Oral health is an important aspect of the overall health status of an individual. DNA damage has been associated with oral health and dental factors due to the increased of oxidative stress (OxS). DNA damage can produce a wide range of effects on human health. These effects could appear immediately, but others do not become evident much later. Chronic diseases have been study to understand their mechanisms, clinical implications, and the development of secondary disease such as cancer. Periodontitis is one of the most common oral diseases. It is an inflammatory chronic infectious disease, which is characterized by the loss of supporting tissues and tooth loss caused by periodontopathogens and long-term release of reactive oxygen species (ROS); thus, oxidative stress is increased during periodontitis. Oxidative stress can produce DNA damage, including the oxidation of nucleosides, which could cause DNA strand break. This oxidative damage leads the formation of micronuclei (MN) a marker of nuclear damage. Also, oxidative stress increased 8-hydroxy-2′-deoxyguanosine levels which are the most common stable product of oxidative DNA damage.
Part of the book: Insights into Various Aspects of Oral Health
The term periodontal disease encompasses a wide variety of chronic inflammatory conditions of the periodontium, including gingivitis and periodontitis. The gingival disease is an infectious process, which occurs due to the progression of untreated gingivitis. It is characterized by a destructive inflammatory process that affects the supporting tissues of the teeth, which causes the loss of the dental organs. As a result of inflammation, a wide range of cytokines and inflammatory mediators together contribute to tissue degradation and bone resorption. However, some molecules that have not been studied in the inflammatory process of this disease, such as the macrophage migration inhibitory factor (MIF) which is considered an important cytokine of the innate immune system; it is expressed constitutively in immune and nonimmune cells, and it is released immediately against bacterial stimuli, hypoxia, and proliferative signals. MIF has been described in some chronic degenerative, inflammatory, and autoimmune diseases. Previous studies have described that in murine models of periodontitis, MIF promotes the activation and differentiation of osteoclasts that could position this cytokine in the immunopathogenesis of gingival disease in humans.
Part of the book: Gingival Disease