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Fibroblast Growth Factor Receptor 2 expression in apical periodontitis in mice.

AIM
Investigate the presence, localization, and the possible correlation of the Fibroblast growth factor receptor-2 (FGFR2) with inflammatory resorption of cementum, periodontal ligament and alveolar bone during development of apical periodontitis in mice.


METHODOLOGY
Apical periodontitis was experimentally induced in mandibular first molars of mice by pulp exposure to the oral environment. Healthy teeth without pulp exposure were used as controls. At 7, 21 and 42 days following pulp exposure, the animals were euthanized and the jaws were prepared for analysis under conventional and fluorescence microscopy, immunohistochemistry (FGFR2), RT-PCR (RNAm levels of RANK, RANKL, OPG, Runx2 and Cathepsin K) and enzymehistochemistry (cementoclasts and osteoclasts). Statistical analysis was performed by Kruskall-Wallis tests and Dunn's post-hoc tests for multiple comparisons (α = 0.05) using SAS 9.4 software.


RESULTS
FGFR2 positive cells were not observed in the tissues surrounding healthy teeth but were observed in teeth with periapical lesions from seven days after root canal contamination. At days 21 and 42 after endodontic infection, the increase in periapical lesion size was accompanied by significant enhanced expression of FGFR2 (p<0.0001), significant increased intensity of inflammatory cells, number of osteoclasts (p<0.0001) and cementoclasts (p<0.0001), and significant enhanced RNAm levels of RANK/RANKL/OPG, Runx2 and Cathepsin K compared to day 0 (p < 0.0001). At 21 and 42 days, FGFR2 was also expressed on osteoblasts, fibroblasts and inside enlarged lacunae of cementocytes along with acute and chronic inflammatory cells (macrophages, plasma cells and neutrophils). At all periods and cells, FGFR2 expression was observed in the cell membrane and cytoplasm, but not in the nucleus.


CONCLUSION
In mice, FGFR2 was not expressed in tissues surrounding healthy teeth but was expressed in apical periodontitis, specifically in the membrane and cytoplasm of osteoblasts, fibroblasts, lacunae of cementocytes, and acute and chronic inflammatory cells (macrophages, plasma cells and neutrophils). Its expression was correlated with the size of the periapical lesions.