CURRENT TOPICS IN GASTRITIS - 2012 Edited by Gyula Mózsik Current Topics in Gastritis - 2012 http://dx.doi.org/10.5772/46056 Edited by Gyula Mózsik Contributors Alejandro H. Corvalan, Gonzalo Carrasco, Kathleen Saavedra, Bruna Maria Roesler, José Murilo Zeitune, Shotaro Enomoto, Kiron Moy Das, Jiro Watari, Kentaro Moriichi, Hiroki Tanabe, Mikihiro Fujiya, Hiroto Miwa, Yutaka Kohgo, Gonzalo Castillo-Rojas, German Aguilar- Gutierrez, Eduardo Mucito-Varela, Stephanie E. Morales-Guerrero, Yolanda López-Vidal, Mohamed Elseweidy, Hanan Alshenawy, Zheming Lu, Dajun Deng, Gyula Mozsik, Jozsef Czimmer, Imre Laszlo Szabo, Janos Szolcsanyi, Kata Cseko, Paolo Arcari, S. Swarnakar, Achariya - Sailasuta Published by InTech Janeza Trdine 9, 51000 Rijeka, Croatia Copyright © 2013 InTech All chapters are Open Access distributed under the Creative Commons Attribution 3.0 license, which allows users to download, copy and build upon published articles even for commercial purposes, as long as the author and publisher are properly credited, which ensures maximum dissemination and a wider impact of our publications. After this work has been published by InTech, authors have the right to republish it, in whole or part, in any publication of which they are the author, and to make other personal use of the work. Any republication, referencing or personal use of the work must explicitly identify the original source. Notice Statements and opinions expressed in the chapters are these of the individual contributors and not necessarily those of the editors or publisher. No responsibility is accepted for the accuracy of information contained in the published chapters. The publisher assumes no responsibility for any damage or injury to persons or property arising out of the use of any materials, instructions, methods or ideas contained in the book. Publishing Process Manager Marija Radja Technical Editor InTech DTP team Cover InTech Design team First published January, 2013 Printed in Croatia A free online edition of this book is available at www.intechopen.com Additional hard copies can be obtained from [email protected] Current Topics in Gastritis - 2012, Edited by Gyula Mózsik p. cm. ISBN 978-953-51-0907-5 free online editions of InTech Books and Journals can be found at www.intechopen.com Contents Preface IX Section 1 History of Gastritis: From Morphology to Etiology and Prognosis 1 Chapter 1 Diagnosis of Gastritis – Review from Early Pathological Evaluation to Present Day Management 3 Imre Laszlo Szabo, Kata Cseko, Jozsef Czimmer and Gyula Mozsik Section 2 Animal Models for Study the Mechanisms of Gastritis 21 Chapter 2 The Role of Helicobacter spp. Infection in Domestic Animals 23 Achariya Sailasuta and Worapat Prachasilchai Section 3 Epidemiology of Gastritis 37 Chapter 3 Helicobacter Pylori Infection and Its Relevant to Chronic Gastritis 39 Mohamed M. Elseweidy Section 4 Afferent Vagal Neural Pathway in the Development and Healing of Chronic Gastritis in Patients 59 Chapter 4 Capsaicin-Sensitive Afferentation Represents a New Mucosal Defensive Neural Pathway System in the Gastric Mucosa in Patients with Chronic Gastritis 61 Jozsef Czimmer, Imre Laszló Szabo, Janos Szolcsanyi and Gyula Mozsik VI Contents Section 5 Diagnostic Backgrounds 77 Chapter 5 The Genetic and Epigenetic Bases of Gastritis 79 Alejandro H. Corvalan, Gonzalo Carrasco and Kathleen Saavedra Chapter 6 Intestinal Metaplasia Related to Gastric Cancer: An Outcome Analysis of Biomarkers for Early Detection 97 Jiro Watari, Kentaro Moriichi, Hiroki Tanabe, Mikihiro Fujiya, Hiroto Miwa, Yutaka Kohgo and Kiron M. Das Chapter 7 Unveiling the Intricacies of Helicobacter pylori-Induced Gastric Inflammation: T Helper Cells and Matrix Metalloproteinases at a Crossroad 113 Avisek Banerjee**, Asish K. Mukhopadhyay**, Sumit Paul, Arindam Bhattacharyya and Snehasikta Swarnakar Chapter 8 Accumulation of DNA Methylation Changes in the Progression of Gastritis to Gastric Cancer 153 Zheming Lu and Dajun Deng Chapter 9 Does Eradication of Helicobacter pylori Decreases the Expression of p53 and c-Myc oncogenes in the Human Gastric Mucosa? 171 Hanan AlSaeid Alshenawy and Amr Mahrous Alshafey Chapter 10 Gastric Cancer Risk Diagnosis Using Molecular Biological and Serological Markers Based on Helicobacter pylori-Related Chronic Gastritis 183 Shotaro Enomoto, Takao Maekita, Kazuyuki Nakazawa, Takeichi Yoshida, Mika Watanabe, Chizu Mukoubayashi, Hiroshi Ohata, Mikitaka Iguchi, Kimihiko Yanaoka, Hideyuki Tamai, Jun Kato, Masashi Oka, Osamu Mohara and Masao Ichinose Section 6 Molecular Phathology, Biochemistry and Genetics in Pathways from H. Pylori Infection to Gastric Cancer 201 Chapter 11 The Role of CagA Protein Signaling in Gastric Carcinogenesis — CagA Signaling in Gastric Carcinogenesis 203 Stephanie E. Morales-Guerrero, Eduardo Mucito-Varela, Germán Rubén Aguilar-Gutiérrez, Yolanda Lopez-Vidal and Gonzalo Castillo-Rojas Contents VII Chapter 12 From Gastritis to Gastric Cancer: The Importance of CagPAI of Helicobacter Pylori on the Development of Early and Advanced Gastric Adenocarcinoma 223 Bruna Maria Roesler and José Murilo Robilotta Zeitune Chapter 13 Gastric Cancer: Molecular Pathology State 241 Filomena Altieri, Paolo Arcari and Emilia Rippa Preface Homeostasis of living organisms is extremelly well regulated by various physiological, hor‐ monal, nutritional, immunological, genetic etc. pathways. We have learnt a lot about these mechanisms during last decades, however, some details remaine to be unknown. The gastric mucosa's function is regulated by many intrinsic (neural, hormonal, immunolog‐ ical, genetic etc. regulations) and extrinsic (different foods or food components, xenobiotics, chemical agents, physical actions) factors, that directly reach the gastric mucosa in both healthy subjects and in patients with gastrointestinal or other diseases. The gastric mucosa is able to reply to these endogenonous and exogenous actions by active and passive (dominantly metabolic) pathways. Many experimental works and clinical obser‐ vations clearly indicate that the macroscopic (and in somewhat microscopic) features of the gastric mucosa to different endogenous and exogenous aggresive agents are very similar. The inflammation, as the general reaction, of gastric mucosa seems to be the same. The role of inflammation in the development of different diseases was suggested by Hyppo‐ crates (B.C. 460-377), who stated that the changes in the blood flow and other body fluids are caused by local irritations of organs („ubi stimulus, idi fluxus”). The appearence of clas‐ sical inflammation were given by Aulus Cornelius Celsus ( B.C. 25- A.C. 50 ) as „tumor,cal‐ or,dolor, rubor” and Claudius Galenos (A.C. 129-200/201) gave the last basic parameter of the inflammation as „functio laesa” to the previously mentinoned characteristic medical phenomena.These terminological questions were accepted by Wirchow in the 19th centrury, and many other famous researchers in our days. Gastritis, as the inflammatory process (or processes), in the gastric mucosa is (are) a patho‐ morphological appearance(s) of inflammation in the gastric mucosa. Acute and chronic gas‐ tritis can be differentiated on the basis of the development and process of the diseases. Chronic gastritis may be caused by different factors such as many chemical, bacterial, viral, physical agents, and one of these is Helicobacter pylori infection, bacterial owergrowth in a hypochlrohydric stomach, autoimmune mechanisms, or chemical agents such as long-term nonsteroidal antinflammatory drug (NSAID) treatment and bile reflux. Nowadays, the importance of Helicobacter pylori infection is increasing . Many of referen‐ ces in the literature used to emphasize the presence of Helicobacter pylori in patients with chronic atrophic gastritis with and without the development of gastric cancer. This bacterium is highly prevalent in many countries and increases the risk for development of gastric and duodenal ulcer diseases, gastric cancer and gastric mucosa-associated lym‐ phoid tissue lymphoma. X Preface So the gastritis (as a pathomorphological event) does not represent a clinically uniform enti‐ ty (as it can be clearly suggested from the difinition of inflammation). Of course, many mechanisms are involved in the development of chronic gastritis, produced by different in‐ trinsic and extrinsic factors (including also the genetic backgrounds). One of the main questions of chronic atrophic gastric is in which pathway(s) leads(lead) to the development of gastric cancer. Because everyone (after Marshall and Warren received the Nobel price in 2005) suggested that the Helicobacter pylori is a main etiological factor in development of gastric and dudenal ulcer, MALToma, gastric cancer and many other non gastrointestinally located disorders. Researchers’ attention was focussed dominantly to the questions of Helicobacter pyloric infection (including the infection, its population spreading out, antibacterial treatment), meanwhile we have forgotten results of the previously carried research observations. The „functio laesa” clinically detactable by the measuremens of gastric basal ( basal acid out‐ put, BAO) and maximal (maximal acid output, MAO) can be obtained without application of any gastric stimulatory agens or with supermaximal doses of pentagastrin or histamine. Unfortunately, these types of measurements disappeared from the everyday medical prac‐ tice. We studied the changes of gastric basal and maximal acid secretiory responses in duo‐ denal ulcer pateints on dependence