Ultrastructural Study of Cultured Human Gingival Fibroblasts Exposed to Endotoxin

Abstract

Our current concept of periodontal disease is that some mediators found in the gingival sulcus are able to penetrate the epithelial barrier and produce tissue destruction in the periodontium. Endotoxin, one such mediator, recently has been the subject of considerable study. The purpose of this investigation was to substantiate the role of endotoxin in the pathogenesis of periodontal disease by ascertaining its action on cellular and subcellular components. In order to accomplish this, cultured human gingival fibroblasts were exposed to media containing either 300 μg/ml or 500 μg/ml of endotoxin and untreated medium for a period of 24 hours. Cells were harvested and prepared for electron microscopy by conventional methods. Electron microscopic examination revealed alterations in mitochondria, Golgi apparatus, lysosomal‐like bodies, cytofilaments and plasma membrane. Relationship of these alterations to pathologic processes is discussed.

Lipopolysaccharide increases cell surface‐associated fibronectin in fibroblasts in vitro

“…Cytotoxic effects of lipopolysaccharide on fibroblasts have been reported. However, the effect apparently occurs at much higher concentrations of lipopolysaccharide (25-200 |ig/ml) than that found in the connective tissue of periodontal disease (5,14,15,19,23). The concentration used in this study was as low as that reported in the tissues from periodontal disease.…”

Effect of aging on expression of nitric oxide and inducible nitric oxide synthase in human gingival fibroblasts

“…Porphyromonas gingivalis (P. gingivalis) is a Gram-negative, anaerobic rod that is considered to be one of the main bacteria associated with adult periodontitis 17) , and its LPS in the cell wall is believed to be one of the virulent factors associated with the development of periodontitis 18) . IFN-γ acts synergistically with LPS to induce the secretion of NO by activating a number of transcription factor signaling cascades 19) .…”

Epithelial cell response to challenge of bacterial lipoteichoic acids and lipopolysaccharides in vitro

“…Furthermore, bacterial surface antigens have been reported to increase epithelial permeability, penetrate healthy gingival sulcular epithelium [16,17], cause complement activation, stimulate leucocyte function and increase cytokine production and bone resorption [10,[18][19][20][21][22][23][24]. In addition, different LPSs show a slight enhancement of gingival fibroblast proliferation at concentrations below 1 ìg=ml, modest to significant suppression of fibroblast proliferation at a concentration range of 10-200 ìg=ml [25][26][27][28][29] and degeneration and death of fibroblasts at concentrations of 300-500 ìg=ml [28,30]. Both growth enhancement and growth inhibition have been described in rat epithelial cells after treatment with LPS from non-oral bacteria [31][32][33][34].…”