Expression and localisation of amelotin, laminin and protein secreted by follicular dendritic cells after ligature-induced experimental periodontitis in rats.

Objective The junctional epithelium (JE) is composed of tightly interconnected layers of squamous epithelial cells that play a crucial role as a defence mechanism. Recently, several enamel-derived proteins have been shown to play a role in the adhesion of JE cells to the mineralised tooth surface. This study aims to explore the in vivo protein expression levels of amelotin (AMTN), laminin (LAM332) and the protein secreted by follicular dendritic cells (FDC-SP) within the JE, both in the presence and absence of experimental periodontitis (EP) in rats.Materials and methods In total, 16 rats were randomly divided into two groups: a control group without EP and a group with induced periodontitis. EP was established by placing cotton ligatures around the cervical region of the lower first molars. Fifteen days after EP induction, all animals were euthanised and mandibles were harvested. Micro-computed tomography, histomorphometric, and immunohistochemistry analyses were employed to assess volumetric bone alterations, architectural bone parameters and number of osteoclasts. The presence of inflammatory cells and enamel protein expression were evaluated by immunofluorescence.Results The results demonstrated that the EP group showed a significant increase in alveolar bone loss, an elevated number of tartrate-resistant acid phosphatase-positive cells, and enhanced inflammatory processes compared to the control group. Immunofluorescence staining revealed a significant increase in the expression of AMTN in the EP group. However, there were no significant differences between the expression of FDC-SP and LAM332. Correlation analysis of AMTN, LAM332 and FDC-SP with the intensity of inflammatory markers (CD45+, CD66b+ and CD8+, CD163+ and CD80+) showed no significant differences for the EP group.Conclusion Our data suggest that the expression of AMTN increased after inflammatory stimuli and that AMTN may be associated with the onset and progression of EP.