BACKGROUND/AIMS: Previously, we reported that SRP resulted in a decrease in mean pocket depth and attachment level and reduced prevalence and levels of Bacteroidesforsythus, Porphyromonas gingivalis, and Treponema denticola at 3 and 6 months post-SRP in 57 subjects with adult periodontitis. 32 of the 57 subjects were monitored at 9 and 12 months. Thus, the purpose of the present investigation was to evaluate the microbial and clinical effects of SRP in 32 (mean age 48+/-11) subjects over a 12-month period. METHOD: Clinical assessments of plaque, gingival redness, suppuration, bleeding on probing, pocket depth and attachment level were made prior to SRP and at 3, 6, 9, and 12 months post-therapy. Subgingival plaque samples were taken at each visit and analyzed using the checkerboard DNA-DNA hybridization technique for the presence and levels of 40 subgingival species. Each subject also received maintenance scaling at each of the subsequent monitoring visits. Differences in clinical parameters and prevalence and levels of bacterial species were analyzed pre- and post-therapy using the Wilcoxon signed ranks test. The Quade test for related samples was used for analysis of multiple visits. RESULTS: Mean pocket depth (mm+/-SEM) decreased from 3.2+/-0.3 at baseline to 2.9+/-0.3 at 12 months (p<0.01). Mean attachment level showed significant reduction at 6 months, but did not diminish further. Bleeding on probing and plaque were significantly reduced at 12 months (p<0.001, p<0.05, respectively). P. gingivalis, B. forsythus and T. denticola decreased in prevalence and levels up to the 6-month visit and remained at these lower levels at 9 and 12 months. Significant increases in levels and prevalence were noted at 12 months for Actinomyces naeslundii genospecies 2, Actinomyces odontolyticus, Fusobacterium nucleatum ss polymorphum, Streptococcus mitis, Capnocytophaga sp, and Veillonella parvula. CONCLUSIONS: The data suggest that the maintenance phase of therapy may be essential in consolidating clinical and microbiological improvements achieved as a result of initial therapy.
BACKGROUND/AIMS: Previously, we reported that SRP resulted in a decrease in mean pocket depth and attachment level and reduced prevalence and levels of Bacteroidesforsythus, Porphyromonas gingivalis, and Treponema denticola at 3 and 6 months post-SRP in 57 subjects with adult periodontitis. 32 of the 57 subjects were monitored at 9 and 12 months. Thus, the purpose of the present investigation was to evaluate the microbial and clinical effects of SRP in 32 (mean age 48+/-11) subjects over a 12-month period. METHOD: Clinical assessments of plaque, gingival redness, suppuration, bleeding on probing, pocket depth and attachment level were made prior to SRP and at 3, 6, 9, and 12 months post-therapy. Subgingival plaque samples were taken at each visit and analyzed using the checkerboard DNA-DNA hybridization technique for the presence and levels of 40 subgingival species. Each subject also received maintenance scaling at each of the subsequent monitoring visits. Differences in clinical parameters and prevalence and levels of bacterial species were analyzed pre- and post-therapy using the Wilcoxon signed ranks test. The Quade test for related samples was used for analysis of multiple visits. RESULTS: Mean pocket depth (mm+/-SEM) decreased from 3.2+/-0.3 at baseline to 2.9+/-0.3 at 12 months (p<0.01). Mean attachment level showed significant reduction at 6 months, but did not diminish further. Bleeding on probing and plaque were significantly reduced at 12 months (p<0.001, p<0.05, respectively). P. gingivalis, B. forsythus and T. denticola decreased in prevalence and levels up to the 6-month visit and remained at these lower levels at 9 and 12 months. Significant increases in levels and prevalence were noted at 12 months for Actinomyces naeslundii genospecies 2, Actinomyces odontolyticus, Fusobacterium nucleatum ss polymorphum, Streptococcus mitis, Capnocytophaga sp, and Veillonella parvula. CONCLUSIONS: The data suggest that the maintenance phase of therapy may be essential in consolidating clinical and microbiological improvements achieved as a result of initial therapy.
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