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Background: The purpose of this study was to compare the prevalence and level of Porphyromonas gingivalis (P. gingivalis) and Tannerella forsythensis (T. forsythensis) in subgingival plaque samples from both healthy individuals and periodontal patients in different age groups. Methods: A total of 498 subgingival plaque samples were studied. These samples were collected from 407 individuals diagnosed with periodontal disease (210 adult periodontitis [AP], 78 rapidly progressive periodontitis [RPP], and 119 refractory periodontitis [Ref-P] cases) and 91 healthy (H) subjects. P. gingivalis and T. forsythensis were detected by indirect immunofluorescent assay using species-specific polyclonal antisera to P. gingivalis strain (FDC 381) and T. forsythensis strain (FDC 335). The prevalence of P. gingivalis and T. forsythensis was compared by chi-square analysis. Differences in P. gingivalis and T. forsythensis levels among various periodontal status and age groups was determined by one-way analysis of variance and Fisher's multiple comparison tests. The association between the presence of P. gingivalis or T. forsythensis in different periodontal status and age groups was measured using odds ratios. Results: P. gingivalis was found in 85.7% (P <0.0001) and T. forsythensis in 60.7% (P = 0.0002) of diseased subjects compared to 23.1% and 39.6%, respectively, in healthy subjects. P. gingivitis, but not T. forsythensis, was detected more frequently in any diseased group than in the H group in every age group (P <0.0001). No significant difference was found in the prevalence of P. gingivalis and T. forsythensis among age groups, except T. forsythensis was more prevalent in the age group of 40 to 59 years than in the age group <20 years (χ² = 3.93, P= 0.047) in the H group. The mean level of P. gingivalis and T. forsythensis was significantly higher in diseased groups than in the H group (P <0.0001). The odds ratio for P. gingivalis in the AP group (25.0) was greater than any other group for P. gingivalis or T. forsythensis compared to the H group. Conclusions: These data suggested that P. gingivalis is closely associated with the pathogenesis of periodontitis and that it may not be a normal inhabitant of periodontally healthy subjects. T. forsythensis is also important in the pathogenesis of periodontal disease; however, whether it causes periodontal disease or is a secondary invader of periodontal lesions remains to be determined. [ABSTRACT FROM AUTHOR]

Areca quid chewing has been linked to oral submucous fibrosis and oral cancer. Arecoline, a major areca nut alkaloid, is considered to be the most important etiologic factor in the areca nut. In order to elucidate the pathobiological effects of arecoline, cytotoxicity assays, cellular glutathione S-transferase (GST) activity and lipid peroxidation assay were employed to investigate cultured human buccal mucosal fibroblasts. To date. there is a large proportion of areca quid chewers who are also smokers. Furthermore, nicotine, the major product of cigarette smoking, was added to test how it modulated the cytotoxicity of arecoline. At a concentration higher than 50 μg/mI, arecoline was shown to be cytotoxic to human buccal fibroblasts in a dose-dependent manner by the alamar blue dye colorimetric assay (P<0.05). In addition, arecoline significantly decreased GST activity in a dose-dependent manner (P<0.05). At concentrations of 100 7mu;g/mI and 400 μg/mI, arecoline reduced GST activity about 21% and 46%. respectively, during a 24 h incubation period. However, arecoline at any test dose did not increase lipid peroxidation in the present human buccal fibroblast test system. The addition of extracellular nicotine acted synergistically on the arecoline-induced cytotoxicity. Arecoline at a concentration of 50 μg/mI caused about 30% of cell death over the 24 h incubation period. However. 2.5 mM nicotine enhanced the cytotoxic response and caused about 50% of cell death on 50 μg/mI arecoline-induced cytotoxicity- Taken together. arecoline may render human buccal mucosal fibroblasts more vulnerable to other reactive agents in cigarettes via GST reduction. The compounds of tobacco products may act synergistically in the pathogenesis of oral mucosal lesions in areca quid chewers. The data presented here may partly explain why patients who combined the habits of areca quid chewing and cigarette smoking are at greater risk of contracting oral cancer. [ABSTRACT FROM AUTHOR]

Background, aims: The habit of betel nut chewing impinges on the daily lives of approximately 200 million people. Betel quid chewers have a higher prevalence of periodontal diseases than non-chewers. This study examined the pathobiological effects of arecoline, a major component of the betel nut alkaloids, on human peri-odontal ligament fibroblasts (PDLF) in vitro. Method: Cell viability, proliferation, protein synthesis, and cellular thiol levels were used to investigate the effects of human PDLF exposed to arecoline levels of 0 to 200mg/ml. In addition, nicotine was added to test how it modulated the effects of arecoline. Results: Arecoline significantly inhibited cell proliferation in a dose-dependent manner. At concentrations of 10 and 30 mg/ml, arecoline suppressed the growth of PDLF by 20% and 50% (p,0.05), respectively. Arecoline also decreased pro-tein synthesis in a dose-dependent manner during a 24-h culture period. A 100 mg/ ml concentration level of arecoline significantly inhibited protein synthesis to only 50% of that in the untreated control (p,0.05). Moreover, arecoline significantly depleted intracellular thiols in a dose-dependent manner. At concentrations of 25 mg/ml and 100 mg/ml, arecoline depleted about 18% and 56% of thiols (p,0.05), respectively. This suggests that arecoline itself might augment the destruction of periodontium associated with betel nut use. Furthermore, the addition of nicotine acted with a synergistic effect on the arecoline-induced cytotoxicity. At a concen-tration of 60 mg/ml, arecoline suppressed the growth of PDLF by about 33%, and 5 mM nicotine enhanced the arecoline-induced cytotoxic response to cause about 66% cell death. Conclusion: During thiol depletion, arecoline may render human PDLF more vulnerable to reactive agents within cigarettes. Taken together, people who combine habits of betel nut chewing with cigarette smoking could be more susceptible to periodontium damage than betel nut... [ABSTRACT FROM AUTHOR]

Betel quid chewing has been linked to oral submucous fibrosis and oral cancer. Cytotoxicity and genotoxicity assays were used to investigate the pathobiological effects of arecoline on cultured human buccal fibroblasts. Arecoline increased double-stranded polynucleic acid at the concentration of 0.1 to 10 μg/ml in a concentration-dependent manner. At a concentration higher than 50 μg/ml, arecoline was cytotoxic to cultured fibroblasts and the cytotoxicity was dose-dependent. No genotoxicity for arecoline was found even at a concentration of 400 μg/ml. On the other hand, 600 μg/ml glutathione (GSH) and 200 μg/ml glycyrrhizin could prevent the arecoline-induced cytotoxicity. These results indicate that arecoline is a cytotoxic agent and no genotoxicity was found to human buccal fibroblasts. Furthermore, increasing consumption of GSH-and glycyrrhizin-rich foods may reduce the oral diseases associated with betel quid chewing. [ABSTRACT FROM AUTHOR]