**5. Neutrophil interactions with symbiotic oral bacteria**

In periodontal health, the interaction between symbiotic microbial community and neutrophils is strongly controlled to prevent tissue damage. This interaction has been evaluated in studies with germ‐free mice and specific pathogen‐free mice. Results of these studies showed that oral sym‐ biotic commensal microbiota has no impact on the structure of gingival tissue of germ‐free mice, while gut commensal microbiota is fundamental on the structural formation of the intestinal tissue [29]. Periodontal tissue recruits neutrophils by means of the chemotactic receptor CXCR2. This receptor has two ligands CXCL1 and CXCL2. Both ligands are expressed in the junctional epithelium of germ‐free and specific pathogen‐free mice, but there is a significant increase on CXCL2 in the epithelium of specific pathogen‐free mice. Therefore, oral bacterial community induces an increase in neutrophil recruitment via CXCL2 [29]. Neutrophils play a key role in preserving oral health, since low neutrophil counts as well as deficiency in neutrophil functional responses have been associated with periodontal disease. As mentioned before, neutrophils kill pathogens by phagocytosis, degranulation, or NETs formation (**Figure 1C**). Neutrophils are very efficient phagocytic cells and have a very efficient antimicrobial mechanism to do so, the respira‐ tory burst response. In this response, high consumption of oxygen results in the production of reactive oxygen species (ROS), through the activation of the NADPH oxidase complex (**Figure 3**) [5]. Patients with chronic granulomatous disease, a rare genetic disorder that consist on muta‐ tions in the NADPH oxidase, are inefficient in mounting a respiratory burst response. As a con‐ sequence, these patients present early in life recurrent infections [30]. These patients present higher bacteria colonization and gingivitis; however, they do not present periodontitis [31].
