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We investigated whether extracellular matrix (ECM) remodeling represents a quantifiable feature of FA-associated OPMDs. A total of 119 participants were included: controls with normal mucosa or oral leukoplakia (OL) and individuals with FA. Histopathological and immunohistochemical analyses (p53, Ki-67, \u03b1-SMA, and elastin), picrosirius red staining, and multiphoton microscopy combining second-harmonic generation and 2-photon fluorescence were performed, complemented by salivary and transcriptomic profiling. Additionally,\n                    <jats:italic toggle=\"yes\">Fanca<\/jats:italic>\n                    -deficient mice were used to assess stromal remodeling. Compared with sporadic OL, FA-OL exhibited reduced collagen density and elastin autofluorescence, a higher collagen-to-elastin ratio, and diminished p53 immunoreactivity. Salivary procollagen type I N-terminal propeptide showed exploratory associations with matrix-derived optical parameters. RNA sequencing of bulk biopsy tissue revealed an altered matrisome transcriptional signature, including enrichment of ECM structural gene sets and downregulation of selected ECM regulatory programs. In FA-related mouse models, collagen and elastin signals were similarly reduced. Collectively, these multimodal data identify ECM disruption as a reproducible feature associated with FA-OL. Matrix disorganization, together with altered epithelial p53 immunoreactivity, supports the hypothesis that epithelial and stromal alterations coexist across the FA-associated oral lesion spectrum.\n                  <\/jats:p>","DOI":"10.1177\/00220345261478636","type":"journal-article","created":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T04:42:31Z","timestamp":1792125751000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Fanconi Anemia: Matrix Remodeling and Oral Carcinogenesis"],"prefix":"10.1177","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9623-7835","authenticated-orcid":false,"given":"T.A.","family":"Silva","sequence":"first","affiliation":[{"name":"Department of Oral Surgery, Pathology and Clinical Dentistry, School of Dentistry, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil"},{"name":"AP-HP, Reference Center for Dental Rare Diseases, Rothschild Hospital (ORARES), Paris, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1220-6300","authenticated-orcid":false,"given":"N.C.M.","family":"Santana","sequence":"additional","affiliation":[{"name":"Department of Oral Surgery, Pathology and Clinical Dentistry, School of Dentistry, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6599-3950","authenticated-orcid":false,"given":"J.A.A.","family":"de Arruda","sequence":"additional","affiliation":[{"name":"Department of Oral Surgery, Pathology and Clinical Dentistry, School of Dentistry, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil"},{"name":"Department of Oral Diagnosis and Pathology, School of Dentistry, Universidade Federal do Rio de Janeiro, Rio de Janeiro, 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