Expression of IL-12 during periodontitis may play an important role in the control of the inflammatory response via the induction of immunosuppressive molecules by hPDL cells. We hypothesize that this immunomodulatory property of IL-12 will serve as a protective mechanism to preserve a population of stem cells under inflammatory conditions.
Interleukin 12 (IL-12) is an inflammatory cytokine that promotes the response of the immune system. This cytokine has been implicated as a potent stimulator of several diseases characterized by inflammatory-induced bone destruction, such as rheumatoid arthritis and periodontitis. Yet, the exact role of IL-12 in the development and progress of periodontitis has not been clarified. Several studies have demonstrated a positive correlation between the level of IL-12 and the severity of periodontal destruction. Deletion of IL-12 in mice with periodontitis significantly suppressed the level of bone destruction. Interestingly, next to a role in modulating the pathogenesis, IL-12 also has immunological-regulatory properties. This cytokine induces expression of immunosuppressive molecules, such as indoleamine-pyrrole 2,3-dioxygenase (IDO). Thus, these findings suggest both negative and positive influences of IL-12 in periodontal disease. It is currently proposed that the diversity of action of cytokines is a molecular key which regulates biological development and homeostasis. Accordingly, the actions of IL-12 might be one of the mechanisms that regulate homeostasis of periodontal tissue during and following inflammation. Therefore, this article aims to review both destructive and protective functionalities of IL-12 with an emphasis on periodontal disease.
Expression of RANKL by hPDL cells significantly increased after IL-12 treatment. Therefore, this study supports a close interrelationship between immune and skeletal systems and suggests an osteolytic role of IL-12 in pathogenesis of periodontal disease.
Background:Chlorhexidine (CHX) is an antiseptic mouthwash widely used as the gold standard for inhibiting plaque formation. However, the bitter taste of CHX limits patient compliance. We developed a 0.12% CHX and 1.5% hydrogen peroxide (H2O2) mouthwash that masked the bitter taste of CHX. This study evaluated the antibacterial activity and subject satisfaction of the developed mouthwash.Materials and Methods:Three mouthwashes were used as follows: (1) a commercial 0.12% CHX mouthwash, (2) a prepared 0.12% CHX mouthwash containing 1.5% H2O2, and (3) a prepared 0.12% CHX mouthwash. A disc diffusion assay was performed to determine the antibacterial activity of each mouthwash against Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans. To assess subject satisfaction with each mouthwash, a satisfaction questionnaire was completed immediately after rinsing with each mouthwash.Results:The antibacterial activities of the three mouthwashes were similar. Moreover, the questionnaire results revealed that the level of satisfaction was significantly higher for the 0.12% CHX/1.5% H2O2 mouthwash compared with the other mouthwashes.Conclusion:The 0.12% CHX/1.5% H2O2 mouthwash revealed a similar antibacterial activity as the CHX standard against periodontal disease pathogens. In addition, the subjects were more satisfied with the new formula compared with 0.12% CHX alone. These data suggest that the 0.12% CHX/1.5% H2O2 formulation is an alternative antibacterial mouthwash to avoid the unpleasant CHX side effects.
Periodontal disease is the most prevalent oral disease. The pathogenesis of this disease is mostly due to the robust host immune response, leading to the destruction of tooth-supporting tissue. Several cytokines have been shown to play roles in pathogenesis of periodontal disease; however, infl ammatory cytokines can also activate the immunomodulatory properties of mesenchymal stem cells (MSCs), the mechanism to protect and maintain cell survival under infl ammatory environment. Therefore, infl ammation can exert both negative and positive effects for regulating tissue homeostasis. Interleukin 12 (IL-12) is one of the potent destructive stimulators in pathogenesis of many infl ammatory diseases. In periodontitis, the increased level of IL-12 in serum and gingival crevicular fl uid was found associated with the severity of the periodontal disease. However, the exact role of IL-12 in periodontitis is still unclear. The aim of this study was to investigate the responses of human periodontal ligament (PDL) cells to exogenous IL-12, especially on the immunomodulatory effects of IL-12. The results demonstrated the presence of IL-12 and IL-12 receptor (IL-12R) in periodontal tissues, and the expression was enhanced in tissues from periodontitis patients. Exogenous IL-12 stimulated the expression of some infl ammatory cytokines as well as the immunomodulatory molecules, such as interferon gamma (IFNγ), human leukocyte antigen (HLA), and indoleamine-pyrrole-2,3-dioxygenase (IDO) enzyme. In conclusion, the data suggested the infl uence of increased IL-12, during periodontal infl ammation, on controlling tissue's homeostasis by upregulating the infl ammatory cytokines and modulating the function of immune cells through the expression of immunosuppressive molecules.
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