Some effects of non-surgical therapy on gingival inflammatory cell subsets in patients with early-onset periodontitis associated with Actinobacillus actinomycetemcomitans

Background: Limited information is available as to whether local cellular immunity in early-onset periodontitis (EOP) subjects harboring Actinobacillus actinomycetemcomitans (Aa) differs from that in patients without Aa. In addition, the effect of scaling and root planing on various lymphocyte subsets is described rather sparsely. Methods: In 10 subjects with early-onset periodontitis harboring Aa (EOP-Aa) and in 10 subjects without Aa (EOP-nonAa), clinical measurements were recorded and gingival biopsies were performed before and after scaling and root planing. The specimens were cut into serial sections; using the alkaline phosphatase-anti-alkaline phosphatase technique, monoclonal antibodies to CD20 (B cells), CD30 (plasma cells), and CD45RO (T-memory cells) were applied as well as polyclonal antibodies to alpha, gamma, and mu chains (Ig A, G, and M). Cells were counted from an area of 0.25 mm(2) in areas showing the largest infiltration. Results: Before therapy, mean counts of all cell phenotypes were found to be markedly enhanced in the EOP-Aa group compared to EOP-nonAa subjects. Following scaling and root planing, the numbers of all phenotypes decreased in both groups. However, comparing the data before and after therapy in the EOP-Aa group, the P value was Conclusions: In EOP subjects harboring Aa, inflammatory cell subsets were detected in 2- to 3-fold higher numbers compared to patients without Aa. Scaling and root planing resulted in a decrease of all cell phenotypes studied in individuals without Aa, whereas in subjects with Aa, the only significant decrease that was seen occurred in plasma cells

Bacterial susceptibility to amoxicillin and potassium clavulanate in advanced periodontitis patients not responding to mechanical therapy

Background, aims: Between 4 and 8% of periodontitis patients are reported to respond poorly to conventional therapy. In these cases, adjunctive use of systemic antibiotics might be a reasonable therapeutic approach. The purpose of this study was to evaluate the effects of systemic amoxicillin/clavulanate as adjunct to periodontal surgery on the predominant subgingival microorganisms in patients not responding to mechanical therapy. Furthermore, the bacterial susceptibility to amoxicillin/clavulanate was analyzed before and after therapy in older to assess the clinical validity of pre-therapeutic susceptibility testing. Methods: In 10 periodontitis subjects with no subgingival detection of Actinobacillus actinomycetemcomitans, the predominant subgingival organisms were identified using the identification system Rapid ID 32 A as well as antibiotic susceptibility was tested utilizing the E test. Results: Porphyromonas gingivalis and Prevotella oralis were detected in 7/10 subjects and could no more recovered after therapy. Fusobacterium nucleatum and Peptostreptococcus micros were present in 5/10 patients before treatment, but could be detected in 6/10, resp. 3/10 after therapy. In 4/10 subjects harboring F. nucleatum and in 3/10 with P. micros, those organisms were not targeted by amoxicillin/clavulanate, although post-treatment testing revealed their alleged susceptibility (MICs varied from 0.023 to 0.032 mu g/ml, resp. from 0.125 to 2.0 mu g/ml). Conclusions: The results of this study suggest that the outcomes of conventional methods of susceptibility testing have to be interpreted very carefully when being used for treatment of plaque-related diseases. Furthermore, since the end point of systemic antibiotic treatment as adjunct to conventional therapy is elimination of F. nucleatum or P. micros in patients harboring these organisms, the use of amoxicillin/clavulanate appears not to be justified