3 resultados para Peptostreptococcus

em BORIS: Bern Open Repository and Information System - Berna - Suiça


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BACKGROUND: There is limited information on infectious and host responses distinguishing older people with or without active periodontitis. This study measured bacterial and serum cytokine and high-sensitivity C-reactive protein (hsCRP) levels in older persons. METHODS: Elders (mean age: 67 years), whose periodontal status had declined most or least (20% worst or 20% best) over 5 years, were enrolled. Two years later, they were classified as periodontally declining (active periodontitis [AP]), if they had at least five teeth with probing depth (PD) > or =5 mm, or stable (stable periodontally [SP]), if they did not. Groups were compared with respect to demographics, PD, clinical loss of attachment, subgingival bacteria, serum hsCRP, interleukin (IL)-1beta and -6, and chronic diseases. RESULTS: Ten AP and 24 SP subjects were identified; 13% of women and 44% of men from the original sample were in the AP group (P <0.05). Most Asians were SP; most whites and all African Americans were classified as having AP (P <0.01). More AP elders had osteoporosis (P <0.01), but the AP and SP groups did not differ with respect to IL-1beta and -6 or hsCRP. Bacterial counts were higher in the AP group for Parvimonas micra (previously Peptostreptococcus micros or Micromonas micros) (7.7 x 10(5) cells versus 3.8 x 10(5) cells; P <0.05), Prevotella intermedia (25.7 x 10(5) cells versus 9.8 x 10(5) cells; P <0.01), Tannerella forsythia (previously T. forsythensis) (16.2 x 10(5) cells versus 8.0 x 10(5) cells; P <0.05), and Streptococcus mutans (6.2 x 10(5) cells versus 2.0 x 10(5) cells; P <0.01). Three risk factors were most predictive of periodontal decline: PD, osteoporosis, and being white or African American. CONCLUSION: Periodontal decline was associated with osteoporosis, ethnicity, PD, gender, serum hsCRP, and levels of four bacterial species.

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BACKGROUND: We investigated clinical and subgingival microbiologic changes during pregnancy in 20 consecutive pregnant women > or =18 years not receiving dental care. METHODS: Bacterial samples from weeks 12, 28, and 36 of pregnancy and at 4 to 6 weeks postpartum were processed for 37 species by checkerboard DNA-DNA hybridization. Clinical periodontal data were collected at week 12 and at 4 to 6 weeks postpartum, and bleeding on probing (BOP) was recorded at sites sampled at the four time points. RESULTS: The mean BOP at week 12 and postpartum was 40.1% +/- 18.2% and 27.4% +/- 12.5%, respectively. The corresponding mean BOP at microbiologic test sites was 15% (week 12) and 21% (postpartum; not statistically significant). Total bacterial counts decreased between week 12 and postpartum (P <0.01). Increased bacterial counts over time were found for Neisseria mucosa (P <0.001). Lower counts (P <0.001) were found for Capnocytophaga ochracea, Capnocytophaga sputigena, Eubacterium saburreum, Fusobacterium nucleatum naviforme, Fusobacterium nucleatum polymorphum, Leptotrichia buccalis, Parvimonas micra (previously Peptostreptococcus micros or Micromonas micros), Prevotella intermedia, Prevotella melaninogenica, Staphylococcus aureus, Streptococcus anginosus, Streptococcus intermedius, Streptococcus mutans, Streptococcus oralis, Streptococcus sanguinis, Selenomonas noxia, and Veillonella parvula. No changes occurred between weeks 12 and 28 of pregnancy. Counts of Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans), Porphyromonas gingivalis, Tannerella forsythia (previously T. forsythensis), and Treponema denticola did not change. Counts of P. gingivalis and T. forsythia at week 12 were associated with gingivitis (P <0.001). CONCLUSIONS: Subgingival levels of bacteria associated with periodontitis did not change. P. gingivalis and T. forsythia counts were associated with BOP at week 12. A decrease was found in 17 of 37 species from week 12 to postpartum. Only counts of N. mucosa increased.

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OBJECTIVE To analyze the subgingival microflora composition of inflammatory bowel disease (IBD) patients with untreated chronic periodontitis and compare them with systemically healthy controls also having untreated chronic periodontitis. METHOD Thirty IBD patients [15 with Crohn's disease (CD) and 15 with ulcerative colitis (UC)] and 15 control individuals participated in the study. All patients had been diagnosed with untreated chronic periodontitis. From every patient, subgingival plaque was collected from four gingivitis and four periodontitis sites with paper points. Samples from the same category (gingivitis or periodontitis) in each patient were pooled together and stored at -70 °C until analysis using a checkerboard DNA-DNA hybridization technique for 74 bacterial species. RESULTS Multiple-comparison analysis showed that the groups differed in bacterial counts for Bacteroides ureolyticus, Campylobacter gracilis, Parvimonas micra, Prevotella melaninogenica, Peptostreptococcus anaerobius, Staphylococcus aureus, Streptococcus anginosus, Streptococcus intermedius, Streptococcus mitis, Streptococcus mutans, and Treponema denticola (P<0.001). CD patients had significantly higher levels of these bacteria than UC patients either in gingivitis or in periodontitis sites (P<0.05). CD patients harbored higher levels of P. melaninogenica, S. aureus, S. anginosus, and S. mutans compared with controls both at gingivitis and at periodontitis sites (P<0.05). UC patients harbored higher levels of S. aureus (P=0.01) and P. anaerobius (P=0.05) than controls only in gingivitis sites. CONCLUSION Our study showed that even with similar clinical periodontal parameters, IBD patients harbor higher levels of bacteria that are related to opportunistic infections in inflamed subgingival sites that might be harmful for the crucial microbe-host interaction.