• Journal of Periodontal and Implant Science
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• v.43 no.1
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• pp.3-11
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• 2013

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.

• Journal of Periodontal and Implant Science
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• v.25 no.1
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• pp.167-178
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• 1995

It has been believed that the increased release of free oxygen radicals and their tissue damaging potency might be a contributing factor in the pathogenesis of periodontal disease. Antioxidant enzymes such as superoxide dismutase(SOD) and catalase can protect the tissue damage from the free oxygen radicals($O_2^-,H_2O_2$, and $OH^-$). In order to investigate the SOD- and catalase - activity in the blood plasma and red blood cells(RBCs) of the patients with perodontitis, 19 male periodontitis patients($25{\sim}35$ years old) who had good general health, more than 10 teeth with severely inflamed gingiva, attachment loss more than 6mm and bone loss were selected as periodontitis group, and 13 male volunteers($22{\sim}29$ years old) with good general and periodontal health were selected as normal group. After blood plasma and RBC were separated from peripheral blood of 2ml collected from antecubital vein of each subject, SOD- activity in blood plasma and RBCs was measured by the same method that Paoletti et al. did, and catalase - activity in RBC was measured by the same method that Beers et al, did. The difference of SOD- and catalase - activity between the normal and the periodontitis groups was statistically analyzed by Student t-test with SPSS/PC program.The results were as follows : 1. SOD activity in blood plasma was significantly lower in the periodontitis group($1.986{\pm}0.893$) than in the normal group($3.324{\pm}1.044$)(p<0.05). 2. There was no statistical significance in the difference of SOD- activity in RBCs between the periodontitis group($7.753{\pm}3.206$) and the normal group($8.116{\pm}1.192$)(p$242.8{\pm}45.6$) than in the normal group($280.2{\pm}32.6$)(p