Areca Nut Usage as a Major Carcinogen
7.6 Pathological Mechanisms of the Malignant Transformation of OSF
7.6.1 Hypoxia
7.6.2 Angiogenesis
7.6.3 Alterations in Cell Cycle
7.6.4 Epithelial-Mesenchymal Transition
7.7 Prognosis of OSF Malignant Transformation
7.8 Conclusion
Summary
References
II: Aetiology of Oral Submucous Fibrosis
8: Lifestyle Factors
8.1 Introduction
8.2 A Review of Methodological Issues
8.3 Epidemiological Studies Contributing to the Evidence
8.3.1 Risk from Betel Quid and Areca Nut without Added Tobacco
8.3.2 Risk from Betel Quid and Areca Nut with Added Tobacco
8.4 Tobacco, Alcohol, and Synergistic Effect
8.5 Dose-Response Effect of Betel Quid and Areca Nut
8.6 Dose-Response of Betel Quid and Areca Nut in Increasing Severity of OSF and Malignant Transformation
8.7 Conclusions
Summary
References
9: Genetic Aspects of Oral Submucous Fibrosis
9.1 Introduction
9.2 Genetic Susceptibility and Gene Expression in Tissue/Organ Fibrosis
9.3 Genetic Susceptibility in Oral Submucous Fibrosis (OSF)
9.3.1 Collagen 1A1 and Collagen 1A2 (COL1A1 and COL1A2) Gene
9.3.2 Matrix Metalloproteinases (MMPs)
9.3.3 Collagenase-1 (COLase-1, MMP-1)
9.3.4 MMP-2 (Gelatinase-A) and MMP-9 (Gelatinase-B)
9.3.5 MMP-3 (Stromelysin-1)
9.3.6 TGF-β and SMAD
9.3.7 Lysyl Oxidase (LOX)
9.3.8 Cystatin C (CST3)
9.3.9 Plasminogen Activator Inhibitor (PAI-1)
9.3.10 TIMPs (Tissue Inhibitor Matrix Metalloproteinases)
9.3.11 Vascular Endothelial Growth Factor (VEGF)
9.3.12 Cytochrome P450 (CYP3A) Gene
9.3.13 DNA Repair Gene Polymorphism
9.3.13.1 X-Ray Cross-Complementing (XRCC) Polymorphism
9.3.13.2 NADPH Quinone Oxidoreductase 1 (NQ01) C609T
9.3.14 Tumor Necrosis Factor-α (TNF-α)
9.3.15 p53 Gene Mutations
9.3.16 Cytotoxic T-lymphocyte-Associated Antigen 4 (CTLA-4); CD 152 (Cluster of Differentiation 152) Gene Polymorphism
9.3.17 Major Histocompatibility Complex (MHC) Class I Chain-Related Gene A (MICA) Polymorphism
9.3.18 Glutathione S-Transferase (GST) Polymorphism
9.3.19 Apoptosis-Associated Genes FAS and FASL Polymorphism
9.3.20 Loss of Heterozygosity (LOH)
9.4 Conclusion
Summary
References
10: Diet and Micronutrients
10.1 Introduction
10.2 Epidemiological Evidence on Diet and Nutrition
10.3 Role of Trace Elements in OSF
10.3.1 Role of Copper
10.3.2 Role of Zinc
10.3.3 Role of Iron
10.3.4 Role of Selenium
10.4 Role of Vitamins
10.5 Interventional Studies
Summary
References
III: Aetiopathogenesis of Oral Submucous Fibrosis
11: In Vivo and In Vitro Experimental Evidence
11.1 Introduction
11.2 In Vivo Experimental Evidence on OSF
11.2.1 In Vivo Animal Models of OSF Induced by ANE/Commercial Areca Nut Products
11.2.2 In Vivo Experimental Evidence of Chili as a Risk Factor of OSF
11.2.3 In Vivo Human Experimental Studies Dealing with OSF Patients
11.2.3.1 Inflammatory Cytokine Production by Peripheral Blood Mononuclear Cells
11.2.3.2 Elevated Levels of Copper from Areca Nut and Drinking Water Reduce Collagen Degradation
11.2.3.3 Genetic Susceptibility in Individuals with OSF
11.2.4 In Vivo Experimental Evidence of Analysis of Areca Nut Alkaloids in Saliva
11.2.4.1 Pro-inflammatory Cytokines in Serum and Saliva in OSF Patients
11.2.4.2 Oxidative Stress Generated by ANE in OSF Patients
11.2.4.3 Involvement of Autoimmunity in the Etiology of OSF
11.2.4.4 Involvement of Micronutrients in the Etiology of OSF
11.3 In Vitro Experimental Evidence Supporting the Role Played by Areca Nut/Betel Quid in OSF
11.3.1 Collagen Synthesis
11.3.2 In Vitro Experimental Evidence Supportive of Inflammation Induced by Arecoline/ANE
11.3.2.1 Contribution of Pro-inflammatory Cytokines
11.3.2.2 Contribution of Pro-inflammatory Enzymes and Molecules
11.3.3 Experimental Evidence Supporting Arecoline/ANE in Stimulating Fibrogenic Cytokines
11.3.4 Experimental Evidence of Areca Nut Extract/Arecoline Contributing to Myofibroblast Activation
11.3.5 Experimental Evidence of Decreased Collagen Degradation and Clearance by Areca Nut
11.3.6 In Vitro Evidence of Oxidative Stress and ROS Generation by Betel Quid
11.3.7 The Role of Arecoline-Induced Autophagy in OSF
11.4 Experimental Evidence-Based Outline of Mechanisms by Which Etiological Agents Contribute to the Development of OSF
11.5 Experimental Evidence That Is Required to Complete the Etiological Picture of OSF
Summary
References
12: Fibrogenic Factors and Molecular Mechanisms
12.1 Introduction
12.2 Areca Nut in the Molecular Pathogenesis of OSF
12.3 Inflammation in Oral Submucous Fibrosis
12.4 Regulation of Inflammatory Mediators in Oral Submucous Fibrosis
12.4.1 Pro-inflammatory Cytokines
12.4.2 Cortisol and Steroids
12.5 Fibrogenic Factors and Signaling Pathways
12.5.1 Transforming Growth Factor-Beta (TGF-β Family)
12.5.1.1 TGF-β Synthesis and Activation
12.5.1.2 TGF-β Receptors
12.5.1.3 TGF-β Signaling and Fibrotic Diseases
12.5.2 Contribution of SMAD and Non-SMAD Signaling Pathways to Fibrosis at the Cellular Level
12.5.2.1 The Role of Areca Nut and Transforming Growth Factor-β in Oral Submucous Fibrosis Progression
12.5.2.2 Transforming Growth Factor-β Regulation by Areca Nut
12.5.2.3 TGF-β in Oral Submucous Fibrosis
12.5.2.4 Epidermal Growth Factor Receptor
12.5.2.5 EGFR Role in Fibrosis
12.5.2.6 Fibroblast Growth Factor Receptor (FGF)
12.5.2.7 Role of FGF in Fibrosis
12.5.2.8 Notch
12.5.2.9 Notch and Myofibroblast Differentiation
12.5.2.10 Notch and Epithelial-Mesenchymal Transition (EMT)
12.5.2.11 Integrins
12.5.2.12 Role of Integrins in Fibrosis
12.6 Extracellular Matrix, and Epithelial-to-Mesenchymal Transition
12.6.1 Molecular Characterization/Molecular Pathogenesis of Oral Submucous Fibrosis
12.6.1.1 Factors Regulating Extracellular Matrix (ECM) Remodeling
12.6.1.2 Matrix Metalloproteinases and Tissue Inhibitors of Matrix Metalloproteinases (MMPs and TIMPs)
12.6.1.3 Alpha-Smooth Muscle Actin (α-SMA)
12.6.1.4 Epithelial-Mesenchymal Transition in Oral Submucous Fibrosis
12.7 Epithelial Factors
12.7.1 E-cadherin
12.7.2 CD147
12.7.3 Cytokeratin
12.7.4 Annexin and Filamin
12.7.5 Loricrin
12.8 Receptor Tyrosine Kinase Pathway
12.9 Transcription Factors
12.10 Wnt Signaling Pathway
12.11 Tissue Injury in Oral Submucous Fibrosis
12.12 Anti-fibrotic Factors: Therapeutic Targets for Oral Submucous Fibrosis
Summary
References
IV: Investigative Techniques for Oral Submucous Fibrosis
13: Noninvasive Diagnostic Techniques in Oral Submucous Fibrosis
13.1 Introduction
13.2 Measurement of Mouth Opening
13.3 Optical Instruments
13.3.1 Tissue Autofluorescence
13.3.2 Ultrasonography
13.3.2.1 Colored Doppler Ultrasonography
13.3.3 ATR-FTIR Spectroscopy
13.3.4 Optical Coherence Tomography
13.3.5 Contact Endoscopy
13.4 Biomarkers in Saliva
13.4.1 Lactate Dehydrogenase
13.4.2 Trace Elements
13.4.3 Oxidative Stress/Micronutrients
13.4.4 Predictive Tumor Markers
13.5 X-Ray (Lateral Cephalometric Analysis)
13.6 Discussion
Summary
References
14: Pathology of Oral Submucous Fibrosis
14.1 Introduction
14.1.1 General Aspects
14.2 Epithelial Changes
14.2.1 Epithelial Thickness
14.2.2 Vesicles and Erosions
14.2.3 Keratinization
14.2.4 Epithelial Dysplasia
14.2.5 Cellular Changes in Keratinocytes and Non-keratinocyte Cells
14.2.5.1 Keratinocytes and Keratinization
14.2.5.2 Non-keratinocytes
Oral Melanocytes
Langerhans Cells
14.3 Connective Tissue Changes
14.3.1 Fibrosis and Hyalinization
14.3.2 Vascularity
14.3.3 Inflammation
14.3.4 Myofibroblast
14.3.5 Mast Cells
14.3.6 Muscles
14.4 Electron Microscopic (EM) Features in OSF
14.5 Special Stains
14.6 Lesions Associated with OSF
14.6.1 Leukoplakia and OSF
14.6.2 Verrucous Hyperplasia and OSF
14.6.3 Coexistence of Lichenoid Features and Fibrosis
14.7 Oral Cancer and OSF
14.7.1 Histological Markers for Genetic Damage and Malignant Transformation in OSF
14.7.1.1 Micronucleus
14.7.1.2 Silver Staining Nucleolar Organizing Region (AgNOR)
Summary
References
15: Biomarkers in Oral Submucous Fibrosis
15.1 Introduction
15.2 Epithelial Markers
15.2.1 Annexin A4 (ANXN A4)
15.2.2 Beta-Catenin (β-Catenin)
15.2.3 CD1a, CD303, and CD207
15.2.4 Cytokeratins (CKs)
15.2.5 E-Cadherin (E-Cad)
15.2.6 Epidermal Growth Factor Receptor (EGFR)
15.2.7 Filamin A (FLNA)
15.2.8 Loricrin
15.3 Connective Tissue Markers
15.3.1 Alpha-Smooth Muscle Actin (α-SMA)
15.3.2 Bone Morphogenetic Protein-7 (BMP7)
15.3.3 CD34
15.3.4 CD68
15.3.5 CD105
15.3.6 CD147
15.3.7 Collagen
15.3.8 Connective Tissue Growth Factor (CTGF)
15.3.9 Decorin
15.3.10 Fibroblast Growth Factor (FGF) and Its Receptors (bFGF, FGF2, FGFR2, and FGFR3)
15.3.11 Fibronectin
15.3.12 Hypoxia-Inducible Factor (HIF)
15.3.13 Mast Cell Tryptase and Mast Cell Chymase
15.3.14 Matrix Metalloproteinase (MMP; MMP-1, MMP-13)
15.3.15 Tissue Inhibitors of Matrix Metalloproteinases (TIMPs; TIMP-1, TIMP-2)
15.3.16 N-Cadherin (N-Cad)
15.3.17 Osteopontin
15.3.18 Podoplanin
15.3.19 S100A4
15.3.20 Syndecan-1
15.3.21 Tenascin-C
15.3.22 Transforming Growth Factor-Beta (TGF-β; TGF-β1, TGF-β2)
15.3.23 Transglutaminase-2 (TGM-2)
15.3.24 TWIST
15.3.25 Vascular Endothelial Growth Factor (VEGF)
15.3.26 Vimentin
15.4 Proliferative, Apoptosis, and Senescence Markers
15.4.1 Bax
15.4.2 Budding Uninhibited by Benzimidazole-Related 1 (BUBR1)
15.4.3 Caspases
15.4.4 C-Jun
15.4.5 Mesenchymal-Epithelial Transition Factor (c-Met)
15.4.6 C-Myc
15.4.7 Cyclin D1
15.4.8 Fragile Histidine Triad Protein (FHIT)
15.4.9 Human Telomerase Reverse Transcriptase (hTERT)
15.4.10 Insulin-Like Growth Factor II mRNA-Binding Protein 3 (IMP3)
15.4.11 Ki67
15.4.12 Microtubule-Associated Protein Light Chain 3 (LC3)
15.4.13 Mouse Double-Minute 2 Homolog (MDM2)
15.4.14 p16
15.4.15 p53
15.4.16 p62
15.4.17 p63
15.4.18 Proliferating Cell Nuclear Antigen (PCNA)
15.4.19 Polo-Like Kinase (PLK)
15.4.20 Phosphatase and Tensin Homolog Deleted on Chromosome 10 (PTEN)
15.4.21 Survivin
15.5 Stemness Markers
15.5.1 Aldehyde Dehydrogenase (ALDH1)
15.5.2 B-Cell-Specific Moloney Murine Leukemia Virus Insertion Site 1 (Bmi1)
15.5.3 CD133
15.5.4 Stage-Specific Embryonic Antigen (SSEA4)
15.5.5 STRO1 (in Fibroblasts and Myofibroblasts)
15.5.6 SRY (Sex-Determining Region on Y Chromosome) Type Homeobox Genes (SOX2)
15.6 Markers of Signaling Pathway Alterations
15.6.1 Dickkopf WNT Signaling Pathway Inhibitor 3 (DKK3)
15.6.2 Phosphorylated Extracellular Signal-Regulated Kinases (pERK)
15.6.3 Glioma-Associated Oncogene Homolog 1 (GLI1)
15.6.4 Sonic Hedgehog (Shh)
15.6.5 WNT Inhibitory Factor 1 (WIF1)
15.7 Inflammatory Markers, Glycoproteins, and Enzymes
15.7.1 Alpha-Enolase (ENO1)
15.7.2 Beta-Integrin (β-Integrin)
15.7.3 Calreticulin
15.7.4 C–C Motif Chemokine Ligand 2 (CCL2)
15.7.5 Cyclooxygenase 2 (COX-2)
15.7.6 Cyclophilin A
15.7.7 Fatty Acid Synthase (FASN)
15.7.8 Fibrinogen Alpha-Chain Precursor (FGA)
15.7.9 Glucose Transporter 1
15.7.10 Heat-Shock Protein 70 (Hsp70)
15.7.11 Hexokinase 2 (HK2)
15.7.12 Hydroxynonenal (4-HNE)
15.7.13 Mucin-1 (MUC1)
15.7.14 Organic Cation Transporter 3 (OCT3)
15.7.15 Secreted Frizzled-Related Proteins (SFRPs)
Summary
References
V: Management of Oral Submucous Fibrosis
16: Medical Management of Oral Submucous Fibrosis
16.1 Introduction
16.1.1 Medical Management of OSF
16.1.1.1 Pharmaceutical Agents
16.1.1.2 Herbal Remedies
16.2 Anti-inflammatory Agents
16.2.1 Corticosteroids
16.3 Immunomodulators
16.3.1 Levamisole
16.3.2 Probiotic Agents
16.4 Proteolytic/Fibrolytic Enzymes
16.4.1 Hyaluronidase
16.4.2 Chymotrypsin
16.4.3 Collagenase
16.5 Antioxidants in OSF
16.5.1 Lycopene
16.5.2 Curcumin (Turmeric)
16.5.3 Tulsi/Holy Basil (Ocimum tenuiflorum/Ocimum sanctum Linn)
16.5.4 Aloe Vera (AV)
16.5.5 Spirulina
16.5.6 Tea Pigments
16.5.7 Salvianolic Acid (Sal-B)
16.5.8 Epigallocatechin Gallate (EGCG)
16.6 Vasodilators
16.6.1 Pentoxifylline (PTX)
16.6.2 Nylidrin Hydrochloride
16.6.3 Isoxsuprine
16.6.4 Xantinol Nicotinate
16.6.5 Buflomedial Hydrochloride
16.7 Biogenic Stimulation
16.7.1 Placental Extract
16.8 Micronutrients (Vitamins and minerals)
16.8.1 Vitamins
16.8.2 Minerals
16.8.3 Oxitard ™
16.8.4 Garlic
16.9 Novel Therapies
16.9.1 Colchicine
16.9.2 Interferon Gamma (IFN-γ)
16.9.3 Anti-TGF-β Drugs
16.9.4 Valdecoxib
16.9.5 Meta analysis of intervention in OSF
Summary and Conclusion
References
17: Curcumin as a Chemopreventive Agent for Oral Submucous Fibrosis
17.1 Introduction
17.2 Turmeric, Curcumin and OSF
17.3 Mechanism of Curcumin on Inflammation and Inflammatory Pathways
17.4 Turmeric and Curcumin Against the Hallmarks of OSF
17.4.1 Cytokines/Interleukins in OSF and Its Inhibition by Turmeric/Curcumin
17.4.2 ECM/Collagen Synthesis in OSF and Its Inhibition by Turmeric/Curcumin
17.4.3 Oxidative Stress in OSF and Its Inhibition by Turmeric/Curcumin
17.4.4 MMPs in OSF and Its Modulation by Turmeric/Curcumin
17.4.5 Fibrosis in OSF and Its Inhibition by Turmeric/Curcumin
17.4.6 TGF-β Signaling in OSF and Its Inhibition by Turmeric/Curcumin
17.5 Experimental Laboratory Studies
17.6 Clinical Studies
17.7 Conclusion
Summary
References
18: Surgical Management of Oral Submucous Fibrosis
18.1 Introduction
18.2 Indications of Surgery
18.3 Principles of Surgery and Surgical Steps
18.3.1 Preoperative Evaluation
18.3.2 Anesthesia, Preparation of the Patient and Intraoperative Evaluation
18.3.3 Incision of Fibrous Bands Followed by Adequate Muscular Release
18.3.4 Masticator Muscle Myotomy
18.3.5 Bilateral Coronoidectomy
18.3.6 Resurfacing of the Surgical Defect
18.3.6.1 Intraoral Flaps
18.3.6.2 Extraoral Flaps
18.3.6.3 Distant Flaps
18.3.6.4 Radial Forearm Free Flap
18.3.6.5 Coverage with Grafts and Membranes
18.4 Pitfalls and Solutions of Resurfacing Techniques
18.5 Postoperative Physiotherapy
18.6 Results of Surgical Intervention
18.7 Post Surgery Surveillance
18.8 Summary and Future Perspectives
18.9 Conclusions
References
VI: Areca Nut Addiction and Treatment
19: Areca Nut Addiction: Tools to Assess Addiction
19.1 Introduction
19.2 Dependence or Addiction to a Substance
19.3 Methods of Assessment of Addiction/Dependence
19.3.1 Diagnostic Criteria and Screening Tools
19.3.2 Biological Assessment Techniques
19.3.3 Limitations of Existing Instruments for Measuring and or Screening for Dependence
19.4 Pharmacology of Areca Nut
19.5 Does Areca Nut Fulfil the Operational Criteria for a Dependence Syndrome?
19.6 Development of Scales to Measure Betel Quid Depeendence/Use
19.6.1 Betel Quid Dependence Scale (BQDS)
19.6.2 Reasons for Betel-Quid Chewing Scale (RBCS)
19.6.3 DSM-5 Betel-Quid Use Disorder
19.6.4 Self-Report Screening Test for Areca Quid Abuser (SSTAA)
19.7 Conclusions and Future Perspectives
Summary
References
20: Behavioural Interventions for Areca Nut Cessation in the Prevention and Management of Oral Submucous Fibrosis
20.1 Introduction
20.2 The Scope of Behavioral Interventions
20.3 Review of the Relevant Intervention Studies
20.3.1 Bangladesh
20.3.2 Guam
20.3.3 India
20.3.4 Pakistan
20.3.5 Sri Lanka
20.3.6 Taiwan
20.4 Discussion
20.5 Conclusion
Summary
References
21: Pharmaceutical Agents for Areca Nut Cessation
21.1 Introduction
21.2 Betel Quid Addiction Beyond Behavioural Therapy
21.2.1 Smokeless Tobacco; Addictive Mechanism
21.2.2 Areca nut; Addictive Mechanisms
21.3 Pharmacotherapy for Areca Nut Cessation
21.3.1 Pharmaco-Therapy for Nicotine Addiction
21.3.2 Pharmaceutical Agents for Arecoline Addiction
21.4 Conclusion
Summary
References
22: World Literature: Bibliography
22.1 Bibliography
22.1.1 Reviews
22.1.2 Epidemiology of OSF Worldwide
22.1.3 Clinical Presentation and Evaluation: Paediatric and Adult Patients of OSF
22.1.4 Classification, Grading and Staging Systems Used in OSF
22.1.5 Etiopathogenesis of OSF as an OPMD
22.1.6 Histopathology and Special Stains in OSF, as OPMD
22.1.7 Molecular Biology and Genetics of OSF, and Malignant Transformation
22.1.8 Immunohistochemistry in OSF
22.1.9 Diagnostic, Serology and Prognostic evaluation
22.1.10 Therapuetics and Treatment of OSF
22.1.11 Relation and Conversion of OSF to OSCC
22.1.12 Research Associated with OSF
Appendix: Prominent Stalwarts in the Study of Oral Submucous Fibrosis
Living Legends
Index