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Heparanase expression in periapical granulomas and radicular cysts
1Department of Oral Medicine, Hebrew University-Hadassah School of Dental Medicine, Jerusalem, Israel. eladhome@md.huji.ac.il
Odontology
|October 25, 2011
Summary
Heparanase expression differs in periapical granulomas (PGs) and radicular cysts (RCs). Epithelial cells strongly express heparanase in RCs, while inflammatory cells show weak expression in PGs.
Area of Science:
- Biochemistry
- Oral Pathology
- Enzymology
Background:
- Heparanase is an enzyme that degrades heparan sulfate in the extracellular matrix and basement membranes.
- Periapical lesions, such as periapical granulomas (PGs) and radicular cysts (RCs), arise from dental pulp infections.
- Understanding the role of heparanase in these lesions may elucidate their distinct pathogenetic mechanisms.
Purpose of the Study:
- To investigate and compare the expression patterns of heparanase in periapical granulomas and radicular cysts.
- To identify the specific cell types responsible for heparanase expression within these periapical lesions.
- To correlate heparanase expression levels with lesion type (PG vs. RC).
Main Methods:
- Immunohistochemistry was employed to detect and quantify heparanase expression.
- Stain intensity, cellular localization, and cell types expressing heparanase were analyzed.
- Periapical granulomas and radicular cysts were categorized based on ordered staining levels.
Main Results:
- Heparanase was detected in both epithelial and inflammatory cells within the periapical lesions.
- Epithelial cells exhibited strong heparanase staining, particularly in radicular cysts.
- Inflammatory cells showed weak heparanase staining, which was predominant in periapical granulomas.
Conclusions:
- Significant differences in epithelial cell heparanase expression exist between radicular cysts and periapical granulomas.
- The distinct cellular sources and levels of heparanase expression suggest specific pathogenetic roles in RCs and PGs.
- Heparanase may play a differential role in the pathogenesis of these common periapical inflammatory conditions.
