Front Cover -- Epigenetics of Chronic Pain -- Copyright -- Contents -- Contributors -- Preface -- Chapter 1: Epigenetic Tools in Chronic Pain Studies -- Introduction -- Measurement of Molecular Changes -- Sample Preparation -- DNA Methylation/Demethylation -- Genome-wide association studies -- Methylation -- Demethylation -- Gene-specific studies -- Chromatin Remodeling/Histone Modifications -- Global versus genome wide detection -- Gene specific studies of histone modification -- Noncoding RNA -- miRNA assay -- Studies of miRNA functions -- Studies of lncRNAs -- Fourth Epigenetic Mechanism -- Manipulation of Epigenetic Mechanisms -- Pharmacological Tools -- Inhibition of enzymes for DNA methylation/demethylation -- Activator and inhibitor for histone acetylation and deacetylation -- Inhibitor for histone methylation and demethylation -- Genetic Modification of Epigenetic Components -- Classic approaches -- EpiEditors -- Closing Remark -- Acknowledgements -- References -- Chapter 2: Epigenetic Regulation of Peripheral Macrophages in Neuropathic Pain -- Introduction -- Peripheral Sensitization in Neuropathic Pain -- Macrophage Infiltration and Cytokine Production -- Macrophage Polarization in Neuropathic Pain -- Chemokine Systems and Inflammation -- Peripheral Chemokines in Neuropathic Pain -- Epigenetic Regulation of Gene Expression -- Histone Modifications and Chemokine Production -- Epigenetic Regulation of Chemokines and Neuropathic Pain -- Conclusions and Future Directions -- Acknowledgments -- Conflicts of Interest -- References -- Chapter 3: Emphasizing Histone-Related Chromatin Remodeling in the Central Nervous System of Animal Models of Chronic Pain -- Histone-Related Chromatin Remodeling -- Neuropathic Pain Model -- Partial Sciatic Nerve Ligation (PSL) Model (Table 1) -- Spinal Nerve Ligation (SNL) Model (Table 1).

Chronic Constriction Injury (CCI) Model (Table 2) -- Spared Nerve Injury (SNI) Model (Table 2) -- Chemotherapy-Induced Neuropathic Pain Model (Table 2) -- Inflammatory Pain Model -- CFA-Induced Inflammation Model (Table 3) -- MIA-Induced Inflammation Model (Table 4) -- Other Pain Model -- Opioid-Induced Hyperalgesia Model (Table 5) -- Hindpaw Incision Model (Table 5) -- Conclusions and Perspectives -- Acknowledgment -- References -- Chapter 4: Role of Histone Modifications in Chronic Pain Development -- Histone Methylation -- H3K9me2 and H3K9me3 -- H3K27me3 -- H3K4me3 -- Histone Acetylation -- Histone Variants -- Other Histone-Modifying Factors -- Perspectives -- Chapter 5: Role of DNA Methylation in Chronic Pain -- Introduction -- The Process of DNA Methylation -- DNA Methylation and Neuropathic Pain -- DNA Methylation and Inflammatory Pain -- DNA Methylation and Cancer Pain -- Methyl-CpG-Binding Domain Proteins (MBDs) and Chronic Pain -- DNA Methylation and Clinical Painful Diseases -- Conclusion & Future Perspective -- References -- Chapter 6: Pain-Induced Chromatin Modifications -- Introduction -- Chromatin Modifications for Transcriptional Regulations -- Histone Modifications -- Noncoding RNAs -- DNA Methylation -- Histone Modifications in Chronic Pain -- Noncoding RNAs in Chronic Pain -- DNA Methylation in Chronic Pain -- Conclusion and Future Directions -- References -- Chapter 7: DNA Methylation/Demethylation Homeostasis and Various Pain Conditions -- Introduction -- DNA Methylation and Demethylation -- Emerging Technologies for Studying DNA Methylation and Demethylation -- DNA Methylation/Demethylation and Transcriptional Regulation -- DNA Methylation and Transcriptional Repression -- DNA Demethylation and Transcriptional Activation -- Role of DNA Methylation in Chronic Pain: An Imbalance Between Methylation and Demethylation.

Mechanisms Underlying the DNA Methylation and Demethylation -- Enhanced Binding Ability of the Demethylated Gene With the Transcription Factor -- Future Treatment Options by Drugging the DNA Methylome -- Concluding Remarks -- Acknowledgements -- References -- Chapter 8: Epigenetic Modulation of Visceral Pain -- Introduction -- Visceral Pain -- Types of Visceral Pain -- Characteristics of Visceral Pain -- Visceral Pain Pathways -- Monitoring Methods of Visceral Pain -- Animal Models of Visceral Pain -- Epigenetic Mechanisms in Visceral Pain -- DNA Methylation in Visceral Pain -- Histone Acetylation in Visceral Pain -- MicroRNA Activities in Visceral Pain -- Conclusion and Future Strategies -- Acknowledgments -- References -- Chapter 9: Noncoding RNAs Are New Players in Chronic Pain -- Introduction -- miRNAs in Chronic Pain -- Long Noncoding RNAs in Chronic Pain -- Circular RNAs in Chronic Pain -- Conclusion -- References -- Chapter 10: Epigenetics of Chronic Visceral Nociception -- Chronic Visceral Pain: A Major Health Care Concern -- Neurobiology of Visceral Nociception -- Modulating Factors of Afferent Input -- Epigenetic Alterations -- Conclusions -- References -- Chapter 11: An Overview of Epigenetic Correlates of Human Chronic Pain Conditions -- Introduction -- Epigenetic Marks and Chronic Pain -- Fibromyalgia and Chronic Widespread Pain -- Role of DNA methylation -- Role of microRNAs -- Headache -- Cancer Pain -- Low Back Pain -- Diabetic Neuropathy -- Chronic Postsurgical Pain -- Neonatal Stress-Related Pain -- Visceral Pain-Irritable Bowel Syndrome (IBS) and miRNA Profiles -- Complex Regional Pain Syndrome and miRNA Profiles -- Sex Differences in miRNA Profiles in Trauma/Stress Pain -- Transient Receptor Potential Cation Channel A1 (TRPA1) and Neuropathic Pain -- Opioid Receptors -- Epigenetics in Painful Disease Conditions.

Rheumatoid Arthritis -- DNA hypomethylation -- Histone code -- Osteoarthritis -- Endometriosis -- Myalgic Encephalomyelitis/Chronic Fatigue Syndrome -- Inflammatory Bowel Diseases and Crohn's Disease -- Periodontal Disease -- Translation and Therapeutic Potential -- General Comments and Concluding Remarks -- Blood-Based Analysis and Brain Epigenetics -- Cell and Tissue-Specificity of Altered Epigenetics -- Implications of Differential Genomic Methylation -- Confounding Factors in Human Epigenetic Studies -- Age -- Sex -- Other factors -- Concluding Remarks -- Acknowledgments -- References -- Index -- Back Cover.