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Helicobacter pylori and the Oral Environment

Helicobacter pylori (H. pylori) are gram-negative bacteria responsible for chronic gastritis, and they assume a significant role in ulcerous disease, gastric carcinoma, and duodenal disease. While approximately 70% to 90% of the world's population carry H. pylori, infection rates are generally reduced in developed countries (20% to 40%). These statistical differences are primarily the result of socioeconomic conditions that affect food consumption in high-risk children.1

 

Physical Characteristics

Helicobacter pylori are motile, spiriliform, curvilinear, microaerophilic, and often manifest in the gastric epithelium. These bacteria produce various enzymes in abundance--urease is one of the most common enzymes associated with H. pylori and has an essential role in the colonization and subsequent damage of the gastric mucosa. The secretion of urease often indicates the presence of infection by H. pylori and can therefore be utilized for diagnostic purposes. Helicobacter pylori bacteria enter the gastric epithelium through oral transmission. Urease creates a nonacidic microambiance that allows the bacteria to survive the sterilizing effect of hydrochloric acid. Aided by the secretion of protease and phospholipase, the bacteria travel through the viscous mucus film that protects the gastric epithelium, adhere to the epithelial cells, and begin to replicate. An immune response is subsequently initiated by neutrophils, which results in gastric tissue alteration.

 

Transmission

Helicobacter pylori are common pathogens that cause gastritis, peptic ulcers, gastric adenocarcinoma, and lymphoma.2 Although the modes of transmission are not well documented,3 a recent study distinguished four potential means of transmission that include: 1) a facial route in which the bacteria colonize in a water source and are subsequently transmitted to humans; 2) an oral route whereby H. pylori colonize in dental plaque and saliva; 3) a gastro-oral route (particularly in children) in which the mucous achlorhydric vomitus is used by H. pylori to infect a new host; and 4) via endoscopic procedures.4 Although gastroenterologists who are exposed to gastric secretion and saliva have a high prevalence of H. pylori infection, recent studies do not indicate significant levels in dental professionals. 5

Diagnosis

A variety of endoscopic and noninvasive examinations are utilized to diagnose H. pylori. Endoscopic examination of gastric tissue includes histological analysis (eg, optical microscopy, electronic microscopy, immunohistochemistry, DNA, and PCR polymerase chain reaction), culture, and rapid urease testing. Endoscopic methods are relatively expensive, require the involvement of specialists, and pose risk and discomfort to the patient. Noninvasive techniques include rapid in-office tests, laboratory examinations with serologic tests to detect antibodies (ie, IgG, IgAX, IgM), and the urea breath test.6 Experimental means of diagnosis include the analysis of antibodies in urine and saliva and the 14 C-urea blood test. Based on the literature, 7,8 it has been concluded that rapid, accurate, and inexpensive tests do exist as an in-office option for clinicians and laboratories who desire immediate feedback yet do not have the volume of H. pylori testing to justify ELISA test formats.

 

Treatment

An effective treatment regimen against H. pylori infection includes a 7-day prescription of Omeprazole (20 mg), Clarithromycin (250 mg), and Tinidazole (500 mg). 9 The combinations of Lansoprazole (30 mg) and amoxicillin or Omeprazole (30 mg) and amoxicillin have been proven to be equally efficacious in clinical study 10; patients in whom eradication was not achieved following dual therapy were successfully treated by quadruple therapy. Standard low-dose triple therapy remains the recommended initial treatment for infection by H. pylori and has demonstrated an acceptable eradication rate. 11 Although the definitions of resistance and clinical relevance are complicated, the failure of antibiotics to eradicate bacteria can be attributed to the inherent resistance of H. pylori.12  

 

Detection of Dental Plaque

It remains undetermined whether H. pylori are resident or transient oral microorganisms. 13 Although the results of studies suggest that H. pylori select the gastric mucosa as a preferred site, detection in dental plaque could indicate that the oral cavity may act as a sanctuary for the transient organism. In an additional study,14 a sensitive immunoperoxidase method was employed to assess the presence of H. pylori in dental plaque. Even if the H. pylori are not generally present in dental plaque, the oral transmission could be attributed to intermittent esophageal reflux. The potential ability of H. pylori to colonize the oral cavity may be related to the selective, specific adhesion between H. pylori, Fusobacterium nucleatum, and Fusobacterium periodontium (human dental plaque).15 These selective coaggregations may indicate that dental plaque serves as a reservoir for this pathogen outside of the stomach.

 

An additional characteristic of H. pylori is the capacity to bind to salivary mucins that cover the oral epithelia.16 Enzyme-linked immunosorbent assay and immunoblotting tests demonstrated that H. pylori adhered more to a sulfated subpopulation of high molecular weight salivary mucins secreted from the palatine glands, and less to mucins secreted by the sublingual and the submandibular salivary gland. This study indicated that sulfated oligosaccharides on salivary mucins may provide receptor structures for adhesion of H. pylori to oral surfaces, and that colonizations--although rare--do occur.17

 

Efficacy of Antimicrobial Oral Health

Studies of antimicrobial mouthrinses have demonstrated their ability to kill microorganisms (eg, methicillin-resistant Staphylococcus aureus, H. pylori, Candida albicans) in 10 to 30 seconds,18 which verified their application for reliable infection control. Oral immunization with H. pylori lysates or with H. pylori urease can protect against contraction of the disease and provide potential vaccination against development of H. pylori infections.19

 

Conclusion

Serology forms are a useful means of monitoring diagnosis, treatment, and follow-up upon the completion of antibiotic treatment for an H. pylori infection.20 These qualitative serological tests are recommended due to their specificity, simplicity, and reduced expense. Helicobacter pylori are an important consideration for the proper diagnosis of a disease managed in close cooperation between general practitioners and specialists. The microorganism can be transmitted orally and has been detected in dental plaque. All standard professional hygiene procedures should be followed to avoid oral transmission of H. pylori during dental treatment.

 

* Former lecturer, University of Paris, Paris, France; Scientific Consultant, Milan, Italy.

 

References

  1. Vigneri S, Termini R, Scialabba A. Helicobacter pylori: A Successful Pathogen. Vicenza, Italy: Lego Press, 1993.
  2. Cave DR. How is Helicobacter pylori transmitted? Gastroenterolgy 1997;113(suppl 6):S9-S14.
  3. Dunn BE, Cohen H, Blaser MJ. Helicobacter pylori. Clin Microbiol Rev 1997;10(4):720-741.
  4. Tursi A, Cammarota G, Papa A, et al. The modes of transmission of Helicobacter pylori infection. Recenti Prog Med 1997;88(5):232-236.
  5. Lin SK, Lambert JR, Schembri MA, et al. The prevalence of Helicobacter pylori in practising dental staff and dental students. Aust Dent J 1998;43(1):35-39.
  6. Peura DA, Pambianco DJ, Dye KR, et al. Microdose 14 C-urea breath test offers diagnosis of Helicobacter pylori in 10 minutes. Am J Gastroenterol 1996;91(2):233-238.
  7. Sadowski D, Cohen H, Laine L, et al. Evaluation of the FlexSure HP whole blood antibody test for diagnosis of Helicobacter pylori infection. Am J Gastroenterol 1998;93(11):2119-2123.
  8. Graham DY, Evans DJ, Peacok J, et al. Comparison of rapid serological tests (FlexSure HP and QuickVue) with conventional ELISA for detection of Helicobacter pylori infection. Am J Gastroenterol 1996;91(5):942-948.
  9. Moayyedi P, Ragunathan PL, Mapstone N, et al. Relevance of antibiotic sensitivies in predicting failure of omeprazole, clarithromycin and tinidazole to eradicate Helicobacter pylori. J Gastroenterol 1998;33(suppl 10):62-65.
  10. Kayser S, Flury R, Zbinden R, et al. Comparative effect of lansoprazole/amoxicillin with omeprazole/amoxicillin for the eradication of Helicobacter pylori in patients with duodenal ulcer. Schweiz Med Wochenschr 1997;127(17):722-727.
  11. Fraser AG, Moore L, Ali MR, et al. An audit of low dose triple therapy for eradication of Helicobacter pylori. N Z Med J 1996;109(1027):290-292.
  12. MŽgraud F. The most important dignostic modalities for Helicobacter pylori, now and in the future. Eur J Gastroenterol Hepatol, 1997;(suppl 1):S13-S15.
  13. Oshowo A, Gillam D, Botha A, et al. Helicobacter pylori: The mouth, stomach, and gut axis. Ann Periodontol 1998;3(1):276-280.
  14. Savoldi E, Marinone MG, Negrini R, et al. Absence of Helicobacter pylori in dental plaque determined by immunoperoxidase. Helicobacter 1998;3(4):283-287.
  15. Andersen RN, Ganeshkumar N, Kolenbrander PE. Helicobacter pylori adheres selectively to Fusobacterium spp. Oral Microbiol Immunol 1998;13(1):51-54.
  16. Veerman EC, Bank CM, Namavar F, et al. Sulfated glycans on oral mucin as receptors for Helicobacter pylori. Glycobiology 1997;7(6):737-743.
  17. Oshowo A, Tunio M, Gillam D, et al. Oral colonization is unlikely to play an important role in Helicobacter pylori infection. Br J Surg 1998;85(6):850-852.
  18. Okuda K, Adachi M, Iijima K. The efficacy of antimicrobial mouth rinses in oral health care. Bull Tokyo Dent Coll 1998;39(1):7-14.
  19. Michetti P. Oral immunization against Helicobacter pylori - A future concept. J Gatroenterol 1998;33(suppl 10):66-68.
  20. Laheij RJ, Witteman EM, Bloembergen P, et al. Short-term follow-up by serology of patients given antibiotic treatment for Helicobacter pylori infection. J Clin Microbiol 1998;36(5):1193-1196.
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