Abstract
Background
Helicobacter pylori (H. pylori) infection is one of the most prevalent infectious diseases worldwide. Dental plaque and saliva are major reservoirs for this microorganism, and some studies have shown that oral‒oral transmission is possible through close contact between physicians and dentists and their patients. This study aimed to investigate the occupational risk of gastrointestinal H. pylori infection among physicians and dentists.
Methods
A comprehensive search of PubMed, Scopus, and Web of Science was conducted up to May 1st 2025. Irrelevant articles were excluded in three stages on the basis of their title, abstract, and full text. Finally, data were extracted following predefined eligibility criteria, and methodological quality was assessed using the Newcastle–Ottawa Scale.
Results
A total of 28 primary studies were ultimately included (21 in the medical group and 7 in the dental group). The prevalence of H. pylori infection ranged from 6.8 to 77.2% in the medical group and 16.67‒70% in the dental group. In 16 of the articles (13 from the medical group and 3 from the dental group), the H. pylori infection rate was reported to be higher in healthcare workers than in the control group.
Conclusion
Current evidence indicates a potential occupational association among healthcare workers. However, the existing evidence is not sufficient for a definitive conclusion, and more well-designed cohort studies are needed, particularly among dentists.
Clinical trial number
Not applicable.
Supplementary Information
The online version contains supplementary material available at 10.1186/s12879-026-13662-3.
Keywords: Helicobacter pylori, Dentists, Physicians, Occupational risk
Introduction
Helicobacter pylori is one of the most widespread chronic bacterial infections worldwide, colonizing approximately half of the global population [1, 2]. Although many infected individuals remain asymptomatic, the organism is a well-established etiological factor for chronic gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric adenocarcinoma [3–5]. The World Health Organization classifies H. pylori as a Group I carcinogen, reflecting its major contribution to global gastrointestinal morbidity and mortality [2–4]. Concurrently, increasing antimicrobial resistance has reduced the effectiveness of standard eradication therapies, further emphasizing the need to identify populations at elevated risk and elucidate potential transmission routes [4].
In addition to the gastric niche, accumulating evidence indicates that the oral cavity may function as an important extragastric reservoir of H. pylori [6]. Detection of the organism in saliva, dental plaque, and periodontal pockets suggests that oral colonization may influence patterns of person‒person transmission and contribute to persistence or recurrence following gastric eradication [7, 8]. Recent evidence has also highlighted the potential relationship between periodontal disease, oral H. pylori reservoirs, and gastric carcinogenesis, emphasizing the possible clinical importance of oral colonization [9]. Oral–oral transmission is particularly plausible in settings characterized by close interpersonal contact or procedures generating saliva-containing or blood-containing aerosols. These findings highlight the potential relevance of oral health environments and raise important questions regarding exposure among dental professionals [5].
Multiple studies over recent decades have examined whether healthcare workers face an increased risk of acquiring H. pylori through occupational exposure. Gastroenterologists and endoscopy staff are frequently identified as high-risk groups, likely because of direct contact with gastric secretions and aerosols generated during upper endoscopic procedures [10–12]. Elevated infection rates have also been reported among intensive-care nurses and other professionals who are routinely exposed to bodily fluids, including long-term care facilities for individuals with intellectual disabilities [12, 13].
Despite the clinical relevance of this question, previous reviews have focused primarily on global epidemiology or broadly addressed occupational risk across heterogeneous professions, without providing a structured synthesis specifically targeting medical and dental personnel. To date, no systematic review has comprehensively evaluated whether physicians, dentists, and their clinical support staff—who routinely encounter patients’ gastric or oral secretions—are at increased occupational risk of H. pylori infection. Clarifying this association is essential for guiding infection-control recommendations, informing workplace safety policies, and identifying groups who may benefit from screening or preventive measures.
This systematic review therefore aims to synthesize the best available evidence on the prevalence and occupational risk of H. pylori infection among physicians, dentists, and their clinical assistants. By comparing infection rates across diverse geographic regions, clinical settings, and diagnostic approaches—and by evaluating differences relative to nonexposed control groups—this review seeks to determine whether healthcare professionals face an elevated risk of acquiring this globally significant infection. These findings have important implications for public health, clinical practice, and the development of evidence-based occupational protection policies.
Methods and materials
Protocol and registration
This systematic review was conducted in accordance with the Cochrane Handbook for Systematic Reviews of Interventions (version 6.4) [14] and reported following the PRISMA 2020 guidelines, and a completed PRISMA checklist is provided as a related file. The review protocol was prospectively registered in the PROSPERO international prospective registry of systematic reviews (Registration number: CRD420261307823). The PROSPERO record has been updated to reflect the current status of the review. To reduce the risk of bias and increase methodological transparency, the research question, eligibility criteria, search strategy, and methodological approach were predefined before study selection and data extraction began.
Study framework (PECO)
The research question and eligibility criteria for this systematic review were formulated using a PECO framework, which is appropriate for observational studies assessing exposure and prevalence. In this framework, the Population (P) included healthcare professionals such as physicians, dentists, and their clinical staff. The Exposure (E) was defined as occupational exposure to patients’ oral or gastric secretions. The Comparator (C), when available, consisted of non-exposed or general population groups. The Outcome (O) was the prevalence of gastrointestinal Helicobacter pylori infection.
Search strategy
A comprehensive literature search was conducted in the PubMed, Scopus, and Web of Science databases to identify studies reporting gastrointestinal Helicobacter pylori infection among medical and dental staff. The final search was conducted on May 1, 2025, which was defined a priori as the cutoff date for study inclusion to ensure consistency and feasibility of the review process.
The search strategy combined Medical Subject Headings (MeSH) and free-text keywords related to Helicobacter pylori, healthcare professionals, and occupational exposure. Following peer-review feedback, the search strategies were refined and re-run in PubMed, Scopus, and Web of Science using the updated syntax while maintaining the same predefined search cutoff date (May 1, 2025). No additional eligible studies were identified through the updated searches. The full electronic search strategies for each database, including Boolean operators and exact search strings, are provided in Supplementary Table S1 to ensure reproducibility.
No restrictions were applied regarding language or year of publication in order to maximize sensitivity. In addition, manual screening of the reference lists of included studies was performed to identify any additional eligible articles.
Inclusion criteria
Studies that examined medical or dental professionals who might be exposed to patients’ oral or gastric secretions at work and provided information on gastrointestinal Helicobacter pylori infection via validated diagnostic techniques such as serology, stool antigen testing, urea breath testing, rapid urease testing, PCR, or histopathology were included in this review. With the aim of obtaining a thorough and sensitive identification of relevant data, no limitations were placed on the year of publication or language, and studies of any sample size were considered.
Exclusion criteria
Studies that did not include medical professionals, did not report gastrointestinal Helicobacter pylori infection, or examined only oral colonization without evaluating stomach involvement were excluded. Studies conducted exclusively on animals or in vitro models were also excluded, as this review focused on human healthcare professionals. Reviews, editorials, letters, case reports, conference abstracts, and other non-original publications were excluded, as were studies with inadequate, missing, or unextractable data. During the full-text review phase, articles with unavailable full texts or unclear or non-validated diagnostic methods were excluded. Studies with insufficient methodological detail or lacking relevant outcome data were also excluded.
Collection and data extraction
All identified records were imported into EndNote, and duplicate entries were removed. Study selection was performed in two stages. In the first stage, two reviewers independently screened the titles and abstracts of all retrieved records based on the predefined eligibility criteria. In the second stage, the same two reviewers independently assessed the full texts of potentially eligible studies. Any disagreements between reviewers at either stage were resolved through discussion, and when necessary, consultation with a third reviewer to reach consensus.
Data extraction was conducted independently by two reviewers using a standardized data extraction form developed for this review. The extracted data included study characteristics such as author, publication year, study design, sample size, country, diagnostic methods, and reported prevalence of Helicobacter pylori infection. The extracted data were cross-checked for accuracy and consistency, and any discrepancies were resolved through discussion among the reviewers. The study selection process is presented in a PRISMA 2020 flow diagram (Fig. 1), which details the number of records identified, screened, assessed for eligibility, and included, along with reasons for exclusion at each stage.
Fig. 1.
PRISMA 2020 flow diagram of study selection process
Quality assessment
The methodological quality and risk of bias of the included studies were assessed using the Newcastle–Ottawa Scale (NOS). Standard NOS criteria were applied for case-control and cohort studies. For cross-sectional studies, a modified version of the NOS adapted for cross-sectional designs was used, based on previously published methodological adaptations [15]. The modified NOS for cross-sectional studies evaluated three domains: selection, comparability, and outcome assessment. The selection domain assessed sample representativeness, sample size adequacy, and ascertainment of exposure. Sample sizes equal to or greater than 100 participants were considered adequate. The comparability domain evaluated whether studies controlled for key confounding variables such as age, sex, and occupational exposure. The outcome domain assessed the validity of outcome measurement methods and statistical reporting. Case-control and cohort studies were evaluated according to the original NOS criteria, including selection of study groups, comparability between groups, and ascertainment of exposure or outcome. Comparability was considered adequate when studies matched or adjusted for major confounding factors such as age, sex, ethnicity, or occupational risk factors. Each included study was independently assessed by two reviewers. Any disagreements were resolved through discussion and, when necessary, consultation with a third reviewer to achieve consensus. NOS scores ranged from 0 to 9 points. Studies scoring 7–9 points were classified as low risk of bias, 4–6 points as moderate risk of bias, and 0–3 points as high risk of bias.
Data synthesis
To display and contrast the characteristics of the included studies, descriptive tables and textual summaries were employed. The first author and publication year, study design and sample size, country of origin, diagnostic techniques for gastrointestinal H. pylori infection, and prevalence reported among the different occupational groups were among the retrieved data. Every extracted field was checked for accuracy, and the extracted data were cross-checked for consistency with the source articles.
A total of 2079 entries were first found in the literature search; 769 of those were duplicates and were eliminated before screening. After removal of duplicates (n = 769), 1310 records were screened by title and abstract, of which 89 were considered potentially relevant and retrieved for full-text assessment. A total of 28 primary studies met the predefined eligibility criteria and were included in the final review. The methodological quality of the included studies was assessed using the Newcastle–Ottawa Scale (NOS); however, no studies were excluded based on quality scores alone. Instead, the risk-of-bias assessment was used to inform the interpretation of the findings.
Results
The quality assessment results are summarized in Table 1, with detailed item-level NOS scoring for each included study provided in Supplementary Tables 2–4 to enhance transparency and reproducibility. Overall, the methodological quality of the included studies was acceptable, with most studies demonstrating low to moderate risk of bias. Among cross-sectional studies, NOS scores ranged from 5 to 6, indicating predominantly moderate methodological quality. The most common limitations identified included limited justification of sample size, lack of reporting of response rates, and insufficient adjustment for potential confounding variables. Additionally, heterogeneity in diagnostic methods used to detect H. pylori infection was frequently observed. Most case-control studies demonstrated strong methodological quality, with NOS scores ranging from 6 to 8. These studies generally provided clear case definitions and appropriate selection of control groups. However, several studies relied on serological testing methods, which may not differentiate between past and active infection, potentially introducing misclassification bias. Among cohort studies, NOS scores ranged from 4 to 7. While several cohort studies demonstrated low risk of bias with appropriate baseline infection assessment and follow-up duration, others were rated as having moderate risk of bias due to limitations in follow-up completeness or study design characteristics. Incomplete reporting of loss to follow-up was identified as a potential limitation in some cohort studies. Overall, higher methodological quality was observed among case-control studies compared with cross-sectional studies, with cohort studies showing variable but generally acceptable methodological quality (Table 1; Supplementary Tables S2–S4).
Table 1.
Quality assessment of included studies using the Newcastle–Ottawa scale
| Author (Year) | Study Design | Selection Domain | Comparability Domain | Outcome / Exposure Domain | Total NOS Score | Risk of Bias |
|---|---|---|---|---|---|---|
| Martinez (2000) | Cross-sectional | 3 | 1 | 2 | 6 | Moderate |
| Gasbarrini (2001) | Cross-sectional | 3 | 1 | 2 | 6 | Moderate |
| Campuzano-Maya (2007) | Cross-sectional | 3 | 1 | 1 | 5 | Moderate |
| Metanat (2010) | Cross-sectional | 3 | 1 | 2 | 6 | Moderate |
| Dutoit (2015) | Cross-sectional | 3 | 0 | 2 | 5 | Moderate |
| Loor (2021) | Cross-sectional | 3 | 0 | 2 | 5 | Moderate |
| Loster (2009) | Cross-sectional | 3 | 1 | 2 | 6 | Moderate |
| Liebana (2016) | Cross-sectional | 3 | 0 | 2 | 5 | Moderate |
| Mikhail (2023) | Cross-sectional | 4 | 0 | 2 | 6 | Moderate |
| Zhou (2000) | Case-control | 4 | 1 | 2 | 7 | Low |
| Upile (2002) | Case-control | 4 | 1 | 2 | 7 | Low |
| Angtuaco (2002) | Case-control | 4 | 1 | 2 | 7 | Low |
| Melo (2003) | Case-control | 4 | 1 | 2 | 7 | Low |
| Mastromarino (2005) | Case-control | 4 | 2 | 2 | 8 | Low |
| Parray (2006) | Case-control | 4 | 1 | 2 | 7 | Low |
| Velasco (2007) | Case-control | 4 | 0 | 2 | 6 | Moderate |
| De Schryver (2008) | Case-control | 4 | 2 | 2 | 8 | Low |
| Kim (2013) | Case-control | 4 | 0 | 1 | 5 | Moderate |
| Mohamed (2014) | Case-control | 4 | 1 | 2 | 7 | Low |
| Abdelrahman (2024) | Case-control | 4 | 2 | 2 | 8 | Low |
| Honda (2001) | Case-control | 4 | 1 | 2 | 7 | Low |
| Matsuda (2005) | Case-control | 4 | 1 | 2 | 7 | Low |
| Liu (2020) | Case-control | 4 | 2 | 2 | 8 | Low |
| Schmid (2001) | Cohort | 4 | 0 | 2 | 6 | Moderate |
| Triantafilidis (2002) | Cohort | 4 | 1 | 2 | 7 | Low |
| Birkenfeld (2004) | Cohort | 3 | 0 | 1 | 4 | Moderate |
| Jonaityte (2021) | Cohort | 3 | 0 | 1 | 4 | Moderate |
| Matsuda & Morizane (2005) | Cohort | 4 | 1 | 2 | 7 | Low |
NOS scores ranged from 0 to 9. Studies scoring 7–9 were considered low risk of bias, 4–6 moderate risk, and 0–3 high risk
Among the 28 studies that met the eligibility requirements and were included in the final analysis, 7 assessed dental professionals or their staff, and 21 investigated medical professionals or their staff. Studies conducted in the medical group mostly included hospital employees, physicians, nurses, medical students, employees of endoscopic units, and staff members working in facilities that provide care for people with cognitive or physical impairments. Physicians and dental workers were evaluated concurrently as subgroups in two of these trials.
Medical staff
The methodological designs of the included primary studies varied considerably: 11 were cross-sectional prevalence studies, 6 were case‒control investigations, and 4 were cohort studies assessing seroconversion or incident infection over time. This distribution illustrates the methodological variety of the literature and represents the wide range of healthcare environments in which H. pylori exposure has been investigated. In addition, one previously published meta-analysis [16] was considered separately to provide contextual insights into occupational risk but was not included in the primary analysis.
Among the six cross-sectional studies that exclusively assessed the prevalence of H. pylori infection in healthcare personnel, only Campuzano-Maya et al. reported a higher prevalence of H. pylori infection among medical staff than among the general population. In contrast, eight of the eleven case‒control studies included in this evaluation reported a higher prevalence of infection in medical personnel than in their respective control groups. Furthermore, three of the four cohort studies reported evidence supporting an increase in the prevalence of H. pylori infection among healthcare professionals over time. Tables 2, 3 and 4 include detailed information about each study’s characteristics, sample descriptions, diagnostic methods, and prevalence. (Tables 2, 3 and 4)
Table 2.
Cross-sectional studies to examine the prevalence of H. pylori infection among medical staff
| Author (Date) | Location | Sample Size | H. pylori Prevalence | H. pylori Diagnosis Method | Conclusion |
|---|---|---|---|---|---|
| Martinez M et al. (2000) | United States | 44 general practitioners | 9.8% | Serology test | Prevalence is not higher in the general population, and routine screening is not recommended for them |
| Gasbarrini A et al. (2001) | Italy | 655 healthcare workers | 30% | UBT* with Carbon 13 | Prevalence is higher in some parts of the healthcare workers’ population |
| Campuzano-Maya G et al. (2007) | Colombia | 422 physicians | 77.2% | UBT with Carbon 13 | High prevalence in physicians |
| Metanat M et al. (2010) | Iran | 97 healthcare workers | 32% | ELISA antibody test | Prevalence is higher in asymptomatic individuals, and the risk in this group of the population is higher, but work in the endoscopy unit cannot be considered as a job risk factor |
| Dutoit T et al. (2015) | South Africa | 92 endoscopy unit staff | 59% | Serology test | Prevalence is higher in asymptomatic individuals, and the risk in this group of the population is higher, but work in the endoscopy unit cannot be considered as a job risk factor |
| Loor A et al. (2021) | Romania | 150 medical students | 25.33% | UBT with Carbon 13 | This study added to the collection of observations related to H. pylori prevalence in medical students |
*UBT = Urea Breath Test
Table 3.
Case‒control studies to examine the prevalence of H. pylori infection in medical staff
| Author (Date) | Location | Sample Size | H. pylori Prevalence | H. pylori Diagnosis Method | Conclusion |
|---|---|---|---|---|---|
| Zhou P et al. (2000) | China | 633 physicians and 85 non-physician as control | H. pylori prevalence is higher and significant in medical staff (P < 0.05) and is significantly higher in dentists and gastroenterologists (P < 0.05) | ELISA antibody test | Medical and dental staff, especially gastroenterologists, are at occupational risk of H. pylori |
| Upile T et al. (2002) | England | 70 surgery staff (40 ENT surgeons and 30 anesthetist) | 50% in the case group and 25.7% in the control group (P < 0.0001) | ELISA antibody test | Surgical staff are at occupational risk of H. pylori, and practical guidelines are needed to reduce this risk |
| Angtuaco T et al. (2002) | United States | 107 medical staff | 17% in the gynecologist/obstetrician group (P < 0.05) | Serology test | Occupational risk of H. pylori in congenital disability centers was higher than endoscopy |
| Melo ET et al. (2003) | Brazil | 405 medical students and residents | 48.68% in residents (33.5% in medical students) (Statistically significant difference) | ELISA antibody test | The higher infection rate among medical residents indicated that greater contact with infected patients may be considered a risk factor |
| Mastromarino P et al. (2005) | Italy |
249 People in 3 Groups: 1. Endoscopy unit staff 2. Hospital staff without contact with patients 3. Hospital staff with contact with patients |
10.93% in endoscopy unit staff (P > 0.05) | ELISA antibody test (Along with stool test) | Nurses are at higher risk of H. pylori due to their direct contact with patients compared to those who do not have this direct contact |
| Parray S et al. (2006) | Pakistan | 150 healthcare workers from different fields | 54.6% of healthcare workers (P < 0.05) | Serology test | In addition to the higher prevalence in healthcare professionals, it also appears to be higher in endoscopy and dentistry professionals (not necessarily significant) |
| Velasco Elizade C et al. (2007) | Cuba | 38 endoscopy staff and 38 control individuals |
39.47% Endoscopist 7.89% Control Group (P < 0.05) |
Serology test | The prevalence of H. pylori in endoscopists is significantly higher than in the control group |
| De Schryver A et al. (2008) | Belgium | 671 Medical staff of centers for physical and mental disabilities and 439 control group |
Odds Ratio = 1.68 Increased Occupational risk by 49.5% |
Serology test | In the reviewed medical staff, H. pylori infection is considered an independent occupational risk |
| Kim H.Y et al. (2013) | South Korea | 110 physicians, 362 nurses, 179 control group from hospital, 359 nonhospital control group |
Overall = 38.7% (P > 0.05) |
Serology test | Medical professions are not associated with occupational infection risk of H. pylori |
| Mohamed SM et al. (2014) | Egypt | 30 people from endoscopy department, 30 people from other departments of hospital, 30 people as control group |
76.7% Hospital Endoscopy 73.3% Hospital Other Departments 76.7% Control Group (P > 0.05) |
Serology test | The medical profession is not a risk factor for infection, but the way infection is controlled affects the increased risk of infection in the hospital |
| Abdelrahman AA et al. (2024) | Egypt | 200 physicians, nurse and other jobs occupied people | Overall = 58.5%, Physicians = 31.5%, Nurses = 53%, other occupied people = 15.5%, (P < 0.05 for physicians, nurses and other occupied people) | Serology test + stool antigen test | Medical staff are at high risk for H. pylori infection |
Table 4.
Cohort studies to examine the prevalence of H. pylori infection in medical staff
| Author (Date) | Location | Sample size ‒evaluation period | Results | H. pylori Diagnosis Method | Conclusion |
|---|---|---|---|---|---|
| Schmid K and Schoerner C. (2001) | Germany | 165 German and immigrant nurses ‒ 30 months | Annual incidence: 2.3% | Serology test | Nursing is a risk factor for H. pylori |
| Triantafillidis JK et al. (2002) | Greece | 437 people ‒ 5 years | Overall = 45.5%, After the end of the study period, 24.8% of negative cases became positive, Overall seroconversion = 4.95% | ELISA antibody test | In the nursing group, the risk factor is significant compared to the technical and clerical groups |
| Birkenfeld S et al. (2004) | Israel |
191 Gastroenterology staff 98 Primary care clinic staff 4633 Symptomatic control group with no history of H. pylori infection |
73% gastroenterology staff, 71% primary care clinic staff, 53% symptomatic controls with no history of H. pylori infection | UBT with Carbon 13 | The prevalence of H. pylori infection in the two groups of healthcare personnel studied was higher than in the general population |
| Jonaityte LR et al. (2021) | Lithuania | 120 to 262 25-year-old medical students |
51.7% (1995) 30.4% (2012) 26.3% (2016) 14.2% (2020) |
Serology test | During this evaluation period, the rate of positivity for H. pylori infection in these students has decreased |
Peters and colleagues (2011) conducted the sole meta-analysis considered in this study that assessed the occupational risk of Helicobacter pylori infection among gastroenterologists and their assistants, on the basis of a final assessment of 15 studies. Eight of these studies reported that gastroenterologists had a significantly higher risk of infection, whereas five reported that medical assistants had a significantly higher risk. For physicians and medical assistants, the pooled relative risk (RR) of H. pylori infection was 1.6 (95% CI: 1.3–2.0) and 1.4 (95% CI: 1.1–1.8), respectively. These results suggest that medical professionals who treat patients with gastrointestinal disorders have a higher reported prevalence of H. pylori infection.
The reported prevalence of H. pylori infection varied from 6.8% to 77.2% across all included studies on medical staff, with the lowest prevalence recorded in the study by Martinez et al. (2000) and the highest in the study by Campuzano-Maya et al. (2007). In terms of sample size, cross-sectional studies examining prevalence solely among medical personnel included between 44 and 655 participants, whereas the sample size in case‒control studies ranged from 70 to 1,110 people. In terms of geographic distribution, the final review included 21 studies featuring medical personnel (not including the meta-analysis by Peters et al., which was not geographically restricted), with the largest number originating in Europe (n = 9), followed by the Americas (n = 5), Asia (n = 4), and Africa (n = 3).
Significant methodological diversity was identified across the included studies, particularly in terms of study design, diagnostic procedures, and professional subgroups. The majority of studies involving medical staff were cross-sectional surveys, supplemented by a few case‒control studies comparing healthcare workers with nonclinical populations and a smaller number of cohort studies evaluating seroconversion over time. This variability also extends to diagnostic techniques where serological tests are the most widely used test for detecting gastrointestinal H. pylori infection, followed by urea breath tests and, less frequently, stool antigen tests or PCR-based evaluations. This methodological diversity, along with variations in sample size, clinical condition, and comparison group characteristics, led to a great deal of variation in reported prevalence estimates and emphasized the need for careful, context-sensitive interpretation of the data.
Several occupational and demographic variables were also assessed in connection with H. pylori infection. Four studies (Triantafillidis et al. (2002), Gasbarrini et al. (2001), Abdelrahman et al. (2024), and Parray et al. (2006)) examined the relationship between age and occupational H. pylori infection. According to Triantafillidis et al., the prevalence was 57.5% in the 41–60 years age group and 40.6% in the 23–40 years age group (P = 0.001). The age group of 20‒35 years had the highest rate of seroconversion (defined as the transition from seronegative to seropositive status over time) in the Parray et al. study, with a reported rate of 57.47%. Only the study by Parray et al. examined the relationship with sex; among women, the difference in seroconversion rates between the treatment and control groups was statistically significant (P < 0.05). Furthermore, Abdelrahman et al. (2024) reported a correlation between H. pylori infection and work experience. Additionally, a correlation between infection and educational level was found in three studies: Triantafillidis et al. (2002), Metanat et al. (2010), and Gasbarrini et al. (2001). However, in the study by Gasbarrini et al., this parameter specifically referred to the fathers’ educational level rather than the participants’ own.
Dental staff
Across the included studies on dental personnel, a wide range of diagnostic techniques were used, and the H. pylori infection prevalence was reported. Although urea breath testing and PCR-based saliva analysis have been used in a few studies, serological evaluation continues to be the most commonly used diagnostic technique, indicating methodological variation within this body of evidence. The reported prevalence among dentists ranged from 16.67% to 70%; Liu et al. (2020) reported the lowest estimate, whereas Honda et al. (2001) reported the highest. Notably, most studies revealed that dental professionals had higher infection rates than did the control group, but not all of the differences were statistically significant. Furthermore, the sample sizes ranged widely, from 46 to 236 participants, suggesting variation in study design throughout the included literature. Table 5 lists each study’s specific characteristics, sample descriptions, diagnostic techniques, and prevalence information. (Table 5)
Table 5.
Studies to examine the prevalence of H. pylori infection in dental staff
| Author (Date) | Location | Sample size ‒evaluation period | H. pylori Prevalence | H. pylori Diagnosis Method | Conclusion |
|---|---|---|---|---|---|
| Honda K et al. (2001) | Japan |
60 dentists 60 control group |
Dentists 70% Control group 38% Odds Ratio = 3.8 95% CI = 1.76–8.02 |
ELISA antibody test | Mouth-to-mouth transmission is probably the most common method |
| Matsuda R et al. (2005) | Japan |
116 dentists 116 nonclinical control group |
Dentists 42.3% Nonclinical control group 40% |
Serological test | The dental profession does not increase the risk of H. pylori infection in its employees |
| Matsuda R & Morizane T. (2005) | Japan |
236 dentists 59 assistants 59 nonclinical staff |
Adjusted Odds Ratio with 95% CI Dentists 2.68 (0.55–19.67) Family history of digestive problems 4.84 (0.83–26.72) Age over 40 years 8.83 (1.26-177.24) Risk of infection 1.12% per year with a relative risk of 4 in dental staff |
Serological test | The dental profession is at high risk for H. pylori infection |
| Loster BW et al. (2009) | Poland | 46 dentists | Dentists 65% | Carbon-13 UBT | The incidence of H. pylori infection in dentists is not higher than in the general population |
| Liebana J et al. (2016) | Spain |
35 first-year dental students 35 third-year dental students 35 from other fields |
Statistically significant difference between groups 1 and 2 and between groups 2 and 3 in terms of H. pylori colonization | Carbon-13 UBT, stool antigen test, serological test | H. pylori colonization has decreased over a 4-month period |
| Liu Q et al. (2020) | China |
90 dentists 110 control group |
Dentists 16.67% Control group 7.27% (P = 0.038) |
H. pylori PCR from saliva samples | Dentists are at high risk for H. pylori infection |
| Mikhail CRG et al. (2023) | Egypt | 83 dental students | Dental students 22.9% | Saliva ELISA | Risk factors for H. pylori infection include middle income, previous history of infection, and clinical signs of dyspepsia |
Numerous occupational and demographic characteristics have been investigated as possible causes of H. pylori infection in dentistry studies, although the results have not always been consistent across studies. A number of studies have shown that age is a repeated factor linked to increased infection rates, with older dentists or those with more work experience exhibiting a notably higher incidence of infection. Long-term contact with oral secretions may increase occupational risk, according to several studies that also suggested a potential link between work time, cumulative patient exposure, and elevated seropositivity. On the other hand, gender seems to have little to no impact on the majority of research, with only a few findings suggesting that male practitioners had greater infection rates. Despite these variations, the overall trend indicated that occupational exposure in dental environments, especially over long periods of practice, may affect the risk of H. pylori infection.
Quantitative meta-analysis was not performed due to substantial methodological and clinical heterogeneity across study designs, diagnostic approaches, and control definitions. The narrative synthesis methodology allowed for a comparison of trends, diagnostic procedures, and prevalence estimates across various medical and dentistry occupational groups.
Discussion
This systematic review aimed to synthesize the most reliable evidence on the occupational risk of Helicobacter pylori infection among dentistry and medical staff. A review of the research conducted on medical staff (n = 21) revealed that in the majority of investigations (n = 13), the prevalence of H. pylori infection among healthcare workers was significant and greater than that in nonmedical control groups. Nurses (reported in the studies by Mastromarino, Schmid and Schoerner, and Triantafillidis), gastroenterologists (reported in the studies by Parray, Zhou, and Elizade-Velasco), surgical staff (Upile), and medical residents (Melo) were the professional subgroups most frequently identified as being at increased risk [17–24]. The authors of these studies primarily attributed the higher infection rates to close and direct contact with patients, implying that occupational exposure plays an important role in transmission within clinical environments.
The remaining studies involving medical staff can be divided into two categories. In the first group, whereas a somewhat high prevalence of H. pylori infection was found among healthcare workers, this prevalence was not always assessed significantly higher than that in the general population. In the second group, the concept that medical professions are individual risk factors for H. pylori infection was rejected. Martinez, Du Toit, Mohamed, and Kim reported that working in healthcare settings should not be regarded as an independent risk factor for infection [25–28]. Furthermore, Mohamed et al. emphasized the importance of adhering to hospital infection control measures in reducing transmission risk, whereas Kim et al. proposed that institutional health policies and individual socioeconomic conditions may have a greater impact on seropositivity than occupational exposure itself [27, 28].
Compared with the pattern shown in medical personnel, the body of research pertaining to dentistry professionals (7 studies) shows a more varied trend. Only three investigations, conducted by Honda, Matsuda and Morizane, and Liu, reported that the dentistry profession is related to an increased occupational risk of H. pylori infection [29–31]. Liebana’s and Mikhail’s studies, on the other hand, found no conclusive evidence to indicate such a connection [10, 32]. Moreover, two other studies by Matsuda and Loster clearly reported that dental practice did not increase the incidence of H. pylori infection, indicating that the prevalence among dentists is not much higher than that of the general population [33, 34].
Although Honda et al. suggested that oral-to-oral transmission might be one of the most frequent ways that H. pylori spreads from patients to dentists, a comparison of research conducted in dentistry and medical environments revealed multiple significant differences [29]. First, there is far more research with medical professionals accessible, and these studies cover a wider variety of clinical settings, including operating rooms, endoscopic units, and outpatient clinics. Second, a greater number of studies in the medical field support the idea that professional exposure increases vulnerability to H. pylori infection when the proportion of studies supporting versus rejecting the occupational-risk hypothesis is compared, while evidence in dental settings is still less consistent and more limited.
The current study reveals a significant degree of variation in the existing research. The majority of the included studies were cross‒sectional or case‒control in design (23 out of 28 final studies), Although cohort studies provide the most appropriate level of evidence for assessing incidence, they were relatively limited in number. Only one of the five cohort studies that were found focused on dental professionals, whereas the other four were carried out among medical professionals. Notably, the results of four of these five cohort studies supported the hypothesis that working in medical and dental fields may be associated with a higher incidence of H. pylori infection; Jonaityte et al. reported the only contradictory data [35].
One of the most significant contributors to study heterogeneity was the vast range of diagnostic procedures employed to confirm H. pylori infection. Serological evaluation, specifically the determination of serum IgG antibodies against H. pylori, has been used in the majority of investigations, including those involving medical professionals. Additional techniques included the urea breath test (UBT), polymerase chain reaction (PCR), and microbial culture. In studies involving dental professionals, greater diversity in diagnostic techniques was observed, which may be attributed to the more routine use of salivary-based assessments in dental research; notably, only Liu and Mikhail used saliva samples specifically for H. pylori detection [31, 36].
A number of studies have also examined occupational and demographic factors, such as age and job experience. Ages ranging from 25 to 60 years, with a mean age of approximately 35 years, made up the majority of the research population in the majority of investigations. Triantafillidis et al. reported a strong link between increasing age and H. pylori infection among medical staff, indicating that cumulative occupational exposure over time may increase infection risk; however, Parray et al. reported the opposite results. Similar discrepancies were found in studies involving dental professionals: Matsuda et al. reported a significant correlation between H. pylori positivity and age among dental students who were 20 years of age or younger, however a different study by Matsuda and Morizane reported a significant correlation in people over 40 years of age. This discrepancy could be partially explained by variations in dietary habits [30, 33]. As a result, it is impossible to make firm conclusions on how age affects the likelihood of H. pylori infection. Additionally, a related parameter, occupational duration, was addressed in only a few studies; among dental professionals, only Honda et al. reported a significant association between work experience and infection, whereas Abdelrahman et al. made a similar observation exclusively in medical personnel [29, 37].
In addition to clinical and methodological criteria, occupational and behavioral characteristics have been proposed as potential contributors to infection risk. Hospital employees who provide care for people with intellectual disabilities have noticeably higher rates of H. pylori infection, according to De Schryver et al., who identified contact with fecal matter as an independent occupational risk factor [38]. On the other hand, Liu et al. reported that the prevalence of H. pylori infection among dentists was greater than that among controls even after adjusting for confounding variables such as personal hygiene, lifestyle choices, and the ability to share food with infected people. Liebana et al. proposed that better oral hygiene practices in senior dental students were linked to decreases in plaque accumulation and the gingival index [31, 32].
Beyond occupational epidemiology, the broader biological role of Helicobacter pylori should also be considered when interpreting these findings. While Helicobacter pylori is widely recognized as a major pathogen associated with gastrointestinal diseases, its role within the human microbiome remains complex and continues to be debated. Emerging evidence suggests that H. pylori may exhibit commensal or even symbiotic characteristics in certain populations, particularly in individuals at low risk for H. pylori-associated diseases [39, 40]. In addition, recent studies have highlighted the potential protective roles of H. pylori in several conditions, including esophageal and inflammatory diseases, further complicating its clinical interpretation.
Given this complexity, a cautious and individualized approach to the management of H. pylori infection is warranted. Rather than adopting universal eradication strategies, clinical decision-making should consider patient-specific factors, including disease status, risk of complications, and overall health profile. Recent evidence also underscores the importance of occupational exposure, with healthcare workers showing distinct epidemiological patterns, including altered symptom profiles and potential antibiotic resistance concerns [41]. In addition, recent genomic studies have emphasized the importance of phenotypic and genotypic characterization of Helicobacter pylori strains for improving antibiotic resistance prediction and optimizing eradication strategies [42].
Furthermore, the presence of H. pylori in the oral cavity and its potential role in oral–gastric transmission pathways highlight the need for a broader clinical perspective when evaluating infection sources [43]. A personalized approach may therefore help balance the potential benefits of eradication against the broader biological role of H. pylori, emphasizing the need for tailored screening and treatment strategies.
Interpretation of methodological limitations
Several methodological limitations should be considered when interpreting the results of the included studies: First, there was significant heterogeneity in the diagnostic methods used to detect H. pylori infection, which included serological testing, urea breath testing, stool antigen testing, polymerase chain reaction, and histopathological examination. Although serological testing is widely used, it may overestimate infection prevalence by detecting prior exposure rather than active infection, leading to potential misclassification bias. Second, many cross-sectional studies failed to account for important confounding factors such as socioeconomic status, household exposure, hygiene practices, and geographic variation in infection prevalence. In many cases, no matching at the design stage or multivariable adjustment during analysis was performed, which could have influenced the observed associations between occupational exposure and H. pylori infection. Finally, incomplete response rate reporting in cross-sectional studies and loss to follow-up in some cohort studies may have introduced selection bias, limiting the findings’ generalizability.
Despite these limitations, the overall methodological quality of the included studies was deemed acceptable, with the majority exhibiting a low to moderate risk of bias, recommending cautious interpretation of the review findings.
Recommendations
Healthcare staff who have frequent patient contact should strictly follow basic infection-control procedures, such as regular hand washing and the use of personal protective equipment including gloves, masks, and face shields. As the danger of occupational exposure is greater in gastrointestinal endoscopic units, improved infection control is especially crucial. Given the probability of asymptomatic carriage, high-risk healthcare workers—particularly those receiving gastrointestinal and endoscopy—may benefit from at least one periodic H. pylori screening test. In addition, increasing basic hygiene standards and maintaining safe water supplies may help reduce transmission. Future studies should pay close attention to the selection of appropriate control groups, and there is a definite need for the creation of standardized guidelines to reduce occupational exposure to H. pylori among both medical and dental professionals.
Conclusion
This systematic review suggests that working in medical or dental environments may represent an occupational risk factor for H. pylori infection. Although the overall prevalence among healthcare professionals does not consistently exceed that of the general population, a significant proportion of the included case‒control studies reported higher infection rates in medical and dental personnel than in their respective control groups, a finding that is more commonly observed in the medical field. Notably, the majority of the limited cohort evidence also suggested increased occupational risk, emphasizing the possible cumulative effect of prolonged clinical exposure. Given the heterogeneity of study designs and diagnostic methods, as well as the scarcity of high-quality prospective investigations, particularly among dental professionals, well-designed cohort studies are strongly advised to clarify the true magnitude and mechanisms of H. pylori occupational transmission in healthcare environments.
Supplementary Information
Below is the link to the electronic supplementary material.
Supplementary Material 1: Supplementary Table S1. Full Search Strategy
Supplementary Material 2: Supplementary Tables S2-S4. Detailed Risk of Bias Assessment Using Newcastle–Ottawa ScaleDescription: Detailed Risk of Bias Assessment Using Newcastle–Ottawa Scale
Acknowledgements
Not applicable.
Abbreviations
- H. pylori
Helicobacter pylori
- NOS
Newcastle–Ottawa Scale
- UBT
Urea Breath Test
- PCR
Polymerase Chain Reaction
- MALT
Mucosa-Associated Lymphoid Tissue
- PRISMA
Preferred Reporting Items for Systematic Reviews and Meta-Analyses
- RR
Relative Risk
- ELISA
Enzyme-Linked Immunosorbent Assay
Author contributions
Conceptualization: Danial Saleh (ORCID number: https://orcid.org/0009-0007-4682-7758), Nader Navabi (ORCID number: https://orcid.org/0000-0001-6321-0089). Methodology: Danial Saleh, Nader Navabi, Raziyehsadat Rezvaninejad (ORCID number: https://orcid.org/0000-0003-2061-7326); writing—original draft preparation: Danial Saleh, Nader Navabi, Raziyehsadat Rezvaninejad; Writing—review and editing: Danial Saleh, Sara Emarloo (ORCID number: https://orcid.org/0009-0006-2292-2868); Visualization: Nader Navabi, Raziyehsadat Rezvaninejad, Sara Emarloo. Supervision: Danial Saleh; Project administration: Danial Saleh, Nader Navabi; All the authors have read and agreed to the published version of the manuscript.
Funding
The authors declare that no funds, grants, or other support was received during the preparation of this manuscript.
Data availability
The data are available from the corresponding author (saleh.danial79@gmail.com) upon request.
Declarations
Ethics approval and consent to participate
Not applicable. This systematic review analyzed data from previously published studies and did not involve human participants or collection of primary data.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
References
- 1.Graham DY. Helicobacter pylori. Curr Top Microbiol Immunol. 2024;445:127–54. [DOI] [PubMed] [Google Scholar]
- 2.Shirani M, Pakzad R, Haddadi MH, Akrami S, Asadi A, Kazemian H, et al. The global prevalence of gastric cancer in Helicobacter pylori-infected individuals: a systematic review and meta-analysis. BMC Infect Dis. 2023;23(1):543. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Crowe SE. Helicobacter pylori Infection. N Engl J Med. 2019;380(12):1158–65. [DOI] [PubMed] [Google Scholar]
- 4.FitzGerald R, Smith SM. An Overview of Helicobacter pylori Infection. Methods Mol Biol. 2021;2283:1–14. [DOI] [PubMed] [Google Scholar]
- 5.Zhang L, Chen X, Ren B, Zhou X, Cheng L. Helicobacter pylori in the Oral Cavity: Current Evidence and Potential Survival Strategies. Int J Mol Sci. 2022;23:21. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Tsami A, Petropoulou P, Kafritsa Y, Mentis YA, Roma-Giannikou E. The presence of Helicobacter pylori in dental plaque of children and their parents: is it related to their periodontal status and oral hygiene? Eur J Paediatr Dent. 2011;12(4):225–30. [PubMed] [Google Scholar]
- 7.Abdul NS, Khalid Alkhelaiwi A, Awadh Alenazi A, Fehaid Alrashidi R, Ghaleb Salma R. The Association of Helicobacter pylori in the Oral Cavity With Dental Caries in Patients With and Without Gastric Infection: A Systematic Review. Cureus. 2023;15(5):e38398. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Duan M, Li Y, Liu J, Zhang W, Dong Y, Han Z, et al. Transmission routes and patterns of helicobacter pylori. Helicobacter. 2023;28(1):e12945. [DOI] [PubMed] [Google Scholar]
- 9.Straka M, Borecová P, Csóková K, Gerža E, James IJ, Straka M, Periodontitis. Oral Helicobacter pylori Reservoirs, and Gastric Cancer: Implications for Adjunctive Periodontal Therapy. Neuro Endocrinol Lett. 2026;47(1):53–63. [PubMed] [Google Scholar]
- 10.Kheyre H, Morais S, Ferro A, Costa AR, Norton P, Lunet N, et al. The occupational risk of Helicobacter pylori infection: a systematic review. Int Arch Occup Environ Health. 2018;91(6):657–74. [DOI] [PubMed] [Google Scholar]
- 11.Navabi N, Arabpoor A, Mirshekari tr. Helicobacter pylori Infection in General Dentist and Dental Assistants: A Pilot Serological Study in Kerman. J Res Dent Sci. 2022;19(3):250–9. [Google Scholar]
- 12.De Schryver AA, Van Winckel MA. Helicobacter pylori infection: epidemiology and occupational risk for health care workers. Ann Acad Med Singap. 2001;30(5):457–63. [PubMed] [Google Scholar]
- 13.De Schryver AA, Van Hooste WL, Van Winckel MA, Van Sprundel MP. Helicobacter pylori infection: a global occupational risk for healthcare workers? Int J Occup Environ Health. 2004;10(4):428–32. [DOI] [PubMed] [Google Scholar]
- 14.Higgins JPTTJ, Chandler J, Cumpston M, Li T, Page MJ, Welch VA, editors. Cochrane Handbook for Systematic Reviews of Interventions version 6.4 (updated August 2023). Cochrane, 2023.
- 15.Herzog R, Álvarez-Pasquin MJ, Díaz C, Del Barrio JL, Estrada JM, Gil Á. Are healthcare workers’ intentions to vaccinate related to their knowledge, beliefs and attitudes? A systematic review. BMC Public Health. 2013;13:154. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Peters C, Schablon A, Harling M, Wohlert C, Costa JT, Nienhaus A. The occupational risk of Helicobacter pylori infection among gastroenterologists and their assistants. BMC Infect Dis. 2011;11:154. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 17.Mastromarino P, Conti C, Donato K, Strappini PM, Cattaruzza MS, Orsi GB. Does hospital work constitute a risk factor for Helicobacter pylori infection? J Hosp Infect. 2005;60(3):261–8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 18.Schmid K, Schoerner C. [Increased incidence of immunoglobulin G antibodies against Helicobacter pylori among trainee nurses]. Dtsch Med Wochenschr. 2001;126(41):1127–31. [DOI] [PubMed] [Google Scholar]
- 19.Triantafillidis JK, Gikas A, Hyphantis T, Cheracakis P, Rokkas T, Konstantellou E, et al. Helicobacter pylori infection in hospital workers over a 5-year period: correlation with demographic and clinical parameters. J Gastroenterol. 2002;37(12):1005–13. [DOI] [PubMed] [Google Scholar]
- 20.Parray S, Malik S, Basu J, Rashid S, Malik GM. Helicobacter pylori prevalence in professional workers in main teaching hospitals of Kashmir Valley. JK Practitioner. 2006;13:95–7. [Google Scholar]
- 21.Zhou P, Fan G, Deng S. [The study on serological epidemiology of Helicobacter pylori infection in medical staffs]. Hunan yi ke da xue xue bao = Hunan yike daxue xuebao = Bulletin of Hunan Medical University. 2000;25:341–2. [PubMed]
- 22.Elizalde C, Ferrer M, Muñiz N. Serologic diagnosis of Helicobacter pylori in endoscopy personnel: Serology in endoscopists. Revista española de enfermedades digestivas: organo oficial de la Sociedad Española de Patología. Digestiva. 2007;99:88–93. [DOI] [PubMed] [Google Scholar]
- 23.Upile T, East C, Paun S, Patel N, Battacharyya A. Helicobacter pylori infection in surgical personnel. Clin Otolaryngol Allied Sci. 2002;27(5):310–3. [DOI] [PubMed] [Google Scholar]
- 24.Melo ET, Lopes EP, Almeida JR, Albuquerque MF, Moura IM. Seroprevalence of Helicobacter pylori antibodies in medical students and residents in Recife, Brazil. J Clin Gastroenterol. 2003;36(2):134–8. [DOI] [PubMed] [Google Scholar]
- 25.Martinez M, Kordisch F, Lesser S. The prevalence of Helicobacter pylori: are emergency medicine residents at risk? J Emerg Med. 2000;19(3):213–5. [DOI] [PubMed] [Google Scholar]
- 26.du Toit T, Buchel OC, Smit SJ. Helicobacter pylori as an occupational hazard in the endoscopy room. S Afr J Surg. 2015;53(3):23–5. [PubMed] [Google Scholar]
- 27.Mohamed S, El Touny M, Ahmed O, Hafez H. Prevalence of Helicobacter pylori among healthcare workers in endoscopy units. Egypt Liver J. 2014;4:94–8. [Google Scholar]
- 28.Kim HY, Kim N, Kim SM, Seo JH, Park EH, Lee DH. Seroprevalence of Helicobacter pylori Infection in Korean Health Personnel. Gut Liver. 2013;7(6):648–54. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 29.Honda K, Ohkusa T, Takashimizu I, Watanabe M, Amagasa M. High risk of Helicobacter pylori infection in young Japanese dentists. J Gastroenterol Hepatol. 2001;16(8):862–5. [DOI] [PubMed] [Google Scholar]
- 30.Matsuda R, Morizane T. Helicobacter pylori infection in dental professionals: a 6-year prospective study. Helicobacter. 2005;10(4):307–11. [DOI] [PubMed] [Google Scholar]
- 31.Liu Q, Zhang Y, Xu C, Chen B, Xu H, Cao Y, et al. Dentists Are at a Higher Risk for Oral Helicobacter pylori Infection. Biomed Res Int. 2020;2020:3945189. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 32.Liébana J, García-Casas V, Liébana-Cabanillas F, Arias-Moliz MT. Prevalence of the colonization of Helicobacter pylori among students of the school of dentistry, University of Granada, Spain. Med Oral Patol Oral Cir Bucal. 2016;21(5):e573–8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 33.Matsuda R, Morizane T, Tsunematsu S, Kawana I, Tomiyama M. Helicobacter pylori prevalence in dentists in Japan: a seroepidemiological study. J Gastroenterol. 2002;37(4):255–9. [DOI] [PubMed] [Google Scholar]
- 34.Loster BW, Czesnikiewicz-Guzik M, Bielanski W, Karczewska E, Loster JE, Kalukin J, et al. Prevalence and characterization of Helicobacter pylori (H. pylori) infection and colonization in dentists. J Physiol Pharmacol. 2009;60(Suppl 8):13–8. [PubMed] [Google Scholar]
- 35.Jonaityte IR, Ciupkeviciene E, Jonaitis P, Kupcinskas J, Petkeviciene J, Jonaitis L. Changes in the seroprevalence of Helicobacter pylori among the Lithuanian Medical Students over the last 25 years and its relation to dyspeptic symptoms. Med (Kaunas). 2021;57(3). [DOI] [PMC free article] [PubMed]
- 36.Mikhail CRG, Abd El Maksoud Mohamed A, Shaker OG, El Desouky E, Shalaby RH. Frequency and risk factors of H. pylori infection among dental students: an observational cross-sectional study. Sci Rep. 2023;13(1):14264. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 37.Abdelrahman AA, Ahmed ESD, Moustafa EFA. Prevalence of Helicobacter pylori infection among healthcare workers in Aswan University Hospital. Arab J Gastroenterol. 2024;25(3):250–6. [DOI] [PubMed] [Google Scholar]
- 38.De Schryver A, Cornelis K, Van Winckel M, Moens G, Devlies G, Derthoo D, et al. The occupational risk of Helicobacter pylori infection among workers in institutions for people with intellectual disability. Occup Environ Med. 2008;65(9):587–91. [DOI] [PubMed] [Google Scholar]
- 39.Reshetnyak VI, Burmistrov AI, Maev IV. Helicobacter pylori: Commensal, symbiont or pathogen? World J Gastroenterol. 2021;27(7):545–60. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 40.Elghannam MT, Hassanien MH, Ameen YA, Turky EA, GM EL, AA EL, et al. Helicobacter pylori and oral-gut microbiome: clinical implications. Infection. 2024;52(2):289–300. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 41.Xie D, Cheng J, Zhao X, Fan C. Determinants of Helicobacter pylori infection and eradication failure among healthcare workers in a high-exposure clinical setting: a single-centre retrospective cohort study in China. BMJ Open. 2026;16(1):e105915. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 42.Martínez-Martínez FJ, Chiner-Oms Á, Furió V, et al. Genomic determinants of antibiotic resistance for Helicobacter pylori treatment: a retrospective phenotypic and genotypic observational study. Lancet Microbe. 2025;7:101217. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 43.Hamada M, Nomura R, Ogaya Y, Nishiyama K, Kadota T, Nakano K. Distribution of Helicobacter pylori in the Oral Cavity of Patients With Tooth Extractions at Various Locations and Ages. Int Dent J. 2026;76(1):103977. [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Supplementary Material 1: Supplementary Table S1. Full Search Strategy
Supplementary Material 2: Supplementary Tables S2-S4. Detailed Risk of Bias Assessment Using Newcastle–Ottawa ScaleDescription: Detailed Risk of Bias Assessment Using Newcastle–Ottawa Scale
Data Availability Statement
The data are available from the corresponding author (saleh.danial79@gmail.com) upon request.

