|
No. | Authors | Year | Target gene | Sample size | Prevalence of H. pylori |
|
1 | Momtaz et al. [52] | 2012 | ureC, cagA, and vacA | 300 patients with gastroduodenal diseases | None of the plaque samples showed presence of H. pylori |
2 | Agarwal and Jithendra [31] | 2012 | 16S rRNA | 30 H. pylori positive and 20 H. pylori negative patients | Overall-42%; in H. pylori positive group-60%; in H. pylori negative group-15%. |
3 | Bago et al. [41] | 2011 | 16S rDNA | 56 patients with chronic periodontitis and gastric H. pylori positive | 37.5% |
4 | Chaudhry et al. [53] | 2011 | 16srRNA and 860 bp DNA region | 89 dyspeptic patients reporting for endoscopy | 51.6% for both genes; 62.9% for 16srRNA; 61% for 860 bp DNA region and 73% if either of the 2 regions are considered |
5 | Gao et al. [44] | 2011 | ureC and cagA genes | 96 patients with H. pylori infection | 82.3% |
6 | Wichelhaus et al. [54] | 2011 | 860bp DNA | 11 orthodontic patients | 36% |
7 |
Assumpção et al. [48] | 2010 | vacA and cagA | 99 adult patients who underwent upper gastrointestinal endoscopy | 72% samples were positive for H. pylori. 63 of 71 positive dental plaque samples were positive for vacA and cagA. 58/71 were positive for cagA while vacA genotypes had a prevalence ranging from 13–59% |
8 | Rasmussen et al. [55] | 2010 | Genomic DNA | 78 dyspeptic patients | 47.4% |
9 | Eskandari et al. [56] | 2010 | 16S rRNA | 67 patients with chronic periodontitis-23 with H. pylori positive gastritis | 5.97% |
10 | Silva et al. [57] | 2010 | vacA and 16S rDNA | 30 dyspeptic patients | 20% by 16S rDNA and 6.7% by vacA |
11 | Silva et al. [58] | 2010 | 16S rRNA | 115 patients | 11.3% |
12 | Silva et al. [59] | 2009 | 16s ribosomal and cagA genes | 32 with H. pylori positive with gastric disease and 32 with H. pylori positive with no gastric disease | Overall-17.7%. Among cases, H. pylori DNA detected in 36.6% and cagA gene detected in 3 out of 11 (27.3%) samples. In control group 0% |
13 |
Gonçalves et al. [60] | 2009 | JW22 and JW23 primers/16S rRNA | 23, HIV seropositive individuals of whom 13 with chronic periodontitis and 10 with periodontally healthy and 31 HIV seronegative individuals of whom 17 had chronic periodontitis and 14 were periodontally healthy | Not specified |
14 | Liu et al. [61] | 2009 | 860 bp fragment | 443 dyspeptic patients | 59.4% |
15 |
Bürgers et al. [36] | 2008 | 16S rDNA | 94 patients who underwent upper gastrointestinal endoscopy | 5.4% |
16 | Liu et al. [62] | 2008 | 860 bp fragment | 214 children | 58.9% |
17 | Teoman et al. [25] | 2007 | Urease A | 67 dyspeptic patients | 28.3% |
18 | Olivier et al. [63] | 2006 | urease AB gene; phosphoglucosamine mutase (glmM) gene; and 860 bp DNA region | 74 healthy members of a rural community | 0 |
19 | Kignel et al. [64] | 2005 | 16S rRNA | 49 dyspeptic patients | 2% |
20 | Fritscher et al. [65] | 2004 | 860 bp fragment | 53 patients with recurrent aphthous stomatitis and 52 patients without RAS | Overall-3.8%; 5.7% in cases and 1.9% among controls |
21 | Gebara et al. [66] | 2004 | 16S rDNA | 30 dentate patients with gingivitis/periodontitis and H. pylori infection | 20% in supra-gingival plaque and 26.6% in subgingival plaque |
22 | Umeda et al. [37] | 2003 | 16S rRNA | 56 dental patients | 25% |
23 | Goosen et al. [67] | 2002 | | | |
24 | Berroteran et al. [39] | 2002 | Urease genes | 32 dyspeptic patients and 20 asymptomatic controls | Overall-28.9%; 37.5% among dyspeptic patients and 15% among controls |
25 | Suk et al. [45] |
2002 | cagA | Sixty-five patients with dyspeptic symptoms | 43.1% |
26 | Miyabayashi et al. [43] | 2000 | ureA | 47 patients with chronic gastritis or peptic ulcer | 38.3% |
27 | Song et al. [68] | 2000 | 860 bp fragment | Forty-two patients who underwent upper gastrointestinal endoscopy | Overall 97% (82% in molar region, 64% in premolar region and 59% in incisor region) |
28 | Song et al. [69] | 2000 | 860 bp fragment | 20 dyspeptic patients | Not specified |
29 | Song et al. [70] | 2000 | 860 bp fragment | 21 patients | 100% |
30 | Song et al. [71] | 1999 | Urease A, 16S rRNA, and 860 bp fragment | 40 dental patients | |
31 | Dowsett et al. [18] | 1999 | | | Not specified |
32 | Oshowo et al. [32] | 1998 | 16S rRNA | 208 dyspeptic patients-116 H. pylori positive and 92 H. pylori negative | Overall 6.25% all in H. pylori positive |
33 | Hardo et al. [24] | 1995 | 16S rRNA | 62 dyspeptic patients | 1.6% |
34 | Mapstone et al. [72] | 1993 | 16S rRNA | 21 dyspeptic patients-13 with H. pylori associated gastritis and 8 who had normal histology | Overall-9.5%; 15.4% in gastritis group and 0 in histologically normal group-overall prevalence-9.5% |
35 | Nguyen et al. [73] | 1993 | 16S rRNA | 25 dyspeptic patients | Overall 28% all in H. pylori positive; among H. pylori positive individuals 38.8%. |
|