Treponema denticola alters cell vitality and induces HO-1 and Hsp70 expression in porcine aortic endothelial cells.

Treponema denticola is an oral spirochete that is associated with periodontal disease and detected occasionally in extraoral lesions associated with systemic disorders such as cardiovascular diseases. The effect of specific bacterial products from oral treponemes on endothelium is poorly investigated. This study analyzed the ability of components of the outer membrane of T. denticola (OMT) to induce apoptosis and heat shock proteins (HO-1 and Hsp70) in porcine aortic endothelial cells (pAECs), compared with results obtained with classical pro-inflammatory lipopolysaccharide (LPS) treatment. Cellular apoptosis was detected when pAECs were treated with either OMT or LPS, suggesting that OMT can damage endothelium integrity by reducing endothelial cell vitality. Stimulation with OMT, similarly to LPS response, increased HO-1 and Hsp-70 protein expression in a time-dependent manner, correlating with a rise in HO-1 and Hsp-70 mRNA. Collectively, these results support the hypothesis that T. denticola alters endothelial cell function. Moreover, our in vitro experiments represent a preliminary investigation to further in vivo study using a pig model to elucidate how T. denticola leaves the initial endodontic site and participates in the development of several systemic diseases.