Modulação do sistema purinérgico e do estresse oxidativo em soro e plaquetas de pacientes com doença periodontal

Abstract

Introduction: Periodontal disease (PD) is characterized by chronic inflammation of the periodontium that leads to structural loss. The relationship between the activation of the purinergic system, oxidative stress (OS), and periodontium inflammation has been increasingly studied. Methodology: This was a cross-sectional, observational study with quantitative analysis, in which platelet and serum samples from 58 PD patients and 25 control individuals were evaluated. A collection of 30 mL of peripheral blood was performed using vacuum tubes with sodium citrate and EDTA. The activity of the enzymes E-NTPDase (CD39) and E-5'-nucleotidase (CD73) was determined as described by LEAL et al. (2005). OS was analyzed by quantifying superoxide dismutase (SOD), thiobarbituric acid-reactive species (TBARS), and reactive species (RS), as described by MCCORD and FRIDOVICH (1969), JENTZSCH et al. (1996), and ALI, LEBEL and BONDY (1992), respectively. Statistical analysis was performed using the Mann-Whitney test, with normality assessment by the Shapiro Wilk and correlation by Pearson's test and Spearman's test, considering results with p ≤ 0.05 as significant. Results: The hydrolysis of ATP by CD39 in serum (p=0.0003) and in platelets (p=0.0025) was greater in the PD group compared to the control group. The analysis of AMP hydrolysis by CD73 showed higher levels in the PD group compared to controls, both in serum (p=0.0004) and platelets (p=0.0053). The hydrolysis of ADP by CD39, in both samples, did not show statistical significance (p=0.4289 in serum, and p=0.1667 in platelets). The quantification of TBARS (p<0.0001) and ROS (p=0.0190) were higher in the PD group, while SOD (p<0.0001) was higher in the control group. Discussion: We observed greater activity of CD39 in the PD group, due to high levels of extracellular ATP in these patients, stimulating the release of pro-inflammatory cytokines. The pronounced activity of CD73 is justified by the greater availability of AMP to be hydrolyzed into adenosine. Moreover, the presence of an inflammatory response in the platelet analysis indicates a higher risk of thrombotic events in PD patients. The increase of pro-oxidant molecules concurrent with the decrease in SOD contributes to the inflammatory and aggregating process. Conclusion: Given the results presented, we observed a strong presence of purinergic signaling and OS in the onset of inflammation in PD, as well as the risk of thrombotic events due to platelet activation induced by inflammation. Further studies are needed to better elucidate the situation and develop therapeutic strategies.