Human gingival fibroblast cytoskeleton is a target for volatile smoke components

Citation
Mt. Rota et al., Human gingival fibroblast cytoskeleton is a target for volatile smoke components, J PERIODONT, 72(6), 2001, pp. 709-713
Citations number
25
Categorie Soggetti
Dentistry/Oral Surgery & Medicine","da verificare
Journal title
JOURNAL OF PERIODONTOLOGY
ISSN journal
00223492 → ACNP
Volume
72
Issue
6
Year of publication
2001
Pages
709 - 713
Database
ISI
SICI code
0022-3492(200106)72:6<709:HGFCIA>2.0.ZU;2-5
Abstract
Background: Several in vitro investigations have indicated that the particu late phase of cigarette smoke as nicotine affects many cell types including gingival fibroblasts, but few studies have examined the effect of volatile fraction on cellular structures involved in cell functions such as adhesio n and proliferation. Since gingival fibroblast survival and reproduction ar e fundamental to maintaining the oral connective tissue as well as to wound healing, the effects of acrolein and acetaldehyde, volatile fractions of c igarette smoke, on cytoskeleton were examined in human gingival fibroblasts (HGFs) in vitro. Methods: Human gingival fibroblast (HGF) strains from healthy subjects with non-inflamed gingiva were utilized. The cells were incubated in different concentrations of acrolein and acetaldehyde. Cell adhesion was evaluated af ter 3 hours. The influence of both substances on cytoskeletal structures, t ubulin and vimentin intermediate filaments (VIF), was investigated using in direct immunofluorescence technique. Results: The results show that both substances produced similar effects, re sulting in a dose-dependent inhibition of HGF adhesion. Disturbance of HGF cytoskeleton consisted of a disruption of microtubules and vimentin microfi laments with alterations in cell shape. Conclusions: Our experimental findings suggest that volatile fractions of c igarette smoke such as acrolein and acetaldehyde, because their ability to bind and interact with the cytoskeleton, prevent HGF adhesion. Consequently the maintenance of the oral connective tissue and integrity and remodeling could be impaired. According to our morphological evidence, these findings confirm other clinical and epidemiological investigations reporting that v olatile components of cigarette smoke could lead to the initiation and prog ression of periodontal disease.