作者: Omar Valero-Monroy , Gabriel Garcia-Cervantes , Luis F. Marquez-Corrales , Ana G. Leija-Montoya , Jorge Sandoval-Basilio
DOI: 10.1016/J.MEHY.2016.08.010
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摘要: Periodontal disease can be initiated by a shift from symbiotic to dysbiotic microbial community. An increase in the recruitment of leukocytes and production inflammatory cytokines, chemokines oxidative stress are generated this shift. In periodontitis, an exacerbated, poorly specific effective response is mounted. Moreover, failure inflammation resolving mechanism leads establishment chronic process, resulting progressive destruction bone soft tissue. different diseases presenting some important players immune defectives. Thus, immunosuppressive environment could induced during inflammation. Myeloid derived suppressor cells (MDSC), heterogenic group immature myeloid with potent suppressive activity, increased several acute diseases. Dysbiosis-mediated induce frequency MDSC. addition, mediators diverse have demonstrated promote expansion, activation MDSC, similar been described periodontal disease. MDSC generation nitric oxide (NO) reactive oxygen species (ROS). Furthermore, differentiate functional osteoclasts. We hypothesize that Review literature evaluating hypothesis possible implications assed work. It encourages study common