Open Journal of Stomatology, 2013, 3, 318-322 OJST Published Online September 2013 (
Helicobacter Pylori and Periodontal diseases: An update
and proposal of a multidisciplinary clinical protocol
Sophie Marbaix1, Assem Soueidan1, Maya Romani2, Guillaume Campard1, Gilles Amador3,
Zahi Badran1
1Department of Periodontology (Inserm U791/UIC Odontologie/CHU de Nantes), Faculty of Dental Surgery, Nantes, France
2Department of Family medicine, American University of Beirut-Medical Centre, Beirut, Lebanon
3Department of Dental public health, Faculty of Dental Surgery (CHU de Nantes), Nantes, France
Received 13 June 2013; revised 14 July 2013; accepted 1 August 2013
Copyright © 2013 Sophie Marbaix et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Helicobacter Pylori has been closely linked to chronic
gastritis, peptic ulcers and increased risk of gastric
carcinoma. Oral cavity, in particular dental plaque in
periodontal pockets, may be a possible reservoir har-
boring H. Pylori, and may therefore be involved in the
gastric reinfection by the bacterium, even after triple
therapy regimen. This report is an update of scientific
data showing the potential localization of H. Pylori in
the oral cavity of periodontitis patients. A multidisci-
plinary clinical protocol combining full-mouth disin-
fection and triple therapy is also suggested. This pro-
tocol could permit to enhance oral H. Pylori eradica-
Keywords: Periodontal; Triple Therapy; Full-Mouth
Periodontal diseases are inflammatory chronic diseases
affecting teeth supportive tissues, and have infectious
bacterial etiology. It is initiated by oral bacterial biofilms
developing on dental roots. Early stage of the disease is
gingivitis, and is characterized by gingival inflammation
(swelling, redness, bleeding···). Individually susceptible
patients could develop Periodontitis, which implies al-
veolar bone loss and periodontal pockets formation
around affected teeth (Figure 1). Periodontopathogenic
bacteria (PB) are mainly anaerobic, Gram negative
strains developing subgingivally in periodontal pockets.
This subgingival environment is particularly favorable
for the survival and proliferation of non-aerobic strains.
Also, many locations in the oral cavity (OC), such as the
dorsum of the tongue are oxygen-poor sites. Helico-
Figure 1. Periodontitis affecting teeth supportive
bacter Pylori (HP), as a gram-negative, microaerophilic,
spiral-shaped bacterium; could find adequate conditions
for colonization and proliferation in the OC. HP has been
implicated in the etiology of gastritis and peptic ulcers.
Its presence is also a risk factor for gastrointestinal can-
cers. Human infection by this pathogen could involve an
oral route, and the OC is an anatomical region with a
potential to harbor HP, in particular dental plaque (oral
Thus, it seems conceivable that oral health status and
different gingival clinical conditions may have an effect
on the presence of HP in oral biofilms, hence influencing
the process of HP gastric infection or reinfection [1,2] .
Many reports found that HP could colonize the healthy
OC or the subgingival periodontal pockets area. The lat-
ter could eventually serve as a bacterial reservoir. Ac-
cording to Savita et al. [3], subjects with periodontitis
harbor a number of HP significantly higher than subjects
without periodontitis. Also, reinfection of the gastroin-
testinal tract by HP from dental plaque could occur after
proper eradication regimen. Triple therapy (TT) has been
successfully used to eradicate gastric HP. TT is the most
common first line treatment recommended for H. Pylori
S. Marbaix et al. / Open Journal of Stomatology 3 (2013) 318-322 319
eradication, it consists of a proton pump inhibitor (PPI)
(lansoprazole 30 mg twice daily, omeprazole 20 mg twice
daily, pantoprazole 40 mg twice daily, rabeprazole 20 mg
twice daily) plus amoxicillin 1 gram twice daily and
clarithromycin 500mg twice daily for 7 to 14 days. Met-
ronidazole (500 mg twice daily) can be substituted for
amoxicillin in penicillin-allergic patients. A longer dura-
tion of treatment (14 versus 7 days) may be more effective
in curing infection, but this remains controversial. TT is
currently considered the gold standard reaching an eradi-
cation rate up to 80% [1,4]. However, in many cases, HP
is not completely eliminated after a single treatment, and
the recurrence of the HP infection has been well-docu-
mented [5]. Therefore, the OC has been suspected to be a
common source for reinfection of the stomach [2,6]. In
fact, bacteria developing in biofilm configuration (such
as in dental plaque) are much more resistant to antibiot-
ics than freely circulating bacteria [7].
Full mouth disinfection (FMD) is a periodontal clini-
cal protocol, combining mechanical antibacterial therapy
(scaling/root planning of dental roots) and antiseptic re-
gimen (chlorhexidine) to obtain PB eradication [8,9].
The mechanical debridement of all teeth is performed
within 24 h, in order to eradicate rapidly PB present in
dental biofilms, and thus preventing reinfection of treated
sites. Also, the adjunction of a systemic antibiotic pre-
scription to FMD (amoxicillin/metronidazole or azithro-
mycin) has been found to successfully enhance clinical
outcomes [10-12].
This article focuses on the specific association of
periodontal status and oral HP in the published scientific
literature. The rationale of considering periodontitis as a
risk factor for HP infections/reinfection will also be dis-
cussed, with an emphasis on the eventual clinical impli-
cations of this assumption. Finally, we suggest the merg-
ing of both FMD and TT regimen, in order to enhance
periodontal therapy outcome as well as eradication of HP.
2.1. Helicobacter Pylori in Periodontally Ill and
Healthy Patients
Several studies have evaluated the correlation between
the prevalence of HP and periodontal diseases. Conflict-
ing results could be observed in the literature, this could
be attributed to the diversity of the studied populations,
sample collection methods, and the specificity of the
methods used for HP detection [2,13]. Although it may
affect the presence of HP in dental plaque, few studies
have separately investigated supra and subgingival plaque,
which corresponds to different microenvironments when
availability of nutrients, oxygen and host mechanisms
are considered [14].
Souto et al. [2] performed a full-mouth clinical ex-
amination (six sites per tooth) to determine periodontal
health status and examined subjects with no history of
gastric symptoms, their results showed a higher preva-
lence of HP in subgingival biofilm of subjects with pe-
riodontitis compared to individuals with periodontal
health (50% versus 11% respectively), suggesting that
periodontal pockets and inflammation may favor HP
colonization. Another study by Riggio and Lennon [15]
examined the presence of H. Pylori in subgingival plaque
(sites with periodontal pocket depth 5 mm) of perio-
dontitis patients with no symptoms of gastritis or peptic
ulcer disease. This study found that 38% of subjects with
deep periodontal pockets were positive for HP. Conse-
quently, the authors concluded that subgingival plaque in
individuals presenting periodontitis may function as a
reservoir for HP.
Gebara et al. [14], found that more than 26% of HP
was detected in the OC of periodontitis patients (all posi-
tive for gastric HP), periodontitis and gingivitis showed a
high prevalence; however, no control group with healthy
patients were included. Al Asqah et al. [13] found that
periodontitis patients had a significantly higher percent-
age of HP in subgingival plaque samples in comparison
to periodontally healthy controls (79% versus 43% re-
spectively). Other studies failed to detect HP in the sub-
gingival plaque [16,17] or found no association between
periodontal status and the prevalence of the bacterium in
OC [18].
2.2. Relation between Gastric Infection and
Periodondal Disease
Umeda et al. [19] showed that more than 40 % of pa-
tients with history of gastritis or peptic ulcers had perio-
dontal pockets (>4 mm). Bruce et al. (54) found that
periodontal pockets 5 mm are associated with increased
odds of HP seropositivity. Also, a large epidemiological
investigation performed over 10,000 subjects [20], found
a positive link between HP associated gastric infection
and periodontal diseases. The latter may facilitate the HP
oro-gastric transmission and colonization of the bacteria
in the digestive tract. Also, periodontitis microenviron-
ment conditions could be favorable for HP multiplication,
thus increasing sufficiently to cause gastric infection
On the other hand, many studies [23-25] failed to es-
tablish a positive correlation between periodontal disease
and gastric infection.
3.1. Effect of Triple Therapy on Oral HP
It is still unclear whether TT affects HP in dental plaque.
Song et al. [26] found plaque samples negative for HP
Copyright © 2013 SciRes. OPEN ACCESS
S. Marbaix et al. / Open Journal of Stomatology 3 (2013) 318-322
only in patients who had recently been treated with TT.
But many reports, found a persistent oral HP after TT
[27-29]. More recently, a meta-analysis [30] confirmed
the close relationship between HP infection in the OC
and the stomach, and concluded that oral HP is more
difficult to eradicate than gastric HP and it may be a
source of reinfection. On the other hand, Umeda et al.
[19] reported that subjects with periodontal pockets re-
tained HP in the OC even after eradication of the bacte-
rium from the stomach. Similarly, Gebara et al. [1]
showed that 60% of subjects with periodontal disease
were still positive for HP DNA in their OC, whereas only
10% were positive in the stomach after triple therapy. In
a same way, Zarik et al. [5] revealed that 3 months after
triple therapy in the group of participants who did not
harbor HP in periodontal pockets, the eradication rate
was 87.4%. In contrast, the group positive for HP in the
subgingival plaque exhibited a significantly lower rate of
eradication (47.6%). Also, polyantibiotic systemic ther-
apy was considerably less efficient in the eradication of
HP from periodontal pockets, compared with its elimina-
tion in the stomach (33% and 87% respectively).
3.2. Effect of Periodontal Therapy on Prevention
of Gastric Helicobacter Pylori Recurrence
Few studies investigated the effect of periodontal therapy
on eradication of gastric HP. Zarik et al. [5], evaluated
the effectiveness of periodontal treatment and TT in
achieving complete elimination of gastric HP infection.
Participants positive for HP in the subgingival biofilm,
who had undergone basic periodontal therapy and a TT
regimen, showed a higher elimination rates compared to
the group who underwent TT alone (77.3% and 47.6%
respectively), thus suggesting that systemic antibiotic
polytherapy alone is not as effective in preventing the
reappearance of gastric HP in subjects positive for the
oral form of HP. A meta-analysis [31] concluded that
periodontal therapy reduces the relative risk of persis-
tence of gastric HP by 63%. Similar results were found
in a study with a two years follow-up [32].
Recently, a case series of 9 patients [33], investigated
whether full mouth ultrasonic debridement can eradicate
persistent oral HP after TT. Periodontal debridement was
able to eradicate HP from 88.3% of patients with gingi-
vitis, while it failed in eradicating the bacteria from the
OC of periodontitis group. Within the limits of this case
series, a single session of oral hygiene instruction com-
bined with full mouth periodontal debridement seemed to
promote a positive effect in eradicating HP only from
supragingival sites.
Actual consensus in Periodontology suggests that antibi-
otic regimen should be started immediately after me-
chanical periodontal treatment [34]. Thus, a complete
elimination of calculus and disorganization of bacterial
biofilms must be achieved prior to any antibiotic therapy
in order to disrupt the biofilm configuration forming a
barrier to antibiotic molecules. For periodontal treatment
we suggest a full mouth disinfection (FMD) approach, as
described in the periodontal literature [9]. The FMD con-
sists of a total scaling/mechanical debridement of teeth
root surfaces. An antiseptic irrigation of the pockets, the
dorsum of the tongue and the tonsils is also performed
[8]. The whole procedure should be finalized in one ses-
sion (or two sessions within 24 h). Immediately after
FMD, an antibiotic regimen (+ antiseptic chlorhexidine
mouth-washes/oral gels) has been found to significantly
enhance periodontal outcome [10]. A combination of
amoxicillin/metronidazole is the most tested combina-
tion after FMD [11]. On the other hand, clarithromycin
has shown an excellent availability in the gingival area
[35]. Hence, the antibiotic regimen in TT could substitute
periodontal prescription as soon as the mechanical treat-
ment is accomplished. This approach could enhance PP
and HP elimination (in the OC and the gastric tract). In
fact, the antibiotics used to eradicate HP are also effi-
cient against the anaerobic PB. Hence, the merging of the
periodontal FMD protocol and the TT (Figure 2) permits
to treat both pathologies in an optimal manner, and could
significantly boost oral HP eradication.
For maintaining long-term results, routine dental/peri-
odontal supportive therapy and daily oral hygiene pro-
cedures should be performed without interruption [6].
Although contradictory results are found in the scientific
Oral h
iene instructions
Tooth brushing, interdental plaque removal, tongue scrapping
Full mouth disinfection(1 or 2 sessions
erformed in 24 h)
Mechanical scaling/root planning (or ultrasonic debridement)
Subgingival chlorhexidine irrigation
Tongue disinfection with chlorhexidine gel
le the ra
+2 weeks chlorhexidine mouthwashes
Starting immediately following the last session of full mouth
Periodontal full mouth disinfection is immediately followed by triple
therapy regimen and antiseptic regimen, in order to enhance the eradi-
cation of periodontopathogenic bacteria as well as oral/gastric H. Py-
Figure 2. Multidisciplinary clinical protocol.
Copyright © 2013 SciRes. OPEN ACCESS
S. Marbaix et al. / Open Journal of Stomatology 3 (2013) 318-322 321
literature, many reports have associated periodontal dis-
ease (periodontal pockets formation) to an increased
prevalence of oral HP. Its bacterial load is increased by
periodontal disease and periodontal pockets formation.
The assumption that subgingival oral biofilm could act as
a suitable reservoir for HP is plausible and supported by
consistent evidence from preliminary clinical trials. The
presence of oral HP in patients with periodontal disease
(Periodontitis and gingivitis) may cause refractoriness of
gastric infection to triple therapy alone [5,31].
The mechanisms that confer the ability of HP to es-
cape systemic treatment are not well understood, but
there is evidence indicating that biofilms provide de-
fense from the host immunological response and the ac-
tion of antimicrobials agents [36]. Hence, antimicrobials
cannot be efficient if the biofilm is not mechanically
disrupted [37] shortly prior to prescription. The subgin-
gival dental biofilm is particularly suspected, due to the
favorable micro-ecological conditions provided by the
periodontal pockets. The biofilm is known to provide
protection from the host’s immunological response, and
bacteria growing in biofilms exhibit high resistance to
antimicrobial agents [5]. We therefore suggest a simple
multidisciplinary clinical management protocol, merging
the triple therapy to periodontal mechanical treatment
and chemical antiseptic disinfection. A joint coordination
between the periodontist and the gastroenterologist is a
perquisite for the success of this treatment regimen.
Adopting this protocol has two objectives; treating pe-
riodontal disease and enhancing the efficacy of the anti
HP therapy.
On the other hand, it should be considered that the ef-
ficacy of non-surgical treatment modalities is related to
the pocket depth. Hence, surgical periodontal procedures
like open flap debridement could be needed in some
cases to eliminate deep bacterial biofilms potentially har-
boring HP [33]. To our knowledge, no research has been
conducted in this field.
In conclusion, the efficacy of the combined proposed
protocol should be investigated in future controlled, ran-
domized clinical trials. If confirmed, it could be inte-
grated in the standard clinical management of HP infec-
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