Periodontal disease has been recently linked to a variety of systemic conditions such as diabetes, cardiovascular disease, preterm delivery, and oral cancer. The most common bacteria associated with periodontal disease, Porphyromonas gingivalis (P. gingivalis) has not yet been studied in the malignant gingival tissues. The objective of this study was to investigate the presence of P. gingivalis in specimens from squamous cell carcinoma patients. We have performed immunohistochemical staining to investigate the presence of P. gingivalis and Streptococcus gordonii (S. gordonii), a non invasive oral bacteria, in paraffin embedded samples of gingival squamous cell carcinoma (n=10) and normal gingiva (n=5). Staining for P. gingivalis revealed the presence of the bacteria in normal gingival tissues and gingival carcinoma, with higher levels (more than 33%, P<0.05) detected in the carcinoma samples. The staining intensity was also significantly enhanced in the malignant tissue by 2 folds (P<0.023) compared to specimens stained for the non‐invasive S. gordonii. P. gingivalis is abundantly present in malignant oral epithelium suggesting a potential association of the bacteria with gingival squamous cell carcinoma.

Increasing evidence suggests an association between periodontal disease and adverse pregnancy outcomes. Although infection is considered as a risk factor for preterm delivery, the localization of oral bacteria or their antigens in chorioamnionitis placental tissue has never been demonstrated. This study was devised to test the hypothesis that periodontal pathogens may be present and affect human placenta in cases of chorioamnionitis. Using immunocytochemistry, we have identified the presence of Porphyromonas gingivalis antigens in placental tissues. The antigens were detected in the placental syncytiotrophoblasts, chorionic trophoblasts, decidual cells, and amniotic epithelial cells, as well as the vascular cells. There was a substantial increase in immunostaining intensity of the tissues sectioned from women with chorioamnionitis compared to those experiencing normalterm pregnancy, p < 0.019 (Mann‐Whitney test). These results suggest that P. gingivalis may commonly colonize placental tissue, and that the presence of the organism may contribute to preterm delivery.

Background: Clinical and epidemiological data strongly support a link between smoking and periodontal disease. The mechanism by which smoking contributes to the destruction of periodontal tissue is not clear and cannot be attributed solely to the vasoconstrictive effects of nicotine. Our hypothesis is that nornicotine, a metabolite of nicotine, upregulates the expression of the receptor for the advanced glycation end products (RAGE) in the gingiva of smokers and triggers the proinflammatory effects of AGE by stimulating the secretion of cytokines and reactive oxygen species which directly cause destruction of the periodontal apparatus.Methods: Human gingival cells grown in tissue culture were exposed to 1 µM nornicotine for 72 hours. Following the nornicotine pretreatment, some of the cells were also treated with AGE that was generated with nornicotine for 48 hours and another group was continued on nornicotine only for 48 hours. Control cells that were not exposed to either nornicotine or AGE were also cultured. The cells were harvested and RNA was extracted for reverse transcription‐polymerase chain reaction (RT‐PCR) and RAGE mRNA was amplified.Results: The nornicotine‐treated cells increased their expression of RAGE by approximately 4‐fold (P <0.05, Student t test). These data suggest that nornicotine, a byproduct of cigarette smoke, can induce RAGE expression in gingival tissues. Therefore, our data support the hypothesis that RAGE potentially plays a significant role in the progression of periodontal disease exacerbated by smoking.Conclusion: Nornicotine, AGE, and upregulation of RAGE may be involved in the pathogenesis of periodontal disease associated with smoking. J Periodontol 2005;76:1171‐1174.