Participation of osteoclastogenic factors in immunopathogenesis of human chronic periapical lesions

Abstract

Background

Chronic periapical lesions (CPLs) are common lesions of the oral cavity and are the result of caries, tooth fracture, iatrogenic causes or factors causing contamination and pulp necrosis. Inflammatory cells participate in the expansion of CPLs by releasing factors that stimulate or inhibit osteolytic activity. The objective of this study was to investigate the participation of RANKL, TNF-α, cathepsin K, IL-33 and OPG in the development of radicular cysts (RCs) and periapical granulomas (PGs).

Methods

Paraffin-embedded sections of 30 RCs and 22 PGs were submitted to immunohistochemistry.

Results

Immunoexpression of the proteins studied was observed in the epithelium and capsule of RCs, as well as in connective tissue of PGs. The expression of the osteoclastogenic factors studied differed significantly in RCs and PGs (p<0.001), with lower expression of OPG in RCs. In PGs, the lowest expression was observed for cathepsin K. Comparison of the two lesions showed a similar participation of RANKL and IL33, while a significant difference was observed for OPG (p<0.001), TNF-α (p=0.002) and cathepsin K (p=0.016). No association of proteins expression with lesions size was observed.

Conclusions

This study demonstrated the participation of RANKL, TNF-α, IL-33, cathepsin K and OPG in the development of RCs and PGs, with emphasis on the highest immunoreactivity of cathepsin in RCs and TNF-α and OPG in PGs. OPG possibly determines the slower growth of PGs compared to RCs.

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