Innate immune response to oral bacteria and the immune evasive characteristics of periodontal pathogens.

Periodontitis is a chronic inflammation of periodontal tissue caused by subgingival plaque-associated bacteria. Periodontitis has long been understood to be the result of an excessive host response to plaque bacteria. In addition, periodontal pathogens have been regarded as the causative agents that induce a hyperinflammatory response from the host. In this brief review, host-microbe interaction of nonperiodontopathic versus periodontopathic bacteria with innate immune components encountered in the gingival sulcus will be described. In particular, we will describe the susceptibility of these microbes to antimicrobial peptides (AMPs) and phagocytosis by neutrophils, the induction of tissue-destructive mediators from neutrophils, the induction of AMPs and interleukin (IL)-8 from gingival epithelial cells, and the pattern recognition receptors that mediate the regulation of AMPs and IL-8 in gingival epithelial cells. This review indicates that true periodontal pathogens are poor activators/suppressors of a host immune response, and they evade host defense mechanisms.

Innate immune response to oral bacteria and the immune evasive characteristics of periodontal pathogens

Periodontitis is a chronic inflammation of periodontal tissue caused by subgingival plaque-associated bacteria. Periodontitis has long been understood to be the result of an excessive host response to plaque bacteria. In addition, periodontal pathogens have been regarded as the causative agents that induce a hyperinflammatory response from the host. In this brief review, host-microbe interaction of nonperiodontopathic versus periodontopathic bacteria with innate immune components encountered in the gingival sulcus will be described. In particular, we will describe the susceptibility of these microbes to antimicrobial peptides (AMPs) and phagocytosis by neutrophils, the induction of tissue-destructive mediators from neutrophils, the induction of AMPs and interleukin (IL)-8 from gingival epithelial cells, and the pattern recognition receptors that mediate the regulation of AMPs and IL-8 in gingival epithelial cells. This review indicates that true periodontal pathogens are poor activators/suppressors of a host immune response, and they evade host defense mechanisms.

A Novel Mutation of the Cathepsin C Gene in Papillon-Lefévre Syndrome.

BACKGROUND: Papillon-Lefévre syndrome (PLS) is a disorder that involves destruction of the periodontium and abnormal hyperkeratosis of the palms of the hands and soles of the feet. Mutations of the lysosomal protease cathepsin C gene (CTSC) have been associated with PLS. However, genotypic and phenotypic correlation has not been established. In the present study we investigated the CTSC gene in a Brazilian cohort affected by PLS. METHODS: Eight consanguineous members of a kindred with PLS were studied. DNA was extracted and all exons of the gene amplified by the polymerase chain reaction (PCR) using specific primers. Mutations were identified by DNA sequencing of the coding region and introns of the CTSC gene. RESULTS: Sequence analysis of CTSC from subjects affected by PLS identified a novel mutation (587T → C) in exon 4, predicted to cause a Leu196Pro amino acid substitution. Three of 3 subjects were homozygous for cathepsin C mutations inherited from a common ancestor. One patient was heterozygous and showed plantar hyperkeratosis without periodontal disease. Two other family members were also heterozygous but did not present palmoplantar hyperkeratosis and/or periodontal disease. CONCLUSIONS: This study describes a novel mutation of the cathepsin C gene in a Brazilian kindred with Papillon-Lefévre syndrome. J Periodontol 2002;73:307-312.