Skip to main content
NCBI home page
JGH Open: An Open Access Journal of Gastroenterology and Hepatology logoLink to JGH Open: An Open Access Journal of Gastroenterology and Hepatology
. 2026 Oct 11;10(10):e70483. doi: 10.1002/jgh3.70483

Halitosis and Helicobacter pylori Infection: A Systematic Review and Meta‐Analysis

Yu Xia 1, Jun‐Da Zhu 1, Tong Su 1, Bing‐Jie Jin 1, Shu‐Lei Zhao 1, Hong‐Wei Xu 1, Chang‐Qin Xu 1,✉
PMCID: PMC13655304  PMID: 42865798

ABSTRACT

Background

Halitosis, a common clinical condition, is frequently associated with Helicobacter pylori infection. Numerous studies have highlighted a significant reduction in halitosis following successful H. pylori eradication.

Aim

This meta‐analysis aimed to investigate the association between H. pylori infection and halitosis, as well as the effect of H. pylori eradication on halitosis resolution.

Methods

We searched major databases, including PubMed, EMBASE, the Cochrane Library, and the Science Citation Index, up to March 2025. Literature screening and data extraction were conducted according to strict inclusion and exclusion criteria. Study quality was assessed using appropriate tools according to study design. Heterogeneity and risk of bias were analyzed using Stata 12.0. Subgroup analyses were performed to examine the relationship between H. pylori infection and halitosis, including infection prevalence, symptom incidence, and treatment outcomes.

Results

Of the 154 articles screened, 24 met the inclusion criteria, involving 5872 patients. The analysis revealed a significantly higher H. pylori infection rate in the halitosis group compared with the non‐halitosis group (OR = 3.42; 95% CI: 1.13–10.33). The prevalence of halitosis was higher in H. pylori ‐positive individuals than in H. pylori ‐negative individuals (OR = 1.91; 95% CI: 1.28–2.86). The prevalence of halitosis was lower in the successful eradication group compared with the unsuccessful eradication group (OR = 0.17; 95% CI: 0.04–0.73). Moreover, pre‐eradication halitosis rates were higher than post‐eradication rates (OR = 4.39; 95% CI: 1.99–9.68).

Conclusion

The findings suggest a significant observational association between H. pylori infection and halitosis, and eradication therapy may be associated with alleviation of halitosis.

Keywords: H. pylori eradication, H. pylori infection, halitosis, Helicobacter pylori , meta‐analysis

1. Introduction

Halitosis, characterized by abnormal odors emanating from the oral or nasal cavity, is a prevalent condition affecting individuals across all age groups [1]. It is estimated that approximately 50% of adults worldwide experience halitosis, with a significant occurrence also observed in children [2, 3]. Beyond its negative impact on social interactions and mental well‐being, halitosis may signal underlying pathological conditions. Halitosis is categorized into two main types: intraoral and extraoral [1]. Intraoral halitosis accounts for 80%–90% of cases, primarily caused by volatile sulfur compounds (VSCs) such as hydrogen sulfide (H2S), methyl mercaptan (CH3SH), and dimethyl sulfide (CH3SCH3), which are metabolic byproducts of oral bacteria [4]. Key contributing factors include tongue coating, periodontal disease, and gingivitis [5]. Extraoral halitosis, on the other hand, is often linked to systemic disorders like gastrointestinal diseases, respiratory infections, metabolic conditions, or hepatic/renal dysfunction [6, 7]. Accurate diagnosis of the underlying etiology is crucial for developing targeted therapeutic strategies.

Helicobacter pylori , a chronic bacterial infection with a global prevalence of approximately 50%, is strongly associated with conditions such as gastritis, peptic ulcers, and gastric cancer [8, 9]. Recent evidence suggests a potential link between H. pylori infection and halitosis. A 2016 meta‐analysis indicated that H. pylori infection might be correlated with halitosis, with eradication therapy providing symptomatic relief in refractory cases [10]. However, recent studies, including those by Yang et al., have reported no significant difference in H. pylori positivity rates between halitosis and non‐halitosis groups [11]. This study systematically reviewed high‐quality English literature and conducted a meta‐analysis to assess whether H. pylori infection is associated with halitosis and whether eradication therapy effectively alleviates symptoms, thereby offering evidence‐based guidance for clinical practice.

2. Methods

This systematic review and meta‐analysis was registered in PROSPERO (registration number: CRD420261327983; registered on February 27, 2026).

2.1. Data Sources and Search Strategy

A systematic search of major databases (PubMed, EMBASE, MEDLINE, and Web of Science) was conducted up to March 2025 to identify articles investigating the association between halitosis and H. pylori . The detailed search strategy for PubMed was as follows: (“Halitosis”[MeSH] OR “Halitosis”[Title/Abstract] OR “Halitoses”[Title/Abstract] OR “bad breath”[Title/Abstract] OR “oral malodor”[Title/Abstract]) AND (“ Helicobacter pylori ”[MeSH] OR “ Helicobacter pylori ”[Title/Abstract] OR “ H. pylori ”[Title/Abstract] OR “ Campylobacter pylori ”[Title/Abstract] OR “ Campylobacter pyloridis ”[Title/Abstract]). Similar strategies were applied to EMBASE, MEDLINE, and Web of Science.

Initial screening of titles and abstracts excluded records that did not meet the inclusion criteria or were deemed irrelevant to the research focus. Additionally, the reference lists of selected articles were reviewed to identify further relevant studies.

2.2. Inclusion and Exclusion Criteria

This study implemented rigorous screening criteria: H. pylori positivity required confirmation by at least two validated methods (urea breath test, histology, or PCR). Halitosis diagnosis required objective measurement (organoleptic score ≥ 2 or gas chromatography VSC ≥ 110 μg/L) or validated questionnaires; studies relying solely on subjective questionnaires were excluded. Inclusion also required extractable data on halitosis prevalence, H. pylori infection rates, and halitosis prevalence before and after eradication. Exclusions comprised studies with fewer than 10 patients, guidelines, letters, reviews, abstracts without full text, or insufficient data. Two investigators independently assessed full texts, resolving disagreements through discussion and consensus. All included studies reported H. pylori prevalence rather than incidence, as infection status was assessed at a single time point or at baseline, and no study prospectively tracked new infections over time.

2.3. Quality Assessment

Methodological quality of the included studies was assessed using design‐specific tools: the Newcastle–Ottawa Scale (NOS) for cohort studies and the Agency for Healthcare Research and Quality (AHRQ) checklist for cross‐sectional studies. The NOS evaluates selection, comparability, and outcome (0–9 points), with scores ≥ 7 indicating high quality. The AHRQ checklist evaluates 11 items (0–11 points), with scores ≥ 9 indicating high quality.

2.4. Data Extraction

Using a predefined data extraction form, data were extracted by two investigators (Y.X., J.D.‐Z., T.S.) and confirmed by two others (B.J.‐J., S.L.‐Z.). Disagreements were addressed by consulting a third investigator (H.W.‐X., C.Q.‐X.). The data collected included publication year, first author, sample size, sex, mean age, study type, data source, and intervention measures.

2.5. Statistical Analysis

Based on study design, the included studies were systematically categorized into four analytical groups to examine the bidirectional relationship between H. pylori infection and halitosis: (1) H. pylori prevalence in halitosis versus non‐halitosis populations, (2) halitosis prevalence in H. pylori ‐positive versus negative populations, (3) halitosis resolution rates following successful versus unsuccessful eradication therapy in H. pylori ‐infected patients, and (4) halitosis prevalence before and after H. pylori eradication in infected individuals. All statistical analyses were performed using Stata version 12.0 (StataCorp). Study heterogeneity was evaluated using Cochran's Q test (significance threshold p < 0.1) and I 2 statistics (indicating heterogeneity when I 2 > 50%). Depending on heterogeneity, either fixed‐effects or random‐effects models were applied for meta‐analysis. For analyses with zero events in one or more cells, a continuity correction of 0.5 was added to each cell of the 2 × 2 table to enable calculation of the odds ratio (OR). Deek's funnel plot asymmetry test was used to assess publication bias, with statistical significance set at p < 0.05 for all inferential analyses. This comprehensive approach ensured a robust evaluation of both the epidemiological association and therapeutic impact between H. pylori infection and halitosis.

3. Results

A total of 154 potential studies were identified through electronic database searches, of which 101 were excluded due to duplication, conference abstracts, reviews, or commentaries. Among the remaining 53 articles, 29 were excluded from the meta‐analysis due to sample sizes of fewer than 10 participants, insufficient data, or non‐English literature. The final 24 studies were deemed eligible for further analysis [11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34]. These included 13 retrospective studies, 9 prospective cohort studies, and 2 cross‐sectional studies. Figure 1 displays the literature screening flowchart and subgroup classification design. Table 1 summarizes the main characteristics of the included studies. Quality assessment results are presented in Supplementary Table 1. The 24 studies were rated as moderate to high quality. Supplementary Table 2 provides a study‐by‐outcome matrix showing the contribution of each included study to the four subgroup analyses. Supplementary Table 3 contains the extracted 2 × 2 data for each included study. This meta‐analysis includes a total of 5872 participants (Group 1: 2305, Group 2: 2389, Group 3: 376, Group 4: 802).

FIGURE 1.

FIGURE 1

Open in a new tab

Literature screening flowchart and subgroup classification design.

TABLE 1.

Characteristics of the studies included in this meta‐analysis.

First author Publication year Country Study type Case number Sex (M/F) Mean age Halitosis test H. pylori test (location) Eradication therapy of H. pylori
Ierardi 1998 Italy Prospective 58 29/29 45.3 Halimeter/organoleptic UBT/histology (stomach) Double‐drug for 2 weeks (omeprazole + amoxicillin), and Triple‐drug for 10 days in case of eradication failure (omeprazole + clarithromycin + metronidazole)
Gasbarrini 1998 Italy Retrospective 116 50/66 35 ± 11 Questionnaire UBT (stomach) ——
Gasbarrini 1999 Italy Prospective 31 18/13 39 ± 12 Questionnaire UBT (stomach) Triple‐drug for 1 week for IDDM patients (pantoprazol + amoxicillin + clarithromycin)
Shashidhar 2000 USA Prospective 32 13/19 11 Questionnaire RUT/histology (stomach) Triple‐drug for 2 weeks (lansoprazol + amoxicillin + clarithromycin)
Werdmuller 2000 The Netherlands Retrospective 404 188/216 50 (H. pylori+) 46 (H. pylori−) Questionnaire Histology, culture and gram stain, RUT, ELISA (stomach) ——
Hoshi 2002 Japan Retrospective 80 34/46 44.7 (H. pylori+) 33.8 (H. pylori−) Organoleptic UBT (stomach) ——
Serin 2003 Turkey Prospective 148 69/79 38.2 Questionnaire histology (stomach) Triple‐drug for 2 weeks (omeprazole + amoxicillin + clarithromycin)
Candelli 2003 Italy Retrospective 121 65/56 14.8 ± 5.6 Questionnaire UBT (stomach) ——
Adler 2005 Argentina Retrospective 124 40/84 56.5 Halimeter PCR (stomach) ——
Katsinelos 2007 Greece Prospective 18 10/8 40.7 ± 10.9 Questionnaire UBT/histology (stomach) Triple‐drug for 10 days (omeprazole + amoxicillin + clarithromycin), and quadruple‐drug for 10 days in case of eradication failure (omeprazole + bismuth + metronidazole + tetracycline)
Suzuki 2008 Japan Retrospective 326 130/196 45.3 ± 15 Gas chromatography PCR (saliva) ——
Lee 2009 Korea Prospective 88 39/49 47.7 ± 10.4 Halimeter UBT (stomach) Triple‐drug for 1 week or Red ginseng for 10 weeks
Tangerman 2012 The Netherlands Retrospective 78 7/4阳性 18/20 60 (H. pylori+) 52.9 (H. pylori−) Organoleptic CLO‐test/histology/culture (stomach) ——
Dore 2012 Italy Cross‐sectional 1741 Unknown 6–15 Questionnaire ELISA (stomach) ——
Yilmaz 2012 Turkey Retrospective 108 54/54 8 Organoleptic Stool antigen test (stomach) ——
HajiFattai 2015 Iran Retrospective 44 20/22 34.29 ± 13.71 Organoleptic test RUT (stomach) ——
Zaric 2015 India Retrospective 98 42/56 19–78 Organoleptic test Nestde‐PCR Triple‐drug for 1 week (amoxicillin + clarythromycin + pantoprazol)
Aksit 2017 Turkey Retrospective 100 47/53 10.22 ± 3.44 Organoleptic and the BANA test. PCR (dental biofilm and saliva) ——
Suzuki 2020 Japan Prospective 12 Unknown 59.5 Organoleptic and gas chromatograph RUT (stomach) Triple‐drug for 1 week (lansoprazole + amoxicillin + clarithromycin) and (lansoprazole + amoxicillin + metronidazole) in case of eradication failure
Kudo 2022 Japan Prospective 77 21/56 64.2 ± 11.5 Total gas detector system RUT/UBT/histology/serum antibody Triple‐drug for 1 week (PPI + amoxicillin + clarithromycin/metronidazole)
Zhou 2024 China Retrospective 574 259/315 45.3 Questionnaire UBT (stomach) ——
Chen 2024 China Prospective 100 45/55 33.37 ± 6.35 Organoleptic UBT (stomach) Quadruple‐drug for 2 weeks (rabeprazole + bismuth + amoxicillin + clarithromycin)
Karakas 2024 Japan Cross‐sectional 543 302:241 3.92 Questionnaire ELISA (feces) ——
Yang 2025 China Retrospective 108 44/64 38.74 ± 8.42 Organoleptic UBT (stomach) ——
Open in a new tab

3.1. Group 1 (n = 7): H. pylori Prevalence in Halitosis vs. Non‐Halitosis Populations

Figure 2 shows an overall OR = 3.42 (95% CI: 1.13, 10.33), indicating that the H. pylori infection rate was significantly higher in the halitosis group compared with the non‐halitosis group, with statistical significance. Heterogeneity metrics (I 2 = 89.9%, p = 0.000) revealed substantial heterogeneity across studies. A random‐effects model was employed to account for this heterogeneity and minimize its impact on the pooled estimate. The variability in H. pylori detection methods, testing sites, broad age range of subjects, and geographic distribution may introduce confounding factors, considering regional variations in prevalence rates and strain virulence.

FIGURE 2.

FIGURE 2

Open in a new tab

H. pylori prevalence in halitosis versus non‐halitosis populations.

3.2. Group 2 (n = 10): Halitosis Prevalence Between H. pylori ‐Positive and ‐Negative Populations

Figure 3 shows an overall OR = 1.91 (95% CI: 1.28, 2.86), demonstrating that the prevalence of halitosis in the H. pylori ‐positive group is significantly higher than in the H. pylori ‐negative group (p < 0.05), suggesting that H. pylori infection may be a risk factor for halitosis. Heterogeneity analysis revealed I 2 = 65.6% (p = 0.002), indicating moderate heterogeneity among studies (I 2 > 50% and p < 0.05). A random‐effects model was applied to mitigate the impact of heterogeneity. Heterogeneity may arise from local oral factors and gastrointestinal comorbidities, which could independently influence the occurrence of halitosis and introduce bias into effect size estimation.

FIGURE 3.

FIGURE 3

Open in a new tab

Halitosis prevalence in H. pylori ‐positive versus ‐negative populations.

3.3. Group 3 (n = 5): Halitosis Resolution Rates Following Successful vs. Unsuccessful Eradication Therapy in Infected Patients With Halitosis

Figure 4 shows an overall OR = 0.17 (95% CI: 0.04, 0.73), indicating a significantly lower halitosis rate in the H. pylori eradicated group compared with the unsuccessful eradication group. The event was defined as the presence of halitosis after treatment; an OR < 1 favors successful eradication. This suggests that H. pylori eradication may reduce the risk of halitosis. Heterogeneity analysis revealed I 2 = 77.2% (p = 0.002), indicating substantial heterogeneity across the studies. A random‐effects model was employed to mitigate the impact of this heterogeneity. Variability in H. pylori eradication regimens, lack of standardization in defining eradication success, differences in halitosis assessment timing, and potential confounding from oral H. pylori colonization or other causes of halitosis contribute to the observed heterogeneity.

FIGURE 4.

FIGURE 4

Open in a new tab

Halitosis resolution rates following successful versus unsuccessful eradication therapy in infected patients with halitosis.

3.4. Group 4 (n = 7): Halitosis Prevalence Before and After H. pylori Eradication in Infected Individuals

Figure 5 demonstrates an overall OR = 4.39 (95% CI: 1.99, 9.68). The event was defined as the presence of halitosis after treatment; an OR > 1 therefore indicates higher odds of halitosis before eradication than after eradication. These results indicate that halitosis prevalence was significantly lower following H. pylori eradication compared with pre‐eradication levels. Heterogeneity analysis revealed I 2 = 76.7% (p = 0.000), suggesting substantial heterogeneity among studies. A random‐effects model was applied to minimize its influence. All studies in this group used a self‐controlled before‐after design without parallel control groups, which could not exclude time‐dependent confounders, such as improvements in oral hygiene during the study period. Additionally, variations in follow‐up duration further increased the uncertainty of the results.

FIGURE 5.

FIGURE 5

Open in a new tab

Halitosis prevalence before and after H. pylori eradication in infected individuals.

4. Discussion

Halitosis, a prevalent clinical symptom, affects approximately 10%–30% of adults in the United States and EU, and 30%–60% in developing countries, significantly impairing quality of life [2]. Its etiology is multifactorial, encompassing oral diseases, gastrointestinal disorders, and systemic conditions [1, 6]. H. pylori , a Gram‐negative bacterium that colonizes the stomach, is a well‐established cause of gastritis, peptic ulcers, gastric adenocarcinoma, and gastric MALT lymphoma [35]. Recent studies suggest a potential link between H. pylori infection and halitosis. Building upon Dou's 2016 meta‐analysis that demonstrated a significant correlation between H. pylori infection and halitosis [10], this study has incorporated updated evidence through May 2025, with a larger sample size of 5872 cases, thereby enhancing statistical power and minimizing random error. The findings further support an observational association between H. pylori infection and halitosis, providing clinical support for H. pylori screening and eradication therapy in patients with refractory halitosis and no apparent oral or otolaryngological pathology.

As research progresses, numerous studies have sought to elucidate the mechanisms by which H. pylori contributes to halitosis. Tonzetich et al. identified the formation of odorous VSCs, such as H2S and CH3SH, by bacteria in the oral cavity—especially within the tongue coating—as a primary cause of oral malodor [7, 36, 37]. In 2009, Lee et al. found significantly higher VSC concentrations in the oral cavity of H. pylori ‐positive patients compared with H. pylori ‐negative patients [23]. Gastric H. pylori can metabolize urea to produce ammonia and VSCs, or indirectly contribute to halitosis by triggering gastric acid reflux, which alters the oral microenvironment [12, 22, 28]. The high urease activity of H. pylori breaks down urea into ammonia and carbon dioxide. Ammonia entering the oral cavity elevates pH, facilitating the proliferation of anaerobic bacteria, which in turn produce VSCs—the primary chemical markers of halitosis [38]. Additionally, H. pylori infection can lead to gastric disorders, such as delayed gastric emptying, abnormal gastric acid secretion, and gastroesophageal reflux. Reflux materials may emit foul odors or alter the oral bacterial flora, while inflammatory mediators generated by gastric inflammation can also influence the oral microenvironment [39]. Notably, the relationship between H. pylori infection, GERD, and halitosis is complex. Some studies have reported an inverse association between H. pylori and GERD, possibly due to H. pylori ‐induced gastric atrophy reducing acid secretion [40]. Meanwhile, GERD itself is a recognized cause of halitosis through regurgitation of gastric contents [41]. This apparent paradox suggests that the association between H. pylori and halitosis may not be simply mediated by GERD. In our analysis, GERD was not consistently adjusted for in the included primary studies, which we have acknowledged as a limitation. H. pylori can also colonize the oral cavity, where oral biofilms provide an optimal environment for its survival, including suitable pH, temperature, and microaerobic conditions. Moreover, oral H. pylori can directly produce ammonia and VSCs through urease activity. Its presence in the oral cavity may also serve as a “reservoir” for gastric reinfection, complicating long‐term halitosis management [42, 43].

Currently, the primary treatment for halitosis centers on oral hygiene interventions, but there is no consensus regarding eradication therapy for H. pylori ‐positive patients. In 2003, Serin et al. studied 148 H. pylori ‐positive patients and observed changes in halitosis rates before and after eradication therapy, finding that 97.2% of those with successful eradication experienced complete resolution of halitosis symptoms [18]. Recent research has increasingly focused on the impact of H. pylori eradication on halitosis relief. A 2022 study by Kudo et al. demonstrated that patients with significant halitosis before treatment showed a marked reduction in symptoms post‐eradication, with improvements persisting up to 2 years after treatment, confirming the long‐term benefits of successful eradication in halitosis management [31]. The present study conducted a longitudinal analysis of halitosis rates before and after successful H. pylori eradication, alongside a cross‐sectional comparison between successfully eradicated and unsuccessful eradication subgroups. The results indicated an 83% reduction in halitosis prevalence (OR = 0.17, 95% CI: 0.04–0.73), with the pre‐eradication risk of halitosis being 4.4 times higher than post‐eradication (OR = 4.39, 95% CI: 1.99–9.68). These findings highlight the significant clinical value of H. pylori eradication in preventing or treating halitosis, particularly in refractory cases with concurrent H. pylori infection [31]. However, some have suggested that the reduction in oral malodor may be attributed to the effects of antibiotics on the oral microbiota. Yet, a 2020 study by Suzuki et al. showed that while antibiotic treatment altered the composition of the salivary bacterial community, it returned to baseline levels within 7 weeks. The improvement in halitosis was not linked to a direct antibiotic effect on oral bacteria, as post‐eradication bacterial composition did not differ significantly from pre‐eradication, and the total bacterial count in the oral cavity showed no substantial change [30]. This finding, however, should be interpreted with caution. The comparison between successful and unsuccessful eradication in Group 3 was observational rather than randomized, and may be confounded by factors such as antibiotic adherence, regimen choice, drug resistance, follow‐up duration, and baseline disease severity. These factors were not systematically controlled in the included studies, and may have influenced the observed treatment effects.

Although multiple clinical studies confirm that successful H. pylori eradication significantly improves halitosis symptoms, therapeutic efficacy exhibits individual variability. Meta‐analyses indicate persistent halitosis in some patients post‐eradication. Potential mechanisms for this include: (1) transient suppression of the oral microbiota during eradication therapy, followed by recolonization by bacteria such as Porphyromonas gingivalis , which continue to produce VSCs [44]; (2) a 2020 meta‐analysis demonstrating a significantly higher prevalence of gastroesophageal reflux in the eradication group compared with controls (RR = 1.54), with gastroesophageal reflux disease correlating with halitosis (OR = 2.24), and a severity‐dependent escalation of risk [45, 46]; and (3) persistent oral infections (e.g., periodontitis, dental caries, tongue coating accumulation) left untreated during eradication therapy [47]. Therefore, a comprehensive evaluation of halitosis etiology is crucial in clinical practice, incorporating both oral treatments and screening for systemic diseases when necessary.

This systematic review and meta‐analysis offers several key strengths. By incorporating 24 studies (total sample size: 5872) published up to 2025, it provides the most current evidence on the association between H. pylori infection and halitosis. The sample size notably exceeds that of prior meta‐analyses [10], establishing this as the largest contemporary dataset on the subject. Additionally, the inclusion of studies on H. pylori eradication therapy strengthens the evidence base, offering valuable insights for managing refractory halitosis in H. pylori ‐infected patients. Methodologically, rigorous criteria for disease diagnosis, study selection, and data extraction enhance the reliability of the conclusions.

However, this meta‐analysis has certain limitations. The restriction to English‐language studies may have led to the omission of research from regions with high H. pylori prevalence (e.g., China), resulting in underrepresentation of data from these areas and potential selection bias. Therefore, the pooled estimates should be interpreted with caution in a global context. Future research should include multilingual evidence to improve geographical representation. The included studies exhibited heterogeneity in sample sources, detection methods, and treatment protocols, which could affect result accuracy. However, the limited number of studies in some subgroups precluded further subgroup or sensitivity analyses to explore the sources of heterogeneity. Additionally, most included studies were observational and did not systematically adjust for important confounders such as periodontal disease, tongue coating, oral hygiene, smoking, reflux disease, functional dyspepsia, diabetes, age, sex, or recent antibiotic use. Thus, our findings reflect an observational association rather than a causal relationship. Future prospective studies with larger sample sizes, standardized diagnostic criteria, and rigorous adjustment for these confounders are needed to establish causality and identify which patient subgroups might benefit most from H. pylori eradication therapy.

In conclusion, the current evidence presented here confirms an observational association between H. pylori infection and halitosis, with eradication therapy showing potential in alleviating oral malodor. However, due to the observational nature of most included studies and lack of adjustment for important confounders, these findings should be interpreted as associative rather than causal.

Funding

This work was supported by the Young Elite Sponsorship Program of Shandong Provincial Medical Association under Grant Number: 2024‐GJ‐0131.

Ethics Statement

This meta‐analysis used only published literature and did not involve human subjects, patient data, or animal experiments. Therefore, ethical approval and informed consent were not required.

Conflicts of Interest

The authors declare no conflicts of interest.

Supporting information

Data S1: PRISMA 2009 checklist.

JGH3-10-e70483-s001.docx (31.9KB, docx)

Supplementary Table 1. Quality assessment results.

JGH3-10-e70483-s003.docx (19KB, docx)

Supplementary Table 2. Study‐by‐outcome matrix.

JGH3-10-e70483-s002.docx (13.5KB, docx)

Supplementary Table 3. Extracted 2 × 2 data for each included study.

JGH3-10-e70483-s004.docx (14.8KB, docx)

Data Availability Statement

The data supporting this meta‐analysis are from previously published studies. All extracted data are presented in this article and its Supplementary Files. The original studies are accessible via PubMed, EMBASE, MEDLINE, and Web of Science, and are cited in the references. No new primary data were generated.

References

  • 1. Li Z., Li J., Fu R., Liu J., Wen X., and Zhang L., “Halitosis: Etiology, Prevention, and the Role of Microbiota,” Clinical Oral Investigations 27, no. 11 (2023): 6383–6393, 10.1007/s00784-023-05292-9. [DOI] [PubMed] [Google Scholar]
  • 2. Barrak I., Stájer A., Gajdács M., and Urbán E., “Small, but Smelly: The Importance of Solobacterium moorei in Halitosis and Other Human Infections,” Heliyon 6, no. 10 (2020): e05371, 10.1016/j.heliyon.2020.e05371. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3. Ueno M., Ohnuki M., Zaitsu T., Takehara S., Furukawa S., and Kawaguchi Y., “Prevalence and Risk Factors of Halitosis in Japanese School Children,” Pediatrics International 60, no. 6 (2018): 588–592, 10.1111/ped.13561. [DOI] [PubMed] [Google Scholar]
  • 4. Lu H. X., Tang C., Chen X., Wong M. C., and Ye W., “Characteristics of Patients Complaining of Halitosis and Factors Associated With Halitosis,” Oral Diseases 20, no. 8 (2014): 787–795, 10.1111/odi.12198. [DOI] [PubMed] [Google Scholar]
  • 5. Newman M. G., Takei H. H., Klokkevold P. R., and Carranza F. A., Carranza's Clinical Periodontology, 11th ed. (Elsevier Saunders, 2012), 331–338. [Google Scholar]
  • 6. Bollen C. M. and Beikler T., “Halitosis: The Multidisciplinary Approach,” International Journal of Oral Science 4, no. 2 (2012): 55–63, 10.1038/ijos.2012.39. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7. Tangerman A., “Halitosis in Medicine: A Review,” International Dental Journal 52 (2002): 201–206, 10.1002/j.1875-595x.2002.tb00925.x. [DOI] [PubMed] [Google Scholar]
  • 8. Hooi J. K. Y., Lai W. Y., Ng W. K., et al., “Global Prevalence of Helicobacter pylori Infection: Systematic Review and Meta‐Analysis,” Gastroenterology 153, no. 2 (2017): 420–429, 10.1053/j.gastro.2017.04.022. [DOI] [PubMed] [Google Scholar]
  • 9. Al Asqah M., Al Hamoudi N., Anil S., Al Jebreen A., and Al‐Hamoudi W. K., “Is the Presence of Helicobacter pylori in Dental Plaque of Patients With Chronic Periodontitis a Risk Factor for Gastric Infection?,” Canadian Journal of Gastroenterology 23, no. 3 (2009): 177–179, 10.1155/2009/950527. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10. Dou W., Li J., Xu L., et al., “Halitosis and helicobacter pylori Infection: A Meta‐Analysis,” Medicine 95, no. 39 (2016): e4223, 10.1097/MD.0000000000004223. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11. Yang L., Gong J. J., Mo X. J., and Qian X. X., “Extraoral Halitosis in Functional Dyspepsia and Its Association With Small Intestinal Bacterial Overgrowth,” Journal of Breath Research 19, no. 2 (2025): 026006, 10.1088/1752-7163/adb208. [DOI] [PubMed] [Google Scholar]
  • 12. Ierardi E., Amoruso A., La Notte T., et al., “Halitosis and Helicobacter pylori : A Possible Relationship,” Digestive Diseases and Sciences 43, no. 12 (1998): 2733–2737, 10.1023/a:1026619831442. [DOI] [PubMed] [Google Scholar]
  • 13. Gasbarrini A., Ojetti V., Pitocco D., et al., “ Helicobacter pylori Infection in Patients Affected by Insulin‐Dependent Diabetes Mellitus,” European Journal of Gastroenterology and Hepatology 10, no. 6 (1998): 469–472, 10.1097/00042737-199806000-00006. [DOI] [PubMed] [Google Scholar]
  • 14. Gasbarrini A., Ojetti V., Pitocco D., et al., “Insulin‐Dependent Diabetes Mellitus Affects Eradication Rate of Helicobacter pylori Infection,” European Journal of Gastroenterology and Hepatology 11, no. 7 (1999): 713–716, 10.1097/00042737-199907000-00005. [DOI] [PubMed] [Google Scholar]
  • 15. Shashidhar H., Peters J., Lin C. H., Rabah R., Thomas R., and Tolia V., “A Prospective Trial of Lansoprazole Triple Therapy for Pediatric Helicobacter pylori Infection,” Journal of Pediatric Gastroenterology and Nutrition 30, no. 3 (2000): 276–282, 10.1097/00005176-200003000-00012. [DOI] [PubMed] [Google Scholar]
  • 16. Werdmuller B. F., van der Putten T. B., Balk T. G., Lamers C. B., and Loffeld R. J., “Clinical Presentation of Helicobacter pylori ‐Positive and ‐Negative Functional Dyspepsia,” Journal of Gastroenterology and Hepatology 15, no. 5 (2000): 498–502, 10.1046/j.1440-1746.2000.02080.x. [DOI] [PubMed] [Google Scholar]
  • 17. Hoshi K., Yamano Y., Mitsunaga A., Shimizu S., Kagawa J., and Ogiuchi H., “Gastrointestinal Diseases and Halitosis: Association of Gastric Helicobacter pylori Infection,” International Dental Journal 52 (2002): 207–211, 10.1002/j.1875-595x.2002.tb00926.x. [DOI] [PubMed] [Google Scholar]
  • 18. Serin E., Gumurdulu Y., Kayaselcuk F., Ozer B., Yilmaz U., and Boyacioglu S., “Halitosis in Patients With Helicobacter pylori ‐Positive Non‐Ulcer Dyspepsia: An Indication for Eradication Therapy?,” European Journal of Internal Medicine 14, no. 1 (2003): 45–48, 10.1016/s0953-6205(02)00206-6. [DOI] [PubMed] [Google Scholar]
  • 19. Candelli M., Rigante D., Marietti G., et al., “ Helicobacter pylori , Gastrointestinal Symptoms, and Metabolic Control in Young Type 1 Diabetes Mellitus Patients,” Pediatrics 111 (2003): 800–803, 10.1542/peds.111.4.800. [DOI] [PubMed] [Google Scholar]
  • 20. Adler I., Denninghoff V. C., Alvarez M. I., Avagnina A., Yoshida R., and Elsner B., “ Helicobacter pylori Associated With Glossitis and Halitosis,” Helicobacter 10, no. 4 (2005): 312–317, 10.1111/j.1523-5378.2005.00322.x. [DOI] [PubMed] [Google Scholar]
  • 21. Katsinelos P., Tziomalos K., Chatzimavroudis G., et al., “Eradication Therapy in Helicobacter pylori ‐Positive Patients With Halitosis: Long‐Term Outcome,” Medical Principles and Practice 16, no. 2 (2007): 119–123, 10.1159/000098364. [DOI] [PubMed] [Google Scholar]
  • 22. Suzuki N., Yoneda M., Naito T., et al., “Detection of Helicobacter pylori DNA in the Saliva of Patients Complaining of Halitosis,” Journal of Medical Microbiology 57, no. pt. 12 (2008): 1553–1559, 10.1099/jmm.0.2008/003715-0. [DOI] [PubMed] [Google Scholar]
  • 23. Lee J. S., Kwon K. A., Jung H. S., Kim J. H., and Hahm K. B., “Korea Red Ginseng on Helicobacter pylori ‐Induced Halitosis: Newer Therapeutic Strategy and a Plausible Mechanism,” Digestion 80, no. 3 (2009): 192–199, 10.1159/000229997. [DOI] [PubMed] [Google Scholar]
  • 24. Tangerman A., Winkel E. G., de Laat L., van Oijen A. H., and de Boer W. A., “Halitosis and Helicobacter pylori Infection,” Journal of Breath Research 6, no. 1 (2012): 017102, 10.1088/1752-7155/6/1/017102. [DOI] [PubMed] [Google Scholar]
  • 25. Dore M. P., Fanciulli G., Tomasi P. A., et al., “Gastrointestinal Symptoms and Helicobacter pylori Infection in School‐Age Children Residing in Porto Torres, Sardinia, Italy,” Helicobacter 17, no. 5 (2012): 369–373, 10.1111/j.1523-5378.2012.00955.x. [DOI] [PubMed] [Google Scholar]
  • 26. Yilmaz A. E., Bilici M., Tonbul A., Karabel M., Dogan G., and Tas T., “Paediatric Halitosis and Helicobacter pylori Infection,” Journal of the College of Physicians and Surgeons–Pakistan 22, no. 1 (2012): 27–30. [PubMed] [Google Scholar]
  • 27. HajiFattahi F., Hesari M., Zojaji H., and Sarlati F., “Relationship of Halitosis With Gastric Helicobacter pylori Infection,” Journal of Dentistry 12, no. 3 (2015): 200–205. [PMC free article] [PubMed] [Google Scholar]
  • 28. Zaric S., Bojic B., Popovic B., and Milasin J., “Eradication of Gastric Helicobacter pylori Ameliorates Halitosis and Tongue Coating,” Journal of Contemporary Dental Practice 16, no. 3 (2015): 205–209, 10.5005/jp-journals-10024-1662. [DOI] [PubMed] [Google Scholar]
  • 29. Aksit Bıcak D., Akyuz S., Kıratlı B., et al., “The Investigation of Helicobacter pylori in the Dental Biofilm and Saliva Samples of Children With Dyspeptic Complaints,” BMC Oral Health 17, no. 1 (2017): 67, 10.1186/s12903-017-0361-x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 30. Suzuki N., Beppu R., Yoneda M., et al., “Effects of Eradication of Helicobacter pylori on Oral Malodor and the Oral Environment: A Single‐Center Observational Study,” BMC Research Notes 13, no. 1 (2020): 406, 10.1186/s13104-020-05253-5. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 31. Kudo Y., Kudo S. E., Miyachi H., et al., “Changes in Halitosis Value Before and After Helicobacter pylori Eradication: A Single‐Institutional Prospective Study,” Journal of Gastroenterology and Hepatology 37, no. 5 (2022): 928–932, 10.1111/jgh.15835. [DOI] [PubMed] [Google Scholar]
  • 32. Zhou J. K., Zheng Y., Wang Y. P., and Ji R., “Prevalence and Associated Risk Factors of Helicobacter pylori Infection in Community Households in Lanzhou City,” World Journal of Gastroenterology 30, no. 47 (2024): 5018–5031, 10.3748/wjg.v30.i47.5018. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 33. Chen Y. and Qian X. X., “Gastric Helicobacter pylori Infection Does Not Contribute to Extraoral Halitosis and Its Eradication Cannot Achieve Substantial Reduction of Halitosis,” Helicobacter 29, no. 1 (2024): e13047, 10.1111/hel.13047. [DOI] [Google Scholar]
  • 34. Karakas H., Tarcin G., Ozbey D., et al., “Frequency and Clinical Correlation of Helicobacter pylori Positivity in Children Admitted to a University Hospital in Türkiye: A Cross‐Sectional Study,” Turkiye Klinikleri Journal of Pediatrics 32, no. 2 (2023): 83–90. [Google Scholar]
  • 35. Kao C. Y., Sheu B. S., and Wu J. J., “ Helicobacter pylori Infection: An Overview of Bacterial Virulence Factors and Pathogenesis,” Biomedical Journal 39, no. 1 (2016): 14–23, 10.1016/j.bj.2015.06.002. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 36. Tonzetich J., “Production and Origin of Oral Malodor: A Review of Mechanisms and Methods of Analysis,” Journal of Periodontology 48, no. 1 (1977): 13–20, 10.1902/jop.1977.48.1.13. [DOI] [PubMed] [Google Scholar]
  • 37. Rosenberg M., “Clinical Assessment of Bad Breath: Current Concepts,” Journal of the American Dental Association (1939) 127, no. 4 (1996): 475–482, 10.14219/jada.archive.1996.0239. [DOI] [PubMed] [Google Scholar]
  • 38. Kumar R., Mirza M. A., Naseef P. P., Kuruniyan M. S., Zakir F., and Aggarwal G., “Exploring the Potential of Natural Product‐Based Nanomedicine for Maintaining Oral Health,” Molecules 27, no. 5 (2022): 1725, 10.3390/molecules27051725. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 39. Mogilnicka I., Bogucki P., and Ufnal M., “Microbiota and Malodor‐Etiology and Management,” International Journal of Molecular Sciences 21, no. 8 (2020): 2886, 10.3390/ijms21082886. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 40. Wang H., Qu Y., Lin Y., et al., “ Helicobacter pylori Infection and Eradication in Relation to Gastroesophageal Reflux Disease,” Journal of Gastroenterology and Hepatology 40, no. 10 (2025): 2391–2401, 10.1111/jgh.70009. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 41. Viana K. S. S., Eleutério F. H. P. F., Maciel V. G., et al., “Association Between Halitosis and Gastrointestinal Disorders: A Review,” Journal of the California Dental Association 52, no. 1 (2024): 2426249, 10.1080/19424396.2024.2426249. [DOI] [Google Scholar]
  • 42. Anand P. S., Nandakumar K., and Shenoy K. T., “Are Dental Plaque, Poor Oral Hygiene, and Periodontal Disease Associated With Helicobacter pylori Infection?,” Journal of Periodontology 77, no. 4 (2006): 692–698, 10.1902/jop.2006.050163. [DOI] [PubMed] [Google Scholar]
  • 43. Bürgers R., Schneider‐Brachert W., Reischl U., et al., “ Helicobacter pylori in Human Oral Cavity and Stomach,” European Journal of Oral Sciences 116, no. 4 (2008): 297–304, 10.1111/j.1600-0722.2008.00543.x. [DOI] [PubMed] [Google Scholar]
  • 44. Kadota T., Ogaya Y., Hatakeyama R., Nomura R., and Nakano K., “Comparison of Oral Flora Before and After Triple Therapy for Helicobacter pylori Eradication in Patient With Gastric Disease,” Odontology 107, no. 2 (2019): 261–267, 10.1007/s10266-018-0393-y. [DOI] [PubMed] [Google Scholar]
  • 45. Mou W. L., Feng M. Y., and Hu L. H., “Eradication of Helicobacter pylori Infections and GERD: A Systematic Review and Meta‐Analysis,” Turkish Journal of Gastroenterology 31, no. 12 (2020): 853–859, 10.5152/tjg.2020.19699. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 46. Struch F., Schwahn C., Wallaschofski H., et al., “Self‐Reported Halitosis and Gastro‐Esophageal Reflux Disease in the General Population,” Journal of General Internal Medicine 23, no. 3 (2008): 260–266, 10.1007/s11606-007-0486-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 47. Anand P. S., Kamath K. P., and Anil S., “Role of Dental Plaque, Saliva and Periodontal Disease in Helicobacter pylori Infection,” World Journal of Gastroenterology 20, no. 19 (2014): 5639–5653, 10.3748/wjg.v20.i19.5639. [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

Data S1: PRISMA 2009 checklist.

JGH3-10-e70483-s001.docx (31.9KB, docx)

Supplementary Table 1. Quality assessment results.

JGH3-10-e70483-s003.docx (19KB, docx)

Supplementary Table 2. Study‐by‐outcome matrix.

JGH3-10-e70483-s002.docx (13.5KB, docx)

Supplementary Table 3. Extracted 2 × 2 data for each included study.

JGH3-10-e70483-s004.docx (14.8KB, docx)

Data Availability Statement

The data supporting this meta‐analysis are from previously published studies. All extracted data are presented in this article and its Supplementary Files. The original studies are accessible via PubMed, EMBASE, MEDLINE, and Web of Science, and are cited in the references. No new primary data were generated.

Articles from JGH Open: An Open Access Journal of Gastroenterology and Hepatology are provided here courtesy of Wiley

RESOURCES