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Updated: Jun 22, 2026

Isolation, Processing and Analysis of Murine Gingival Cells

Isolation, Processing and Analysis of Murine Gingival Cells

Published on: July 2, 2013

B-1a cells in experimental gingivitis in humans.

Mauro Donati¹, Birgitta Liljenberg, Nicola U Zitzmann

¹Department of Periodontology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden. mauro.donati@odontologi.gu.se

Journal of Periodontology

|July 1, 2009

Summary

Autoreactive B cells (B-1a cells) increase during plaque accumulation in periodontitis patients. These cells play an active role in the host immune response to microbial challenges in chronic periodontitis.

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Isolation, Characterization and Functional Examination of the Gingival Immune Cell Network

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Published on: February 16, 2016

Area of Science:

Immunology
Periodontology
Oral Microbiology

Background:

Previous studies identified autoreactive B cells (B-1a cells) in periodontitis lesions.
The active role of B-1a cells in the host response to microbial challenge remained unclear.

Purpose of the Study:

To investigate the reaction of B-1a cells to de novo plaque formation.
To assess the involvement of B-1a cells in the host response in treated severe chronic periodontitis patients.

Main Methods:

Subjects with severe chronic periodontitis underwent surgical periodontal therapy.
Gingival biopsies were collected from healed sites (baseline) and after 3 weeks of experimental gingivitis (plaque accumulation).
Immunohistochemical analysis was performed to quantify cell populations.

Main Results:

Biopsies with 3 weeks of plaque accumulation showed increased proportions of B-1a cells (CD19+ and CD5+) compared to baseline.
Significantly higher tissue fractions of T cells (CD3+), B cells (CD19+), and cells expressing Bcl2 were observed after plaque accumulation.

Conclusions:

Autoreactive B cells (B-1a cells) are actively involved in the host response to microbial challenge in chronic periodontitis.
The findings highlight the role of B-1a cells in the inflammatory process of periodontitis.