Molecular factors associated with compartmentalization of gingival immune responses and transepithelial neutrophil migration.

PMN migration into the gingival sulcus is a tightly regulated process aimed at selectively increasing leukocyte availability at the site of bacterial plaque aggression, i.e. the superficial portion of the junctional epithelium. The evidence reviewed in this paper indicates that, besides the action of complement fragments, arachidonic acid metabolites, formyl peptides and other bacterial products, the establishment of a gradient of ICAM-1 expression across the junctional epithelium and the expression of IL-8 in its superficial layers probably represent important regulatory mechanisms leading to PMN migration into the gingival sulcus. Such mechanisms can be regulated by the autocrine and paracrine action of some pro-inflammatory cytokines and could, possibly be initiated by specific bacteria-keratinocyte interactions. The advantage of such a redundant regulatory mechanism leading to PMN transepithelial migration is probably related to the key role of the neutrophil in the maintenance of a local host-parasite equilibrium on one side, and on the tissue injury associated with PMN persistence or random migration within periodontal tissues on the other. Several investigations are in progress aimed at identifying the initial environmental stimuli leading to PMN recruitment into the gingival sulcus and at further exploring the important regulatory events.