The purpose of this study was to assess the serum antibody levels to periodontal bacteria in patients with periodontal disease, and to explore the diagnostic uses of the serum antibody assessment and its potential as a therapeutic guide. One hundred twenty-nine patients were clinically examined for the type and extent of periodontal destruction and serum IgG antibody levels to Actinobacillus actinomycetemcomitans (Aa), Actinomyces israelii (Ai), A. viscosus (Av), Bacteroides asaccharolyticus (Ba), B. corporis (Bc), B. denticola (Bd), B. gingivalis (Bg), B. intermedius (Bi), B. loescheii (BI), Capnocytophaga gingivalis (Cg), C. ochracea (Co), and Fusobacterium nucleatum (Fn). Clinical and serological data were subjected to correlation analyses. A small group of patients was monitored during the progress of periodontal treatments. The IgG antibody levels were assessed with an enzyme-linked immunosorbent assay (ELISA). Significantly elevated IgG antibody levels were manifested to Aa, Ai, Bg, and Fn in all forms of periodontal disease, additionally to Cg and Co in juvenile periodontitis, and to Bi in adult periodontitis. There were some correlations between a few clinical parameters and the antibody levels. Successful periodontal treatment significantly decreased the antibody levels to all of the micro-organisms; however, during periodontal treatment, there were no marked differences between pre- and post-treatment levels. The antibody reactivities to the periodontopathic micro-organisms may be of diagnostic and predictive value in patients.

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Tumorigenesis is a complex process involving genetic, epigenetic, and metabolic alterations. Gestational arsenic exposure has been shown to increase hepatic tumors in adult male offspring of C3H mice, which spontaneously develop hepatic tumors often harboring activating Ha-ras mutation. We explored tumor-promoting changes by gestational arsenic exposure with a focus on Ha-ras mutation and gene expression changes. The results of this study demonstrated that gestational arsenic exposure particularly increased hepatic tumors with a C61A Ha-ras mutation. Real-time PCR analyses on the adult normal livers showed that two genes (Creld2, Slc25a30), whose expression are induced by endoplasmic reticulum stress and cellular oxidative stress, respectively, were significantly upregulated and two genes (Fabp4, Ell3), whose products are involved in lipid efflux and apoptosis, respectively, were significantly downregulated more than twofold by gestational arsenic exposure compared with control mice. The expression changes in the four genes were shown to be late-onset events and to some extent to be associated with corresponding histone modifications, and not with DNA methylation changes. The gene expression changes suggested alterations in lipid metabolism and associated oxidative stress augmentation. Consistently, expression of an oxidative-stress-inducible gene heme oxygenase-1 (HO-1) was upregulated in the livers of the arsenic group. We also found increased expression of retrotransposon L1 mRNA in the tumor-bearing livers of the arsenic group in comparison with control mice. These results suggested that gestational arsenic exposure induces tumor-augmenting changes, including oxidative stress and L1 activation, in a late-onset manner, which would particularly promote tumorigenic expansion of cells with a C61A Ha-ras mutation.

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