Enterococcus faecalis is the main pathogen causing refractory apical periodontitis (RAP). This bacterium can tolerate harsh environments and trigger periapical immune inflammatory responses that result in persistent infection inside and outside the root canal. Adhesion to the dentin wall of root canals and the subsequent formation of biofilms significantly enhances the drug resistance and anti-erosion ability of Enterococcus faecalis, which is the key factor mediating its pathogenesis. The adhesion of Enterococcus faecalis to dentin involves non-specific adhesion and specific adhesion, and the latter is mediated by adhesion-related virulence factors, mainly including the adhesin of collagen from enterococci (Ace), extracellular surface protein (Esp), gelatinase (GelE), serine protease (SprE), endocarditis and biofilm associated pilus (Ebp) and aggregation substance (AS), which is regulated by multiple two-component systems. The two-component system Fsr can promote the expression of gelE and sprE when the cell population density increases. GelE can further reduce Ace, while the two-component system GrvRS directly downregulates ace expression in response to the serum environment. The two-component systems CroRS and WalRK may also promote and inhibit the expression of various virulence factors, including ace and gelE, thus affecting the adhesion of Enterococcus faecalis. In addition, the mechanochemical preparation and the internal environment of the root canal can also influence the adhesion of Enterococcus faecalis to dentin. Avoiding the introduction of Enterococcus faecalis and using adhesion-interfering medications during root canal treatment can effectively prevent the adhesion of Enterococcus faecalis, and a variety of activated irrigation protocols can also be effective at increasing the clearance of Enterococcus faecalis from the root canal. The design of rational drugs targeting key factors involved in and regulators of the adhesion of Enterococcus faecalis to dentin is expected to provide new ideas and strategies for root canal infection control. The present paper reviews the adhesion of Enterococcus faecalis to dentin and its influencing factors.

Oral bacteria directly affect the disease status of dental caries and periodontal diseases. The dynamic oral microbiota cooperates with the host to reflect the information and status of immunity and metabolism through two-way communication along the oral cavity and the systemic organs. The oral cavity is one of the most important interaction windows between the human body and the environment. The microenvironment at different sites in the oral cavity has different microbial compositions and is regulated by complex signaling, hosts, and external environmental factors. These processes may affect or reflect human health because certain health states seem to be related to the composition of oral bacteria, and the destruction of the microbial community is related to systemic diseases. In this review, we discussed emerging and exciting evidence of complex and important connections between the oral microbes and multiple human systemic diseases, and the possible contribution of the oral microorganisms to systemic diseases. This review aims to enhance the interest to oral microbes on the whole human body, and also improve clinician’s understanding of the role of oral microbes in systemic diseases. Microbial research in dentistry potentially enhances our knowledge of the pathogenic mechanisms of oral diseases, and at the same time, continuous advances in this frontier field may lead to a tangible impact on human health.