Mechanisms of innate and adaptive immunity work both separately and in concert within the oral cavity, where the oral mucosa serves as the primary barrier to a multitude of environmental and microbial challenges. In the periodontium, the sulcular and junctional epithelium represent an anatomic entry point highly susceptible to microbial translocation from dental biofilm. This barrier is only several cells thick and deteriorates in states of inflammation.
Neutrophil recruitment and homeostasis are essential to maintaining a functional state of innate immune surveillance. In sites of infection or inflammation, peripheral clearance of apoptotic neutrophils is performed by macrophages and dendritic cells, suppressing the release of proinflammatory cytokines interleukin (IL)-23 and IL-17. IL-17 is produced by conventional adaptive T helper 17 (TH17) cells and innate-acting lymphocyte populations, both of which are present in mucosal surfaces.
Physiologic mechanical stimulation, such as the low-level trauma incurred during mastication, influences gingival TH17 cells to aid in the recruitment of neutrophils and production of antimicrobial peptides, thus serving to regulate tissue homeostasis in an IL-17 dependent manner. IL-17 plays a key role in periodontal immunity and has been shown to be required for immunologic defense against oral infections such as candidiasis. Alternatively, TH17 cells can influence osteoblasts to produce the osteoclastogenic cytokine, RANKL, and TH17 cells can even produce RANKL themselves. Excessive TH17 is associated with periodontitis, in which a dysbiotic microbiome triggers the pathogenic TH17/IL-17 response associated with periodontal tissue destruction and bone loss.