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Updated: Sep 13, 2025

Isolation, Processing and Analysis of Murine Gingival Cells
Published on: July 2, 2013
Association of Mast Cell Activity With Chronic Gingivitis, Chronic Periodontitis, and Aggressive Periodontitis in
Manisha Mallik1, Anindita Banerjee1, Dipankar Samaddar2
1Department of Periodontology, Buddha Institute of Dental Sciences and Hospital, Patna, IND.
Introduction:
Periodontal diseases, including chronic gingivitis, chronic periodontitis, and aggressive periodontitis, are driven by complex immune responses, with mast cells (MCs) playing a pivotal role through the release of mediators during degranulation. Although MC involvement in chronic periodontal conditions has been documented, its role in aggressive periodontitis and the relationship between MC degranulation and inflammation intensity remain poorly understood. This study aimed to quantify MCs and assess their degranulation in gingival tissues across healthy gingiva, chronic gingivitis, chronic periodontitis, and aggressive periodontitis using histochemical staining to elucidate their role in periodontal inflammation and disease progression.
Materials And Methods:
This cross-sectional study included 120 systemically healthy subjects recruited from the Periodontology Outpatient Department. The groups included healthy periodontium (n = 30), chronic gingivitis (n = 30), chronic periodontitis (n = 30), and aggressive periodontitis (n = 30) groups. Gingival biopsies were obtained, fixed, sectioned, and stained with toluidine blue to identify intact and degranulated MCs in juxta-epithelial (Z1) and deep connective tissue (Z2) zones. MC counts were performed under 40x magnification, with examiner calibration to ensure reliability (intraclass correlation (ICC) ≥ 0.85). Nonparametric tests (Kruskal-Wallis with Dunn's test) were used to analyze MC density and degranulation, with a significance level of p < 0.05.
Results:
MC counts were highest in chronic periodontitis (7.10 ± 2.50 in Z1, 6.70 ± 2.10 in Z2) and aggressive periodontitis (6.10 ± 1.70 in Z1, 6.50 ± 2.00 in Z2), followed by chronic gingivitis and healthy gingiva (p < 0.00001). Degranulated MCs were significantly elevated in diseased groups, particularly chronic periodontitis (4.69 ± 2.09 in Z1, 4.51 ± 1.89 in Z2) compared to healthy controls (p = 0.0001). Intact MCs showed less variation, with significant differences between the healthy and aggressive periodontitis groups (p = 0.045).
Conclusion:
Increased MC degranulation was associated with periodontal disease severity, particularly in chronic and aggressive periodontitis, suggesting a key role of MC degranulation in inflammatory progression. These findings highlight the potential of MCs as therapeutic targets in periodontal management.

