Eradication of Gastric Helicobacter pylori Ameliorates Halitosis and Tongue Coating

Background: The influence of gastric Helicobacter pylori infection on the development of oral pathoses remains unclear. The aim of this study is to examine the influence of gastric H. pylori infection on occurrence of halitosis and coated tongue. Materials and methods: Ninety-eight patients with dyspepsia were included in the study and their salivary samples and gastric biopsies were analyzed for the presence of H. pylori by Nested-PCR. Halitosis and coated tongue were assessed at the initial examination and 3 months after systemic eradication therapy against H. pylori. Results: Gastric biopsies of 66 patients were positive for H. pylori. Only one saliva sample was H. pylori positive. At initial examination, halitosis was observed in 20 patients (30.3%) out of 66 who had gastric H. pylori infection and in only 3 patients (9.4%) out of 32 without H. pylori infection (p = 0.0236). Coated tongue was diagnosed in 18 (27.2%) patients with the infection compared to only 2 (6.25%) patients negative for gastric H. pylori (p = 0.0164). Patients with gastric infection were treated with the triple eradication therapy (Amoxicillin, Clarythromycin, Pantoprazol) and their gastric biopsies and oral status were examined 3 months later. Halitosis was significantly more prevalent in the group of patients with persistent H. pylori infection (42.1%) compared to only 6.4% of patients in the group where infection was successfully eradicated (p = 0.0012). Coated tongue was diagnosed in 47.4% of patients where H. pylori was still present after eradication therapy and in only 6.4% where eradication succeeded (p = 0.0003). Conclusion: Our findings suggest that eradication of gastric H. pylori significantly alleviates halitosis and coated tongue, the two oral conditions that may be considered as extragastric manifestations of this common chronic bacterial infection

Intensive Remodeling of Purkinje Cell Spines after Climbing Fibers Deafferentation Does Not Involve MAPK and Akt Activation

Subtotal lesion of the inferior olive (IO) achieved by treating experimental animals with 3-acetylpyridine (3AP) induces partial Purkinje cells (PCs) deafferentation that leads to PC hyperactivity and new spine formation. Coincidentally, the olivary terminals belonging to the few survived olivary neurons undergo an extensive collateral sprouting resulting in reinnervation of the neighboring denervated PCs. We obtained chemical deafferentation of PCs in adult rats (body weight, 120-170 g; age, 35-40 days) by a single intraperitoneal injection of 3AP (65 mg/kg body weight), and as early as 3 days after 3AP treatment, important morphological changes could be observed on PCs. Mitogen-activated protein kinase (MAPK) cascades and more specifically extracellular signal-regulated kinases 1/2 (ERK1/2) play a critical role in the signaling events underlying synaptic plasticity. For instance, long-term depression (LTD) in the adult hippocampus and long-term potentiation (LTP) in cerebellum both involve ERK activation. Since PCs deprived of their climbing fibers (CFs) afferents initiate an intensive remodeling of the spines and rapid recall of the remaining CFs, it prompted us to see whether the observed phenomena correlated with MAPK and Akt activation. Immunohistochemistry and Western blotting were done at various time points after 3AP application (from 24 h to 6 days), as the exact dynamics of CF loss is not precisely known. As judged by Western blotting, there was no increase of activated ERK in the cerebellum. However, immunohistochemistry revealed increased ERK phosphorylation in the "pinceaux" of basket cells in 3AP animals. Similarly, stress-activated protein kinase(SAPK)/c-Jun N-terminal kinase (JNK), p38 MAPK, and Akt activation were also studied by means of Western blotting and immunohistochemistry. Upon 3AP treatment no changes in phosphorylation status could be seen in the different kinases subjected to analysis. Our results suggest that activation of MAPK and Akt cascades is not essential in this model of neuronal plasticity

The association between apical periodontitis and adverse pregnancy outcomes: a systematic review

BackgroundThe association between adverse pregnancy outcomes (APOs) and maternal apical periodontitis remains unclear as it has not been examined rigorously or reviewed systematically.ObjectiveTo systematically review and critically evaluate the available evidence on the association of maternal apical periodontitis with several APOs.MethodsA literature search was conducted using the following electronic databases: Clarivate Analytics’ Web of Science, Scopus, PubMed, and Cochrane Central Register of Controlled Trials (CENTRAL), from inception to 25 February 2021, with no language restrictions. Observational studies including longitudinal clinical trials, cohort, case–control and cross-sectional studies of prospective and retrospective design were included. Articles with duplicate or overlapping results, abstract-only papers, case reports, case series, animal studies and reviews were excluded. Two independent reviewers were involved in study selection, data extraction and appraising the included studies; disagreements were resolved by a third reviewer. The Newcastle–Ottawa Scale (NOS) and the adapted form of the NOS were used to assess the quality for case–control and cross-sectional studies, respectively.ResultsTwo case–control and one cross-sectional study were included in the current review. The included studies were published between 2015 and 2017, with a total of 1187 participating individuals with an approximate age range of 15 to 40 years. As the included studies reported different outcomes, the heterogeneity of data prevented a meta-analysis being undertaken. The overall quality of the evidence was ‘Fair’ for two out of three included studies, while one study was categorized as ‘Good’.DiscussionTwo out of three included primary studies had a substantial number of methodological inconsistencies and flaws, and therefore caution should be exercised in interpreting the results of this systematic review because several important covariates were not considered in the original investigations.ConclusionBased on a limited volume and ‘Fair’ and ‘Good’ quality of evidence, a positive association between maternal apical periodontitis and APOs was observed. However, more ‘Good’ quality clinical studies are needed to confirm the results of the current review

The association between apical periodontitis and adverse pregnancy outcomes: a systematic review

BackgroundThe association between adverse pregnancy outcomes (APOs) and maternal apical periodontitis remains unclear as it has not been examined rigorously or reviewed systematically.ObjectiveTo systematically review and critically evaluate the available evidence on the association of maternal apical periodontitis with several APOs.MethodsA literature search was conducted using the following electronic databases: Clarivate Analytics’ Web of Science, Scopus, PubMed, and Cochrane Central Register of Controlled Trials (CENTRAL), from inception to 25 February 2021, with no language restrictions. Observational studies including longitudinal clinical trials, cohort, case–control and cross-sectional studies of prospective and retrospective design were included. Articles with duplicate or overlapping results, abstract-only papers, case reports, case series, animal studies and reviews were excluded. Two independent reviewers were involved in study selection, data extraction and appraising the included studies; disagreements were resolved by a third reviewer. The Newcastle–Ottawa Scale (NOS) and the adapted form of the NOS were used to assess the quality for case–control and cross-sectional studies, respectively.ResultsTwo case–control and one cross-sectional study were included in the current review. The included studies were published between 2015 and 2017, with a total of 1187 participating individuals with an approximate age range of 15 to 40 years. As the included studies reported different outcomes, the heterogeneity of data prevented a meta-analysis being undertaken. The overall quality of the evidence was ‘Fair’ for two out of three included studies, while one study was categorized as ‘Good’.DiscussionTwo out of three included primary studies had a substantial number of methodological inconsistencies and flaws, and therefore caution should be exercised in interpreting the results of this systematic review because several important covariates were not considered in the original investigations.ConclusionBased on a limited volume and ‘Fair’ and ‘Good’ quality of evidence, a positive association between maternal apical periodontitis and APOs was observed. However, more ‘Good’ quality clinical studies are needed to confirm the results of the current review

Somatic genomic imbalances in ‘tumour-free’ surgical margins of oral cancer

Up to 30% of oral squamous cell carcinoma (OSCC) patients develop local recurrence and distant metastasis. The molecular status of histologically cancer-free tumour margins could be a critical factor in predicting tumour behaviour. The aim of this study was to detect somatic genomic imbalances in OSCC with emphasis on the surgical margins. DNA was isolated from tumour tissues, margin tissues, and blood samples (used as control) obtained from 11 OSCC patients, and genome-wide array comparative genomic hybridization was performed. Imbalances were present in both tumours and margins, although, as expected, they were more prevalent in tumours (duplications, P = 0.0002; deletions, P = 0.0001). Duplications were more frequent than deletions in both tumours and margins, but without statistical significance. Fifteen imbalances in tumour tissues were recurrent and all of them were duplications. Four of these were found both in tumours and margins and involved chromosomes 1q, 8p, Xp, Yp, and Yq. Four imbalances were recurrent in margin tissue and all of them were duplications (autosomes 8 and 17 and both sex chromosomes). Histologically ‘cancer-free’ margins hide genomic alterations consistent with unexplained OSCC recurrences. Establishing the molecular status of the margins could improve outcome prediction

A point mutation in the 5'splice site of the dystrophin gene first intron responsible for X-linked dilated cardiomyopathy.

I.F.9.04

Linkage of familial dilated cardiomyopathy to chromosome 9. Heart Muscle Disease Study Group.

Idiopathic dilated cardiomyopathy is a heart muscle disease of unknown etiology, characterized by impaired myocardial contractility and ventricular dilatation. The disorder is an important cause of morbidity and mortality and represents the chief indication for heart transplantation. Familial transmission is often recognized (familial dilated cardiomyopathy, or FDC), mostly with autosomal dominant inheritance. In order to understand the molecular genetic basis of the disease, a large six-generation kindred with autosomal dominant FDC was studied for linkage analysis. A genome-wide search was undertaken after a large series of candidate genes were excluded and was then extended to two other families with autosomal dominant pattern of transmission and identical clinical features. Coinheritance of the disease gene was excluded for > 95% of the genome, after 251 polymorphic markers were analyzed. Linkage was found for chromosome 9q13-q22, with a maximum multipoint lod score of 4.2. There was no evidence of heterogeneity. The FDC locus was placed in the interval between loci D9S153 and D9S152. Several candidate genes for causing dilated cardiomyopathy map in this region

Tetraploidy in a 26-month-old girl (cytogenetic and molecular studies)

Liveborn infants with tetraploidy are very rare in human pregnancies and usually die during the first days or months. Seven cases of liveborn infants with tetraploidy have previously been reported. Among them only two 92, XXXX infants survived for longer than 12 months. Here we report on the case of a 26-month-old girl with tetraploidy. The main clinical features of tetraploidy are facial dysmorphism, severely delayed growth and developmental delay. On the basis of molecular studies we discuss the possible origin of the additional chromosome sets in our proband. To our knowledge, this infant is the first reported case of tetraploidy who lived up to 26 months

Molecular genetics of dilated cardiomyopathies.

The application of molecular genetics in cardiology is currently producing important results in the study of the pathogenetic mechanisms underlying cardiomyopathies. Recent clinical surveys have indicated that genetic factors play a major pathogenetic role in idiopathic dilated cardiomyopathy (IDC). Familial IDC is frequent (20-30\%) and is probably a heterogeneous entity, as suggested by the clinical variability and the different pattern of inheritance in the affected families. Molecular genetic studies have demonstrated the existence of heterogeneity also at the genetic level. In a series of families with X-linked IDC, the disease gene has been identified as the dystrophin gene. In familial right ventricular cardiomyopathy (or right ventricular dysplasia), a new nosological entity characterized by isolated right ventricular involvement that can mimic IDC, the disease gene has been localized in the long arm of chromosome 14. In families with matrilineal transmission, the cardiomyopathy could be linked to mitochondrial DNA alterations. Autosomal dominant familial IDC, considered to be the most frequent form, is currently under active investigation. Our preliminary data have excluded a large series of candidate genes, among which are the cardiac beta-myosin heavy chain and several other genes encoding for cardiac contractile proteins, genes of the HLA region, and about 60 genes involved in the immune regulation