Periodontal Disease Shortens the Telomere Length in Human Gingival Crevicular Epithelium Cells and Human Umbilical Endothelial Cells

Abstract

Background: Telomere length, a biomarker of cellular aging, is decreased by inflammation. It is uncertain whether chronic inflammation, such as periodontal disease (PD), shortens telomere lengths. We compared the telomere lengths of gingival crevicular epithelium cells from both the healthy side and the diseased side of patients with PD and investigated whether lipopolysaccharide derived from a periodontal bacterium, Porphyromonas gingivalis (Pg-LPS) shortened the telomere lengths of human umbilical endothelial cells (HUVECs). Methods: We extracted genomic DNA from gingival crevicular epithelium cells on the diseased and healthy sides collected from 25 patients with PD (mean age 72.4 years, 17 females. 8 males) and measured the telomere lengths by the polymerase chain reaction (PCR) method. After stimulating HUVECs with Pg-LPS at concentrations of 0.05, 0.1, and 1.0 µg/mL, we extracted genomic DNA and measured the telomere lengths. Results: The telomere lengths on the patients' diseased sides were significantly shorter than those on the healthy sides (392.6 ± 232.8 kb vs. 599.5 ± 467.0 kb, p = 0.004). In the HUVECs, a concentration-dependent but nonsignificant decrease in telomere length was observed in response to Pg-LPS. Expressed as a ratio relative to the telomere lengths of unstimulated HUVECs, the ratio of telomere lengths decreased in a concentration-dependent manner, and the Pg-LPS concentration 1.0 µg/mL significantly decreased the ratio compared to the telomere lengths of unstimulated HUVECs. Conclusions: Gingival crevicular epithelial cells of individuals with PD are believed to undergo aging due to telomere shortening. The involvement of one of the factors of periodontal virulence, LPS, is suspected as the mechanism.