ArticleScientific reports2023
Associations of tissue damage induced inflammatory plasticity in masseter muscle with the resolution of chronic myalgia.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Lymphotoxin-beta receptor controls the development of chronic pain.Cell reports · 2026Article
- Masticatory myalgia to headache-like secondary hypersensitivity induces gene plasticity at dura mater.The journal of headache and pain · 2026Article
- Features of Gene Regulation in Violation of the Inflammatory Response of Monocyte-like Cells Bearing Mitochondrial Mutations Associated with Atherosclerosis.Current medicinal chemistry · 2025Article
- Causal relationships between immunophenotypes, plasma metabolites, and temporomandibular disorders based on Mendelian randomization.Scientific reports · 2024Article
- Degenerative and regenerative peripheral processes are associated with persistent painful chemotherapy-induced neuropathies in males and females.Scientific reports · 2024Article
- Editorial: Mechanisms of orofacial pain.Frontiers in pain research (Lausanne, Switzerland) · 2024Article
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8 authors at 1 institution in 1 country.
Funding
Abstract
Gene plasticity during myogenous temporomandibular disorder (TMDM) development is largely unknown. TMDM could be modeled by intramuscular inflammation or tissue damage. To model inflammation induced TMDM we injected complete Freund's adjuvant (CFA) into masseter muscle (MM). To model tissue damage induced TMDM we injected extracellular matrix degrading collagenase type 2 (Col). CFA and Col produced distinct myalgia development trajectories. We performed bulk RNA-seq of MM to generate gene plasticity time course. CFA initiated TMDM (1d post-injection) was mainly linked to chemo-tacticity of monocytes and neutrophils. At CFA-induced hypersensitivity post-resolution (5d post-injection), tissue repair processes were pronounced, while inflammation was absent. Col (0.2U) produced acute hypersensitivity linked to tissue repair without inflammatory processes. Col (10U) generated prolonged hypersensitivity with inflammatory processes dominating initiation phase (1d). Pre-resolution phase (6d) was accompanied with acceleration of expressions for tissue repair and pro-inflammatory genes. Flow cytometry showed that immune processes in MM was associated with accumulations of macrophages, natural killer, dendritic and T-cells, further confirming our RNA-seq findings. Altogether, CFA and Col treatments induced different immune processes in MM. Importantly, TMDM resolution was preceded with muscle cell and extracellular matrix repairs, an elevation in immune system gene expressions and distinct immune cell accumulations in MM.
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