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-antialkaline 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 mm2 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 <0.05 only for CD30-positive cells. In the EOP-nonAa group, the differences before and after therapy reached statistical significance (P<0.05) for all cell counts, except for IgM-positive cells. Furthermore, reduction of probing depth and gain of clinical attachment reached the 0.05 level of statistical significance only in EOP-nonAa subjects.


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.
Kleinfelder
J W
JW
Department of Periodontology, Medical Center St Radboud, University of Nijmegen, The Netherlands. j.kleinfelder@dent.kun.nl
Sculean
A
A
Lange
D E
DE
D000328:Adult; D016976:Aggregatibacter actinomycetemcomitans / Q000472:pathogenicity; D010520:Aggressive Periodontitis / Q000276:immunology* / Q000382:microbiology / Q000628:therapy*; D001402:B-Lymphocytes / Q000276:immunology; D003773:Dental Plaque / Q000382:microbiology*; D012534:Dental Scaling; D005260:Female; D006801:Humans; D007132:Immunoglobulin Isotypes / Q000032:analysis; D007150:Immunohistochemistry; D007156:Immunologic Memory; D016130:Immunophenotyping; D017730:Ki-1 Antigen / Q000032:analysis; D016131:Lymphocyte Subsets / Q000276:immunology*; D008297:Male; D010950:Plasma Cells / Q000276:immunology; D018709:Statistics, Nonparametric; D013601:T-Lymphocytes / Q000276:immunology; D016896:Treatment Outcome
D007132:Immunoglobulin Isotypes; D017730:Ki-1 Antigen