Generation of inflammatory stimuli: how bacteria set up inflammatory responses in the gingiva

Abstract

Objectives: The primary aetiologic factor of periodontal disease is the bacterial biofilm. Gram-positive and gram-negative bacteria possess a plethora of structural or secreted components that may cause direct destruction to periodontal tissues or stimulate host cells to activate a wide range of inflammatory responses. These responses are intended to eliminate the microbial challenge, but may often cause further tissue damage.

Methods: This review has been divided into three parts: (a) bacterial virulence factors, which includes basic information on bacterial virulence factors, and the principle inflammatory responses that host cells elicit against these factors, (b) main receptors and signalling pathways, which includes basic information about the main receptors that interact with the bacterial virulence factors, the nature of these interactions, and the activated signalling pathways that lead to inflammatory responses, and (c) initiation of inflammation, which includes a model by which the virulence factors may interact with host cells and lead to inflammatory responses in the gingiva.

Findings and conclusions: Bacterial components/virulence factors may be involved in modulating inflammatory responses and include: lipopolysaccharides (LPS), peptidoglycans, lipotechoic acids, fimbriae, proteases, heat-shock proteins, formyl-methionyl peptides, and toxins. Potential host cell receptors involved in recognizing bacterial components and initiating signalling pathways that lead to inflammatory responses include: Toll-like receptors (TLRs), CD14, nucleotide-binding oligomerization domain proteins (Nod) and G-protein-coupled receptors, including formyl-methionyl peptide receptors and protease-activated receptors. Of the above bacterial and host molecules, evidence from experimental animal studies implicate LPS, fimbriae, proteases, TLRs, and CD14 in periodontal tissue or alveolar bone destruction. However, evidence verifying the involvement of any of the above molecules in periodontal tissue destruction in humans does not exist.