Antimicrobial peptides represent an important aspect of the innate defense system that contributes to the control of bacterial colonization and infection. As studies have progressed it has become clear that antimicrobial peptides manifest other functions in addition to their antimicrobial effects. These functions include chemotaxis of numerous types of host cells involved in both the innate and adaptive response. In this review the antimicrobial activity, regulation, and the contribution to host homeostasis of α-defensins and LL-37 as well as β-defensins are discussed in context of their specific tissue locations in the junctional and oral epithelium respectively.

The oral microbial community is the best-characterized bacterial ecosystem in the human host. It has been shown in the mouse that oral commensal bacteria significantly contribute to clinically healthy periodontal homeostasis by influencing the number of neutrophils that migrate from the vasculature to the junctional epithelium. Furthermore, in clinically healthy tissue, the neutrophil response to oral commensal bacteria is associated with the select expression of the neutrophil chemokine CXCL2 but not CXCL1. This preliminary study examined the contribution of commensal bacteria on neutrophil location across the tooth/gingival interface. Tissue sections from the root associated mesial (anterior) of the second molar to the root associated distal (posterior) of the second molar were examined for neutrophils and the expression of the neutrophil chemokine ligands CXCL1 and CXCL2. It was found that both the number of neutrophils as well as the expression of CXCL2 but not CXCL1 was significantly increased in tissue sections close to the interdental region, consistent with the notion of select tissue expression patterns for neutrophil chemokine expression and subsequent neutrophil location. Furthermore, mice gavaged with either oral Streptococcus or Lactobacillus sp. bacteria induced a location pattern of neutrophils and CXCL2 expression similar to the normal oral flora. These data indicate for the first time select neutrophil location and chemokine expression patterns associated with clinically healthy tissue. The results reveal an increased inflammatory load upon approaching the interproximal region, which is consistent with the observation that the interproximal region often reveals early clinical signs of periodontal disease.

Background Oral gingival tissue, especially the junctional epithelium (JE), is constantly exposed to sub‐gingival plaque. A key component of gingival health is the regulation of the number of neutrophils that migrate into the gingival crevice to counteract its harmful effects. This report investigates the contribution of innate defense receptors, Toll‐like receptor (TLR)2, TLR4, and both (TLR2/4) to the maintenance of neutrophil homeostasis in the JE. Methods Bacterial composition was analyzed from whole oral swabs collected from 12‐ to 14‐week‐old TLR2, TLR4, TLR2/4 double knock‐out (KO) mice using a MiSeq platform targeting the V3‐V4 region of the 16S ribosomal RNA gene. Mandibles were histologically examined for quantification of neutrophils in the JE and bone loss. Lastly, total bacterial load was quantitated using quantitative real‐time PCR. Results Compared with wild‐type, all TLR KO mice displayed significantly increased recruitment of neutrophils (P = 0.0079) into the JE. In addition, TLR4 and TLR2/4 KO mice demonstrated a significant increase in the number of bacteria (P = 0.0022 and P = 0.0152, respectively). Lastly, comparative compositional analyses of the oral microbiome revealed that each KO strain harbored unique microbial communities that are distinct from each other but maintained similar levels of alveolar bone. Conclusions Neutrophil migration into healthy mouse JE does not require TLR2 or TLR4. However, a significant increase in the number of neutrophils as well as a significant change in the oral microbial composition in both TLR2 and TLR4 KO mice demonstrate that these TLRs contribute to the homeostatic relationship between bacteria and the host in healthy mice periodontal tissue.