Scientific Reports: Associations of tissue damage induced inflammatory plasticity in masseter muscle with the resolution of chronic myalgia (Lai)

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 the 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 the initiation phase (1d). Pre-resolution phase (6d) was accompanied with the acceleration of expressions for tissue repair and pro-inflammatory genes. Flow cytometry showed that immune processes in MM were 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 by muscle cell and extracellular matrix repairs, an elevation in immune system gene expressions, and distinct immune cell accumulations in MM.

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Since 2004, UT Health San Antonio, Greehey Children’s Cancer Research Institute’s (Greehey CCRI) mission has been to advance scientific knowledge relevant to childhood cancer, contribute to understanding its causes, and accelerate the translation of knowledge into novel therapies. Greehey CCRI strives to have a national and global impact on childhood cancer by discovering, developing, and disseminating new scientific knowledge. Our mission consists of three key areas — research, clinical, and education.