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Short-chain fatty acids and chronic temporomandibular joint pain

短链脂肪酸与慢性颞下颌关节疼痛

基本信息

批准号：
10341250
负责人：
Feng Tao
金额：
$ 35.98万
依托单位：
TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR
依托单位国家：
美国
项目类别：
财政年份：
2022
资助国家：
美国
起止时间：
2022-01-05 至 2026-12-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10341250
关键词：
Acetic Acids Address Affect Anti-Inflammatory Agents Arthralgia Butyric Acids Carbohydrates Chronic Development Epigenetic Process Facial Pain Fermentation Freund&apos s Adjuvant Genes Genetic Transcription Germ-Free Glutamate Decarboxylase Goals Health Personnel Histone Acetylation Histone Deacetylase Histone Deacetylation Histones Inflammatory Injections Knockout Mice Ligation Maintenance Masseter Muscle Mediating Medical Mus Neurons Nociception Oral health Pain Pathogenesis Patients Play Promoter Regions Property Propionic Acids Publishing Regulation Research Resveratrol Role Signal Transduction Structure of trigeminal nerve spinal tract nucleus System Temporomandibular Joint Temporomandibular Joint Disorders Tendon structure Testing Therapeutic Effect Trigeminal System Vagotomy Vagus nerve structure Volatile Fatty Acids Work base chronic pain epigenetic regulation fatty acid supplementation fecal transplantation gut bacteria gut microbiome gut microbiota innovation microbiome alteration mouse model non-opioid analgesic pain inhibition receptor vagus nerve stimulation

项目摘要

Project Summary: Temporomandibular disorders (TMDs) are the most common temporomandibular joint (TMJ) pain condition; however, the underlying mechanisms remain poorly understood. As such, TMJ pain has long confounded medical and dental health care providers, and current treatment of chronic TMJ pain are often unsatisfactory. Our recent work suggests that gut microbiome perturbation and reduction of short-chain fatty acids (SCFAs) in the gut may be involved in the pathogenesis of TMJ pain and recovering SCFAs to normal levels could be developed into a new complementary non-opioid therapy for such pain. Our preliminary results further suggest that SCFAs may contribute to TMJ pain via an epigenetic mechanism. In this project, we will reveal specific epigenetic mechanisms by which SCFAs regulate chronic TMJ pain. Our hypothesis is that gut microbiome perturbation-produced SCFA reduction enhances chronic TMJ pain by epigenetically suppressing Gad2 transcription, and that SCFA supplementation inhibits such pain via normalizing the epigenetic regulation. To address this central hypothesis, we will conduct the studies proposed in three specific aims. In Aim 1, we will determine the therapeutic effect of SCFA supplementation on chronic TMJ pain. In Aim 2, we will identify the epigenetic mechanism that underlies the role of SCFAs in chronic TMJ pain. In Aim 3, we will define the role of vagus nerve in SCFA-mediated epigenetic regulation of chronic TMJ pain. Together, we expect to reveal a critical epigenetic mechanism that underlies the role of SCFAs in TMJ pain. The proposed research is significant since it will demonstrate whether and how SCFAs regulate TMJ pain. The proposed studies are innovative since these studies will identify a previously unrecognized role for SCFAs in the epigenetic regulation of TMJ pain.

项目总结: