Periodontitis is epidemiologically associated with oral squamous cell carcinoma (OSCC), but the tissue-cell states shared by the two diseases are unknown. We integrated seven public droplet-based scRNA-seq datasets into an atlas of 498,185 cells from 111 oral mucosal samples using scVI/scANVI, benchmarked with scIB. Each disease was compared only with matched control tissue, using patient-level analyses. Both diseases expanded activated inflammatory and matrix fibroblast states. Activated and resting fibroblasts differed in a similar way in both diseases (ρ = 0.53; patient-bootstrap 95% CI 0.42–0.57), also within lesional tissue (ρ = 0.51). Disease-versus-control fibroblast responses, however, were only weakly shared (ρ = 0.24) and not within the oral cavity, so this similarity reflects a generic activated-stroma phenotype rather than a disease-specific fibroblast programme. Endothelial and mural responses were shared more strongly, whereas immune responses diverged. B/plasma-cell expansion was the only abundance change credible in both diseases. Periodontitis showed classical-monocyte influx and a lower share of C1Q+ macrophages. TREM2+ lipid-associated macrophages rose from leukoplakia to carcinoma, but their gain over tumour-adjacent tissue appeared in only one of two cohorts. SPP1–CD44 signalling passed significance thresholds only in OSCC. This cross-sectional study is hypothesis-generating and does not show causation.