RESUMEN
OBJECTIVE: The oral cavity undergoes frequent stress caused by repeated mechanical trauma, and the constant contact of the injured oral mucosa with bacteria leads to the production of various pro-inflammatory cytokines and chemokines. Neutrophils play essential roles in the acute inflammation against the invasive microbiota, and compromised neutrophil recruitment hinders the bacterial clearance and worsens periodontitis. In this study, we aimed to explore whether wounding at the oral cavity would have an impact on the neutrophil lineage, and, if so, whether microbial contamination of the wounded surface plays significant roles. METHODS: We developed a surgical model of an oral wound (palate wound), by a small incision in the hard palate of the mice. We also evaluated the effect of chlorhexidine on oral wound-induced neutrophilia of bone-marrow. RESULTS: We demonstrated an increased neutrophilia in the bone-marrow of the oral wound group, as well as decreasedex vivoneutropoietic potential, in both IL-3 and GM-CSF-driven bone-marrow cultures. Washing of the entire oral cavity with chlorhexidine before surgery abolished the bone-marrow neutrophilia in the oral wound group and increased neutropoiesis in culture, relative to the saline-treated oral wound control group. Co-located treatment (both chlorhexidine treatment and wound on the right side of the palate) resulted in significantly reduced bone-marrow neutrophilia, compared to the mismatched treatment (chlorhexidine treatment and wound on opposite sides of the palate). Neither neutrophilia nor decreased neutropoiesis were dependent on glucocorticoid signaling. CONCLUSIONS: The prophylactic use of chlorhexidine ameliorates the neutrophilic response on the bone marrow, restoring the neutrophil numbers.