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Background and Purpose: This study analyses whether first‐line antihypertensive drugs ameliorate the dysbiosis state in hypertension, and to test if this modification contributes to their blood pressure (BP) lowering properties in a genetic model of neurogenic hypertension. Experimental Approach: Twenty‐week‐old male Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were untreated or treated with captopril, amlodipine or hydrochlorothiazide. A faecal microbiota transplantation (FMT) experiment was also performed by gavage of faecal content from donor SHR‐treated groups to SHR recipients for 3 weeks. Key results: Faeces from SHR showed gut dysbiosis, characterized by lower acetate‐ and higher lactate‐producing bacteria and lower strict anaerobic bacteria. All three drugs increased the anaerobic bacteria proportion, captopril and amlodipine restored the proportion of acetate‐producing bacterial populations to WKY levels, whereas hydrochlorothiazide decreased butyrate‐producing bacteria. Captopril and amlodipine decreased gut pathology and permeability and attenuated sympathetic drive in the gut. Both drugs decreased neuroinflammation and oxidative stress in the hypothalamic paraventricular nuclei. Hydrochlorothiazide was unable to reduce neuroinflammation, gut sympathetic tone and gut integrity. FMT from SHR‐amlodipine to SHR decreased BP, ameliorated aortic endothelium‐dependent relaxation to acetylcholine, lowered NADPH oxidase activity, aortic Th17 infiltration and reduced neuroinflammation, whereas FMT from SHR‐hydrochlorothiazide did not have these effects. Conclusions and Implications: First‐line antihypertensive drugs induced different modifications of gut integrity and gut dysbiosis in SHR, which result in no contribution of microbiota in the BP lowering effects of hydrochlorothiazide, whereas the vasculo‐protective effect induced by amlodipine involves gut microbiota reshaping and gut‐immune system communication. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to analyze the effects of periodontal treatment on markers of atherosclerotic coronary artery disease and circulating levels of periostin. Background: Periostin is necessary for periodontal stability, but it is highly present in atherosclerotic plaques. Treatment of periodontal disease, with low levels of local periostin, is thought to reduce systemic levels of periostin. Thus, this may contribute to cardiovascular health. Methods: A pilot randomized controlled clinical trial was designed to include patients with severe periodontal disease and history of atherosclerotic coronary artery disease. Samples of gingival crevicular fluid (GCF) and serum were collected before and after periodontal treatment by periodontal surgery or non‐surgical therapy. The levels of several markers of inflammation and cardiovascular damage were evaluated including CRP, IFN‐γ, IL‐1ß, IL‐10, MIP‐1α, periostin, and TNF‐α in GCF and CRP, Fibrinogen, IFN‐γ, IL‐1ß, IL‐6, IL‐10, L‐Selectin, MIP‐1α, Periostin, TNF‐α, and vWF in serum. Results: A total of 22 patients with an average of 56 years old were recruited for participating in this study. Twenty of them were male. Most of them (82%) had suffered an acute myocardial event and underwent surgery for placing 1, 2, or 3 stents in the coronary arteries more than 6 months ago but less than 1 year. The treatment of periodontal disease resulted in an overall improvement of all periodontal parameters. Regarding the evaluation of GCF and serum, a significant increase of periostin in the GCF was observed after periodontal surgery. In contrast, although other markers in GCF and serum improved, no significant correlations were found. Conclusion: Treatment of periodontal disease through periodontal surgery induces a local and transient increase in the levels of periostin in the gingival crevicular fluid. The effects on systemic markers of inflammation and cardiovascular function have not been confirmed. [ABSTRACT FROM AUTHOR]

Purpose: To determine clinical parameters, histologic features, and radiographic linear bone width changes of regenerated bone using different biomaterials for ridge preservation following tooth extraction. Materials and Methods: For this pilot study, five patients were grafted with anorganic bovine bone and collagen plus recombinant human platelet-derived growth factor-BB (rhPDGF-BB), five patients were grafted with anorganic bovine bone and collagen alone, and five patients did not receive any biomaterial (control) after tooth extraction. Clinical, histologic, and radiographic evaluations were carried out 4 months postextraction. Results: Differences in terms of buccolingual width were found when comparing the control group to the group grafted with anorganic bovine bone and collagen plus rhPDGF-BB (P = .012). No statistical differences were observed between the groups in terms of mineralized or nonmineralized tissue formation or in terms of the number of osteoblasts or osteocytes per mm2 after 4 months of healing. Interestingly, the number of vessels in the grafted area was found to be significantly different among the three groups (P = .005). The number of Musashi-1 positive cells was also different among groups, both in the mineralized and the nonmineralized areas of the grafted bone (P = .024 and .005, respectively). Conclusion: Anorganic bovine bone with bovine collagen is an efficient biomaterial to avoid postextraction resorption of the alveolar ridge. The addition of rhPDGF-BB appears to improve the biologic features of the newly formed bone and decrease bone resorption; further studies are needed for confirmation. [ABSTRACT FROM AUTHOR]

In order to re‐evaluate the safest area to incise skin and the flexor retinaculum (FR) when performing a carpal tunnel release (CTR), we carried out a mapping study of the nerve endings in the skin and FR on cadaver specimens, which, unlike previous studies for the first time, includes histomorphometry and image digital analysis. After dividing the skin and FR into 20 and 12 sections, respectively, we carried out a histomorphological analysis of nerve endings. The analysis was performed by two neutral observers on 4‐μm histological sections stained with hematoxylin–eosin (H‐E), and Klüver–Barrera with picrosirius red (KB + PR) methods. A semi‐automatic image digital analysis was also used to estimate the percentage of area occupied per nerve. We observed a lower quantity of nerve endings in the skin of the palm of the hand in line with the ulnar aspect of the 4th finger. The ulnar aspect of the FR was the most densely innervated. However, there are no statistically significant differences between sections in the percentage of area occupied per nerve both in the skin and in the FR. We concluded that there is not a safe area to incise when performing carpal tunnel surgery, but taking into account the quantity of nerve endings present in skin and FR, we recommend an incision on the axis of the ulnar aspect of 4th finger when incising skin and on the middle third of the FR for CTR. [ABSTRACT FROM AUTHOR]

Purpose: To examine differences in morphology and in immunophenotype subsets between chronic periodontitis (CP) and peri-implantitis (P-I) lesions and to test the diagnostic agreement (CP vs P-I) among three independent observers, based on histopathological features. Materials and methods: This observational cross-sectional study included 15 gingival biopsies of CP lesions and 15 biopsies of P-I lesions for double-blinded examination by three independent pathologists. Inflammatory infiltrate intensity was assessed semiquantitatively on a 4-point scale, determining the percentage of lymphocytes, plasma cells, monocytes/macrophages, and granulocytes and the presence/absence of bacterial colonies. Immunohistochemical analyses were performed to verify the inflammatory infiltrate subset data (CD45, CD38, CD68 and myeloperoxidase [MPO]-positive), and number of vessels. Kappa statistic was used to evaluate the degree of diagnostic concordance among examiners. Results: Inflammatory infiltrate was significantly more severe in P-I cases (P = 0.01), which showed a significantly higher percentage of plasma cells (P = 0.004) than in CP cases. Immunohistochemically, the percentage of leukocyte subsets was generally lower in CP (CD38: 32.05%; CD68: 6.45% and MPO: 8.62%) than in P-I (CD38: 61.13%; CD68: 9.09% and MPO: 7.47%) (CD38 P = 0.001, P = 0.955 and P = 0.463, for remaining subsets, respectively; Mann-Whitney U-test). The interobserver diagnostic agreement was poor or slight (kappa = -0.18 to 0.13). Conclusions: Despite the significantly more severe general inflammatory infiltrate and plasma cells in P-I cases, it proved difficult to detect reliable differential morphological features based on histopathological images of these CP and P-I soft-tissue samples, obtaining low inter-observer and intraobserver diagnostic agreement. [ABSTRACT FROM AUTHOR]