Periodontitis is associated with systemic inflammation and vascular endothelial dysfunction in patients with lacunar infarct.

Abstract

Periodontitis has been associated with lacunar infarct (LI), a type of cerebral small vessel disease. The objective of this study was to ascertain whether periodontitis is associated with increased circulating levels of systemic inflammation and endothelial dysfunction biomarkers in patients with LI. One hundred twenty patients with LI and 120 healthy controls underwent a full-mouth periodontal examination. The periodontal inflamed surface area (PISA) was calculated for each participant. Demographic, medical, and neurological information were recorded from all of them. In addition, blood samples were collected in order to investigate differences in terms of interleukin (IL)-6, IL-10, pentraxin (PTX) 3, soluble fragment of tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and amyloid-beta (Aβ) peptides (i.e., Aβ1-40 , and Aβ1-42 ) measured in serum. Periodontitis was independently associated with increased levels of IL-6 (R2 =0.656, P<0.001), PTX3 (R2 =0.115, P<0.001), sTWEAK (R2 =0.527, P<0.001), and Aβ1-40 (R2 =0.467, P<0.001) in patients with LI. Within patients with poor outcome, PISA positively correlated with IL-6 (r=0.738, P<0.001), PTX3 (r=0.468, P=0.008), sTWEAK (r=0.771, P<0.001), and Aβ1-40 (r=0.745, P<0.001). Our data suggest a link between periodontitis, systemic inflammatory response, and disruption of the vascular endothelial function in patients with LI. Experimental studies are needed to elucidate possible pathways through which periodontitis could lead to this systemic inflammatory state with impairment of the endothelial function in LI. Further longitudinal studies with large samples are warranted to confirm our findings.