The Role of Nrf2 in the Regulation of Periodontitis, Peri-implantitis, Dentin Infection, and Apical Periodontitis

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

The most frequent dental infections happen when bacteria enter the pulp and spread to the tissues. Dental caries arise from the dissolution of enamel and dentin by the acidic metabolites of oral streptococci. Dissolution leads to cavitation, which allows oral germs to enter the bloodstream. If left untreated, cavitation develops into bacterial invasion of the dental pulp. Dental plaque, also called dental biofilm, is associated with periodontitis. When the pulp is exposed, significant inflammation and necrotic foci occur as bacteria infect the tissue. Intravascular bacteria were identified in all instances, which may indicate an essential pathway for transmitting the infection via the pulp tissue. Also, bacteria buildup around a dental implant can result in peri-implantitis (PI), harming the adjacent bone and gums. Reactive oxygen species (ROS) are produced in excess when pathogens incite host immunological responses. Furthermore, osteogenic differentiation and bone formation depend on the regulated generation of ROS. Cells have complex antioxidant systems that carefully control the amount of ROS and prevent its harm. This mechanism activates transcription for multiple genes involved in antioxidant and cytoprotective functions through specific DNA sequences called antioxidant response elements (AREs). Nuclear factor erythroid-2-related factor-2 (Nrf2) is vital in safeguarding c

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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