Denture-related stomatitis is associated with endothelial dysfunction

Oral inflammation, such as periodontitis, can lead to endothelial dysfunction, accelerated atherosclerosis, and vascular dysfunction. The relationship between vascular dysfunction and other common forms of oral infections such as denture-related stomatitis (DRS) is unknown. Similar risk factors predispose to both conditions including smoking, diabetes, age, and obesity. Accordingly, we aimed to investigate endothelial function and major vascular disease risk factors in 44 consecutive patients with dentures with clinical and microbiological features of DRS (n = 20) and without DRS (n = 24). While there was a tendency for higher occurrence of diabetes and smoking, groups did not differ significantly in respect to major vascular disease risk factors. Groups did not differ in main ambulatory blood pressure, total cholesterol, or even CRP. Importantly, flow mediated dilatation (FMD) was significantly lower in DRS than in non-DRS subjects, while nitroglycerin induced vasorelaxation (NMD) or intima-media thickness (IMT) was similar. Interestingly, while triglyceride levels were normal in both groups, they were higher in DRS subjects, although they did not correlate with either FMD or NMD. Conclusions. Denture related stomatitis is associated with endothelial dysfunction in elderly patients with dentures. This is in part related to the fact that diabetes and smoking increase risk of both DRS and cardiovascular disease

Periodontitis as an inflammatory trigger in hypertension: from basic immunology to clinical implications

Hypertension and periodontitis are both highly prevalent co-morbidities worldwide, and their occurrence increases with age. Multiple observational epidemiological studies have shown that periodontitis is associated with an increased cardiovascular disease (CVD) occurrence. Large systematic reviews and metanalyses further show that periodontitis increases the risk of hypertension and is associated with increased systolic and diastolic blood pressure. Genetic and clinical evidence, utilizing mendelian randomization and randomized clinical trials, support the causal role of periodontitis in hypertension. The mechanisms of this link remain unclear. Critical components of immune and inflammatory pathogenesis of periodontitis considerably overlap with immune mechanisms of hypertension. Clinical studies support that both C-reactive protein (CRP) levels and white blood cell counts (WBC) mediate the relationship between periodontal disease and high blood pressure. In particular, activation of Th1, Th17, T regulatory cells, and proinflammatory monocytes has been shown to be essential in both conditions. Immunosenescent dysregulated CD28null T cells have been implicated, along with key effector cytokines such as interleukin 6 (IL-6), TNF-alpha (TNF-α), interferon-gamma (IFN-γ), and interleukin 17 (IL-17). A better understanding of the relationships between hypertension and periodontitis is essential not only for possible utilization of this knowledge for a non-pharmacological approach to improving blood pressure control. It may also provide valuable pathogenetic clues linking inflammation and hypertension, which has become particularly relevant in the light of links between hypertension and autoimmune disorders or, more recently, COVID-19

Th1-type immune responses to Porphyromonas gingivalis antigens exacerbate angiotensin II-dependent hypertension and vascular dysfunction

Background and Purpose: Emerging evidence indicates that hypertension is mediated by immune mechanisms. We hypothesized that exposure to Porphyromonas gingivalis antigens, commonly encountered in periodontal disease, can enhance immune activation in hypertension and exacerbate blood pressure elevation, vascular inflammation and vascular dysfunction. Experimental Approach: Th1 immune response were elicited through immunizations using Porphyromonas gingivalis lysate antigens (10ug) conjugated with aluminium oxide (50ug) and IL‐12 (1ug). The hypertension and vascular endothelial dysfunction evoked by sub‐pressor doses of Angiotensin II (0.25mg/kg/day) were studied and vascular inflammation was quantified by flow cytometry and real time polymerase chain reaction. Key Results: Systemic T cell activation, characteristic for hypertension, was exacerbated by P. gingivalis antigen stimulations. This translated into increased aortic vascular inflammation with enhanced leukocytes, in particular, T cell and macrophage infiltration. Expression of the Th1 cytokines, Interferon‐γ and Tumour Necrosis Factor‐α and the transcription factor TBX21 was increased in aortas of P. gingivalis/Interleukin‐12/aluminium oxide immunized mice, while IL‐4 and TGF‐β were unchanged. These immune changes in mice with induced T helper type 1 immune responses were associated with enhanced blood pressure elevation and endothelial dysfunction compared to control mice in response to two weeks infusion of a sub‐pressor dose of Angiotensin II. Conclusion and Implications: These studies support the concept that Th1 immune responses induced by bacterial antigens such as P. gingivalis can increase sensitivity to sub‐pressor pro‐hypertensive insults such as low dose Angiotensin II, therefore providing a mechanistic link between chronic infection such as periodontitis and hypertension

Medycyna i Społeczeństwo. Materiały konferencyjne

Ze wstępu: "Z inicjatywy i pod patronatem Krakowskiej Szkoły Wyższej im. Andrzeja Frycza Modrzewskiego w Krakowie odbyła się w styczniu 2003 r. konferencja naukowa lekarzy, farmaceutów, biochemików, filozofów, fizjopatologów, farmakologów i klinicystów, których rozważania skupiały się wokół obszernego tematu „MED YCYNAISPOŁECZEŃSTWO Spotkanie otworzył JM Rektor Prof. KSW dr hab. Zbigniew Maciąg. Rektor wyraził podziękowanie wykładowcom i wyraził głęboką nadzieję, że kolejny numer wydawnictwa Szkoły Acta Academiae Modrevianae, złożony z wybranych prac prezentowanych na konferencji, służył będzie społeczeństwu."(...