Biotechnology & Biotechnological Equipment

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Oral Cavity and Systemic Diseases—Helicobacter

Pylori and Dentistry

Assya Krasteva, Vladimir Panov, Adriana Krasteva & Angelina Kisselova

To cite this article: Assya Krasteva, Vladimir Panov, Adriana Krasteva & Angelina Kisselova
(2011) Oral Cavity and Systemic Diseases—Helicobacter�Pylori and Dentistry, Biotechnology &
Biotechnological Equipment, 25:3, 2447-2451, DOI: 10.5504/BBEQ.2011.0078

To link to this article: https://doi.org/10.5504/BBEQ.2011.0078

© 2011 Taylor and Francis Group, LLC

Published online: 16 Apr 2014.

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 REVIEW DOI: 10.5504/bbeq.2011.0078 MB

ORAL CAVITY AND SYSTEMIC DISEASES – HELICOBACTER PYLORI AND

DENTISTRY
Assya Krasteva1, Vladimir Panov2, Adriana Krasteva3, Angelina Kisselova1
1
Medical University – Sofia, Faculty of Dental Medicine, Department of Imaging and Oral Diagnostics, Sofia, Bulgaria
2
Medical University “Prof. Dr. P. Stoyanov”, Faculty of Dental Medicine, Department of Conservative and Pediatric Dentistry,
Varna, Bulgaria
3
Medical University – Sofia, Faculty of Pharmacy, Department of Pharmacology and Toxicology, Sofia, Bulgaria
Correspondence to: Assya Krasteva
E-mail: asyakrasteva@gmail.com

ABSTRACT
Helicobacter pylori is a Gram-negative microorganism and an important factor in the pathogenesis of numerous diseases
including gastro-intestinal perturbations (peptic ulcer, gastric carcinoma, gastric mucosa-associated lymphoid tissue lymphoma),
metabolic, autoimmune, vascular and systemic disorders.
The isolation of H. pylori from dental plaque and saliva is of great interest in order for the role of the oral cavity in its transmission
to be examined. It is considered that the oral cavity is the main extragastric “reservoir” and an entry of the infection and
reinfection. Virulent H. pylori strains can be present, although seldom and probably transitory, in oral specimens from patients
with chronic dental or gastroduodenal diseases or both.
In the present review we would like to elaborate on the place of H. pylori in the oral cavity and the role of the dentists in
limiting the transmission of infection and consequently helping to reduce the risk of patient’s reinfection. On the other hand,
the possibility dental practitioners to be at a higher risk for H. pylori infection is discussed, possible oral manifestations of the
disease and some practical recommendations are given.

Biotechnol. & Biotechnol. Eq. 2011, 25(3), 2447-2541
Keywords: Helicobacter pylori, oral cavity as reservoir, dental
recommendations
Background
H. pylori is an important factor in the pathogenesis of
numerous diseases including gastro-intestinal, metabolic,
autoimmune, vascular and systemic disorders (atherosclerosis,
Raynaud’s disease; headache and migraine; artritis, immune
thrombocytopenia, Henoch-Schönlein disease, Sjögren
syndrom, autoimmune thyroiditis; rosacea, chronic urticaria,
atopic dermatitis, alopecia areata, iron deficiency anemia,
amenorrhea, halitosis, oral ulcer or aphtosis) (3, 5, 16, 17,
19, 22).
Epidemiology
This infection affects more than half of the human population.
The prevalence is however unbalanced between rural
developing areas (more than 80%) and urban developed areas
(less than 40%) (25). At birth, the rate of H. pylori positivity is
81% in breast-milk and 96% in maternal and infant sera (12).
H. pylori is found in gastric mucosa in 90 to 100% of
patients with duodenal ulcer and 70 to 90% in patients with
gastric ulcer (11).
Risk factors for H. pylori
Risk factors for H. pylori infection are:
• poor social and economic development;
Biotechnol. & Biotechnol. Eq. 25/2011/3
• poor hygienic practices;
• absence of hygienic drinking water;
• unsanitary food preparation.
The presence of H. pylori in sheep stomach in the absence
of associated gastritis and recovery of H. pylori from sheep
milk and gastric tissue suggest that sheep may be a natural host
for H. pylori (6). Helicobacter DNA was demonstrated in 60%
of milk samples and in 30% of sheep tissue samples. Sardinian
shepherds have almost a 100% prevalence of H. pylori and
the prevalence is higher than that of their same-household
siblings (6).
Transmission of H. pylori
Main routes of infections are: oral-oral, gastro-oral and faecal-
oral transmission, however no predominant mechanism
of transmission has been yet identified. Transmission may
occur in a vertical mode (e.g. from parent to child) or in a
horizontal mode (across individuals or from environmental
contamination). In either case, the involvement of water and
food cannot be excluded as sources of infection. The likelihood
of the transmission pathway in developing rural and developed
urban areas appears to be different. In developed areas,
person-to-person transmission within families appears to be
dominant, while in the rural developing areas the transmission
pathway appears to be more complex. In this latter case, the
transmission by contaminated food, water, or via intensive
contact between infants and non-parental caretakers may have
a greater influence than within-family transmission (25).
2447
 Oral H. pylori has been detected in periodontal pockets of
various depths and the dorsum of the tongue by nested PCR.
Overall, 58% of the subjects had a positive fingernail result,
with a significant positive relationship between fingernail and
tongue positivity. The authors have suggested that oral carriage
of H. pylori may play a role in the transmission of infection
and that the hand may be instrumental in transmission (7).
Oral cavity as reservoir of infection
Recent studies have shown that patients with chronic gastritis
are with a higher prevalence of H. pylori in the dental plaque
than in the stomach (60% in the gastric mucosa and 90% in the
poster) (21). This shows that oral cavity may be the first place
for colonization and then the infection may involve the gastric
mucosa.
The bacterium has been detected in saliva, supragingival
and subgingival plaque, suggesting that these sites may be
considered reservoirs for H. pylori not only in urease-positive
patients, but in healthy volunteers and thus be involved in the
reinfection of the stomach (14).
The eradication therapy is more effective in the absence
of H. pylori in the oral cavity (92%), compared to that in its
presence (52%). The “reservoir” in the stomach facilitates the
reinfection (2, 8, 23).
It is of a great importance that oral H. pylori might cause
gastric reinfection even after the eradication therapy (2, 8, 20).
H. pylori has also been found in the palatine tonsils. Some
authors have observed that patients with IgA nephropathy had
tonsillar H. pylori (P < 0.01) (18). Assumpção et al. have found
that H. pylori was detected in 96% of gastric mucosa samples
and in 72% of dental plaque samples. Sixty-three (89%) of
71 dental plaque samples that were H. pylori -positive also
exhibited identical vacA and cagA genotypes in the gastric
mucosa. The most common genotype was vacAs1bm1 and
cagA positive, either in the dental plaque or the gastric mucosa.
The conclusion of this survey was that the gastric infection
was correlated with the presence of H. pylori in the mouth (1).
These data were also seen by Eskandari et al. (9).
It is difficult a niche in the oral cavity, specific to H. pylori,
to be defined. The bacteria has been detected in all areas of
the mouth, but those data are not comparable because of the
different methods performed (24).
Thirty-six specimens from the oral cavity of 25 patients
with dental and/or gastroduodenal diseases have been
evaluated by culture and rapid urease test and afterward, for the
HLO (Helicobacter-like organisms), by immunofluorescence
with monoclonal antibodies and PCR. One H. pylori strain
was isolated from a 9-year-old child with gingivitis and
chronic gastritis. The strain was H. pylori positive by the
immunofluorescence and PCR for H. pylori gene ureA and
carried the virulence gene cagA as well as the more toxigenic
genotype vacA s1 m2. Two other HLO strains were isolated from
2448
adults and were positive by the immunofluorescence, however
without a PCR confirmation, they could not be identified at
the species level. The second dental plaque specimen from the
previously (two years ago) positive child was negative by the
culture and PCR directly in the oral specimen. This can suggest
a transitory presence of H. pylori in the oral cavity (4).
Dental practitioners as a risk contingent for H.
pylori
Dentists and dental professionals may be at increased risk due
to the contact with oral cavity of patients with presence of H.
pylori in the oral cavity where it may serve as reservoir for
gastric infections and participate in the pathogenesis of oral
mucosal lesions and ulceration. However, evidence regarding
the occurrence of H. pylori infections and colonization in
dentists is conflicting, but has been based mainly on serological
studies, which carry significant limitations (19).
It has been found that Japanese dentists are at a high
risk for H. pylori infection than controls, with the oral-oral
transmission route being possibly the most common (13, 19).
H. pylori and oral health
Regarding oral health it has been demonstrated that greater
plaque index and a higher incidence rate for gingivitis is
observed in individuals with gastric H. pylori infection (1).
Some authors have found that H. pylori was scarce in patients
with periodontitis (9).
Silva et al. (23) studied 115 individuals, divided in 4 groups:
(A) with gastric diseases and periodontal disease; (B) with
gastric diseases and no periodontal disease; (C) without gastric
diseases and without periodontal disease, (D) without gastric
diseases and with periodontal disease. H. pylori was detected
in the supragingival plaque and there was an association
between the supragingival colonization of H. pylori and oral
hygiene parameters such as the presence of plaque and gingival
bleeding (23).
Oral manifestations and symptoms in patients
with H. pylori infection
In some patients different nonspecific oral signs of H. pylori
infections can often be seen, such as:
• gingivitis (Fig. 1);
• periodontitis (Fig. 2);
• aphthous stomatitis (Fig. 3);
• tongue coating (Fig. 4);
• halitosis.
Many patients complain of subjective symptoms such as
month and tongue burning, numbness in the mouth, altered
taste, dry mouth, even in the absence of common typical
clinical symptoms of infection.
Biotechnol. & Biotechnol. Eq. 25/2011/3
Fig. 1. Gingivitis.
Fig. 2. Periodontitis.
Fig. 3. Aphthous stomatitis.
Biotechnol. & Biotechnol. Eq. 25/2011/3
Fig. 4. Tongue coating.
General treatment rules
In 56 patients with chronic periodontitis and gastric H. pylori
1-week eradication therapy with amoxycilin 1 g, clarithromycin
500 mg, and proton pump inhibitor 20 mg twice a day was
performed. Almost 40% of the patients with gastric H. pylori
harbored the bacterium in the oral cavity. After the eradication
therapy, H. pylori was not detected in the oral cavity, which
suggests high effectiveness of the therapy protocol in the oral
cavity, or it is possible that oral H. pylori is of a transient
character (2).
In contrast, Zaric et al. (26) communicated that periodontal
treatment in combination with systemic therapy could be a
promising approach to increasing the therapy efficacy and
decreasing the risk of infection recurrence. 77.3% of the
patients treated with combined periodontal therapy exhibited
successful eradication of gastric H. pylori, compared with
47.6% who underwent only triple therapy (26). Similar results
2449
were obtained by Jia et al. (15). Long-term professional dental
plaque control was associated with less gastric reinfection
by H. pylori, suggesting that dental plaque control may help
preventing H. pylori-induced gastric disease or reinfection.
The prevalence of H. pylori in the gastric mucosa was 20%
in patients who received dental plaque control, which was
significantly lower than in those without dental plaque control
(84%) (15).
Some studies have shown that H. pylori could be transmitted
more often through household contact (kissing) than with
consumption of contaminated foods.
Good nutrition, frequent fruits and vegetables consumption
and foods rich in vitamin C, protect against infection with H.
pylori.
Treatment protocol
One-week eradication therapy with:
1. Amoxycilin caps. 1 g, twice daily, after meal;
2. Clarithromycin tabl. 500 mg, twice daily, after meal;
3. Proton pump inhibitor tabl. 20 mg - twice daily, 15 min
before meal;
4. Colloidal bismuth subcitrate (De-Nol tabl. 120 mg) 4
times daily (3 times before meal and 1 capsule at bed time).
Practical dental recommendations
Individuals positive for H. pylori in their gastric or oral
samples, as determined by nested PCR, were treated either
with periodontal and triple therapy or with triple therapy alone.
Results indicate that 77.3% of those treated with the combined
therapy exhibited successful eradication of gastric H. pylori,
compared to 47.6% who underwent only triple therapy.
Analysis of these data suggests that periodontal treatment
in combination with systemic therapy could be a promising
approach to increase the efficacy of the treatment and to
decrease the risk of infection recurrence (10).
Based on the literature data and on our experience we
recommend:
1. Professional plaque and tartar removal (by scaling)
– at the beginning of eradication, as well as during therapy
(5-7 days at the beginning of the treatment) and after medical
therapy (10 to 30 days after treatment) to reduce the possibility
of reinfection;
2. New tooth brush to be used (in order for further infection
to be prevented);
3. Special care to the “removal” of denture plaque – daily
brushing with toothpaste, soaking in a desinfection solution,
sometimes even replacement with new dentures;
4. Daily care for good oral hygiene: at least 3 min teeth
cleaning on all surfaces;
5. Cleaning of the tongue – use of a toothbrush with special
equipment (the cracked surface of the tongue can become
2450
friendly, except for the healthy bacterial flora, also for harmful
bacteria); and cleaning the hard palate;
6. Cleaning the intradental spaces – with dental floss and
intradental brushes;
7. Mouthwash usage – twice daily – during the treatment to
chemical plaque control (water inhibits the plaque formation,
prevents its attachment to the teeth or facilitates its decay, and
thus favors the mechanical cleaning);
8. Some studies have shown that chewing gum has an
antibacterial effect against H. pylori.
Conclusions
The presence of H. pylori in the oral cavity could be
considered as main extragastric reservoir and possible source
of reinfection. It has been confirmed in some patients with
gingivitis, periodontitis, stomatitis aphthosa, halitosis and
tongue coating. The dental treatment in combination with
systemic therapy could be a promising therapeutical approach.
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