Role of dental plaque, saliva and periodontal disease in Helicobacter pylori infection

Table 1 Studies evaluating the presence of Helicobacter pylori in dental plaque

Ref.	Method of H. pylori detection in dental plaque	Sample population and sample size	Prevalence of H. pylori in dental plaque
Agarwal and Jithendra[84], 2012	PCR	India; 30 H. pylori-positive and 20 H. pylori-negative patients	Overall-42% (n = 21); in H. pylori-positive group-60% (18/30); in H. pylori-negative group-15% (3/20)
Momtaz et al[85], 2012	PCR	Iran; 300 patients with gastro-duodenal diseases	0
Wichelhaus et al[86], 2011	PCR	Germany; 11 orthodontic patients	36% (n = 4)
Gao et al[46], 2011	PCR	China; 96 patients with H. pylori infection	82.30%
Chaudhry et al[45], 2011	PCR	Pakistan; 89 dyspeptic patients reporting for endoscopy	51.6% (n = 46) for both genes; 62.9% (n = 56) for 16srRNA; 61.7% (n = 55) for 860-bp DNA region; 73% (n = 65) if either of the 2 regions were considered
Bago et al[81], 2011	PCR	Croatia; 56 patients with chronic periodontitis and gastric H. pylori-positive	37.5% (n = 21)
Silva et al[71], 2010	PCR	Brazil; 115 patients-36 with dyspepsia and periodontal disease, 31 with dyspepsia but no periodontal disease, 22 with neither dyspepsia nor periodontal disease, 26 with periodontal disease and without dyspepsia	11.3% (n = 13)
Silva et al[87], 2010	PCR	Brazil; 30 dyspeptic patients	20% (n = 6) by 16S rDNA and 6.7% (n = 2) by vacA
Eskandari et al[88], 2010	PCR	Iran; 67 patients with chronic periodontitis-23 with H. pylori-positive gastritis	5.97% (n = 4/67)
Assumpção et al[89], 2010	PCR	Brazil; 99 adult patients who underwent upper gastro-intestinal endoscopy	72% (71) samples were positive for H. pylori. Overall, 63 (89%) of 71 positive dental plaque samples were positive for vacA and cagA. 58/71 (82%) were positive for cagA, while vacA genotypes had a prevalence ranging from 13%-59%
Medina et al[90], 2010	PCR	Argentina; 98 patients-43 dyspeptic patients and 55 asymptomatic controls	10.2% (n = 10)
Liu et al[70], 2009	PCR	China; 443 dyspeptic patients	59.4% (n = 263)
Gonçalves et al[69], 2009	PCR	Brazil; 23 HIV seropositive individuals (13 who had chronic periodontitis and 10 who were periodontally healthy) and 31 HIV seronegative individuals (17 who had chronic periodontitis and 14 who were periodontally healthy)	Not specified; frequency of detection was significantly higher in chronic periodontitis groups compared with periodontally healthy groups
Silva et al[91], 2009	PCR	Brazil; 30 individuals who were H. pylori-positive with gastric disease (cases) and 32 individuals who were H. pylori-positive with no gastric disease (controls)	Overall-17.7% (n = 11). Among cases, DNA detected in 36.6% (11/30); control group-0%
Morales-Espinosa et al[62], 2009	PCR	Mexico; 66 hospitalized patients and 65 dental patients	Overall-19.9% (n = 26); 24% (n = 16) among hospitalized patients and 15% (n = 10) among dental patients
Souto and Colombo[68], 2008	PCR	Brazil; 225 patients-56 periodontally healthy and 169 chronic periodontitis patients	50% in patients with chronic periodontitis and 11.4% in periodontally healthy individuals
Liu et al[92], 2008	PCR	China; 214 children	58.9% (n = 126)
Bürgers et al[93], 2008	PCR	Germany; 94 patients who underwent upper gastro-intestinal endoscopy	5.4% (n = 5/92 dentate patients)
Teoman et al[94], 2007	PCR	Turkey; 67 dyspeptic patients	28.3% (n = 19)
Olivier et al[95], 2006	PCR	South Africa; 74 healthy members of a rural community	0
Kignel et al[96], 2005	PCR	Brazil; 49 dyspeptic patients	2% (n = 1)
Gebara et al[53], 2004	PCR	Brazil; 15 gingivitis and 15 periodontitis patients-all were H. pylori-positive in antral mucosa	20% (n = 6) in supra-gingival plaque and 26.6% (n = 8) in sub-gingival plaque
Fritscher et al[97], 2004	PCR	Brazil; 53 patients with recurrent aphthous stomatitis (cases) and 52 patients without recurrent aphthous stomatitis (controls)	Overall-3.8%; 5.7% (n = 3) in cases and 1.9% (n = 1) among controls
Umeda et al[35], 2003	PCR	Japan; 56 dental patients	25% (n = 14)
Suk et al[98], 2002	PCR	Taiwan; 65 patients with dyspeptic symptoms	43.1% (n = 28)
Berroteran et al[99], 2002	PCR	Venezuela; 32 dyspeptic patients and 20 asymptomatic controls	Overall-28.9%; 37.5% (n = 12) among dyspeptic patients and 15% (n = 3) among controls
Goosen et al[100], 2002	PCR	South Africa; 58 clinically healthy volunteers	1.7% (n = 1)
Song et al[63], 2000	PCR	Germany; 15 dyspeptic patients and 6 orthodontic patients	100% (n = 21)
Song et al[101], 2000	PCR	Germany; 20 dyspeptic patients	In dental plaque-not specified; 100% in oral samples (plaque and saliva)
Song et al[58], 2000	PCR	Germany; 42 patients who underwent upper gastro-intestinal endoscopy	97% (n = 41)-82% in molar region, 64% in premolar region and 59% in incisor region
Miyabayashi et al[79], 2000	PCR	Japan; 47 patients with chronic gastritis or peptic ulcer	38.3% (n = 18)
Agarwal and Jithendra[84], 2012	Culture	India; 30 H. pylori-positive and 20 H. pylori-negative patients	Overall-18% (n = 9); in H. pylori-positive group-30% (9/30); in H. pylori-negative group-0
Loster et al[49], 2009	Culture	Poland; 46 dentists without known co-morbidities	48%
Sudhakar et al[102], 2008	Culture	India; 50 patients with duodenal and gastric ulcer (study group) and 25 students (control group)	Overall 6.7% (n = 5); in study group-10% (n = 5), in control group-0%
Teoman et al[94], 2007	Culture	Turkey; 67 dyspeptic patients	0
Czesnikiewicz-Guzik et al[47], 2005	Culture	Poland; 100 female patients	48.3%
Czesnikiewicz-Guzik et al[48], 2004	Culture	Poland; 100 female patients	48.3%
Umeda et al[35], 2003	Culture	Japan; 18 dental patients	5.6% (n = 1)
Goosen et al[100], 2002	Culture	South Africa; 58 clinically healthy volunteers	13.8% (n = 8)
Checchi et al[103], 2000	Culture	Italy; 35 patients from a Periodontology clinic	8.6% (n = 3)
Sambashivaiah et al[73], 2011	RUT/CLO test	India; 36 patients in 3 groups-group I, healthy subjects, group II, chronic periodontitis patients, group III, chronic periodontitis patients with type II diabetes mellitus	Overall-66.7% (n = 24); among group I-41.7% (n = 5), group II-75% (n = 9), group III-83.3% (n = 10)
Bali et al[65], 2010	RUT/CLO test	India; 124 dyspeptic patients of which 60 were H. pylori-positive (cases) and 64 were H. pylori-negative (controls)	Overall-51.6% (n = 64); among cases-86.7% (n = 52)
Assumpção et al[89], 2010	RUT/CLO test	Brazil; 99 adult patients who underwent upper gastro-intestinal endoscopy	52% (n = 48/93)
Al Asqah et al[64], 2009	RUT/CLO test	Saudi Arabia; 62 dyspeptic patients with periodontitis and 39 dyspeptic patients without periodontitis	Overall-65%; 79% in periodontitis group and 43% in non-periodontitis group
Sudhakar et al[102], 2008	RUT/CLO test	India; 50 patients with duodenal and gastric ulcer (study group) and 25 students (control group)	Overall 49.3% (n = 37); in study group-70% (n = 35), in control group-8% (n = 2)
Chitsazi et al[40], 2006	RUT/CLO test	Iran; 88 dyspeptic patients-44 with H. pylori infection and 44 without H. pylori infection	Overall 18.2% (16/88); 36.4% (16/44) in H. pylori-positive group
Anand et al[104], 2006	RUT/CLO test	India; 65 dyspeptic patients with H. pylori infection (cases) and 69 dyspeptic patients without infection (controls)	Overall-79.9% (n = 107/134); 89.2% (n = 58) among cases and 71% (n = 49) among controls
Gürbüz et al[39], 2003	RUT/CLO test	Turkey; 75 dyspeptic patients	91.7% (n = 68)
Choudhury et al[67], 2003	RUT/CLO test	India; 124 patients with dyspepsia	43% (n = 54)
Al-Refai et al[105], 2002	RUT/CLO test	Saudi Arabia; 75 dyspeptic patients and 60 healthy controls	Overall-88.1% (n = 119); among dyspeptic patients-89.3% (n = 67); among controls-86.7% (n = 52)
Butt et al[74], 2002	RUT/CLO test	Pakistan; 78 dyspeptic patients	100%
Suk et al[98], 2002	RUT/CLO test	Taiwan; 65 patients with dyspeptic symptoms	100%
Ozdemir et al[106], 2001	RUT/CLO test	Turkey; 81 dyspeptic patients	79% (n = 64)
Avcu et al[75], 2001	RUT/CLO test	Turkey; 241 H. pylori-positive patients with gastric histologic changes	44.8% (n = 108)
Namiot et al[107], 2010	EIA	Poland; 155 patients	65.6% (n = 101)
Leszczyńska et al[108], 2009	EIA	Poland; 164 dyspeptic patients referred for endoscopy-95 H. pylori infected and 69 non-infected	82.1% in H. pylori-positive subjects and 17.7% in H. pylori-negative subjects
Checchi et al[103], 2000	EIA	Italy; 35 patients from a Periodontology clinic	11% (n = 4)
Butt et al[74], 2002	Cytology	Pakistan; 78 dyspeptic patients	88%
Butt et al[82], 2001	Cytology	Pakistan; 135 dyspeptic patients	81.5% (n = 110)
Rasmussen et al[109], 2010	Southern blot	Brazil; 78 dyspeptic patients	47.4% (n = 37)

HIV: Human immunodeficiency virus; PCR: Polymerase chain reaction; RUT: Rapid urease test; CLO: Campylobacter-like organism; EIA: Enzyme immunoassay; H. pylori: Helicobacter pylori.

Table 2 Studies evaluating the presence of Helicobacter pylori in saliva

Ref.	Method of detection of H. pylori in saliva	Sample population and sample size	Prevalence of H. pylori in saliva
Momtaz et al[85], 2012	PCR	Iran; 300 patients with gastro-duodenal diseases	8.3% (n = 25)
Gao et al[46], 2011	PCR	China; 96 patients with H. pylori infection	51.10%
Momtaz et al[110], 2010	PCR	Iran; 250 dyspeptic patients	14.4% (n = 36)
Silva et al[87], 2010	PCR	Brazil; 30 dyspeptic patients	30% (n = 9) by 16S rDNA and 6.7% (n = 2) by vacA
Medina et al[90], 2010	PCR	Argentina; 98 patients-43 dyspeptic patients and 55 asymptomatic controls	9.2% (n = 9)
Silva et al[91], 2009	PCR	Brazil; 30 individuals who were H. pylori positive with gastric disease (cases) and 32 individuals who were H. pylori positive with no gastric disease (controls)	Overall-25.8% (n = 16). Among cases, H. pylori DNA detected in 53.3% (16/30); in control group-0%
Morales-Espinosa et al[62], 2009	PCR	Mexico; 66 hospitalized patients and 65 dental patients	Overall-35.9% (n = 47); 52% (n = 34) among hospitalized patients and 20% (n = 13) among dental patients
Suzuki et al[111], 2008	PCR	Japan; 326 non-dyspeptic subjects	6.4% (n = 26)
Bürgers et al[93], 2008	PCR	Germany; 94 patients who underwent upper gastro-intestinal endoscopy	7.4% (n = 7)
Kignel et al[96], 2005	PCR	Brazil; 49 dyspeptic patients	0
Gebara et al[53], 2004	PCR	Brazil; 15 gingivitis and 15 periodontitis patients-all were H. pylori-positive in antral mucosa	10% (n = 3)
Goosen et al[100], 2002	PCR	South Africa; 58 clinically healthy volunteers	3.4% (n = 2)
Song et al[101], 2000	PCR	Germany; 20 dyspeptic patients	In saliva-not specified; 100% in oral samples (plaque and saliva)
Song et al[58], 2000	PCR	Germany; 42 patients who underwent upper gastro-intestinal endoscopy	55% (n = 23)
Miyabayashi et al[79], 2000	PCR	Japan; 47 dyspeptic patients and 10 healthy controls	34% (n = 16) among dyspeptic patients
Umeda et al[35], 2003	PCR and culture	Japan; 15 dyspeptic patients	26.7% (n = 4)
Czesnikiewicz-Guzik et al[47], 2005	Culture	Poland; 100 female patients	54.10%
Cześnikiewicz-Guzik et al[48], 2004	Culture	Poland; 100 female patients	54%
Rasmussen et al[109], 2010	Southern blot	Brazil; 78 dyspeptic patients	42.3% (n = 33)

PCR: Polymerase chain reaction; H. pylori: Helicobacter pylori.

Table 3 Studies evaluating the association of oral hygiene status and gingival/periodontal status with Helicobacter pylori infection

Ref.	Oral health status evaluated	Definition of oral hygiene/periodontal status	Sample population and sample size	Association with oral H. pylori	Association with gastric H. pylori
Sambashivaiah et al[73], 2011	Periodontal status	Mean probing depth > 5 mm	India; 36 patients in 3 groups-group I, healthy subjects, group II, chronic periodontitis patients, group III, chronic periodontitis patients with type II diabetes mellitus	Significant	Not evaluated
Silva et al[71], 2010	Periodontal status	At least 4 teeth with PD ≥ 5 mm and CAL > 3 mm	Brazil; 115 dyspeptic patients	Significant	Not evaluated
Namiot et al[107], 2010	Oral hygiene/periodontal status	Oral Hygiene index/Russell’s periodontal index	Poland; 155 dyspeptic patients	Non-significant	Not evaluated
Bali et al[65], 2010	Oral hygiene status/periodontal status	Oral hygiene index-simplified/probing pocket depth	India; 124 dyspeptic patients of which 60 were H. pylori positive (cases) and 64 were H. pylori negative (controls)	Not evaluated	Significant
Gonçalves et al[69], 2009	Periodontal status	At least 3 sites with PD ≥ 5 mm and/or CAL ≥ 4 mm and BOP	Brazil; 23 HIV seropositive patients of whom 13 had periodontitis and 10 were periodontally healthy; 31 HIV seronegative patients of whom 17 had periodontitis and 14 were periodontally healthy	Significant	Not evaluated
Al Asqah et al[64], 2009	Periodontal status	BOP + PD ≥ 3 mm on at least 4 teeth	Saudi Arabia; Dyspeptic patients-62 patients with periodontitis and 39 without periodontitis	Significant	Significant
Liu et al[70], 2009	Gingival status	Gingival index	China; 443 dyspeptic patients	Significant	Not evaluated
Zaric et al[72], 2009	Gingival and periodontal status	Mean PD, CAL and gingival index scores	Serbia; 66 dyspeptic patients with H. pylori infection of gastric mucosa	Significant for mean PD but not for CAL and gingival index scores	Not evaluated
Bürgers et al[93], 2008	Periodontal status	Periodontal Screening Index	Germany; 94 dyspeptic patients	Non-significant	Non-significant
Souto and Colombo[68], 2008	Periodontal status	≥ 10% of teeth with probing depth and/or clinical attachment loss ≥ 5 mm, or ≥ 15% of teeth with probing depth and/or clinical attachment loss ≥ 4 mm, and > 10% of sites with bleeding on probing	Brazil, 225 patients-56 periodontally healthy and 169 chronic periodontitis patients	Significant	Not evaluated
Namiot et al[112], 2007	Periodontal status	Russell’s periodontal index	Poland; 137 H. pylori-positive patients with peptic ulcer	Not evaluated	Non-significant
Anand et al[104], 2006	Oral hygiene status/periodontal status	Oral hygiene index-simplified/patients with one or more sites with a PD ≥ 3 mm and CAL ≥ 3 mm at the same site	India; 65 dyspeptic patients with H. pylori infection (cases) and 69 dyspeptic patients without H. pylori infection (controls)	Not evaluated	Non-significant
Gebara et al[53], 2004	Gingival and periodontal status	Gingivitis group-patients with PD ≤ 3 mm and BOP on at least 4 sites; periodontitis group- BOP + PD ≥ 5 mm on at least 4 teeth	Brazil; 15 gingivitis and 15 periodontitis patients-all were H. pylori-positive in antral mucosa	Non-significant	Not evaluated
Gürbüz et al[39], 2003	Oral hygiene/periodontal status	Plaque index/Russell’s index	Turkey; 75 dyspeptic patients	Significant	Significant
Umeda et al[35], 2003	Periodontal status	Presence of periodontal pockets ≥ 4 mm	Japan; 28 patients who harbored H. pylori in stomach/duodenum	Significant	Not evaluated
Choudhury et al[67], 2003	Periodontal status	CPI	India; 124 dyspeptic patients	Significant	Not evaluated
Butt et al[74], 2002	Oral hygiene status/periodontal status	Community Periodontal Index of treatment needs	Pakistan; 78 dyspeptic patients	Significant with amount of dental plaque but not with gingival or periodontal inflammation	Not evaluated
Dye et al[66], 2002	Periodontal status	Presence of 1 dental site with PD ≥ 5 mm	United States; data from 4504 participants of National Health and Nutrition Examination III Survey	Not evaluated	Significant
Berroteran et al[99], 2002	Gingival status	Gingival index-scoring from 0-3	Venezuela; 32 dyspeptic patients and 20 asymptomatic controls	Non-significant	Non-significant
Al-Refai et al[105], 2002	Oral hygiene/gingival/ periodontal status	Plaque index/gingival index/Community Periodontal Index of treatment needs	Saudi Arabia; 75 dyspeptic patients and 60 healthy controls	Non-significant	Non-significant

PD: Pocket depth; CAL: Clinical attachment level; BOP: Bleeding on probing; CPI: Community periodontal index; H. pylori: Helicobacter pylori.

Table 4 Studies evaluating the effects of systemic Helicobacter pylori eradication therapy on oral Helicobacter pylori

Ref.	Sample population and sample size	Prevalence of H. pylori in dental plaque	Type of anti-H. pylori therapy	Prevalence of H. pylori in dental plaque after anti-H. pylori therapy	Effect on H. pylori infection
Gao et al[46], 2011	China; 80 patients with H. pylori infection-37 treated with anti-H. pylori therapy (gp A) and 43 treated with anti-H. pylori therapy and periodontal therapy (gp B)	82.3% in dental plaque and 51.1% in saliva	Gp A-2 wk proton pump inhibitor or triple therapy; gp B-2 wk triple therapy and initial periodontal therapy (oral hygiene education and scaling)	After 4 wk-29.7% (n = 11) in gp A and 4.7% (n = 2) in gp B; after 1 yr-43.2% (n = 16) in gp A and 18.6% (n = 8) in gp B	Eradication rate of gastric H. pylori After 4 wk-73% (27/37) in gp A and 81.4% (35/43) in gp B After 1 yr-32.4% (11/37) in gp A and 62.8% (27/43) in gp B
Bago et al[81], 2011	Croatia; 56 patients with chronic periodontitis and gastric H. pylori-positive	37.5% (n = 21)	One week therapy consisting of amoxicillin 1 g, clarithromycin 500 mg, and omeprazole 20 mg twice a day	0	Eradication rate in stomach was 76.2% (16/21)
Zaric et al[72], 2009	Serbia; 44 patients-21 patients positive for H. pylori in subgingival dental plaque and gastric mucosa (G+O+t) and 23 patients who were positive for H. pylori only in gastric mucosa (G+O-t)- all 44 received only anti-H. pylori (triple) therapy	47.7%	Triple therapy consisting of amoxicillin 2 g/d, clarithromycin 1 g/d, and pantoprazole 80 mg/d for 7 d	In G+O+t-66.7% (14/21)	In the G+O+t group, only 47.6% (10/21) showed eradication of gastric H. pylori compared with 87.4% (20/23) in G+O-t
Gebara et al[80], 2006	Brazil; 30 dentate patients with gingivitis/periodontitis and H. pylori infection who received anti-H. pylori therapy	20% (n = 6) in supra-gingival plaque and 26.6% (n = 8) in sub-gingival plaque	Triple therapy consisting of amoxicillin 1 g, clarithromycin 500 mg, and lansoprazole 30 mg twice a day for 7 d	30% (n = 9) in supra-gingival plaque and 46.7% (n = 14) in sub-gingival plaque	Eradication rate of 90%
Gürbüz et al[39], 2003	Turkey; 75 dyspeptic patients of which 61 were H. pylori-positive and also had H. pylori in dental plaque	90.7% (n = 68); 81.3% (n = 61) had co-infection	Amoxicillin 1 g, clarithromycin 500 mg, and ranitidine bismuth citrate 400 mg twice a day for 7 d	100% in 61 patients	Eradication rate of 83%
Suk et al[98], 2002	Taiwan; 65 patients with dyspeptic symptoms	Overall-43.1% (n = 28), 73.7% (28/38) among H. pylori-positive patients	Colloidal bismuth subcitrate 1 g, amoxicillin 500 mg, and metronidazole 250 mg four times daily for 2 wk or cimetidine 200 mg, amoxicillin 500 mg, and metronidazole 250 mg 4 times a day for 2 wk	92.9% (26/28)	H. pylori eradicated from 84.2% (n = 32/38) H. pylori infected individuals
Butt et al[82], 2001	Pakistan; 82 patients positive for H. pylori in dental plaque-27 received only anti-H. pylori therapy (gp 1); 25 received anti-H. pylori therapy+periodontal therapy (gp 2); 30 received only periodontal therapy (gp 3)	100%	Gp 1-twice daily omeprazole 20 mg, clarithromycin 500 mg and metronidazole 400 mg; gp 2-triple therapy and dental scaling and chlorhexidine mouthwashes twice daily for 7 d; gp 3-only dental treatment	100% in gp 1; 16% in gp 2 (4/25); 10% in gp 3 (3/30)	Not evaluated
Miyabayashi et al[79], 2000	Japan; 47 patients with chronic gastritis or peptic ulcer-48.9% (n = 23) were positive for oral H. pylori and 38.3% (n = 18) had H. pylori in plaque	48.9% (n = 23) were positive for oral H. pylori and 38.3% (n = 18) had H. pylori in plaque	Lansoprazole 30 mg/d, metronidazole 750 mg/d, and clarithromycin 400 mg/d for 2 wk	Oral prevalence at 4 wk-34% (16/47)	At 4 wk-91.6% (22/24) of subjects negative for oral H. pylori were successfully eradicated of H. pylori infection compared to 52.2% (12/23) in oral H. pylori-positive patients. At 2 years, 95.8% (23/24) of subjects negative for oral H. pylori were successfully eradicated of H. pylori infection compared with 69.5% (16/23) in oral H. pylori-positive patients

H. pylori: Helicobacter pylori.

Table 5 Studies evaluating the effect of periodontal therapy on oral and gastric Helicobacter pylori

Ref.	Sample population and sample size	Prevalence of H. pylori in dental plaque	Details of periodontal therapy	Prevalence of H. pylori in dental plaque after periodontal therapy	Effect on H. pylori infection
Gao et al[46], 2011	China; 80 patients with H. pylori infection-37 treated with anti-H. pylori therapy (gp A) and 43 treated with anti-H. pylori therapy and periodontal therapy (gp B)	82.3% in dental plaque and 51.1% in saliva	Gp A-2 wk proton pump inhibitor or triple therapy; gp B-2 wk triple therapy and initial periodontal therapy (oral hygiene education and scaling)	After 4 wk, 29.7% (n = 11) in gp A and 4.7% (n = 2) in gp B; after 1 yr, 43.2% (n = 16) in gp A and 18.6% (n = 8) in gp B	Eradication rate of gastric H. pylori After 4 wk, 73% (27/37) in gp A and 81.4% (35/43) in gp B, after 1 year, 32.4% (11/37) in gp A and 62.8% (27/43) in gp B
Sambashivaiah et al[73], 2011	India; 36 patients in 3 groups-group I, healthy subjects, group II, chronic periodontitis patients, group III, chronic periodontitis patients with type II diabetes mellitus	Overall-66.7% (n = 24); among group I-41.7% (n = 5), group II-75% (n = 9), group III-83.3% (n = 10)	Group II and III patients received full mouth scaling and root planning	Group II, 0 and group III, 8.3% (n = 1)	Not evaluated
Zaric et al[72], 2009	Serbia; 43 patients positive for H. pylori in sub gingival dental plaque and gastric mucosa-21 received only anti-H. pylori (triple) therapy (G+O+t); 22 received anti-H. pylori (triple) therapy)+periodontal therapy (G+O+tp)	100%	Triple therapy consisting of amoxicilin 2 g/d, clarithromycin 1 g/d, and pantoprazole 80 mg/d for 7 d. Periodontal therapy included oral hygiene orientation, plaque and calculus removal with an ultrasonic device, scaling, and root planing, as well as irrigation of periodontal pockets with 0.12% chlorhexidine-gluconate performed during triple therapy, in one sitting	In G+O+t-66.7% (14/21); in G+O+tp-27.3% (6/22)	In the G+O+tp group, 77.3% (17/ 22) showed eradication of gastric H. pylori compared with 47.6% (10/21) in G+O+t
Jia et al[83], 2009	China; 107 dyspeptic patients in whom H. pylori was eradicated from the gastric mucosa-56 received dental plaque control (test) and 51 did not (control)	Not evaluated	Full-mouth scaling, root planning and polishing, and dental plaque control instructions by dentist	Not evaluated	Prevalence of H. pylori in gastric mucosa was 19.64% (11/56) in test group and 84.31% (43/51) in control group
Butt et al[82], 2001	Pakistan; 82 patients positive for H. pylori in dental plaque-27 received only anti-H. pylori therapy (gp 1); 25 received anti-H. pylori therapy+periodontal therapy (gp 2); 30 received only periodontal therapy (gp 3)	100%	Gp 1-twice daily omeprazole 20 mg, clarithromycin 500 mg and metronidazole 400 mg; gp 2-triple therapy and dental scaling and chlorhexidine mouthwashes twice daily for 7 d; gp 3-only dental treatment	100% in gp 1; 16% in gp 2 (4/25); 10% in gp 3 (3/30)	Not evaluated

H. pylori:Helicobacter pylori.