The increased expression of Fib-8 in smoking-related periodontitis also suggests a shift in fibroblast subpopulation dynamics.52 Notably, the smoking-induced upregulation of genes associated with ageing, apoptosis, and cell migration, such as S100A8 and S100A9, aligns with earlier findings that smoking promotes fibroblast dysfunction and impaired wound healing.53,54 The expression of genes involved in wound healing pathways in the SP group was elevated, primarily due to the ongoing damage and chronic inflammatory response induced by smoking. This evidence concerns the gene S100A9 and periodontitis.