[70, 71] proposed a mechanistic hypothesis, involving the brain–b

[70, 71] proposed a mechanistic hypothesis, involving the brain–blood barrier

disruption with the release of proinflammatory and vasoactive substances and the induction of apoptosis. Zullo et al. [72] compiled the results of the six available studies [73-78] in an editorial and did not find any significant difference in the H. pylori prevalence between glaucoma patients and controls. They concluded that there was limited evidence supporting the role Osimertinib of H. pylori in glaucoma pathogenesis. This editorial was followed by numerous comments but with no new data confirming or invalidating this hypothesis [79, 80]. A single open-labeled noncomparative study showed that H. pylori eradication may have favorable effects Crizotinib mouse on the outcome of chronic central serous chorioretinopathy [81], but the authors considered this result in the context of a possible spontaneous regression of this pathology. Another controversy concerned the implication of H. pylori infection as a risk factor in laryngeal cancer. Whereas

Pajic-Penavic et al. [82] did not detect H. pylori DNA in healthy laryngeal mucosa, Izadi et al. [83] identified H. pylori DNA in 9% (5/55) patients with benign laryngeal lesions. Then Gong et al. [84] compared H. pylori DNA detection between 81 patients with laryngeal squamous cell carcinoma and 75 control subjects in a case–control study. After adjusting for confounding factors, regression analysis indicated that the presence of the bacteria was an independent risk factor for laryngeal cancer (OR = 7.15, 95% CI [3.29, 15.53], p < .001). To test the Verteporfin in vitro relationship between H. pylori and laryngopharyngeal

reflux, Cekin et al. [85] studied 43 patients with a laryngeal lesion; H. pylori DNA was detected in larynx samples from 24 patients (55.8%); however, they found no association between H. pylori, laryngopharyngeal reflux and malignant/premalignant laryngeal lesion status. Several studies compared H. pylori strains isolated simultaneously in the oral cavity (including dental plaque or squamous cell cancer) and gastric mucosa (neoplasia, chronic gastritis) [86-89]. All of these studies suggested that the oral cavity could represent a reservoir of H. pylori with the risk of recolonization of the stomach after systemic eradication therapy. H. pylori was also suggested as one of the etiologic agents of recurrent aphthous stomatitis. Tas et al. [90] studied the impact of H. pylori eradication on the clinical course of recurrent aphthous stomatitis with a follow-up of 6 months. In the successfully eradicated group (n = 18), vitamin B12 levels were significantly increased, and the mean number of aphtous lesions was significantly decreased. A possible beneficial effect of H. pylori eradication in patients with recurrent aphthous stomatitis due to an increase in vitamin B12 levels after eradication was hypothesized. No association was found between H. pylori and oral lichen planus [91].

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