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Oxidative stress in the local and systemic events of apical periodontitis

dc.contributor.authorHernández-Ríos P.
dc.contributor.authorPussinen P.J.
dc.contributor.authorVernal R.
dc.contributor.authorHernández M.
dc.date.accessioned2020-09-02T22:20:26Z
dc.date.available2020-09-02T22:20:26Z
dc.date.issued2017
dc.identifier10.3389/fphys.2017.00869
dc.identifier.citation8, NOV, -
dc.identifier.issn1664042X
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4870
dc.descriptionOxidative stress is involved in the pathogenesis of a variety of inflammatory disorders. Apical periodontitis (AP) usually results in the formation of an osteolytic apical lesion (AL) caused by the immune response to endodontic infection. Reactive oxygen species (ROS) produced by phagocytic cells in response to bacterial challenge represent an important host defense mechanism, but disturbed redox balance results in tissue injury. This mini review focuses on the role of oxidative stress in the local and associated systemic events in chronic apical periodontitis. During endodontic infection, ligation of Toll-like receptors (TLRs) on phagocytes' surface triggers activation, phagocytosis, synthesis of ROS, activation of humoral and cellular responses, and production of inflammatory mediators, such as, cytokines and matrix metalloproteinases (MMPs). The increment in ROS perturbs the normal redox balance and shifts cells into a state of oxidative stress. ROS induce molecular damage and disturbed redox signaling, that result in the loss of bone homeostasis, increased pro-inflammatory mediators, and MMP overexpression and activation, leading to apical tissue breakdown. On the other hand, oxidative stress has been strongly involved in the pathogenesis of atherosclerosis, where a chronic inflammatory process develops in the arterial wall. Chronic AP is associated with an increased risk of cardiovascular diseases (CVD) and especially atherogenesis. The potential mechanisms linking these diseases are also discussed. © 2017 Hernández-Ríos, Pussinen, Vernal and Hernández.
dc.language.isoen
dc.publisherFrontiers Media S.A.
dc.subjectApical lesion
dc.subjectApical periodontitis
dc.subjectAtherosclerosis
dc.subjectOxidative stress
dc.subjectROS
dc.subjectgelatinase A
dc.subjectgelatinase B
dc.subjectimmunoglobulin G antibody
dc.subjectimmunoglobulin M antibody
dc.subjectmatrix metalloproteinase
dc.subjectosteoclast differentiation factor
dc.subjectoxidized low density lipoprotein
dc.subjecttoll like receptor
dc.subjectAggregatibacter actinomycetemcomitans
dc.subjectapical periodontitis
dc.subjectatherogenesis
dc.subjectcardiovascular disease
dc.subjectchronic inflammation
dc.subjectcoronary artery disease
dc.subjectcytokine production
dc.subjectcytokine release
dc.subjectendothelial dysfunction
dc.subjecthuman
dc.subjectmouth infection
dc.subjectnonhuman
dc.subjectosteoclastogenesis
dc.subjectoxidative stress
dc.subjectperiodontal ligament
dc.subjectperiodontitis
dc.subjectphagocytosis
dc.subjectPorphyromonas endodontalis
dc.subjectPorphyromonas gingivalis
dc.subjectShort Survey
dc.subjectvitamin D deficiency
dc.titleOxidative stress in the local and systemic events of apical periodontitis
dc.typeShort Survey


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