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Submitted: 01 Sep 2014
Revision: 26 Oct 2014
Accepted: 02 Nov 2014
ePublished: 20 Mar 2015
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Avicenna J Dent Res. 2015;7(1): 3.
  Abstract View: 1410
  PDF Download: 631

Research Article

The Possible Role of Helicobacter pylori in the Development of Sjogren's Syndrome and Chronic Sialadenitis

Alireza Monsef Esfahani 1, Soussan Irani 2*, Shahram Sabeti 3, Farahnaz Bidari Zerehpoush 3

1 Department of Pathology, Hamadan University of Medical Sciences, Hamadan, IR Iran
2 Department of Oral Pathology, Hamadan University of Medical Sciences, Hamadan, IR Iran
3 Department of Pathology, Loghman Hospital, Shahid Beheshti University of Medical Sciences, Tehran, IR Iran
*Corresponding Author: *Corresponding author: Soussan Irani, Department of Oral Pathology, Hamadan University of Medical Sciences, P. O. Box: 65178-38741, Hamadan, IR Iran. Tel: +98-8118354250, Fax: +98-8118354220, E-mail: , Email: Address:sousanirani@gmail.com

Abstract

Background: Sjogren’s syndrome (SS) is a chronic autoimmune disease characterized by lymphocytic infiltration of exocrine glands, which can be triggered by environmental factors such as viral infection. Chronic obstructive sialadenitis is the most common type of chronic sialadenitis and many different bacterial infections develop as a result of ductal obstruction.

Objectives: This study was conducted to assess the association of these lesions with the presence of Helicobacter pylori.

Patients and Methods: A total of 56 biopsies diagnosed as Sjögren's syndrome (SS) and chronic sialadenitis (CS) due to sialolithiasis in submandibular glands, sublingual and minor salivary glands were selected (56 samples as examined group and 20 samples as control group). All the paraffin blocks were cut for hematoxylin and eosin (H and E) staining to confirm the diagnoses and then the samples were prepared for immunohistochemistry (IHC) staining to detect H. pylori. Chi-squared test was used for statistical analysis.

Results: Chi-squared test showed a significant difference between H. pylori positivity in the groups examined (P = 0.046) and between SS group and normal tissue samples (P = 0.013). There was no significant difference between gender and H. pylori positivity in examined groups examined (P = 0.574, P = 0.543, respectively). In addition, there was no significant difference between gender and H. pylori positivity in SS group (P = 0.119, P = 0.331, respectively) also in CS group (P = 0.981, P = 0.571).

Conclusions: Bacterial infection has been suggested in the pathogenesis of both SS and CS. In addition, H. pylori is a resident of the oral cavity, thus may be involved in the development and progression of these lesions. Hence, search for H. pylori antibody in blood of patients with SS is suggested.

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