Huang, Z.; Yang, D.; Zhang, R.; Chen, Q.; Zhao, H.; Xu, H.

Spatial transcriptomics is often interpreted with tools that do not explicitly encode tissue-scale physical priors such as finite ligand diffusion, density-based state stability, or self-exciting spatial recruitment. We introduce three compact computational methods and apply them to a 326,554-cell spatial atlas of human oral mucosal carcinogenesis spanning normal mucosa, hyperplasia, oral lichen planus, and dysplasia. DC3 (Diffusion-Constrained Cell Communication) replaces distance-blind ligand-receptor co-expression with a ligand-specific exponential distance kernel. It down-weights short-range ECM-class interactions by three to four orders of magnitude relative to traditional scoring, remains rank-stable under diffusion-length perturbation and dys2 removal (Spearman rho >= 0.93), and better matches COMMOT than traditional co-expression on the dys2 benchmark. A within-section label-permutation null indicates that only 0.5-6.6% of the top MRB-autocrine DC3 signal is attributable to spatial clustering alone. A log-density landscape, reported in nats rather than thermodynamic units, places the Malignant_risk_basal (MRB) cluster in a high-density epithelial region with a reverse barrier of 2.43 nats from stress-proliferative basal cells on the full atlas, 1.93 nats after dys2 removal, and 1.0-1.9 nats under Silverman/Scott bandwidth rules. MRB local neighborhood entropy is stable at 0.67-0.68 bits across bandwidth and PCA-dimension choices. A spatial Hawkes model separates immune-cell background density from self-excitation; apparent dysplasia-level adaptive-immune attenuation is not significant by 10,000 label permutations (all FDR q = 1.00) and is retained only as a section-level observation. External checks in CELLxGENE Census and Puram 2017 reposition the MRB signature as a dysplasia-restricted aberrant-basal-differentiation phenotype rather than a marker preserved in fully malignant OSCC. The methods are presented as lightweight, interpretable tools, and the biological findings as hypotheses requiring independent validation.