Journal of periodontology · 2009
B-1a cells in experimental gingivitis in humans.
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Donati Mauro, Liljenberg Birgitta, Zitzmann Nicola U, Berglundh Tord
Аннотация
BACKGROUND: Although previous studies revealed the presence of autoreactive B cells (B-1a cells) in periodontitis lesions, no evidence was provided for an active role of such cells in the host response to microbial challenge. The aim of the present investigation was to study the reaction of B-1a cells to de novo plaque formation in subjects who were treated for severe chronic periodontitis.
METHODS: Fifteen white subjects with generalized, severe chronic periodontitis volunteered. Surgical periodontal therapy was performed in all quadrants of each subject after a period of infection control. After 6 months of healing (baseline), two gingival biopsies were harvested from each patient (probing depth <4 mm and no bleeding on probing; healed sites). The experimental gingivitis model was applied, and plaque accumulation was allowed for 3 weeks. Two additional biopsies were collected and prepared for immunohistochemical analysis on day 21.
RESULTS: The biopsies retrieved after 3 weeks of plaque accumulation contained larger proportions of CD19+ and CD5+ cells (B-1a cells) than biopsies representing baseline (healed sites) (7.38% +/- 2.80% versus 5.96% +/- 2.48%). The tissue fraction of cells carrying the markers for CD3 (T cells), CD19 (B cells), and Bcl2 (apoptosis-associated marker) were significantly larger in tissue samples collected after 3 weeks of plaque accumulation than in specimens from baseline (healed sites).
CONCLUSION: Autoreactive B cells (B-1a cells) are involved in the host response to microbial challenge in subjects with chronic periodontitis.
METHODS: Fifteen white subjects with generalized, severe chronic periodontitis volunteered. Surgical periodontal therapy was performed in all quadrants of each subject after a period of infection control. After 6 months of healing (baseline), two gingival biopsies were harvested from each patient (probing depth <4 mm and no bleeding on probing; healed sites). The experimental gingivitis model was applied, and plaque accumulation was allowed for 3 weeks. Two additional biopsies were collected and prepared for immunohistochemical analysis on day 21.
RESULTS: The biopsies retrieved after 3 weeks of plaque accumulation contained larger proportions of CD19+ and CD5+ cells (B-1a cells) than biopsies representing baseline (healed sites) (7.38% +/- 2.80% versus 5.96% +/- 2.48%). The tissue fraction of cells carrying the markers for CD3 (T cells), CD19 (B cells), and Bcl2 (apoptosis-associated marker) were significantly larger in tissue samples collected after 3 weeks of plaque accumulation than in specimens from baseline (healed sites).
CONCLUSION: Autoreactive B cells (B-1a cells) are involved in the host response to microbial challenge in subjects with chronic periodontitis.