A central role for reactive oxygen species (ROS) in the pathogenesis of temporomandibular joint disorders: All roads lead to ROS
Abstract
Temporomandibular joint disease (TMD) is a musculoskeletal pain disorder occurring at the temporomandibular joint (TMJ), the interface of the skull’s temporal bone and the mandible1. This literature review examines the anatomy, epidemiology, biochemistry and cellular biology of TMD in order to frame underlying biochemical and cellular events within the human context of the disease. This review identifies several key elements pertaining to TMD pathogenesis, including mechanical stress-induced hypoxia-reperfusion, disruption of mitochondrial function, arachidonic acid catabolism (through prostaglandins and leukotrienes), cartilage degradation, bone resorption, and breakdown of joint lubrication. Based on a thorough analysis of established correlations and causations we propose an overarching mechanism that provides a holistic representation of TMD, something noticeably absent in the literature to-date. This mechanism clearly highlights the central role of reactive oxygen species (ROS) in the pathogenesis of TMD, a conclusion holding significant implications for both treatment and our understanding of the disease.
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