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Year : 2014  |  Volume : 1  |  Issue : 2  |  Page : 62-64

Helicobacter pylori and its role in oral diseases: A note on pathogenesis

Department of Microbiology and Pathology, Thai Moogambigai Dental College, Chennai, Tamil Nadu, India

Date of Web Publication31-Dec-2014

Correspondence Address:
Dr. J Sunitha
Department of Oral pathology and Microbiology, Thai Moogambigai Dental college, Golden George Nagar, Chennai - 600107, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2229-3019.148260

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Helicobacter pylori belongs to a family of bacteria that colonize the mammalian stomach present in half of the world's population. It has been causally linked to chronic gastritis, peptic ulceration, and gastric adenocarcinoma. This review is about the pathogenesis and oral-related lesions associated with H. pylori infection.

Keywords: Aphthous ulcer, gastrointestinal tract, Helicobacter pylori, oral lesions

How to cite this article:
Dayanathi AR, Sunitha J, Ramamoorthy A, Jeddy N, Jeeva S. Helicobacter pylori and its role in oral diseases: A note on pathogenesis. J Indian Acad Dent Spec Res 2014;1:62-4

How to cite this URL:
Dayanathi AR, Sunitha J, Ramamoorthy A, Jeddy N, Jeeva S. Helicobacter pylori and its role in oral diseases: A note on pathogenesis. J Indian Acad Dent Spec Res [serial online] 2014 [cited 2019 Jun 25];1:62-4. Available from: http://www.jiadsr.org/text.asp?2014/1/2/62/148260

  Introduction Top

Helicobacter pylori (H. pylori) previously called 'Campylobacter pylori' is a gram-negative, microaerophilic bacteria present in the gut. It was first isolated by Marshal and Warren, which ushered in a new era in gastric microbiology. [1] H. pylori belongs to a family of bacteria that colonize the mammalian stomach, and is causally linked to chronic gastritis, peptic ulceration, and gastric adenocarcinoma. [2] This bacterium colonizes over half of the world's population. Infection is usually acquired in childhood and in the absence of antibiotic therapy, persists for lifetime of the host. H. pylori is the only known bacteria that can persistently colonize the normal stomach, and is able to tolerate the harsh conditions of the stomach. [3]

Dental plaque is recognized as a reservoir of H. pylori by some researchers. It is considered to be a normal commensal by some, though being difficult to isolate due to the meager presence. There isevidently an increase in the number of oral H. pylori in chronic gastritis patients. Further, H. pylori can promote the development of oral mucosal lesions likerecurrent aphthous ulcer and may function as an intermediary in the route of oral to gastric infection. [4] H. pylori infection contributes to the pathogenesis of periodontal diseases, recurrent aphthous ulcers, glossitis, burning mouth syndrome, and some dermatological diseases. [5]

Risk factors for H. Pylori

The risk factors for H. pylori include poor social economic status, poor hygiene practice, absence of hygienic drinking water, and unsanitary food preparation. [6],[7]

Transmission of H. Pylori

The main route of organism entry has been charted as the following - oral to oral, gastro to oral, and fecal to oral. Transmission may occur in a vertical or horizontal mode. Oral carriage of H. pylori may play a role in the transmission of infection. [7]


H. pylori is well adapted to withstand low pH to gain entry to its preferred territory, the mucus layer of the mucous membrane. One of the survival capabilities is its ability to resist mucosa and migration towards epithelial cell. Once there, the bacterium resists the local and systemic immune responses. Colonization persists for life in the host if there is no exposure to antibiotics. [5] Once it escapes from the lumen, it modifies the bioenvironment in the area and starts releasing collagenases which degrade the collagen in the host enabling more space for the movement of the bacteria. The Fas Ag pathway of apoptosis is activated during H. pylori infection. The combined action of the collagenases and stimulation of apoptosis leads to ulceration of the mucosa. [8]

Oral lesions associated with H. Pylori

Recurrent aphthous stomatitis

Recurrent aphthous stomatitisis one of the most common oral mucosal conditions presenting as recurrent, multiple, small, round ulcers, with circumscribed margins, having yellow or gray floors, and are surrounded by an erythematous halo. The predisposing factors implicated include genetics, trauma, tobacco, drugs, hematinic deficiency, celiac disease, inflammatory bowel disease, hormonal changes, stress, and microorganisms. [9]

Recently, H. pylori has been proposed to be one of the important etiological agents in the pathogenesis of recurrent aphthous stomatitis. [10] It has been showed that patients with recurrent oral ulcerations appear to suffer from active H. pylori infection in a high percentage of cases. [11] Surprisingly, eradication of H. pylori may have a reducing effect on the recurrence and healing period of recurrent aphthous stomatitis. Studies by Meleki et al., and Fritscher et al., have proved contradictory to the same. [12]


Dental plaque typically forms on the supragingival and subgingival tooth surfaces lacking ingood oral hygiene measures. Plaque biofilms can enhance the survivability of some bacteria by providing access to urea reduced by urease-producing microorganisms and neutralizes the effects of acidification. Moderate and severe cases of periodontitis have shown a positive seropositivity to H. pylori. [3] Riggio and Lennon concluded from a study that subgingival plaque, particularly when the pocket depth is more than 5 mm in adult periodontitis cases, may function as a reservoir for H. pylori. [13],[14] The inflammatory markers produced by H. pylori in the oral cavity further addsto the burden on the preexisting inflammation due to chronic periodontitis in the oral cavity. Conclusively, H. pylori is mainly associated with moderate to severe cases of periodontitis, and its role in the contributionto gastric reinfection needs to be substantiated by further research. [4]

Lichen planus

Lichen planusis a relatively common, chronic dermatomucosal disease that often affects the oral mucosa. Lichen planus is an autoimmune disease with a female predilection. Hamideh et al., found that levels of H. pylori using urease breath test was significantly higher in lichen planus patients than in controls. [15] These results support a definitive etiological role for H. pylori in lichen planus, which is in line with study done by Sikander et al. On the contrary, a couple of research findings were totally disagreeing with the concept of any relationship of lichen planus with H. pylori. [16]


Psoriasis is an auto immune inflammatory disease that is often associated with comorbidities such as dyslipidemia, diabetes mellitus, obesity, and cardiovascular disorders. Studies done by Ana et al., [17] Ali et al., [18] Halasz, [19] and Ghada et al., [20] have shown a close association between psoriasis and H. pylori. Further, there has been evidence of psoriatic lesions clearing following eradication of H. pylori. In a largest study, H. pylori showed positive results for moderate to severe cases of psoriasis. Hence, it can be concluded that although no clear association between the two, testing for presence of H. pylori can enhanceviable treatment option for psoriasis.

  Conclusion Top

Thus, there is increasing evidence that the oral cavity acts as a reservoir and may also aid in the transmission of H. pylori. However, further studies have to be performed using controlled conditions, larger samples, and latest diagnostic tests to substantiate the role of this bacterium. Understanding the mechanisms of action of these bacteria offers the exciting hope of newer treatment options for the above diseases.

  References Top

Marshall BJ, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1984;1:1311-5.  Back to cited text no. 1
Lehours P, Yilmaz O. Epidemiology of Helicobacter pylori infection. Helicobacter 2007;12:1-3.  Back to cited text no. 2
Kilmartin CM. Dental implications of Helicobacter pylori. J Can Dent Assoc 2002;68:489-93.  Back to cited text no. 3
Dye BA, Kruszon-Moran D, McQuillan G. The relationship between periodontal disease attributes and Helicobacter pylori infection among adults in the United States. Am J Public Health 2002;92:1809-15.  Back to cited text no. 4
Makola D, Peura DA, Crowe SE. Helicobacter pylori infection and related gastrointestinal diseases. J Clin Gastroenterol 2007;41:548-58.  Back to cited text no. 5
Assya K, Vladimir P, Adriana K, Angelina K. Oral cavity and systemic diseases - Helicobacter pylori and dentistry. Biotechnol 2011;25:2447-57.  Back to cited text no. 6
Dowsett SA, Archila L, Segreto VA, Gonzalez CR, Silva A, Vastola KA, et al. Helicobacter pylori infection in indigenous families of Central America: Serostatus and oral and fingernail carriage. J Clin Microbiol 1999;8:2456-60.  Back to cited text no. 7
Kusters JG, van Vliet AH, Kuipers EJ. Pathogenesis of Helicobacter pylori infection. Clin Microbiol Rev 2006;19:449-90.  Back to cited text no. 8
Jurge S, Kuffer R, Scully C, Porter SR. Mucosal disease series. Number VI. Recurrent apthous stomatitis. Oral Dis 2006;12:1-21.  Back to cited text no. 9
Scully C, Porter S. Recurrent apthous stomatitis: Current concepts of etiology, pathogenesis and management. J Oral Pathol Med 1989;18:21-7.  Back to cited text no. 10
Preeti L, Magesh K, Rajkumar K, Karthik R. Recurrent apthous stomatitis. J Oral Maxillofac Pathol 2001;15:252-6.  Back to cited text no. 11
Maleki Z, Sayyari AA, Alavi K, Sayyari L, Baharvand M. A study of the relationship between Helicobacter pylori and recurrent aphthous stomatitis using a urea breath test. J Contemp Dent Pract 2009;10:9-16.  Back to cited text no. 12
Fritscher AM, Cherubini K, Chies J, Dias AC. Association between Helicobacter pylori and recurrent aphthous stomatitis in children and adolescents. J Oral Pathol Med 2004;33:129-32.  Back to cited text no. 13
Riggio MP, Lennon A. Identification by PCR of Helicobacter pylori subgingival plaque of adult periodontitis patients. J Med Microbiol 1999:48;317-22.   Back to cited text no. 14
Hamideh M, Homa H, Behrooz B, Reza M, Gita MR. Association of Helicobacter pylori with lichen planus. Indian J Dermatol 2007;52:138-40.  Back to cited text no. 15
Khan SS, Syed HA, Faisal R, Jehan A, Muhammad S, Shahana UK. Relationship between Lichen Planus and Helicobacter pylori positive patients in Karachi- Pakistan. Eur Acad Res 2013;1:1309-12.  Back to cited text no. 16
Hernando-harder AC, Booken N, Goerdt S, Singer MV, Harder H. Helicobacter pylori infection and dermatologic diseases. Eur J Dermatol 2009;19:431-44.  Back to cited text no. 17
Ali M, Whitehead M. Clearance of chronic psoriasis after eradication therapy for Helicobacter pylori infection. J Eur Acad Dermatol Venereol 2008;22:753-4.  Back to cited text no. 18
Halasz CL. Helicobacter pylori antibodies in patients with psoriasis. Arch Dermatol 1996;132:95-6.  Back to cited text no. 19
Fathy G, Said M, Abdel-Raheem SM, Sanad H. Helicobacter Pylori infection: A possible predisposing factor in chronic plaque-type psoriasis. J Egypt Women Dermatol Soc 2010;7:39-43.  Back to cited text no. 20


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