Circulation levels of acute phase proteins pentraxin 3 and serum amyloid A in atherosclerosis have correlations with periodontal inflamed surface area

Abstract

ObjectivesOne of the plausible mechanisms in the relationship between periodontitis and coronary artery disease (CAD) is the systemic inflammatory burden comprised of circulating cytokines/mediators related to periodontitis. This study aims to test the hypothesis that periodontal inflamed surface area (PISA) is correlated with higher circulating levels of acute phase reactants (APR) and pro-inflammatory cytokines/mediators and lower anti-inflammatory cytokines/mediators in CAD patients.Material and MethodsPatients aged from 30 to 75 years who underwent coronary angiography with CAD suspicion were included. Clinical periodontal parameters (probing depth - PD, clinical attachment loss, and bleeding on probing - BOP) were previously recorded and participants were divided into four groups after coronary angiography: Group 1: CAD (+) with periodontitis (n=20); Group 2: CAD (+) without periodontitis (n=20); Group 3: CAD (-) with periodontitis (n=21); Group 4: CAD (-) without periodontitis (n = 16). Serum interleukin (IL) −1, −6, −10, tumor necrosis factor (TNF)-α, serum amyloid A (SAA), pentraxin (PTX) 3, and high-sensitivity C-reactive protein (hs-CRP) levels were measured with ELISA.ResultsGroups 1 and 3 showed periodontal parameter values higher than Groups 2 and 4 (p<0.0125). None of the investigated serum parameters were statistically significantly different between the study groups (p>0.0125). In CAD (-) groups (Groups 3 and 4), PISA has shown positive correlations with PTX3 and SAA (p<0.05). Age was found to predict CAD significantly according to the results of the multivariate regression analysis (Odds Ratio: 1.17; 95% Confidence Interval: 1.08-1.27; p<0.001).ConclusionsAlthough age was found to predict CAD significantly, the positive correlations between PISA and APR in CAD (-) groups deserve further attention, which might depend on the higher PISA values of periodontitis patients. In further studies conducted in a larger population, the stratification of age groups would provide us more accurate results.

Increase in serum and salivary neutrophil gelatinase-associated lipocalin levels with increased periodontal inflammation

“…3 Various studies used the PISA to understand the association between systemic diseases and periodontitis. [4][5][6] Considering their results, PISA may be used as a continuous periodontal variable in conjunction with microbiological or biochemical variables (cytokine(s)/mediator(s)) in periodontal medicine studies, to clarify any potential role in the pathogenesis of both periodontal and systemic diseases.…”

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

“…Recently, it has been shown that PISA was positively correlated with PTX3 levels in patients with periodontitis without coronary artery disease (CAD) and IL‐10 was inversely correlated with PD in patients with CAD. However, no association was found with IL‐6 …”

“…However, no association was found with IL-6. 40 It has been suggested that periodontitis might be associated with endothelial dysfunction. 41 Although PTX3 is an APR, it is produced by macrophages or endothelial cells (ECs) in response to an inflammatory stimulus related with atherosclerosis 42,43 and is associated with diminished flowmediated dilatation (FMD), thus, being a more powerful predictor of endothelial dysfunction than C-reactive protein.…”

Time to put periodontal disease on the list of chronic inflammatory diseases contributing to premature atherosclerosis

“…To establish proof, we will need to quantify the specific level of inflammation of oral origin that contributes to the systemic inflammatory burden. Although efforts to do so are underway, 6 there is still work to be done. Long-term intervention studies assessing the effect that ongoing dental therapy (aimed at helping patients achieve and maintain a functioning dentition with minimal inflammation over their life span) has on associated systemic diseases will be necessary before causality can be determined.…”