THE ROLE OF OXIDATIVE STRESS, INFLAMMATION AND GLIAL CELL IN PATHOPHYSIOLOGY OF MYOFASCIAL PAIN

Purpose: The aim of this article is to explain the role of oxidative stress, inflammatory responses, and glial cell in the pathophysiolo-gy of myofascial pain. Therefore the management of myofascial pain can be optimally done by clinicians through blockage of each biomarker in a specific pathway. Views: Myofascial pain is often one of the reasons for patients to visit the doctor with a prevalence of approximately 21-30%. Overused muscle can lead to myofascial trigger points. Activities that cause ongoing muscle contraction can cause an increase in metabolic stress and decreased blood flow resulting in the imbalance of oxidative-antioxidant. Malondialdehyde is one of the biomarkers of oxidative stress. This process also can increase the release of neuropeptides, cytokines, and inflammatory substances. Prostaglandins, especially prostaglandin E2 (PGE2), can increase vascular permeability and cell proliferation that binds to sensory neuron receptors, which facilitate sensitization to the pain nerve. Astrocytes are the most abundant cell type in the central nervous system, which plays an essential role in the induction and persistence of pain. In ischemic conditions, astrocytes will alternate and turn into reactive astrogliosis. This condition will increase the level of glial fibrillary acidic protein. Conclusions: The exact pathophysiology of myofascial pain is not thoroughly clear. Hence, some studies found the total levels of oxidative stress were higher in patients with myofascial pain. Malondialdehyde, PGE2, and GFAP as the biomarkers from those factors are increased in patients with myofascial pain.