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 the elevation in BP, vascular inflammation and vascular dysfunction. Experimental Approach Th1 immune responses were elicited through immunizations using P. gingivalis lysate antigens (10 μg) conjugated with aluminium oxide (50 μg) and IL‐12 (1 μg). The hypertension and vascular endothelial dysfunction evoked by subpressor doses of angiotensin II (0.25 mg·kg−1·day−1) were studied, and vascular inflammation was quantified by flow cytometry and real‐time PCR. Key Results Systemic T‐cell activation, a characteristic of hypertension, was exacerbated by P. gingivalis antigen stimulation. This translated into increased aortic vascular inflammation with enhanced leukocyte, in particular, T‐cell and macrophage infiltration. The expression of the Th1 cytokines, IFN‐γ and TNF‐α, and the transcription factor, TBX21, was increased in aortas of P. gingivalis/IL‐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 an enhanced elevation of BP and endothelial dysfunction compared with control mice in response to 2 week infusion of a subpressor dose of angiotensin II. Conclusions and Implications These results support the concept that Th1 immune responses induced by bacterial antigens such as P. gingivalis can increase sensitivity to subpressor pro‐hypertensive insults such as low‐dose angiotensin II, thus providing a mechanistic link between chronic infection, such as periodontitis, and hypertension. Linked Articles This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc

IntroductionThe presence of oral inflammation has recently been linked with the pathogenesis of cardiovascular diseases. While numerous studies have described links between periodontitis and endothelial dysfunction, little is known about the influence of denture-related stomatitis (DRS) on cardiovascular risk. Therefore, the aim of this study was to determine whether the treatment of DRS can lead to improvement of the clinical measures of vascular dysfunction.Material and methodsThe DRS patients were treated with a local oral antifungal agent for 3 weeks. Blood pressure, flow-mediated dilatation (FMD) and nitroglycerine-mediated vascular dilatation (NMD) were measured during three study visits: before treatment, one day and two months after conclusion of antifungal therapy.ResultsFlow-mediated dilatation measurements showed significant improvement of endothelial function 2 months after treatment (FMD median 5%, 95 CI: 3–8.3 vs. 11%, 95% CI: 8.8–14.4; p < 0.01), while there was no difference in control, endothelium-independent vasorelaxations (NMD; median = 15.3%, 95% CI: 10.8–19.3 vs. 12.7%, 95% CI: 10.6–15; p = 0.3). Other cardiovascular parameters such as systolic (median = 125 mm Hg; 95% CI: 116–129 vs. 120 mm Hg, 95% CI: 116–126; p = 0.1) as well as diastolic blood pressure and heart rate (median = 65.5 bpm, 95% CI: 56.7–77.7 vs. 71 bpm, 95% CI: 66.7–75; p = 0.5) did not change during or after the treatment.ConclusionsTreatment of DRS is associated with improvement of endothelial function. Since endothelial dysfunction is known to precede the development of severe cardiovascular disorders such as atherosclerosis and hypertension, patients should be more carefully screened for DRS in general dental practice, and immediate DRS treatment should be advised.

Despite continuous efforts to prevent cardiovascular diseases (CVDs), heart failure prevails as the number one cause of death in developed countries. To properly treat CVDs, scientists had to take a closer look at the factors that contribute to their pathogenesis and either modernize current pharmaceuticals or develop brand new treatments. Enhancement of current drugs, such as tolvaptan and omecamtiv mecarbil, sheds new light on already-known therapies. Tolvaptan, a vasopressin antagonist, could be adopted in heart failure therapy as it reduces pre- and afterload by decreasing systolic blood pressure and blood volume. Omecamtiv mecarbil, which is a myosin binding peptide, could aid cardiac contractility. The next generation vasodilators, serelaxin and ularitide, are based on naturally occurring peptides and they reduce peripheral vascular resistance and increase the cardiac index. In combination with their anti-inflammatory properties, they could turn out to be extremely potent drugs for heart failure treatment. Cardiotrophin has exceeded many researchers’ expectations, as evidence suggests that it could cause sarcomere hypertrophy without excessive proliferation of connective tissue. Rapid progress in gene therapy has caused it to finally be considered as one of the viable options for the treatment of CVDs. This novel therapeutic approach could restore stable heart function either by restoring depleted membrane proteins or by balancing the intracellular calcium concentration. Although it has been set back by problems concerning its long-term effects, it is still highly likely to succeed.

Background Two clinical parameters, the gingival thickness (GT) and the width of keratinized tissue (WKT), describe the gingival phenotype, which is defined as the 3-dimensional volume of the gingiva. The periodontal phenotype additionally includes the thickness of the labial plate of the alveolar crest (TLPAC). Material/Methods Thirty patients with healthy periodontium on the upper canines and incisors underwent measurements for crestal, supracrestal, free gingival thickness (FGT), the alveolar crest-gingival margin (AC-GM), alveolar crest-cementoenamel junction distance, and the TLPAC at 2, 4, and 8 mm apically from the edge of the alveolar crest using cone-beam computed tomography (CBCT) with computer-aided design and prosthetic-driven implant planning technology. For each tooth, the gingival and periodontal phenotype was evaluated on the basis of the gingival thickness, width of keratinized tissue (WKT), and TLPAC measurements. Each patient’s periodontal phenotype was evaluated according to the coronal width/length ratio of both the upper central incisors. Results The dentogingival units had varying average values for the 3 periodontal phenotypes (thin phenotype: FGT 0.65±0.06 mm, WKT 4.85±1.18 mm, AC-GM 3.17±0.64 mm, TLPAC2 0.66±0.28 mm; medium phenotype: FGT 0.87±0.07 mm, WKT 5.49±1.23 mm, AC-GM 3.36±0.65 mm, TLPAC2 0.76±0.37 mm; and thick phenotype: FGT 1.20 mm, WKT 6.00 mm, AC-GM 3.90 mm, TLPAC2 0.90 mm). Positive correlations were seen among WKT, FGT, AC-GM, and TLPAC2. Conclusions Positive correlations between the FGT and WKT, and the AC-GM distance confirm that measurements using CBCT with computer-aided design and prosthetic-driven implant planning technology can evaluate the gingival phenotype and TLPAC2 for the periodontal phenotype.

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