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Periodontal disease is a chronic inflammatory disease that results in the breakdown of the tooth-supporting tissues, and can ultimately lead to resorption of the alveolar bone. Recently, several studies have shown a close relationship between increased interleukin-18 (IL-18) levels and the pathogenesis of chronic periodontitis, a major cause of tooth loss. However, it has yet to be shown whether chronic periodontitis results from or causes an increase in IL-18 after bacterial infection. In the present study, we investigated how IL-18 overexpression relates to periodontal disease using IL-18 transgenic (Tg) mice. IL-18Tg and wild-type mice were inoculated intraorally with Porphyromonas (P.) gingivalis, which has been implicated in the etiology of chronic periodontitis. Seventy days after P. gingivalis infection, alveolar bone loss and gingival cytokine levels were assessed using histo-morphological analysis and enzyme-linked immuno-absorbent assay, respectively. Periodontal bone loss was evoked in IL-18Tg mice, but not in wild-type mice. Interestingly, levels of bone-resorptive cytokines, including IL-1α, IL-1β, tumor necrosis factor-α, and IL-6, were unchanged in the gingival tissues of IL-18Tg mice infected with P. gingivalis, although levels of interferon γ (a proinflammatory T-helper 1 cytokine) decreased. RT-PCR analysis showed elevated expression of mRNAs for receptor activator of nuclear factor kappa-B ligand (a key stimulator of osteoclast development and activation) and CD40 ligand (a marker of T cell activation) in the gingiva of IL-18Tg mice infected with P. gingivalis. We conclude that increased IL-18 in the gingival tissues evokes chronic periodontitis after bacterial infection, presumably via a T cell-mediated pathway.

To determine the risk of developing symptoms due to the presence of maxillary and mandibular third molars, we analyzed a reliable population sample by age, and according to third-molar position and impaction level using long-term follow-up data under conditions of good oral hygiene. Of 308 graduates from our dental school, a total of 776 third molars were followed up for periods of 11 to 27 years by means of intraoral radiographs. The development of symptoms, the participant's age, and third-molar angular position and degree of impaction were investigated. For both maxillary and mandibular third molars, the risk of developing a symptom correlated neither with angular position nor with impaction level. The first symptom associated with a third molar developed most frequently in their 20's for both maxilla (16.2%) and mandible (17.5%), with the next highest frequency being in their 30's (12.6%, maxilla; 13.0%, mandible). The status of third molars shows no relation to the subsequent development of symptoms if good oral hygiene is maintained. The low rates of symptom-development do not support removal of asymptomatic third molars.