“…[32][33][34][35][36] In general, the autofluorescence intensity of cancerous and precancerous lesions is lower, due to mucosal thickening and reduced collagen fluorescence. 29 However, tissue autofluorescence has been attributed to many sources, 37 including metabolic molecules (NADH, FAD), [38][39][40] proteins, and other molecules (flavins, collagen, elastin, hemoglobin), 41 breakdown of certain biomolecules (hematoporphyrin, flavins), 42 and induced molecular changes concurrent with inflammation. [43][44][45] Hence, the molecular and histologic basis for AFI is still uncertain.…”