Epigenetic mechanisms and implications in tendon inflammation (Review)

Cellular inflammation is not just an immediate response following pathogenic infections or resulting from damage due to injury, it is also associated with normal physiological functions, including wound healing and tissue repair. The existence of such a definitive role in normal physiology and in disease pathology indicates the presence of a regulatory mechanism that is tightly controlled in normal cells. A tight control over gene expression is associated with regulatory mechanisms in the cells, which can be either inducible or epigenetic. Among other intracellular mechanisms that contribute to epigenetic gene regulation, DNA methylation has been shown to maintain a tight control over gene expression through the actions of DNA methyltransferases (DNMTs). With a clear role in developmental and tissue-specific temporal gene regulation, the involvement of DNMTs is evident in normal and pathological conditions. In this review article, inflammation in tendons associated with disease pathology and tissue repair or regeneration at the musculoskeletal joints is critically reviewed. More specifically, the review focuses on known epigenetic mechanisms and their role in the clinical presentation of the disease in human joint disorders associated with tendon inflammation, with an emphasis on the gene regulatory mechanisms that are controlled through DNA methylation, histone deacetylation, and microRNAs.