, campylobacter pyloridis 1983 Warren Marshall 1. MALT Mucosa Associated Lymphoid Tissue. 5,6 dental plaque subgingival plaque
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1 原 著 , ,2 2, MALT Mucosa Associated Lymphoid Tissue / / / / p= U/ ml 8.7U/mL p=0.015 / /p=0.012 p=0.020 / campylobacter pyloridis 1983 Warren Marshall 1 MALT Mucosa Associated Lymphoid Tissue 2, % ,6 dental plaque subgingival plaque Tel Fax ( 484 ) Vol.29 No
2 / / JMP SAS USA χ 2 Student t 42.2U/mL 8.7U/mL p=0.015 / p= / p=0.020 /p= / 2 5, glycocalyx complex biofilm EPS extracellular polysaccharide 10,11 1 p U/mL) / χ p= p=0.03* Vol.29 No ( 485 )
3 1 / 2 / Zou PCR Miyabayashi ( 486 ) Vol.29 No
4 / 16 / 17,18 IMT 19 CagA cytotoxinassociated-a %2 CagAVacA Vacuolating cytotoxin A CagA 21 VacA / / / / 22,23 PCR / 54 MSD Marshall BJ, Warren JR: Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1984; 1: Parsonnet J, Friedman GD, Vandersteen DP, et al: Helicobacter pylori infection and the risk of gastric carcinoma. N Engl J Med 1991; 325: Uemura N, Okamoto S, Yamamoto S, et al: Helicobacter pylori infection and the development of gastric cancer. N Engl J Med 2001; 345: Brown LM: Helicobacter pylori: epidemiology and routes of transmission. Epidemiol Rev 2000; 22: Umeda M, Kobayashi H, Takeuchi Y, et al: High prevalence of Helicobacter pylori detected by PCR in the oral cavities of periodontitis patients. J Periodontol 2003; Vol.29 No ( 487 )
5 74: Gebara EC, Pannuti C, Faria CM, et al: Prevalence of Helicobacter pylori detected by polymerase chain reaction in the oral cavity of periodontitis patients. Oral Microbiol Immunol 2004; 19: Eskandari A, Mahmoudpour A, Abolfazli N, et al: Detection of Helicobacter pylori using PCR in dental plaque of patients with and without gastritis. Med Oral Patol Oral Cir Bucal 2010; 15: e Riggio MP, Lennon A: Identification by PCR of Helicobacter pylori in subgingival plaque of adult periodontitis patients. J Med Microbiol 1999; 48: Souto R, Colombo AP: Detection of Helicobacter pylori by polymerase chain reaction in the subgingival biofilm and saliva of non-dyspeptic periodontal patients. J Periodontol 2008; 79: Socransky SS, Haffajee AD: Dental biofilms: difficult therapeutic targets. Periodontol 2000; 28: Herrera D, Alonso B, León R, et al: Antimicrobial therapy in periodontitis: the use of systemic antimicrobials against the subgingival biofilm. J Clin Periodontol 2008; 35(8 Suppl): Gürbüz AK, Ozel AM, Yazgan Y, et al: Oral colonization of Helicobacter pylori: risk factors and response to eradication therapy. South Med J 2003; 96: Gebara EC, Faria CM, Pannuti C, et al: Persistence of Helicobacter pylori in the oral cavity after systemic eradication therapy. J Clin Periodontol 2006; 33: Zou QH, Li RQ: Helicobacter pylori in the oral cavity and gastric mucosa: a meta-analysis. J Oral Pathol Med 2011; 40: Miyabayashi H, Furihata K, Shimizu T, et al: Influence of oral Helicobacter pylori on the success of eradication therapy against gastric Helicobacter pylori. Helicobacter 2000; 5: Oishi Y, Kiyohara Y, Kubo M, et al: The serum pepsinogen test as a predictor of gastric cancer: the Hisayama study. Am J Epidemiol 2006; 163: Gunji T, Matsuhashi N, Sato H, et al: Helicobacter pylori infection is significantly associated with metabolic syndrome in the Japanese population. Am J Gastroenterol 2008; 103: Gunji T, Matsuhashi N, Sato H, et al: Helicobacter pylori infection significantly increases insulin resistance in the asymptomatic Japanese population. Helicobacter 2009; 14: Corrado E, Rizzo M, Tantillo R, et al: Markers of inflammation and infection influence the outcome of patients with baseline asymptomatic carotid lesions: a 5-year follow-up study. Stroke 2006; 37: Mayr M, Kiechl S, Mendall MA, et al: Increased risk of atherosclerosis is confined to CagA-positive Helicobacter pylori strains: prospective results from the Bruneck study. Stroke 2003; 34: Poppe M, Feller SM, Römer G, et al: Phosphorylation of Helicobacter pylori CagA by c-abl leads to cell motility. Oncogene 2007; 26: Bouziane A, Ahid S, Abouqal R, et al: Effect of periodontal therapy on prevention of gastric Helicobacter pylori recurrence: a systematic review and meta-analysis. J Clin Periodontol 2012; 39: Elkind MS: Infectious burden: a new risk factor and treatment target for atherosclerosis. Infect Disord Drug Targets 2010; 10: ( 488 ) Vol.29 No
6 Association between H. pylori infection and Dental Disease Yoshiko Mizuno 1,2), Tsutomu Yamazaki 2,3), Daisuke Koide 1), Mikio Takanashi 1), Issei Komuro 2) 1) Department of Clinical Epidemiology & Systems, The University of Tokyo 2) Department of Cardiovascular Medicine, The University of Tokyo 3) Clinical Research Support Center (CresCent), The University of Tokyo Hospital Abstract Objective: Helicobacter pylori (H. pylori) are gram negative, microaerophilic, spiralshaped bacteria found in the gastric mucosa. Infection with this organism is connected with peptic and duodenal ulcers, gastric carcinoma and non-hodgkin s lymphomas of gastric mucosa-associated lymphoid tissue (MALT). On average, 50% of people in the world are infected by this microorganism. The route by which H. pylori infection is transmitted is not yet clear and there are many unanswered questions, among them whether the oral cavity could be considered as a reservoir of these bacteria. We investigated a relationship between H. pylori infection and dental caries/periodontitis. Methods: The population of the study was 68 subjects (34-82 years old, mean age 59) who had undergone esophagogastroduodenoscopy and blood tests. Student s t test and the chi-square test were applied. Results: In line with previous studies, pepsinogen I/II and anti-helicobacter pylori antigens (IgG) were low (gastric disease (+) 4.2, disease (-) 5.8, p=0.023) and high (gastric disease (+) 42.2U/mL, disease (-) 8.7U/mL, p=0.015), respectively, in subjects with gastric disease. However, subjects with dental caries/periodontitis had a low prevalence of gastric disease. Moreover, the pepsinogen I/II ratio was high (p=0.012) and anti-helicobacter pylori antigen levels were low (p=0.020) in subjects with periodontitis. Similar results were seen in those with dental caries, although they were not statistically significant. Conclusions: There was not enough evidence for an association between H. pylori infection and dental disease. Further studies are needed to clarify whether there is a causative link between H. pylori infection and dental disease in the Japanese population. Keywords: Helicobacter pylori, dental caries, periodontitis Vol.29 No ( 489 )
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