Saudi Journal of Gastroenterology
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Year : 1998  |  Volume : 4  |  Issue : 1  |  Page : 13-16
Helicobacter pylori in the dental plaque of healthy Saudis

Department of Internal Medicine, Dentistry and Laboratory Medicine, King Fahd Specialist Hospital, P.O. Box 2290, Qassim, Saudi Arabia

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Date of Submission05-Mar-1997
Date of Acceptance02-Nov-1997


The objective of this study is to determine the presence of Helicobacter pylori in the dental plaque of healthy Saudis and its relation to dental care. One hundred randomly selected healthy Saudis attending the dental clinic were assessed for oral hygiene and periodontal disease by dental examination. Information about the use of toothpaste, chewing stick, smoking and dentures was obtained. Samples of dental plaque were collected after scoring it according to the plaque index. Presence of H. pylori in the plaque was sought by a commercially available rapid urease test with a sensitivity of 94% and a specificity of 100%. The presence of H. pylori was indicated by a positive rapid urease test in 81 %. There was significant correlation of heavy dental plaque (plaque index score 3) with presence of H. pylori (p=0.03). We conclude that H. pylori is present in the dental plaque of most Saudis and this is due to poor oral hygiene.

How to cite this article:
Contractor QQ, Tahir MY, Naseem S, Ahmad S. Helicobacter pylori in the dental plaque of healthy Saudis. Saudi J Gastroenterol 1998;4:13-6

How to cite this URL:
Contractor QQ, Tahir MY, Naseem S, Ahmad S. Helicobacter pylori in the dental plaque of healthy Saudis. Saudi J Gastroenterol [serial online] 1998 [cited 2022 Aug 8];4:13-6. Available from:

Helicobacter pylori Scientific Name Search  one of the world's most common bacterial infections. Human beings are the sole natural host of HP although closely similar organisms have been found in primates [1] . It is difficult to culture from contaminated sources as it grows more slowly in vitro than most other organisms. H. pylori DNA has been detected by polymerase chain reaction in sewage water [2] . It can survive for several days in distilled water, saline and sea water if these are kept cool. However, at room temperature they become non-culturable after one to three days [3]. It is possible that particulate matter could provide a more favorable local environment and increase survival time. It seems certain from available data that human beings are the only source of infection.

Majority of the population of the developing world is infected by HP from an early age [4] . Mode of transmission is important as reinfection after eradication of the organism from the gastric mucosa is a major concern, especially in the developing countries [5] . It is believed that HP could be transmitted by the oro-oral and feco-oral routes. Gastroesophageal reflux can permit access to the mouth, or it can be excreted in the feces [2] . H. pylori has been cultured both from the feces and the dental plaque (DP) in a few studies [6],[7],[8],[9] . Polymerase chain reaction has identified HP in DP of a larger number of subjects, although some controversy still exists [10],[11],[12]­ . Increased rates of infection among children of West African mothers who premasticate their infant's food favors oro-oral transmission while similarity of the seroepidemiology with that of hepatitis A is in support of feco-oral transmission [13],[14] .

The aim of the present study was to obtain evidence indicating the presence or absence of HP in the DP of healthy Saudis and to determine their relation to dental health.

   Patients and Method Top

One hundred Saudi patients attending the dental clinic at King Fahd Specialist Hospital, Qassim were asked to participate in the study. The purpose of the study was explained to the patients and consents were obtained. The study was approved by the ethics committee of the hospital.

Cases were selected in a randomized fashion from three age groups: 0-20, 21-40, 41-60 years. A detailed history and clinical assessment regarding oral care such as teeth cleaning after every meal, use of tooth paste and dentures was obtained. Cleaning of teeth with "miswak"-chewing sticks derived from Salvadora persica, Azadirachta indica and Accacia arabica-is a common habit among Saudis. It is an important part of the ablutions before worship which takes place five times a day. Details of this practice which is common among Saudis, was noted in all subjects (15). Use of antibiotics currently or in the previous two months and history of smoking was recorded.

Oral hygiene was assessed by the oral hygiene index (OHI), on a scale 1 to 3:1=debris present on the gingival third of the tooth-good oral hygiene, 2=debris present on two-thirds of the tooth­- moderate, 3=debris present on the whole tooth surface poor [16] .

Dental plaque was scored according to the plaque index (PI) on a scale I to 3.1; tooth surface looks clean but plaque can be removed with sharp instrument light plaque, 2; visible plaque covering one-third of the crown surface moderate, 3; visible plaque covering two-third or more of the crown surface-heavy [16] ..

The plaque was sampled with the deepest pocket reading and removed with a sterile universal currette. Subgingival and supragingival plaques­where both were present-were sampled. The plaque was taken from the impression surface of the denture if the patient wore a denture.

H. pylori was detected by the commercially available rapid urease test, CP-Test (BROCADES PHARMA spa Milano-Italia). Plaque was immediately placed into the reconstituted vial. Change of color from yellow to red within 20 minutes, upto a maximum of 60 minutes (as recommended by the manufacturer), was considered positive. This test has a sensitivity of 94% and specificity of 100% (17). To confirm this we injected pure proteus (urease producing organism) culture and there was no change in color for upto 24 hours (no further observation was made).

The data were analyzed using SPSS for Windows (Release 6.0) statistical software. Spearman correlation coefficients were calculated and p values of <0.05 were regarded as statistically significant.

   Results Top

None of the subjects have dyspepsia or any major illness. Since minimal periodontal disease is common in the community they were regarded as healthy. The presence of HP in DP was indicated by a positive CP test in 81/100, i.e. 81% of the cases. Correlation of HP in DP to age, sex, dental care and smoking is shown in [Table - 1] and to degree of oral hygiene and nature of DP is shown in [Table - 2].

Most of the subjects (73%) had moderate or poor oral hygiene. Positivity of CP test was higher in this group as compared to those with good oral hygiene, although statistically not significant. Heavy DP (plaque index score 3) was associated with a significantly higher positivity for HP than moderate and light (combined group) DP (p=0.03).

All the subjects responded in the affirmative when questioned regarding cleaning their teeth after every meal. Although 55% were using toothpaste, only 26% were using it daily. Similarly, chewing stick, (miswak), was used by 56% but only 20% were using it appropriately and regularly as recommended [15] .

Seven patients were taking antibiotics for upper respiratory tract infection and four of these had a positive CP test. It thus seems that intake of antibiotics does not alter the results significantly.

   Discussion Top

The present study confirms previous reports that DP harbors HP. Similar to the evidence from another developing country, HP is present in the DP of most Saudis [9] . One hundred subjects were evaluated in the present study and a larger population or studies from other parts of Saudi Arabia could confirm these results. An ideal control subject would be one without dental disease. However, since dental problems are so common in the population it would be difficult to find an ideal control subject. Conflicting results in published works have been attributed to the methods of sample collection or oral contamination caused by gastroesophageal reflux at the time of endoscopy [12] . In the present study, DP was collected with sterile universal currettes and these subjects were not undergoing endoscopies. A good correlation between CLO test and tissue culture has been reported [5],[9] .

It has been suggested that high positive results from developing countries may reflect the local standards of dental care and hygiene, eating habits, sanitation practice, and socioeconomic class [12] . We found a significantly higher rate of positivity for HP in those with a heavy DP (plaque index score 3). Although the positivity was lower in those with good oral hygiene as compared to those with poor oral hygiene, this was not statistically significant.

Identical strains of HP were reported in antral mucosa and DP by DNA fingerprinting [17] . Using nested PCR, which is more sensitive and specific, two-third of 13 HP gastritis patients had HP in DP and saliva respectively [7] . Presence of organism in the mouth has major implications for the spread of HP and identifies a potential source of reinfection following eradication from the stomach.

Using CLO test, HP was detected in DP, gastric body and antral mucosa in 98%, 70% and 67% respectively of 43 Indian patients with dyspepsia [5] .Triple drug therapy (bismuth, tinidazole and amoxicillin or doxycycline) administered for 15 days to 24 patients cleared HP from the gastric mucosa in all but in none from DP. It was concluded that DP is a major and permanent reservoir of HP. Since it was unaffected by systemic therapy it was blamed for reinfection of the gastric mucosa. This is very likely as reinfection occurs with the same strain [8] .

In studies from developed countries, duodenal ulcer relapse rates of 10% at 6 months and 35% at 12 months have been reported, despite eradication of HP [18],[19] . Since reexposure to HP occurs in only 1% per year in healthy population from developed countries, this observation suggests a higher reinfection, possibly from DP in duodenal ulcer patients [20],[21] .

Eradication of HP from the gastric mucosa has limited benefits in developing countries as reexposure is frequent [21] . Since HP in dental plaque is not affected by systemic therapy it is the possible source of reinfection. Presence of HP in DP is related to the standard of oral hygiene. In this regard it was noteworthy that the majority of the subjects in the present study were not using either the toothpaste or the chewing stick, (miswak) appropriately. This could be the cause of poor dental hygiene and the high incidence of HP in DP in the population studied.

   References Top

1.Goodwin CS, McConnell W, McCullough RK, et al. Cellular fatty acid composition of Campylobacter pylori form primates and ferrets compared with those of other campylobacters. J Clin Microbiol 1989;27:938-43.  Back to cited text no. 1    
2.Mendall MA, Northfield TC. Transmission of Helicobacter pylon infection. Gut 1995;37:1-3.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.West AP. Millar AR, Tompkins DS. Survival of Helicobacter pylori in water and saline (Letter). J Chn Pathol 1990;43:609.  Back to cited text no. 3    
4.Graham DY, Adam E, Reedy GT, et al. Seroepidemiology of Helicobacter pylon infection in India. Comparison of developing and developed countries. Dig Dis Sci 1991;36:1084-8.  Back to cited text no. 4    
5.Desai HG, Gill HH, Shankaran K, Mehta PR, Prabhu SR. Dental plaque: permanent reservoir of Helicobacter pylon 3. Scand J Gastroenterol 1991;26:1205-8.  Back to cited text no. 5  [PUBMED]  
6.Thomas JE, Gibson GR, Darboe MK. Dale A, Weaver LT. Isolation of Helicobacter pylori from human feces. Lancet 1992;3,40:1194-5.  Back to cited text no. 6    
7.Mapstone NP, Lynch DAF, Lewis FA, et al. PCR identification of Helicobacter pylori in feces from gastritis patients (letter). Lancet 1993;341:447.  Back to cited text no. 7    
8.Shames B, Krajden S, Fuksa M, Babida C, Penner JL. Evidence for the occurrence of the same strain of Campylobacter pylon in the stomach and dental plaque. J Clin Microbiol 1989;27:2849-50.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Majmudar P, Shah SM, Dhunjibhoy KR, Desai HG. Isolation of Helicobacter pylon from dental plaques in healthy volunteers. Indian J Gastroenterol 1990;9:271-2.  Back to cited text no. 9    
10.Banatvala N, Lopez CR, Owen R, et al. Helicobacter pylon in dental plaque (letter, comment). Lancet 1993;341:380.  Back to cited text no. 10    
11.Nguyen AM, Engstrand L, Genta RM, Graham DY, el Zaatari FAK. Detection of Helicobacter pylon in dental plaque by reverse transcription-polymerase chain reaction. J Clin Microbiol 1993;31:783-7.  Back to cited text no. 11    
12.Hardo PG, Tugnait A, Hassan F, et al. Helicobacter pylori infection and dental care. Gut 1995;37:44-6.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]
13.Albenque M, Tall F, Dabis F, Megraud F. Epidemiological study of transmission from mother to child in Africa. Rev Esp Enferm Dig 1990;78 Suppl 1:48.  Back to cited text no. 13    
14.De Korwin J, Remot P, Hartemann P, Catelle A, Conroy M, Schmitt J. Association of A hepatitis seropositivity with Helicobacter pylori gastric infection supporting a person to person transmission of HP. Irish Med J 1992;161(suppl):60-1.  Back to cited text no. 14    
15.Almas K, Al-Lafi TR. The natural tooth brush. Worl Health Forum 1995;16:206-10.  Back to cited text no. 15    
16.Ainamo J. Epidemiology of Periodontal Disease. ln:Lindhe J, editor. Test book of Clinical Penodontology, 2nd edition, Copenhagen; Munksgaard 1990;70-88.  Back to cited text no. 16    
17.Khandekar K, Palmer KR, Eastwood MA, Scott AC, Desai M, Owen RJ. DNA fingerprints of Helicobacter pylon from mouth and antrum of patients with chronic ulcer dyspepsia (letter). Lancet 1993;342:751.  Back to cited text no. 17    
18.Fiocca R, Solcia E, Santoro B. Duodenal ulcer relapse after eradication of Helicobacter pylori (letter). Lancet 1991;337:1614.  Back to cited text no. 18    
19.Patchett S, Beattie S, Leen E, Kenae C, O'Morain C. Helicobacter pylori and duodenal ulcer recurrence. Am J Gastroenterol 1992;87:24-7.  Back to cited text no. 19    
20.Tytgat GMNJ, Noach LA, Rauws EAJ. Helicobacter pylon in fection and duodenal ulcer disease. Gastroenterol Clin North Am 1993;22:127-39.  Back to cited text no. 20    
21.Shankaran K, Desai HG. Helicobacter pylori in dental plaque. J Clin Gastroenterol 1995; 21:82-4.  Back to cited text no. 21  [PUBMED]  

Correspondence Address:
Qais Qutub Contractor
King Fahd Specialist Hospital, P.O. Box 2290, Buraidah
Saudi Arabia
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Source of Support: None, Conflict of Interest: None

PMID: 19864780

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