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Updated: Apr 26, 2026

Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
Immunoexpression of interleukin 17 in apical periodontitis lesions
Natasha C Ajuz1, Henrique Antunes2, Thais A Mendonça3
1Department of Endodontics and Immunohistochemistry Laboratory, Faculty of Dentistry, Estácio de Sá University, Rio de Janeiro, RJ, Brazil.
Introduction:
Interleukin (IL)-17 expression has been detected in apical periodontitis lesions, but its role in the disease process remains unclear. The present study compared the expression of IL-17 in periradicular cysts and granulomas and evaluated the association of this cytokine with clinical and radiographic findings.
Methods:
Apical periodontitis lesions (18 cysts and 20 granulomas) were obtained from 38 patients subjected to periradicular surgery. Some clinical, radiographic, and cone-beam computed tomographic features were recorded. Silanized slides containing paraffin sections were used for the immunohistochemical reactions using anti-IL-17 antibody. Image analysis was performed using an optical microscope, and each sample was divided into 5 high-power fields, which were evaluated for the expression of IL-17 in the epithelium and connective tissues. Results were evaluated for correlations with the lesion size and the occurrence of symptoms and sinus tract.
Results:
Expression of IL-17 was significantly higher in cysts than in granulomas (P = .02). Among the periradicular cysts, a thin epithelium showed significantly increased labeling for IL-17 when compared with a hyperplastic epithelium (P = .003). IL-17 expression was usually associated with focal accumulations of polymorphonuclear leukocytes. No association of IL-17 expression with symptoms, sinus tract, or lesion size was observed (P > .05).
Conclusions:
The present study reinforces the notion that IL-17 may take part in the pathogenesis of apical periodontitis lesions. A role in the exacerbation of chronic inflammation and cyst formation is suspected. Further studies are required to shed light on the specific functions of IL-17 in periradicular inflammatory processes.
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