Reactive pocket epithelium in untreated chronic periodontal disease: possible derivation from developmental remnants of the enamel organ and root sheath

The pathological lining epithelium of destructive periodontitis was studied by analysis of the expression of intermediate filament proteins in biopsies of untreated advanced periodontitis. The cytokeratin (CK) pair 8/18 characteristic of simple epithelia was expressed consistently in a distribution pattern confined to the reactive pocket epithelium. The pattern of CK8/18 expression was complex with two broad presentations evident. In two-thirds of the advanced disease biopsies, the entire pathological lining epithelium was strongly reactive for both CK8 and CK18. In the remainder, the more superficial lining epithelium was mixed with foci of reactive and unreactive cells, with the deeper epithelium uniformly reactive. Only occasional highly localised reactivity for the simple keratins (CK8/18) was found in the lining epithelia of biopsies from minimally inflamed periodontal tissues. The pathological lining epithelium of advanced periodontitis was further characterised by the co-expression in basal layers of CK14, and of CK13 but not CK4, which are characteristic of suprabasal layers of stratified squamous epithelia. Cytokeratin 17, a marker of high turnover and migrating epithelial cells was extremely variable with no clear association between expression pattern and location of the epithelium ordisease status. There was no reactivity for CK10/11 typical of cornifying cells nor of vimentin, the characteristic intermediate filament of mesenchymal cells. The intermediate filament protein profile of the reactive lining epithelium was indistinguishable from the reactive epithelium present in three of five biopsies of periapical granulomas containing hyperplastic epithelium from activation of the developmental remnants of Hertwig's sheath, known as the cell rests of Malassez. The data reported are compatible with a contribution by remnants of developmental epithelium, including the reduced enamel epithelium and the cell rests of Malassez, to the reactive lining epithelium of the subgingival pocket in the pathogenesis of chronic periodontitis.