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Updated: Aug 19, 2026
Isolation, Characterization and Functional Examination of the Gingival Immune Cell Network
Published on: February 16, 2016
Lymphocyte subpopulations and the expression of intercellular adhesion molecules in chronic periodontitis
Gordan Cindrić1, Andrej Aurer, Darije Plancak
1Dental Studies, School of Medicine, University of Rijeka, Croatia.
Insights
Host immune responses, specifically T and B cell presence, influence chronic periodontitis (CP) treatment outcomes. Cellular adhesion molecule expression did not differ between treatment responders and non-responders.
Area of Science:
- Immunology
- Periodontology
- Cell Biology
Background:
- Immunological responses to bacteria are critical in chronic periodontitis (CP).
- Cellular adhesion molecules (ICAM-1, beta-1 integrins) were hypothesized to influence CP disease course.
- Understanding immune cell profiles in treatment response is crucial.
Purpose of the Study:
- To investigate the expression of cellular adhesion molecules (ICAM-1, beta-1 integrins).
- To compare capillary density and lymphocyte subpopulations in gingival biopsies.
- To correlate these factors with treatment response in chronic periodontitis patients.
Main Methods:
- Immunohistochemical analysis of gingival biopsies from CP patients.
- Categorization into treatment responders (n=20) and non-responders (n=21).
- Assessment of ICAM-1, beta-1 integrins, capillary density, and T/B lymphocyte populations.
Main Results:
- No significant differences in capillary density, ICAM-1, or beta-1 integrin expression between groups.
- Treatment responders exhibited a T cell-predominant inflammatory infiltrate.
- Non-responders showed an approximately equal distribution of T and B cells.
Conclusions:
- Host immune mechanisms, particularly lymphocyte composition, are key determinants of CP treatment outcomes.
- Differential expression of cellular adhesion molecules (ICAM-1, beta-1 integrins) is unlikely to be a major factor in CP treatment response.
Abstract:
Immunological responses to invading bacteria play a major role in the course of inflammatory periodontal diseases, such as CP. It was suggested that one of the major elements in determining the course of the disease is the expression of cellular adhesion molecules. We therefore investigated the expression of cellular adhesion molecules, ICAM-1 and beta-1 integrins, capillary density and lymphocyte subpopulations in gingival biopsies obtained from 20 patients with CP who responded and 21 patient who failed to respond to initial treatment using immunohistochemical methods. We found no differences between the two groups in capillary density, ICAM-1 and beta-1 integrin expression. Patients who responded to treatment had a lymphocytic inflammatory infiltrate consisting predominantly of T cells, while those who failed to respond had an approximately equal number of T and B cells. Our findings support the role of host immunological mechanisms in determining the outcome of CP and argue against a major role of differential cellular adhesion molecule expression.
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