Expression of Interleukin-1 and temporomandibular disorder: Contemporary review of the literature

Sorenson, Adam; Hresko, Kyle; Butcher, Seth; Pierce, Sean; Tramontina, Vinicius Augusto; Leonardi, Rosalia; Loreto, Carla; Bósio, José A.; Almeida, Luís Eduardo

doi:10.1080/08869634.2017.1342890

Cited by 19 publications

(16 citation statements)

References 17 publications

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“…Notably, the complex balance between the molecules and receptors of the IL-1 family significantly impacts the TMJ homeostasis, as indicated in many research, which illustrated the presence of higher degrees of IL-1α and IL-1β in the synovial fluid of patients with TMDs [27]. In this study, the synovial fluid samples were extracted from patients with TMDs at diverse phases, which led to the conclusion that the increased degrees of these cytokines result in the development and progress of TMD [89].…”

Section: Il-1mentioning

confidence: 79%

Biomarkers for Temporomandibular Disorders: Current Status and Future Directions

et al. 2020

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Numerous studies have been conducted in the previous years with an objective to determine the ideal biomarker or set of biomarkers in temporomandibular disorders (TMDs). It was recorded that tumour necrosis factor (TNF), interleukin 8 (IL-8), IL-6, and IL-1 were the most common biomarkers of TMDs. As of recently, although the research on TMDs biomarkers still aims to find more diagnostic agents, no recent study employs the biomarker as a targeting point of pharmacotherapy to suppress the inflammatory responses. This article represents an explicit review on the biomarkers of TMDs that have been discovered so far and provides possible future directions towards further research on these biomarkers. The potential implementation of the interactions of TNF with its receptor 2 (TNFR2) in the inflammatory process has been interpreted, and thus, this review presents a new hypothesis towards suppression of the inflammatory response using TNFR2-agonist. Subsequently, this hypothesis could be explored as a potential pain elimination approach in patients with TMDs.

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Section: Il-1mentioning

confidence: 79%

Biomarkers for Temporomandibular Disorders: Current Status and Future Directions

et al. 2020

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“…The intricate balance of molecules and receptors of the IL-1 family has a deep effect on the TMJ homeostasis. Many studies indicated that higher levels of IL-1α and IL-1β are present in the synovial fluid of patients with TMD 46 .…”

Section: Interleukin-1 (Il-1)mentioning

confidence: 99%

Inflammatory mediators related to arthrogenic temporomandibular dysfunctions

Poluha

Grossmann

2018

Brazilian Journal of Pain

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BACKGROUND AND OBJECTIVES: Inflammatory disorders of the temporomandibular joint present a high prevalence in the population. The knowledge about inflammatory mediators, such as histamine, serotonin, kinins, eicosanoids, platelet-activating factor, nitric oxide, tumor necrosis factor and interleukins, may contribute to a better understanding of these disorders. The objective of this study was to review the literature on the major inflammatory mediators involved in temporomandibular arthralgia. CONTENTS: A search was made in the LILACS, Pubmed/ Medline, Scielo and Science direct databases, crossing the following descriptors in the English and Portuguese language: inflammation, temporomandibular joint, inflammatory mediators, inflammation, temporomandibular joint and inflammatory mediators. Articles of literature review, systematic review, meta-analysis and randomized clinical trials, as well as books with compatible themes, published between September 1990 and June 2017 were included. Clinical reports, open label studies, animal model studies, were excluded. CONCLUSION: The knowledge of the inflammatory process, with the different mediators and mechanisms, can contribute to a better understanding, allowing the selection of the best therapy to be used clinically in cases of arthrogenic temporomandibular joint disorders.

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“…As an important inflammatory cytokine in the initiation and development of TMD, IL-1 β was widely used to simulate the inflammatory microenvironment of TMD in vitro[ 10 , 11 ]. In this study, we showed that IL-1 β inhibited the autophagy and chondrogenic differentiation of SMSCs.…”

Section: Introductionmentioning

confidence: 99%

Rapamycin-Induced Autophagy Promotes the Chondrogenic Differentiation of Synovium-Derived Mesenchymal Stem Cells in the Temporomandibular Joint in Response to IL-1β

Liu

Wang

et al. 2020

BioMed Research International

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Cartilage defects in temporomandibular disorders (TMD) lead to chronic pain and seldom heal. Synovium-derived mesenchymal stem cells (SMSCs) exhibit superior chondrogenesis and have become promising seed cells for cartilage tissue engineering. However, local inflammatory conditions that affect the repair of articular cartilage by SMSCs present a challenge, and the specific mechanism through which the function remains unclear. Thus, it is important to explore the chondrogenesis of SMSCs under inflammatory conditions of TMD such that they can be used more effectively in clinical treatment. In this study, we obtained SMSCs from TMD patients with severe cartilage injuries. In response to stimulation with IL-1β, which is well known as one of the most prevalent cytokines in TMD, MMP13 expression increased, while that of SOX9, aggrecan, and collagen II decreased during chondrogenic differentiation. At the same time, IL-1β upregulated the expression of mTOR and decreased the ratio of LC3-II/LC3-I and the formation of autophagosomes. Further study revealed that rapamycin pretreatment promoted the migration of SMSCs and the expression of chondrogenesis-related markers in the presence of IL-1β by inducing autophagy. 3-Benzyl-5-((2-nitrophenoxy)methyl)-dihydrofuran-2(3H)-one (3BDO), a new activator of mTOR, inhibited autophagy and increased the expression of p-GSK3βser9 and β-catenin, simulating the effect of IL-1β stimulation. Furthermore, rapamycin reduced the expression of mTOR, whereas the promotion of LC3-II/LC3-I was blocked by the GSK3β inhibitor TWS119. Taken together, these results indicate that rapamycin enhances the chondrogenesis of SMSCs by inducing autophagy, and GSK3β may be an important regulator in the process of rapamycin-induced autophagy. Thus, inducing autophagy may be a useful approach in the chondrogenic differentiation of SMSCs in the inflammatory microenvironment and may represent a novel TMD treatment.

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Expression of Interleukin-1 and temporomandibular disorder: Contemporary review of the literature

Abstract: Articles that compared IL-1 concentrations in TMD vs. control groups found significant differences.

Cited by 19 publications

References 17 publications

Biomarkers for Temporomandibular Disorders: Current Status and Future Directions

Biomarkers for Temporomandibular Disorders: Current Status and Future Directions

Inflammatory mediators related to arthrogenic temporomandibular dysfunctions

Rapamycin-Induced Autophagy Promotes the Chondrogenic Differentiation of Synovium-Derived Mesenchymal Stem Cells in the Temporomandibular Joint in Response to IL-1β

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