Reactive pocket epithelium in untreated chronic periodontal disease: possible derivation from developmental remnants of the enamel organ and root sheath
N. Hunter et al., Reactive pocket epithelium in untreated chronic periodontal disease: possible derivation from developmental remnants of the enamel organ and root sheath, J ORAL PATH, 30(3), 2001, pp. 178-186
The pathological lining epithelium of destructive periodontitis was studied
by analysis of the expression of intermediate filament proteins in biopsie
s of untreated advanced periodontitis. The cytokeratin (CK) pair 8/18 chara
cteristic of simple epithelia was expressed consistently in a distribution
pattern confined to the reactive pocket epithelium. The pattern of CK8/18 e
xpression was complex with two broad presentations evident. In two-thirds o
f the advanced disease biopsies, the entire pathological lining epithelium
was strongly reactive for both CK8 and CK18. In the remainder, the more sup
erficial lining epithelium was mixed with foci of reactive and unreactive c
ells, with the deeper epithelium uniformly reactive. Only occasional highly
localised reactivity for the simple keratins (CK8/18) was found in the lin
ing epithelia of biopsies from minimally inflamed periodontal tissues. The
pathological lining epithelium of advanced periodontitis was further charac
terised by the cc-expression in basal layers of CK14, and of CK13 but not C
K4, which are characteristic of suprabasal layers of stratified squamous ep
ithelia, 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 or disease status. There was no reac
tivity for CK10/11 typical of cornifying cells nor of vimentin, the charact
eristic intermediate filament of mesenchymal cells. The intermediate filame
nt protein profile of the reactive lining epithelium was indistinguishable
from the reactive epithelium present in three of five biopsies of periapica
l granulomas containing hyperplastic epithelium from activation of the deve
lopmental remnants of Hertwig's sheath, known as the cell rests of Malassez
. The data reported are compatible with a contribution by remnants of devel
opmental epithelium, including the reduced enamel epithelium and the cell r
ests of Malassez, to the reactive lining epithelium of the subgingival pock
et in the pathogenesis of chronic periodontitis.