In response to damage, the body activates repair mechanisms that increase the expression of wound healing-related genes, whose upregulation subsequently promotes cell proliferation and migration.51 However, prolonged and excessive repair may lead to tissue dysfunction, further exacerbating the progression of periodontitis.55 Furthermore, the communication between fibroblasts and epithelial cells, particularly through the EPGN-EGFR signalling pathway, may drive excessive epithelial proliferation and migration,56,57 which could contribute to the epithelial barrier breakdown observed in smokers. This evidence concerns the gene EPGN and periodontitis.