| Literature DB >> 52857 |
Abstract
It is proposed that oral keratoses appear white because of the ability of abnormal oral keratin to evenly reflect the visible light spectrum because of the hydration of the keratin layer in a manner similar to the reaction of the stratum corneum of the epidermis to water. Thickening of the keratin layer per se or the over-all thickness of the epithelium does not appear to be the primary factor in causing an intraoral lesion to appear white. The white appearance is related to thickness only insofar as it takes a certain amount of abnormal keratin to be clinically evident. It appears that an accumulation of only 10 to 20 microns of abnormal keratin is sufficient to cause a lesion to appear very white. This is about the amount seen on the normal human palate. It seems likely that, when a normally nonkeratinized area, such as the buccal mucosa or floor of the mouth, is stimulated to produce keratin, the keratin thus produced would be different from normally occurring oral keratin. This difference apparently manifests itself clinically as hydration of the keratin layer. A more complete understanding of why white lesions are white awaits further elucidation in regard to the role of lipids, keratohyaline granules, membrane-coating granules, and intercellular cement. Characterization of the oral keratins as to their amino acid residues and types of bondings, as well as insight into the events transpiring when the prickle cell becomes keratinized, may not only shed light on the etiology of these lesions but also have prognostic implications.Entities:
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Year: 1975 PMID: 52857 DOI: 10.1016/0030-4220(75)90375-8
Source DB: PubMed Journal: Oral Surg Oral Med Oral Pathol ISSN: 0030-4220