The oral mucosa: A barrier site participating in tissue‐specific and systemic immunity

Abstract

In the oral cavity, the immune system is constantly exposed to unique tissue-specific signals, including a rich community of commensal microbes and their metabolites, continuous tissue damage from mastication, and antigens from food and airborne particles. How this unique combination of signals participates in the training of specialized immunity at this site is not well understood, yet imbalance of local responses is linked to tissue-specific disease susceptibilities with the prototypic disease being periodontitis. However, the oral mucosa is also well recognized as a site where systemic inflammatory and autoimmune diseases often manifest, indicating that systemic immune deregulation is reflected in the function of the oral immune system. This commentary will discuss both aspects of compartmentalized and systemic immunity at the oral mucosa.

IL‐22–expressing CD4+AhR+ T lymphocytes are associated with RANKL‐mediated alveolar bone resorption during experimental periodontitis

“…Periodontitis results from polymicrobial synergy and dysbiosis; however, periodontal tissue breakdown is mainly determined by the host's immune response, where the T‐lymphocyte subpopulations play a central role in the alveolar bone resorption that leads to tooth loss . In this context, T‐helper (Th)1 and Th17 lymphocytes have been related more to destructive events of periodontitis, while Th2 and T regulatory (Treg) lymphocytes have been related more to the suppression of the Th1 and Th17 responses, periodontitis remission, and periodontal healing …”

“…[3][4][5] In this context, T-helper (Th)1 and Th17 lymphocytes have been related more to destructive events of periodontitis, while Th2 and T regulatory (Treg) lymphocytes have been related more to the suppression of the Th1 and Th17 responses, periodontitis remission, and periodontal healing. 3,4,[6][7][8][9][10][11][12][13] The newly identified Th22 lymphocyte is a subset of CD4 + T cells with specific properties different from the other Th lineages. Indeed, Th22 lymphocytes specifically produce interleukin (IL)-22, but not IL-1β and interferon (IFN)γ or IL-17 and receptor activator of nuclear factor-κB ligand (RANKL) which are predominantly produced by Th1 or Th17 lymphocytes, respectively.…”

“…During periodontal infection, naïve CD4 + T lymphocytes can differentiate into one of distinct subsets, including Th1, Th2, Th17, and Treg, which express specific transcription factor master switch genes and produce particular patterns of cytokines to promote their function. In this context, Th1 and Th17 lymphocytes have been associated with the onset and progression of periodontitis, while Th2 and Treg lymphocytes have been associated with suppression of the Th1 and Th17 responses and disease remission and healing 3,4,[6][7][8][9][10][11][12][13]. In 2009, a new subtype of CD4 + T lymphocyte was discovered and termed Th22.…”

Prevention of infective endocarditis and bacterial resistance to antibiotics: A brief review

“…Additionally, another aspect to be considered is the oral biofilm, which includes several bacterial species and has a structure that depends on the patient's age, dentition type, and systemic medical condition(s) . Furthermore, the biofilm's morphological structure varies from case to case, but a unique pattern for active dental infections has not been identified …”

“…Additionally, another aspect to be considered is the oral biofilm, which includes several bacterial species and has a structure that depends on the patient's age, dentition type, and systemic medical condition(s). [23][24][25] Furthermore, the biofilm's morphological structure varies from case to case, but a unique pattern for active dental infections has not been identified. 24,26 Also, an important point to consider for clinicians is that the time frame (or incubation period) between bacteremia and the onset of IE symptoms is usually 7-14 days; 84% of the cases occur during this period.…”