Periodontal disease is an infection that, in pregnant women, can act as a risk factor for preterm delivery by increasing local and systemic inflammatory responses. Objective. To analyze the presence of periodontal disease, proinflammatory cytokines, and prostaglandin E2 (PGE2) in pregnant patients at high risk for preterm delivery. Materials and Methods. Pilot study for a case-control study. We included 46 pregnant patients (23 patients at risk of preterm delivery as cases and 23 patients without risk of preterm delivery as controls). We excluded patients who received periodontal treatment, antibiotics, or antimicrobials over the last 3 months as well as those with infections or diseases such as diabetes or hypercholesterolemia. The patients underwent a periodontal assessment, and their levels of cytokines (interleukin- [IL-] 2, IL-6, IL-10, and tumor necrosis factor- [TNF-] α) and prostaglandin E2 (PGE2) were quantified. Results. Patients with periodontal disease showed higher levels of cytokines (IL-2, IL-6, IL-10, and TNF-α) and PGE2. Patients at high risk for preterm birth showed higher IL levels compared with patients at low risk for preterm delivery. PGE2 increased with the severity of periodontal disease. PGE2 was higher in patients at low risk for preterm delivery, although this difference was not significant. Conclusion. Periodontal disease can increase the systemic inflammatory response as well as the levels of PGE2 and inflammatory cytokines in pregnant patients.

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Hypertension is associated with chronic inflammation in the tissues and organs that are involved in the regulation of arterial pressure, such as kidneys and blood vessels. Periodontal disease affects systemic inflammatory markers, leading to endothelial dysfunction, atherosclerotic plaque instability, dyslipidaemia, and insulin resistance. These conditions can also cause an increase in the blood pressure. Nonsurgical periodontal therapies, such as scaling and root planning, can affect systemic markers of inflammation. We evaluated the effect of scaling and root planning on serum levels of inflammation biomarkers in hypertensive patients. The sample consisted of 19 hypertensive patients with Periodontitis. The patients underwent laboratory tests that included glycaemia, cholesterol, triglycerides and blood count. Blood pressure was measured before periodontal therapy, and the second blood pressure recording was obtained at the re-evaluation appointment. Quantification of peripheral blood cytokines was performed using the Milliplex Inflammation Human Cytokine kit (Interleukin 1-β, Interleukin-4, Interleukin-6, Interleukin-8, Interleukin-10, Interleukin-12 P70, Interleukin-17A, vascular endothelial growth factor and tumor necrosis factor-alpha). All cytokine levels decreased from the initial examination to reassessment. Cytokines that reflected a statistically significant difference included Interleukin-1β and endothelial vascular growth factor ( P = .04 and P = .004). Hypertensive patients with periodontitis undergoing non-surgical periodontal treatment exhibited a decrease in proinflammatory cytokine levels. Non-surgical periodontal treatment decreases the levels of systemic proinflammatory cytokines in controlled hypertensive patients.

Systemic Th17 response in the presence of periodontal inflammation The relationship between periodontitis and the pathogenesis of other inflammatory diseases, such as diabetes, rheumatoid arthritis and obesity has been an important topic of study in recent decades. The Th17 pathway plays a significant role in how local inflammation can influence systemic inflammation in the absence of systemic pathology. Objective: To determine Th17 biased-cells in systemically healthy patients in the presence of generalized chronic periodontitis. Methodology: A total of 28 patients were recruited without systemic inflammatory pathology, which was determined by clinical history, the Health Assessment Questionnaire (HAQ) and rheumatoid factor detection. Of these patients, 13 were diagnosed as healthy/gingivitis (H/G) and 15 as generalized chronic periodontitis (GCP). Th17 (CD4 + CD161 +) cells and Th17IL23R + (CD4 + CD161 + IL-23R +) cells were quantified by flow cytometry, based on the total cells and on the lymphocyte region, termed the "enriched population" (50,000 events for each). Results: The percentages of Th17 cells of the H/G and periodontitis groups were similar on total cells and enriched population (19 vs 21.8; p=4.134 and 19.6 vs 21.8; p=0.55). However, Th17IL23R+ cells differ significantly between periodontally healthy patients and generalized chronic periodontitis patients in both total cell (0.22% vs 0.65%; p=0.0004) and enriched populations (0.2% vs 0.75%; p=0.0266). Conclusions: GCP patients (otherwise systemically healthy) were characterized by increased Th17-proinflammatory cell phenotype positive for the IL-23 receptor in peripheral blood. The proportion of Th17 cells that are negative for the IL-23 receptor in the peripheral blood of systemically healthy patients seemed to be unaffected by the presence or absence of chronic periodontitis.