Table of Contents Author Guidelines Submit a Manuscript
International Journal of Dentistry
Volume 2017, Article ID 2697210, 6 pages
https://doi.org/10.1155/2017/2697210
Research Article

LPS from P. gingivalis Negatively Alters Gingival Cell Mitochondrial Bioenergetics

1College of Dental Medicine, Roseman University of Health Sciences, South Jordan, UT, USA
2Department of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA

Correspondence should be addressed to Benjamin T. Bikman; ude.uyb@namkib_nimajneb

Received 23 November 2016; Revised 13 February 2017; Accepted 20 March 2017; Published 16 May 2017

Academic Editor: Gianrico Spagnuolo

Copyright © 2017 Kiran Napa et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Objective. Oral inflammatory pathologies are linked to increased oxidative stress, thereby partly explaining their relevance in the etiology of systemic disorders. The purpose of this work was to determine the degree to which LPS from Porphyromonas gingivalis, the primary pathogen related to oral inflammation, altered gingival mitochondrial function and reactive oxygen species generation. Methods. Human gingival fibroblast (HGF-1) cells were treated with lipopolysaccharide of P. gingivalis. Mitochondrial function was determined via high-resolution respirometry. Results. LPS-treated HGF-1 cells had significantly higher mitochondrial complex IV and higher rates of mitochondrial respiration. However, this failed to translate into greater ATP production, as ATP production was paradoxically diminished with LPS treatment. Nevertheless, production of the reactive H2O2 was elevated with LPS treatment. Conclusions. LPS elicits an increase in gingival cell mitochondria content, with a subsequent increase in reactive oxygen species production (i.e., H2O2), despite a paradoxical reduction in ATP generation. These findings provide an insight into the nature of oxidative stress in oral inflammatory pathologies.