Porphyromonas gingivalis infection during pregnancy increases maternal tumor necrosis factor alpha, suppresses maternal interleukin-10, and enhances fetal growth restriction and resorption in mice. (57/333)

Epidemiological studies have shown a potential association between maternal periodontitis and pregnancy complications. We used a pregnant murine model to study the effect of infection with the periodontal pathogen Porphyromonas gingivalis on pregnancy outcomes. Female BALB/c mice were inoculated with heat-killed P. gingivalis (10(9) CFU) in a subcutaneous chamber and mated 2 weeks later. At gestation day (GD) 7.5, mice were challenged with live P. gingivalis (10(7) CFU) (n = 20) or broth (control; n = 8) and sacrificed at GD 16.5. Fetal growth restriction (FGR, <0.46 g) was defined as fetuses with weights 2 standard deviations (SD) smaller than controls (0.56 +/- 0.05 g [mean +/- SD]). Among the 20 challenged mice, 8 had both normal-weight (0.51 +/- 0.11 g) and FGR (0.34 +/- 0.1 g) fetuses within the same litter. All other challenged dams had normal-weight fetuses (0.57 +/- 0.04 g). Maternal liver, uterus, and spleen samples were examined for P. gingivalis DNA using a PCR technique. Of the eight challenged mice with FGR fetuses, three had PCR signals for P. gingivalis in liver and uterus, but not in the spleen. Liver, uterus, and spleen were negative for P. gingivalis DNA among all other challenged and control mice. In serum of dams with FGR fetuses, tumor necrosis factor alpha levels were elevated significantly, while interleukin-10 levels were significantly reduced compared to levels in dams with normal fetuses. P. gingivalis-specific serum immunoglobulin G levels were significantly elevated in dams with FGR fetuses compared to dams without any FGR fetuses. These data demonstrate that P. gingivalis-induced murine FGR is associated with systemic dissemination of the organism and activated maternal immune and inflammatory responses.  (+info)

Porphyromonas gingivalis infection in pregnant mice is associated with placental dissemination, an increase in the placental Th1/Th2 cytokine ratio, and fetal growth restriction. (58/333)

Our previous animal studies showed that maternal Porphyromonas gingivalis infection in a subcutaneous chamber is associated with hepatic and uterine translocation, as well as systemic induction of maternal inflammatory responses, both of which were associated with fetal growth restriction (FGR). However, P. gingivalis-challenged dams had fetuses with either FGR (2 standard deviations below mean weight of nonchallenged dams) or normal weight. Therefore, the objective of this study was to determine whether maternal infection with P. gingivalis compromises normal fetal development via direct placental invasion and induction of fetus-specific placental immune responses characterized by a proinflammatory Th1-type cytokine profile. P. gingivalis-specific DNA was detected in placentas and fetuses of FGR and normal littermates from P. gingivalis-infected dams. Th1- and Th2-type cytokine mRNA as well as tumor necrosis factor alpha and transforming growth factor beta 2 mRNA were examined in placental tissue by using reverse transcription-PCR to determine Th1/Th2 ratios. For eight litters containing both normal-weight and FGR fetuses, P. gingivalis DNA was detected only in the placentas of FGR fetuses. All fetuses and all amniotic fluid samples from infected and control dams were negative for P. gingivalis DNA. mRNA levels of gamma interferon and interleukin-2 (IL-2) were significantly increased in placentas of FGR fetuses, while expression of IL-10 was significantly decreased in the same group. These data indicate that, in P. gingivalis-challenged dams, within each litter there is placenta-specific translocation of P. gingivalis that results in growth restriction of the targeted fetus, which is associated with a shift in the placental Th1/Th2 cytokine balance.  (+info)

Role for periodontitis in the progression of lipid deposition in an animal model. (59/333)

Epidemiologic studies have implicated periodontitis as a risk factor for the development of cardiovascular disease. However, no prospective studies investigating this potential relationship have been carried out. Age- and sex-matched New Zealand White rabbits were maintained on a diet consisting of 0.5% fat for 13 weeks to induce the accumulation of lipid deposits in the aorta as a model for atherogenesis. One-half of the animals received silk ligatures around their mandibular premolars followed by an application of a periodontal pathogen, Porphyromonas gingivalis, to induce periodontitis. Animals were sacrificed after 14 weeks. Periodontal disease severity was quantified radiographically, histologically, and by direct visualization of bone loss on defleshed skulls. Lipid deposition was evaluated by computer-assisted morphometry in the aortas en face after lipid deposits were stained with Sudan IV. Animals with experimentally induced periodontitis had more extensive accumulations of lipids in the aorta than did nonperiodontitis animals (P < 0.05), and there was a positive correlation between the severity of periodontal disease and the extent of lipid deposition (r(2) = 0.9501). The results provide direct evidence that periodontitis may be a risk factor and may contribute to the pathogenesis of atherosclerosis. The data support the concept that infections at remote locations can modulate atherosclerotic events distantly.  (+info)

Gingipains as candidate antigens for Porphyromonas gingivalis vaccine. (60/333)

Porphyromonas gingivalis (P. gingivalis), a gram-negative anaerobe, is involved in the pathogenesis of periodontal disease, and is found frequently in the subgingival flora in patients with periodontitis. This organism possesses a variety of virulence factors including lipopolysaccharide, capsular material, fimbriae and proteases (enzymes). Among the P. gingivalis antigens, enzymes such as Arginine-specific gingipains (RgpA, RgpB) and lysine-specific gingipain (Kgp) have been studied for their ability to induce biologically significant antibodies. This review summarizes recent information on the gingipains and their possible application in the development of an anti-P. gingivalis vaccine.  (+info)

Paronychia due to Prevotella bivia that resulted in amputation: fast and correct bacteriological diagnosis is crucial. (61/333)

Prevotella bivia is mainly associated with endometritis. The case of a patient with paronychia in a thumb due to P. bivia resulting in osteitis and amputation is reported. The species was not acknowledged in the first bacterial culture 2 weeks before surgery.  (+info)

Comparison of real-time PCR and culture for detection of Porphyromonas gingivalis in subgingival plaque samples. (62/333)

Porphyromonas gingivalis is a major pathogen in destructive periodontal disease in humans. Detection and quantification of this microorganism are relevant for diagnosis and treatment planning. The prevalence and quantity of P. gingivalis in subgingival plaque samples of periodontitis patients were determined by anaerobic culture and real-time PCR amplification of the 16S small-subunit rRNA gene. The PCR was performed with primers and a fluorescently labeled probe specific for the P. gingivalis 16S rRNA gene. By the real-time PCR assay, as few as 1 CFU of P. gingivalis could be detected. Subgingival plaque samples from 259 adult patients with severe periodontitis were analyzed. P. gingivalis was detected in 111 (43%) of the 259 subgingival plaque samples by culture and in 138 (53%) samples by PCR. The sensitivity, specificity, and positive and negative predictive values of the real-time PCR were 100, 94, 94, and 100%, respectively. We conclude that real-time PCR confirms the results of quantitative culture of P. gingivalis and offers significant advantages with respect to the rapidity and sensitivity of detection of P. gingivalis in subgingival plaque samples.  (+info)

Effects of a mixed infection with Porphyromonas gingivalis and Treponema denticola on abscess formation and immune responses in mice. (63/333)

Porphyromonas gingivalis and Treponema denticola have been found together in lesions of human periodontitis. We examined the ability of a mixed infection by both bacteria to synergistically form abscesses and disturb immune responses in mice. Absorbance of an invasive P. gingivalis 16-1 strain grown in tryptic soy broth and T. denticola ATCC 33520 strain grown in TYGVS medium were adjusted. BALB/c mice were injected with 200 microliters of the cell suspension at a site on the lateral dorsal area. The sizes of the subsequent subcutaneous abscesses were measured with a caliper gauge, and the area was expressed in square mm. Mixed infections by P. gingivalis and T.denticola produced larger abscesses than those formed after mono-infections by either P. gingivalis or T.denticola. The abscesses caused by mixed infection reached their maxima on the 6th day and maintained that size for the subsequent 5 days. The delayed type hypersensitivities against extracted antigens of P.gingivalis in mixed infection mice were significantly lower than those in the mono-infected mice. However, the IgG response to sonicated antigen of P.gingivalis did not differ between the two groups. The sizes of the abscesses caused by mixed infections in mice immunized with whole cells of P.gingivalis 16-1 were compared to those caused in sham-immunized mice. The average size of the abscess caused by mixed infection in immunized mice did not differ from that in sham-immunized mice, but many of the abscesses in immunized mice ruptured on the 4th or 5th day, followed by recovery in two weeks. These results suggest that mixed infection with P.gingivalis and T.denticola attenuates protective immune responses.  (+info)

Use of insertion sequence element IS1126 in a genotyping and transmission study of Porphyromonas gingivalis. (64/333)

Porphyromonas gingivalis is strongly associated with periodontal diseases and is regarded as one of the risk factors for periodontitis. Insertion sequence element IS1126-based PCR was used to investigate the genetic heterogeneity of P. gingivalis from periodontitis patients and to examine the frequency of the parent-child and spouse-spouse transmission. Two sets of IS1126-specific primers were used for the PCR. The inward primer set (PI1 and PI2), which amplifies the IS1126 fragment of approximately 690 bp, was used to identify P. gingivalis. The outward primer set (PI1RC and PI2RC), which is reverse complementary to PI1 and PI2, respectively, and amplifies the gene fragments between the adjacent IS1126 elements was used to characterize the genotypes of the P. gingivalis strains. PCR of P. gingivalis with PI1RC and PI2RC resulted in the production of two to seven amplicons, which showed a unique electrophoretic pattern in each strain (4 laboratory strains and 37 clinical isolates cultured from 12 patients with aggressive periodontitis). The usefulness of the method for transmission study was confirmed by detecting identical genotypes between the isolates and the plaque samples from which the isolates were cultured and between the plaque samples from different tooth sites in the same patient. Thirty probands with periodontal diseases and their thirty immediate family members were included in the transmission study. In 11 of 14 parent-child pairs (78.6%), P. gingivalis revealed an identical or similar band pattern, whereas 5 of 16 spouse pairs (31.25%) had this similarity. These results show that IS1126-based PCR for genotyping P. gingivalis has a highly discriminating potential with reproducible data and is a simple and reliable method for a transmission study.  (+info)