No full-text available
To read the full-text of this research,
you can request a copy directly from the authors.
Korea Red Ginseng on Helicobacter pylori -Induced Halitosis: Newer Therapeutic Strategy and a Plausible Mechanism
Abstract
Gas chromatographic documentation of volatile sulfur compounds in Helicobacter pylori cultures and the amelioration of halitosis after eradication suggested a causal link between H. pylori infection and halitosis.
We hypothesized that Korea red ginseng can relieve H. pylori-associated halitosis based on their anti-inflammatory and cytoprotective actions in H. pylori-associated gastritis.
Eighty-eight functional dyspepsia patients presenting with either subjective halitosis or objective halimeter levels >100 ppb were recruited, on whom tests were repeated after 10 weeks of red ginseng administration. The expressions of cystathionine gamma-lyase (CSE), cystathionine beta-synthetase (CBS), IL-6, IL-8 and IL-1beta mRNA were compared in H. pylori-infected or NaHS-treated gastric epithelial cells according to red ginseng treatment.
After 10 weeks of red ginseng administration, 38 patients out of 68 H. pylori-positive cases became 'free of halitosis' accompanied with halimeter levels <50 ppb accordant with the subjective resolution of halitosis. Among the remaining 30 patients, 15 cases administered with both eradication regimen and red ginseng supplement showed either higher eradication rates (93.3%) or were found to be completely free of halitosis in comparison to the other 15 patients who were only administered the eradication regimen. Among 20 H. pylori-negative patients, 13 patients became 'free of halitosis' with 10 weeks of red ginseng treatment alone. Red ginseng extracts significantly decreased H. pylori- or NaHS-induced CSE expressions concomitant with attenuated levels of IL-6, IL-8 and IL-1beta mRNA.
The strategy consisting of Korea red ginseng supplementation after the successful eradication of H. pylori could be an effective way to fight troublesome halitosis.
... Therefore, gastroenterologists and microbiologists continue to search for new therapies due to the increasing prevalence of H. pylori infection and the physiological and pharmacoeconomic burden of the second-line therapy. To increase eradication rates of first-line therapy, several clinical trials involving extending treatment duration to more than one week, use of higher doses of per protocol (PP), and/or new antibiotics such as quinolones, use of quadruple therapy, or addition of probiotics, vitamin C, bovine lactoferrin, ginseng, wine, garlic, honey, and cranberry have been carried out [11][12][13][14][15]. Previous studies have suggested that Korean red ginseng 1) inhibits H. pylori colonization, 2) exhibits antioxidative and antiinflammatory effects during H. pylori infection, 3) provides efficient restorative action, 4) inhibits expression of genes associated with generation of volatile sulfur compounds (VSCs), and 5) increases eradication rates in addition to attenuating H. pyloriassociated halitosis [16][17][18][19]. Here, we investigated the effects of supplementation of triple therapy with Korean red ginseng on both H. pylori eradication rates and H. pylori-associated halitosis. ...
... Four subjects in the Korean red ginseng group and one in the eradication-only group were lost to follow-up; we speculated that this was due to a change in medical staff (the clinical trial nurse) after the trial had begun. As we have previously reported eradication rates [18,19] (albeit at differing time points than the data presented here), these data ( Fig. 2a upper and middle panels) are presented together with those of the study described here (Fig. 2a lower panel). Although the eradication plus Korean red ginseng regime resulted in higher eradication rates than the eradication-only regime in each trial, statistical significance was not achieved, most likely due to the small number of subjects in each trial. ...
... Therefore, we inferred that supplementation of traditional therapies with Korean red ginseng would enhance treatment of H. pylori infection, especially in locations with a high incidence of H. pylori-associated gastric malignancy. The prevalence of H. pylori infection is believed to We previously conducted three clinical studies [18,19]. The first [18] was composed of 60 subjects (27 received only eradication therapy and 33 received eradication therapy plus 10 weeks of Korean red ginseng), the main objective of which trial was to measure the change of pathological scores according to group; eradication rate was obtained only as involved parameter (upper panel). ...
This clinical study was performed to evaluate whether supplementation of proton pump inhibitor (PPI)-based triple therapy with Korean red ginseng can enhance Helicobacter pylori (H. pylori) eradication and reduce levels of halitosis-associated volatile sulfur compounds (VSCs) in the stomach. Seventy-six patients were randomized into an eradication regimen-only group (n=45) or an eradication regimen plus 10 weeks of Korean red ginseng supplementation group (n=31). The eradication regimen consisted of PPI b.i.d., clarithromycin 500 mg b.i.d., and amoxicillin 1 g b.i.d.. for seven days. Korean red ginseng supplementation commenced on the last day of the eradication regimen. -urea breath test and halimeter measurements were performed prior to protocol repetition. By intention-to-treat analysis, the H. pylori eradication rate in the Korean red ginseng group (77.4%, 24 of 31) was higher than that in the control group (45.0%, 26 of 45). However, by per protocol analysis, the eradication rate in the Korean red ginseng group was significantly higher than that in the control group (92.3%, 24/26 vs. 69.4%, 26/38; p
... Additional report was followed that Korea red ginseng could relieve halitosis through their anti-inflammatory and cytoprotective actions in patients with H. pylori-infected gastritis. 14 Since halitosis is malordor coming from mouth and stomach, there is high possibility that halitosis is associated with gastroesophageal reflux disease (GERD). In the current study, we hypothesized that halitosis can be an extraesophageal symptom of GERD. ...
... Minimal change lesion; classified as part of NERD based on reference. [14][15][16] gastric juices were aspirated from gastric corpus during the endoscope procedure using aspiration tube inserted onto biopsy channel (Olympus, Tokyo, Japan) and were stored at −70 o C deep freezer until the assay. After several times of trials and errors at different temperature for the evaporating of gastric juices, we could success in final decision that 60 o C were quite ideal for evaporating gastric juices for gas chromatography. ...
... The fact that no significant difference observed in VSC levels according to severity of esophageal mucosal injury defined by LA classification and minimal lesion showed highest VSC concentration leaves possible insights of H2S role in pathogenesis of ERD like intervening of esophageal inflammation before the development of erosive lesions, sloughing of esophageal mucosa, and increased synthesis of VSCs in injured esophageal mucosa. [22][23][24] Currently, minimal change lesion is classified as NERD because of no definite presence of erosive or ulcerative changes in esophagogastric junction, [14][15][16] but there is high possibility that minimal change lesion could be one of early ERD supported with our objective finding that minimal change lesion showed highest levels of VSCs than either NERD or ERD. Hiatal hernia is closely associated with GERD and ERD was seen more frequently in patients with hiatal hernia than in patients without hiatal hernia. ...
In a previous issue published in Gut and Liver, we found that erosive changes in the esophagogastroduodenal mucosa were strongly correlated with increased levels of volatile sulfur-containing compounds (VSC), suggesting that halitosis could be a symptom reflecting the erosive status of the upper gut mucosa. Together with other studies showing a possible association between halitosis and gastroesophageal reflux disease (GERD), under the premise that halitosis could be one of extraesophageal manifestations of erosive GERD (ERD), we investigated the significance of Halimeter ppb levels on ERD compared to non-erosive gastroesophageal reflux disease (NERD).
Subjects were assigned to the NERD group if there was no evidence of esophageal erosive changes on endoscopy, despite reflux symptoms, and to the ERD group if they had GERD A, B, C, or D (according to the Los Angeles classification). The VSC levels were measured in all patients with either a Halimeter (before endoscopy) or by gas chromatography of the gastric juices aspirated during endoscopy.
The VSC level differed significantly between the NERD and ERD groups (p<0.0001), suggesting that this can be used to discriminate between NERD and ERD. However, the VSC level did not differ significantly with the severity of GERD. Even though hiatal hernia and a body mass index of >24 kg/m(2) was significantly associated with ERD, there was no correlation with Halimeter ppb levels. Minimal-change lesions exhibited the highest VSC levels, signifying that minimal change lesions can be classified as ERD based on our finding that halimeter ppb levels were descrimitive of erosive change.
Erosive changes in the esophageal mucosa were strongly associated with VSC levels, supporting the hypothesis that halitosis can be a potential biomarker for the discrimination between ERD and NERD, reflecting the presence of erosive change in the lower esophagogastric junction.
... We found that Korean red ginseng can resolve halitosis through either regulation of the genes responsible for VSC synthesis or direct inhibition of H. pylori infection. The evidence is as follows: H. pylori increased the levels of cystathionine g-lyase (CSE) and cystathionine b-synthase (CBS) mRNA, which encode inflammatory cytokines that promote VSC synthesis, and of the inflammatory mediators IL-1b, IL-8, and IL-6; Korean red ginseng significantly attenuated CSE and CBS mRNA production concomitant with decreased expression of the respective proteins; significant reductions in halimeter ppb levels (<50) were obtained after H. pylori eradication and red ginseng supplementation [47]. Thus, halitosis appears to be mechanistically associated with H. pylori infection, and Korean red ginseng supplementation following a successful eradication regimen could alleviate troublesome halitosis. ...
... Four patients were lost to follow-up in the Korean red ginseng group and one patient in the eradication alone group [68]. In a previous published trial, we assessed the eradication rate under the same protocol (i.e., eradication alone vs. eradication plus 10 weeks of Korean red ginseng supplementation), although over a different time course [47,49]. By combining the data from the current and the previous trial to determine the overall efficacy of Korean red ginseng supplementation on the H. pylori eradication rate, we found that a 10-week course of Korean red ginseng (Jeongkwanjang red ginseng capsule, 2.7 g/day; Korea Ginseng Cooperation, Daejeon, Korea) supplementation significantly augmented eradication rates (eradication alone group 75 of 102, 73.5% vs. eradication plus Korean red ginseng group 82 of 90, 91.1%; p<0.005). ...
Ginseng has been reported to reduce the risk of cancer in diverse organs, including the lip, oral cavity, pharynx, larynx, esophagus, lung, liver, pancreas, ovary, colon, rectum, and stomach, as demonstrated in clinical and epidemiological studies. studies, base on which findings, Panax ginseng has been classified as a "non-organ-specific cancer preventive." However, the recent keen interest in traditional medicinal herbs has been frequently questioned, about exact mode of action and the use of panaceic compounds has been a prime issue discussed in terms of complementary and alternative medicine. Several in vitro and in vivo studies have shown the mitigating effects of Korean red ginseng on Helicobacter pylori (H. pylori)-associated atrophic changes and carcinogenesis; However, evidence-based medicine, consisting of large-scale or well designed clinical studies, is still warranted whether Korean red ginseng is to be recognized as an essential therapeutic strategy regarding a "H. pylori-associated gastric cancer preventive." Specifically, comprehensive clinical trials of Korean red ginseng are needed to demonstrate that mucosal regeneration in patients with atrophic gastritis is feasible using Korean red ginseng supplements after the eradication of H. pylori infection. Ginseng is a good example of a natural herb and its ubiquitous properties may include the reduction or delay of inflammation carcinogenesis. Korean red ginseng contains ample amounts of active ginsenosides and we have demonstrated their effects in in vitro and in vivo studies with positive outcomes. In this review, the quantitative and qualitative benefits of Korean red ginseng in the treatment of H. pylori infection are described.
... In contrast to previous investigations that targeted gastric epithelial cells to document the anti-inflammatory effects of KRGE [19], in the current study, HUVECs were stimulated with H. pylori or the H 2 S donor NaHS to investigate the possible mechanisms underlying the cancer preventive effect of KRGE. We were particularly interested in mechanisms related to angiogenesis because the angiogenesis stimulated by H. pylori infection can cause either inflammation or carcinogenesis. ...
... HUVECs stimulated with 100 mM NaHS exhibited significantly increased CBS and CSE expression (Fig. 1A). On the basis of data from our previous publication [19] that showed that H. pylori infection significantly increased the levels of H 2 S (as indicated by RT-PCR of H 2 S generating genes and gas chromatography to measure H 2 S levels in the gastric juices of H. pyloriinfected gastritis patients), we decided that the administration of 100 mM NaHS could be used in place of live H. pylori bacteria to stimulate H 2 S generation in HUVECs. The use of NaHS instead of H. pylori infection was preferred under the basis that NaHS has no cytotoxicity at concentrations of up to 300 mM (Fig. 1B), whereas 100 multiplicity of infection H. pylori led to significant levels of cytotoxicity (Fig. 1B). ...
Previously, we reported that Helicobacter pylori-associated gastritis and gastric cancer are closely associated with increased levels of hydrogen sulfide (H2S) and that Korean red ginseng significantly reduced the severity of H. pylori-associated gastric diseases by attenuating H2S generation. Because the incubation of endothelial cells with H2S has been known to enhance their angiogenic activities, we hypothesized that the amelioration of H2S-induced gastric inflammation or angiogenesis in human umbilical vascular endothelial cells (HUVECs) might explain the preventive effect of Korean red ginseng on H. pylori-associated carcinogenesis. The expression of inflammatory mediators, angiogenic growth factors, and angiogenic activities in the absence or presence of Korean red ginseng extracts (KRGE) were evaluated in HUVECs stimulated with the H2S generator sodium hydrogen sulfide (NaHS). KRGE efficiently decreased the expression of cystathionine β-synthase and cystathionine γ-lyase, enzymes that are essential for H2S synthesis. Concomitantly, a significant decrease in the expression of inflammatory mediators, including cyclooxygenase-2 and inducible nitric oxide synthase, and several angiogenic factors, including interleukin (IL)-8, hypoxia inducible factor-1a, vascular endothelial growth factor, IL-6, and matrix metalloproteinases, was observed; all of these factors are normally induced after NaHS. An in vitro angiogenesis assay demonstrated that NaHS significantly increased tube formation in endothelial cells, whereas KRGE pretreatment significantly attenuated tube formation. NaHS activated p38 and Akt, increasing the expression of angiogenic factors and the proliferation of HUVECs, whereas KRGE effectively abrogated this H2S-activated angiogenesis and the increase in inflammatory mediators in vascular endothelial cells. In conclusion, KRGE was able to mitigate H2S-induced angiogenesis, implying that antagonistic action against H2S-induced angiogenesis may be the mechanism underlying the gastric cancer preventive effects of KRGE in H. pylori infection.
... After successful treatment, the oral cavity is a reservoir for gastric re-infection [75]. In Korea, applying a general eradication regimen with red ginseng supplementation at the local level showed eradication rates of 93% [76]. Adler's group, based on the case report of a male patient with Hp infection, both in the mouth (BHH) and in the stomach, established triple therapy in their patients at a general level and added oral hygiene teaching, periodontal treatment, cleaning the tongue with a gauze soaked with mouthwash and topical application of metronidazole gel on the dorsum of the tongue, with a decrease in the recurrence rate of Hp after eradication [56,77,78]. ...
Helicobacter pylori (Hp) is one of the most common infections worldwide, with important implications in gastric pathology. Early diagnosis and treatment are essential for the control and prevention of gastric diseases. The role of Hp in the oral cavity has been investigated and studied for the past 30 years, with a growing interest because oral-oral transmission is one of the main routes. In patients with burning, halitosis, and lingual papillary hypertrophy (BHH) in the oral cavity, the dental plaque and lingual dorsum have been identified as Hp reservoirs for colonization. BHH is suggested as an effective marker for early diagnosis of Hp infection, which should be confirmed by molecular techniques and correlated with gastric involvement.
... Korea red ginseng was effective in relieving oral malodour in patients with H pylori because red ginseng extracts significantly reduced H pylori or Sodium hydrosulfide (NaHS)induced ystathionine g-lyase expression as well as attenuated levels of IL-6, IL-8, and IL-1b mRNA. 59 ...
This review discusses the effects of ginseng and its extracts in the treatment of dental caries, periodontal diseases, endodontic diseases, oral cancers, oral mucosal diseases, and some other dental associations. In the meantime, bioavailability and safety application of ginseng products are discussed. All of the articles reviewed were from PubMed, Embase, Cochrane Library, Web of Science, China National Knowledge Infrastructure, Wanfang Data, and VIP Chinese Science and Technology Periodicals Full-Text Database through November 2022, including full-text English or non-English publications. Ginseng and its extracts were shown to have beneficial effects on oral diseases, and further studies are needed to understand the mechanisms and confirm the effects in humans.
... In addition, acidic polysaccharides blocked H. pylori attachment to gastric epithelial cells in an in vitro experiment [45]. In a clinical setting, Korean red ginseng treatment showed beneficial effects on H. pylori-associated halitosis, chronic gastritis, and inflammation carcinogenesis [46][47][48]. These studies show the possible therapeutic use of RGE, a mixture of effective components of Korean red ginseng, for H. pylori-induced gastric diseases, including inflammation. ...
Helicobacter pylori (H. pylori) causes gastric diseases by increasing reactive oxygen species (ROS) and interleukin (IL)-8 expression in gastric epithelial cells. ROS and inflammatory responses are regulated by the activation of nuclear factor erythroid-2-related factor 2 (Nrf2) and the expression of Nrf2 target genes, superoxide dismutase (SOD) and heme oxygenase-1 (HO-1). We previously demonstrated that Korean red ginseng extract (RGE) decreases H. pylori-induced increases in ROS and monocyte chemoattractant protein 1 in gastric epithelial cells. We determined whether RGE suppresses the expression of IL-8 via Nrf2 activation and the expression of SOD and HO-1 in H. pylori-infected gastric epithelial AGS cells. H. pylori-infected cells were treated with RGE with or without ML385, an Nrf2 inhibitor, or zinc protoporphyrin (ZnPP), a HO-1 inhibitor. Levels of ROS and IL-8 expression; abundance of Keap1, HO-1, and SOD; levels of total, nuclear, and phosphorylated Nrf2; indices of mitochondrial dysfunction (reduction in mitochondrial membrane potential and ATP level); and SOD activity were determined. As a result, RGE disturbed Nrf2–Keap1 interactions and increased nuclear Nrf2 levels in uninfected cells. H. pylori infection decreased the protein levels of SOD-1 and HO-1, as well as SOD activity, which was reversed by RGE treatment. RGE reduced H. pylori-induced increases in ROS and IL-8 levels as well as mitochondrial dysfunction. ML385 or ZnPP reversed the inhibitory effect of RGE on the alterations caused by H. pylori. In conclusion, RGE suppressed IL-8 expression and mitochondrial dysfunction via Nrf2 activation, induction of SOD-1 and HO-1, and reduction of ROS in H. pylori-infected cells.
... Thus, the hyperglycemia caused by sub-chronic administration in the high-dose KRG groups may be associated with increased H 2 S synthesis via CBS and CSE in the liver, given that CSE is an important H 2 S-producing enzyme that can be upregulated by NO 26 . Several earlier studies that explored KRG treatment and its association with H 2 S showed, for example, that KRG treatment inhibited H 2 S in vivo and in vitro 32,33 . Choi et al. reported that KRG at doses of 50-100 μg/ ml decreased both CBS and CSE expression in human umbilical vein endothelial cells (HUVECs) 34 . ...
Ginseng (Panax ginseng Meyer) is commonly used as an herbal remedy worldwide. Few studies have explored the possible physiological changes in the liver although patients often self-medicate with ginseng preparations, which may lead to exceeding the recommended dose for long-term administration. Here, we analyzed changes in the hepatic proteins of mouse livers using quantitative proteomics after sub-chronic administration of Korean red ginseng (KRG) extract (control group and 0.5, 1.0, and 2.0 g/kg KRG) using tandem mass tag (TMT) 6‐plex technology. The 1.0 and 2.0 g/kg KRG groups exhibited signs of liver injury, including increased levels of aspartate transaminase (AST) and alanine aminotransferase (ALT) in the serum. Furthermore, serum glucose levels were significantly higher following KRG administration compared with the control group. Based on the upregulated proteins found in the proteomic analysis, we found that increased cystathionine beta-synthase (CBS) and cystathionine gamma-lyase (CSE) levels promoted greater hydrogen sulfide (H2S) synthesis in the liver. This investigation provides novel evidence that sub-chronic administration of KRG can elevate H2S production by increasing protein expression of CBS and CSE in the liver.
... Red Asian ginseng extract in vitro significantly attenuated H. pylori-induced cytotoxicity, inflammation, and DNA damage(Park et al., 2005). Most importantly, several randomized human trials have been conducted, and the results indicated that red Asian ginseng supplementation significantly augmented H. pylori eradication in infection patients(Chung et al., 2010;Kim, Lee, Kim, Lee, & Hahm, 2007;Lee et al., 2009).The above anti-H. pylori researches are all about Asian ginseng either in white or red form, whereas there is relatively limited research that explores American ginseng and notoginseng. ...
Asian ginseng (Panax ginseng C.A. Meyer), American ginseng (Panax quinquefolius) and notoginseng (Panax notoginseng) are the three most commonly used ginseng botanicals in the world. With the increasing interests on antimicrobial properties of plants, the antimicrobial activities of ginseng species have been investigated by a number of researchers worldwide. This overview interprets our present knowledge of the antimicrobial activities of the three ginseng species and some of their bioactive components against pathogenic bacteria (Pseudomonas aeruginosa, Helicobacter pylori, Staphylococcus aureus, Escherichia coli, Propionibacterium acnes, et al.) and fungi (Candida albicans, Fusarium oxysporum, et al). Ginsenosides, polysaccharides, essential oil, proteins, and panaxytriol are all might responsible for the antimicrobial activities of ginseng. The antimicrobial mechanisms of ginseng components could be summarized to the following points: (a) inhibit the microbial motility and quorum‐sensing ability; (b) affect the formation of biofilms and destroy the mature biofilms, which can weaken the infection ability of the microbes; (c) perturb membrane lipid bilayers, thus causing the formation of pores, leakages of cell constituents and eventually cell death; (d) stimulate of the immune system and attenuate microbes induced apoptosis, inflammation, and DNA damages, which can protect or help the host fight against microbial infections; and (e) inhibit the efflux of antibiotics that can descend the drug resistance of the microbial. The collected information might facilitate and guide further studies needed to optimize the use of ginseng and their components to improve microbial food safety and prevent or treat animal and human infections.
... Red arrows and closed-ended lines indicate for stimulatory and inhibitory effects of ginseng, respectively administration of red ginseng improves the H. pylori eradication rate (91.7% in the red ginseng group and 79.4% in the placebo group, P = 0.147), attenuates the gastric inflammation, and reduces the oxidative DNA damage (P < 0.001) and apoptosis (Deog Ki 2007). Administration of red ginseng capsules (2.7 g/day for 5 weeks) also relieves H. pyloriassociated halitosis by suppressing the expression of cystathionine γ-lyase, cystathionine β-synthetase, IL-6, IL-8, and IL-1β (Lee et al. 2009), suggesting that red ginseng is a useful clinical supplement in the eradication of H. pylori and an effective treatment for H. pylori-associated halitosis. ...
Ginseng has been traditionally used as an herbal nutritional supplement in Asian countries, including Korea, China, Japan, and Vietnam for several millennia. Most studies have focused on the role of ginseng on anti-oxidative stress, anti-inflammatory, and anti-cancer activities. Recently, modulator activities of ginseng on the immune responses during pathogenic bacterial and viral infections and beneficial effects of ginseng in infectious diseases have been elucidated. In vivo and in vitro studies revealed the potential of ginseng extracts and ginsenosides Rg1, Rg3, Rb1, Rb2, Rb3, compound K, Re, Rd, Rh2 for treatment of several infectious diseases. The molecular mechanisms of these effects mainly involve inflammatory cytokines (TNF-α, IL-6, IL-1β, IFN-γ, IL-10), apoptotic pathway (bcl-2, bcl-xL), PI3K/Akt pathway, MAPKs pathway, JAK2/STAT5, NF-κB pathway, and the inflammasome. In this review, we will summarize the current knowledge on the effects of ginseng in the immune responses during the infections and its bioactivities on the prevention of infectious diseases as well as its underlying mechanisms. Moreover, the therapeutic potential of ginseng as an anti-bacterial and anti-viral medication and vaccine adjuvant will be discussed as well.
... Since then, H pylori infection has been investigated with regards to a potential relationship with halitosis in the past 20 years in many studies, and inconsistent results from case reports, epidemiological studies, randomized controlled trials, and quasirandomized controlled trials have been reported. [7,[11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29] For example, data from Ierardi et al [13] showed that H pylori eradication could resolve the symptom of halitosis. Serin et al [19] showed that halitosis was a frequent and treatable symptom of H pylori-positive nonulcer dyspepsia and suggested an H pylori eradication therapy for those patients with halitosis. ...
Background:
Halitosis is used to describe any disagreeable odor of expired air regardless of its origin. Numerous trials published have investigated the relation between Helicobacter pylori (H pylori) infection and halitosis, and even some regimes of H pylori eradication have been prescribed to those patients with halitosis in the clinic. We conducted a meta-analysis to define the correlation between H pylori infection and halitosis.
Objectives:
To evaluate whether there is a real correlation between H pylori infection and halitosis, and whether H pylori eradication therapy will help relieve halitosis.
Methods:
We searched several electronic databases (The Cochrane Library, MEDLINE, EMBASE, PubMed, Web of Science, and Wanfangdata) up to December 2015. Studies published in English and Chinese were considered in this review. After a final set of studies was identified, the list of references reported in the included reports was reviewed to identify additional studies. Screening of titles and abstracts, data extraction and quality assessment was undertaken independently and in duplicate. All analyses were done using Review Manager 5.2 software.
Results:
A total of 115 articles were identified, 21 of which met the inclusion criteria and presented data that could be used in the analysis. The results showed that the OR of H pylori infection in the stomach between halitosis-positive patients and halitosis-negative patients was 4.03 (95% CI: 1.41-11.50; P = 0.009). The OR of halitosis between H pylori-positive patients and H pylori-negative patients was 2.85 (95% CI: 1.40-5.83; P = 0.004); The RR of halitosis after successful H pylori eradication in those H pylori-infected halitosis-positive patients was 0.17 (95% CI: 0.08-0.39; P <0.0001), compared with those patients without successful H pylori eradication. And the RR of halitosis before successful H pylori eradication therapy was 4.78 (95% CI: 1.45-15.80; P = 0.01), compared with after successful H pylori eradication therapy.
Conclusions:
There is clear evidence that H pylori infection correlates with halitosis. H pylori infection might be important in the pathophysiological mechanism of halitosis, and H pylori eradication therapy may be helpful in those patients with refractory halitosis.
... The resolution rate among the 15 patients receiving Korea red ginseng along with H. pylori eradication regimen, 93% turned free of halitosis. Interestingly among 20 H. pylori negative patients, also treated with Korea red ginseng, 13 patients became free of halitosis (Lee et al., 2009). ...
Halitosis or mouth malodor is a known problem for many years. The knowledge regarding the possible association of Helicobacter pylori infection is quite limited in literature. A comparative quasi experimental clinical trial study was conducted on 17 H. pylori positive patients and 16 H. pylori negative patients who were complaining of halitosis. All patients, regardless of H. pylori infection, received two-week's treatment of clarithromycin (500 mg BID) and amoxicillin (1 g BID) along with three month's long omeprazole; a pretested questionnaire was used for self-reported measurement of halitosis. Halitosis was assessed after three and six months of continued treatment. Patients were also checked for eradication of H. pylori infection. Mean estimated time for improvement was 74.4 days for H. pylori negative group compared to 46.8 days for H. pylori positive group. 12 out of 17 patients in this group improved during the treatment time, while only 4 of the 16 patients in H. pylori negative group improved (P<0.01). The relative risks of halitosis resolution in H. pylori positive group over H. pylori negative group were 2.8 and 3.3, respectively after 3 and 6 months. H. pylori eradication can resolve halitosis in majority of patients without an oral pathology causing halitosis. H. pylori may be a probable rather than a possible cause of halitosis.
... Loesche et al [110] reported that 74% of the bacteria cultured from the lingual dorsum were Veillonella parvula, Actinomyces odontolyticus, Streptococcus intermedius and Clostridium innocuum. Table 5 shows the different research groups that attempted to relate halitosis to H. pylori [111][112][113][114][115][116][117][118][119][120][121][122][123] . The first were Tiomny et al [111] , who in 1992 in Israel studied 6 patients with halitosis, 5 of whom were H. pylori-positive. ...
Helicobacter pylori (H. pylori) has been found in the oral cavity and stomach, and its infection is one of the most frequent worldwide. We reviewed the literature and conducted a Topic Highlight, which identified studies reporting an association between H. pylori-infection in the oral cavity and H. pylori-positive stomach bacterium. This work was designed to determine whether H. pylori is the etiologic agent in periodontal disease, recurrent aphthous stomatitis (RAS), squamous cell carcinoma, burning and halitosis. Record selection focused on the highest quality studies and meta-analyses. We selected 48 articles reporting on the association between saliva and plaque and H. pylori-infection. In order to assess periodontal disease data, we included 12 clinical trials and 1 meta-analysis. We evaluated 13 published articles that addressed the potential association with RAS, and 6 with squamous cell carcinoma. Fourteen publications focused on our questions on burning and halitosis. There is a close relation between H. pylori infection in the oral cavity and the stomach. The mouth is the first extra-gastric reservoir. Regarding the role of H. pylori in the etiology of squamous cell carcinoma, no evidence is still available.
... The therapy used to treat gastric ulcers includes control of acid secretion as well as the inflammation reversal to the mucosa. Korea red ginseng can assist in the eradication of Helicobacter pylori and alleviate H. pylori-induced halitosis [9] . A recent pharmacological investigation reports the antihistamine and anticytokine releasing effects of ginsenoside Re isolated from the berries of Panax ginseng [7]. ...
The protective effect of ginsenoside Re, isolated from ginseng berry, against acute gastric mucosal lesions was examined in rats with a single intraperitoneal injection of compound 48/80 (C48/80). Ginsenoside Re (20 mg/kg or 100 mg/kg) was orally administered 0.5 h prior to C48/80 treatment. Ginsenoside Re dose-dependently prevented gastric mucosal lesion development 3 h after C48/80 treatment. Increases in the activities of myeloperoxidase (MPO; an index of neutrophil infiltration) and xanthine oxidase (XO) and the content of thiobarbituric acid reactive substances (TBARS; an index of lipid peroxidation) and decreases in the contents of hexosamine (a marker of gastric mucus) and adherent mucus, which occurred in gastric mucosal tissues after C48/80 treatment, were significantly attenuated by ginsenoside Re. The elevation of Bax expression and the decrease in Bcl2 expression after C48/80 treatment were also attenuated by ginsenoside Re. Ginsenoside Re significantly attenuated all these changes 3 h after C48/80 treatment. These results indicate that orally administered ginsenoside Re protects against C48/80-induced acute gastric mucosal lesions in rats, possibly through its stimulatory action on gastric mucus synthesis and secretion, its inhibitory action on neutrophil infiltration, and enhanced lipid peroxidation in the gastric mucosal tissue.
... Diminished halitosis after eradication suggested a causal link between H. pylori infection and halitosis. 98,99 These studies indicate that H. pylori eradication may reduce the production of substances responsible for bad breath. Besides, H. pylori is a common finding in cases of vocal fold minimal lesions, and thus eradication should be considered for vocal fold polyps, vocal fold nodules, posterior granulomas, and right vocal fold nodules. ...
Since the discovery of Helicobacter pylori in 1982, the development of several treatment guidelines has allowed a consensus on the indications for H. pylori eradication. Beyond these currently accepted indications, including various upper gastrointestinal disorders and extragastric diseases, a significant amount of new information regarding H. pylori eradication is emerging. Certain types of acute gastritis, such as nodular gastritis, hypertrophic gastritis, Ménétrier's disease, hemorrhagic gastritis, and granulomatous gastritis are reversible after H. pylori eradication. Further, for chronic gastritis, closed-type atrophic gastritis and complete-type intestinal metaplasia appear to be more reversible after H. pylori eradication than open-type atrophic gastritis and incomplete-type intestinal metaplasia. Eradication can also be considered in subjects younger than 40 years who have a family history of gastric cancer and in subjects with long-term medications that might lead to bleeding (antiplatelet agents) or atrophy (proton pump inhibitors). Emerging evidence indicates that H. pylori eradication could be an effective treatment for some extragastric diseases that are unresponsive to conventional therapy. In such conditions, routine screening for eradication of H. pylori has not previously been recommended; a "test-and-treat" approach is suggested in the aforementioned situations. Given that H. pylori eradication is effective when the gastritis is reversible, future indications should be expanded to include acute gastric lesions that show marked improvement upon H. pylori eradication rather than just focusing on chronic gastric lesions. Future indications for H. pylori eradication should focus more on reversible lesions before preneoplastic conditions develop.
... The patients received a 1-week triple therapy for the eradication of H. pylori and then received either placebo Nutrigenomics for H. pylori infection capsules that were composed of flour, in the case of the placebo group or Korean red ginseng capsules in case of the treatment group, which were randomized and administered for 10 weeks. As a result, the Korean red ginseng group showed a significant improvement in neutrophil infiltrations (P = 0.008), CAG (P < 0.05), and even intestinal metaplasia (P = 0.005) 22,23 Using an affymetrix biochip assay (pooled samples according to group, repeated thrice), we analyzed biomarkers to predict responders and non-responders; that is, four potential biomarkers including HSP70, IGFBP, metallotheionine-1 and defensin-a ( Figure 5). ...
While dietary habits or nutritional intake continue to rank as significant factors influencing the incidence of cancer, there have been considerable scientific uncertainties about who will benefit, but who about will not benefit from nutrition. This might be due to inadequate knowledge about an individual's genetic background, the cumulative effect of nutrients on genetic expression profiles, ambiguous clinical differences between beneficiaries and non-beneficiaries and the lack of information about active protein induction. During the past 200 years of nutrition research, we have experienced revolutionary advances in both chemistry and genomics. According to the high expectations for tailored medicine, a nutrigenomic approach harboring tremendous potential to change the future of dietary guideline and personal recommendations will provide an essential basis for personalized dietary recommendations to prevent common multifactorial diseases decades before their overt clinical manifestation. In the current review, we introduce our efforts to discover Helicobacter pylori (H. pylori)-related disease biomarkers applicable for diagnostic, predictive and therapeutic purposes using several kinds of technology. For instance, based on publications showing the in vitro and in vivo efficacy of Korean red ginseng on mitigating H. pylori-associated gastric atrophy, a nutrigenomic approach allows us to confirm that Korean red ginseng prevents H. pylori-associated gastric cancer in predictable ways.
... Recently we could add more evidence that Korea red ginseng was very efficient in eliminating troublesome halitosis. Since halitosis is closely associated with erosive changes in the stomach [49], the halitosis improving actions of Korea red ginseng were dependent on either direct suppressive action of Korea red ginseng on enzyme responsible for generating volatile sulfure compounds, that is, cystathionine γ-lyase and cystathionine β-synthase, or cytorestorative actions [50]. ...
Key molecular players that link inflammation to carcinogenesis are prostaglandins, cytokines, nuclear factor-kappaB (NF-kappaB), chemokines, angiogenic growth factors, and free radicals, all of which lead to increased mutations and altered functions of important enzymes and proteins, for example, activation of oncogenic products and/or inhibition of tumor suppressor proteins, in inflamed tissues, thus contributing to multi-stage carcinogenesis process. Interpreted reversely, the identification of the molecular mechanisms by which chronic inflammation increases cancer risk or optimal intervention of targeted drugs or agents during the inflammation-associated carcinogenic process could be a necessary basis for developing new strategy of cancer prevention at many sites. In this review, we discuss the possibilities for cancer prevention by controlling inflammation process in Helicobacter pylori (H. pylori)-associated inflamed stomach with Korea red ginseng. Korea red ginseng is a good example of a natural herb that has ubiquitous properties that are conductive to stop inflammatory carcinogenesis that is un wanted outcome of H. pylori infection, rendering rejuvenation of chronic atrophic gastritis.
Nowadays, natural medicines like honey, clove, miswak, and propolis are a part of dental treatment due to their reduced toxicity, wide availability, and cost effectiveness. This chapter gives an insight to the reader about the potential use of natural products in current dentistry. They are in many forms and include chewing sticks, oils, herbal extracts, minerals, animal products (e.g., honey), herbs, herbal materials, herbal preparations, and finished herbal products that contain parts of plants or other plant materials as active ingredients. Natural medicines hold huge benefits as adjunctive therapeutic uses in dentistry. Use of these techniques with suitable dosage would benefit the general population by preventing various dental problems.
Aim: To assess the correlation between bad breath (also known as halitosis) and Helicobacter pylori (H. pylori) infection. Methods: A total of 236 patients or healthy volunteers were randomly seleted. Based on the presence of halitosis or not, the subjects were divided into a halitosis and a no-halitosis group. All patients underwent 14C-urea breath test, and according to the presence of H. pylori infection or not, the subjects were divided into a H. pylori infection group and a no-infection group. The incidence of halitosis in the H. pylori infection and no-infection groups was compared, and the correlation of H. pylori infection with halitosis was analyzed. Results: Of the 236 subjects included, 109 (46.19%) had halitosis, including 74 (67.89%) who were positive for H. pylori infection, and 127 (53.81%) had no halitosis, including 36 (28.35%) who were positive for H. pylori infection. The rate of H. pylori infection between the two groups was statistically significant (χ2 = 31.53, P < 0.05), and there was a significant correlation between halitosis and H. pylori infection (r = 0.33). There were 135 (57.20%) H. pylori positive cases, of which 93 (68.89%) had halitosis. There were 101 (42.80%) H. pylori negative cases, of which only 4 (3.96%) had halitosis. The rate of halitosis between the two groups was statistically significant (χ2 = 52.57, P < 0.05), and there was a significant correlation between H. pylori infection and halitosis (r = 0. 61). Conclusion: In people with halitosis, many have H. pylori infection, and in H. pylori positive people, many have halitosis. There is a close correlation between H. pylori infection and halitosis.
"War on cancer" was declared through the National Cancer Act by President Richard Nixon in 1971, but cancer statistics from the American Cancer Society and other sources indicated the failure of this war, suggesting instead focus on the message that a "prevention strategy" might be much more effective than cancer treatment. While cancer statistics notoriously showed sharp increases in incidence as well as in mortality concurrent with economic growth in Asia, fortunately Asian countries benefit from plentiful resources of natural compounds, which can prevent cancer. Just like cancer chemotherapeutics targeted to kill cancer cells in Western countries, natural agents activating molecular mechanisms for cancer prevention, reversion of premalignant tumors, and even ablation of cancer stem cells, are very abundant in Asia. Currently, these natural agents are under very active investigations targeting the hallmarks of cancer prevention, including selective induction of apoptosis in cancer cells, suppression of growth factors or their signaling, suppression of cell proliferation and of cancer-promoting angiogenesis, induction of mesenchymal-epithelial transition, and disruption of the tumor microenvironment, developing promising cancer preventive agents. However, Asia is the most populous continent in the world and some Asian countries do not have the resources to implement cancer screening programs for early detection or treatment. In addition, despite the excellent cancer preventive screening strategies in some Asian countries, well-designed clinical trials for cancer prevention are somewhat delayed compared to Western countries. In this review article, several phytochemicals/phytoceuticals produced and studied in different Asian countries will be introduced, including Korean red ginseng (pride of Korea), curcumin (Indian spice for life), black or green tea (popular in Japan/Sri Lanka), genistein from tofu (famous Chinese food), diallylsulfide or S-allylcysteine (garlic, popularly consumed as a food ingredient in many Asian countries), capsaicin, 6-gingerol, flavopiridol, and silymarin (abundant in various Asian foods). Whereas in Western countries cancer chemotherapeutics involve strategies not only to block the growth of the primary tumor, but also to inhibit its progression to metastatic disease, the endless pursuit of effective agents for cancer prevention may be a unique and featured strategy in Asia. More active efforts for clinical application of these principles should be supported.
Background:
Ginseng (the roots of Panax ginseng Meyer) is a well-known traditional Oriental medicine and is now widely used as a health food. It contains several types of ginsenosides, which are considered the major active medicinal components of ginseng. It has recently been reported that the qualitative and quantitative properties of ginsenosides found in ginseng may differ, depending on cultivation regions, ages, species, and so on. Therefore, it is necessary to study these variations with respect to cultivation ages and regions.
Methods:
In this study, 3-6-yr-old roots of P. ginseng were collected from three different cultivation regions. The contents of five ginsenosides (Rb1, Rd, Rc, Re, and Rgl) were measured by rapid resolution liquid chromatography coupled with quadruple-time-of-flight mass spectrometry. The Kruskal-Wallis Rank sum test and multiple t test were used for comparative analysis of the data to evaluate the dynamic changes in the accumulation of these ginsenosides affected by cultivation regions and ages.
Results:
The content and composition of ginsenosides varied significantly among specimens collected from different cultivation regions and having different cultivation ages. For all samples, the content of Rg1 and Re ginsenosides increases with age and this rate of increase is different for each sample. The contents of Rb1, Rc, and Rd varied with cultivation ages in samples from different cultivation regions; especially, Rb1 from a 6-yr-old root showed approximately twofold variation among the samples from three cultivation regions. Furthermore, the content of Rb1 highly correlated with that of Rd (r = 0.89 across all locations and ages).
Conclusion:
In our study, only the contents of ginsenosides Rg1 and Re were affected by the root age. Ginsenosides Rb1, Rc, and Rd varied widely with ages in samples from different cultivation regions.
Halitosis is a generally accepted marker of diseases in the oral cavity and of systemic and gastrointestinal disorders. Based on these authors' previous findings (that (1) there is a close association between H. pylori infection and halitosis; (2) Korea red ginseng may suppress the colonization of H. pylori, fight H. pylori-induced cytotoxicity, and impose significant anti-inflammatory actions in patients with chronic gastritis; and (3) H. pylori infection is linked with the generation of significant levels of volatile sulfur compounds (VSCs), and the levels of VSCs correlate significantly with H. pylori-associated mucosal damages), in the current study, the authors documented the molecular mechanisms of Korea red ginseng's efficacy in ameliorating halitosis. When the RAW 264.7 cells were treated with the releasing compound NaHS, the mRNA expression of cystathionine -lyase (CSE), IL-6, COX-2, and iNOS were more significantly induced compared with the vehicle-treated group. The cytoskeletal components of ezrin's and moesin's mRNA expressions were elevated by NaHS treatment accompanied by the activation of MAPK, p38, and ERK. Korea red ginseng pretreatment reduced both the NaHS-induced CSE expression and the proinflammatory genes (e.g., IL-6, COX-2, and iNOS) in a concentration-dependent manner. The ERM expression and the phosphorylation of p38 were also significantly reduced by Korea-red-ginseng pretreatment. Overall, Korea red ginseng pretreatment imposed significant anti-inflammatory effects through the downregulation of the NaHS-triggered proinflammatory gene expression, CSE, and ERM mRNA expression. Korea red ginseng could thus be said to be a key remedy of halitosis and to be effective in relieving gastric inflammation.
Halitosis is a symptom and not a diagnosis. Rather, the topic represents a spectrum of disorders, including intra-oral, otorhinolaryngological, metabolic, systemic, pulmonary, psychological and neurological conditions. Halitosis may be the third most common trigger for patients to seek dental care and can cause significant impact on patient quality of life. About 10% of all genuine halitosis cases are attributed to extra-oral processes. Some authorities have reported that the nasal cavity and the oropharynx are the most common sites of origin of extra-oral halitosis. However, recent evidence appears to suggest that blood borne halitosis may be the most common subtype of extra-oral halitosis. Tangerman and Winkel report that dimethyl sulphide was the main volatile implicated in extra-oral blood borne halitosis. They proposed a hitherto unknown metabolic condition by way of explanation for this finding, resulting in systemic presence of dimethyl sulphide in blood and alveolar breath. This paper reviews the knowledge base regarding the behaviour of dimethyl sulphide in physiological systems and those disorders in which blood borne halitosis secondary to dimethylsulphidemia is thought to have an aetiopathological role.
There is disagreement about a possible relationship between Helicobacter pylori (H. pylori) infection and objective halitosis, as established by volatile sulfur compounds (VSCs) in the breath. Many studies related to H. pylori used self-reported halitosis, a subjective and unreliable method to detect halitosis. In this study a possible relation between H. pylori and halitosis was evaluated, using an objective method (gas chromatography, GC) to detect the VSCs, responsible for the halitosis. The levels of the VSCs hydrogen sulfide (H(2)S), methyl mercaptan (MM) and dimethyl sulfide (DMS) were measured in mouth breath and in stomach air of 11 H. pylori positive patients and of 38 H. pylori negative patients, all with gastric pathology. Halitosis was also established by organoleptic scoring (OLS) of mouth-breath. The levels of H(2)S, MM and DMS in the mouth-breath and stomach air of the H. pylori positive patients did not differ significantly from those of the H. pylori negative patients. OLS of the mouth-breath resulted in 9 patients with halitosis, 1 out of the H. pylori positive group and 8 out of the H. pylori negative group, which is not statistically different. The concentrations of the VSCs in stomach air were in nearly all cases below the thresholds of objectionability of the various VSCs, indicating that halitosis does not originate in the stomach. The patients with gastric pathology were also compared with control patients without gastric pathology and with normal volunteers. No significant differences in VSCs in mouth breath were observed between these groups. Thus, in this study no association between halitosis and H. pylori infection was found. Halitosis, as established by GC and OLS, nearly always originates within the oral cavity and seldom or never within the stomach.
The present article reviews the current knowledge of halitosis with particular emphasis upon the interplay of diet and disease of the gastrointestinal tract upon oral malodour.
Transient-altered breath smell usually reflects the effects of foodstuffs, whereas longstanding halitosis is almost always because of oral disease such as gingivitis or periodontitis. There is, however, increasing evidence that upper gastrointestinal tract disease may give rise to halitosis and that extracts of foodstuffs may be future therapeutic agents for the treatment of halitosis derived from the mouth or upper gastrointestinal tract.
There is some interplay between the halitosis and the gastrointestinal tract, and it is possible that the therapy of halitosis may be aided by investigations of the effects of foodstuffs upon bacteria that give rise to volatile sulphur compounds.
With the aim of investigating a possible relationship between "objective" halitosis (established by sulfide levels in the breath) and Helicobacter pylori, we performed a study in 58 dyspeptic patients reported to suffer from "bad breath." Furthermore, we evaluated the effects on halitosis of eradication therapy (only for H. pylori-positive patients) and chlorhexidine antiseptic mouth rinses (in all patients). Sulfide compound assay indicated objective halitosis in 52/58 patients, 30 of whom were positive and 22 negative for H. pylori. In 19/30 eradication by double therapy provoked a decrease to below the cutoff value of sulfide levels in 15. In the other 11 of the 30 subjects, in whom H. pylori positivity persisted, halitosis parameters did not change. Chlorexidine reduced sulfides to below the cutoff value in 16/22 H. pylori-negative patients, but did not provoke any change in the 11 unsuccessfully treated H. pylori-positive subjects. In these, objective halitosis disappeared only after a successful eradication by triple therapy (9/11). Our results show a possible association between halitosis and H. pylori since bacterial eradication may resolve the symptom. Antiseptic mouthwashes may be effective only in absence of H. pylori, when halitosis may be due to oral putrefactive microbial activity. In a small number of subjects the cause and treatment of halitosis need to be clarified.
The aims of this study were to identify hydrogen sulfide (H2S)-producing bacteria among tongue biofilm microflora and to investigate the relationship between bacterial flora and H2S levels in mouth air. Oral malodour levels in 10 subjects (age 21-56 years) were assessed by gas chromatography, and Breathtron and organoleptic scores. Based on these assessments, subjects were divided into two groups: an odour group and a no/low odour group. Tongue coatings were sampled and spread onto Fastidious Anaerobe Agar plates containing 0.05% cysteine, 0.12% glutathione and 0.02% lead acetate, and were then incubated anaerobically at 37 degrees C for 2 weeks. Bacteria forming black or grey colonies were selected as H2S-producing phenotypes. The numbers of total bacteria (P<0.005) and H2S-producing bacteria (P<0.05) in the odour group were significantly larger than those in the no/low odour group. Bacteria forming black or grey colonies (126 isolates from the odour group; 242 isolates from the no/low odour group) were subcultured, confirmed as producing H2S and identified according to 16S rRNA gene sequencing. Species of Veillonella (38.1% in odour group; 46.3% in no/low odour group), Actinomyces (25.4%; 17.7%) and Prevotella (10.3%; 7.8%) were the predominant H2S-producing bacteria in both the odour and no/low odour groups. These results suggest that an increase in the number of H2S-producing bacteria in the tongue biofilm is responsible for oral malodour, although the bacterial composition of tongue biofilm was similar between the two groups.
Helicobacter pylori is a curved microaerophilic Gram-negative bacterium considered as a risk factor for gastric cancer. The aim of this study was to find an association between burning sensations, acid taste, halitosis, and lingual hyperplasia with the effect of H. pylori on the mouth.
A total of 124 subjects with different gastric diseases were studied: 46 patients with burning, halitosis and lingual dorsum hyperplasia and 78 patients with other diseases.
The detection of H. pylori in the oral cavity by histopathologic diagnosis and molecular biology was confirmed in 40/46 (87%) patients with burning, halitosis, and lingual hyperplasia, and in 2/78 (2.6%) subjects with other diseases. Chi2: 91.26 (p < .001) Mantel-Haenszel.
This trial showed an association between H. pylori and burning, halitosis, and lingual hyperplasia, and further considered this bacterium a risk factor for gastric infection.
Oral malodour (halitosis) is common; most people have some element of transient unpleasant oral odour at some time.1 w1 In the developed world, 8-50% of people perceive that they have persistent recurrent episodes of oral malodour. This article provides a succinct review of oral malodour relevant to medical practitioners.
Oral malodour is common and can affect people of all ages. When severe or longstanding, it may decrease self confidence and social interactions.w2
Oral malodour on awakening is common and generally not regarded as halitosis. Longstanding oral malodour is usually caused by oral, or sometimes nasopharyngeal, disease (box 1). The most likely cause of oral malodour is the accumulation of food debris and dental bacterial plaque on the teeth and tongue, resulting from poor oral hygiene and resultant gingival (gingivitis) and periodontal (gingivitis/periodontitis) inflammation. Although most types of gingivitis and periodontitis can give rise to malodour, acute necrotising ulcerative gingivitis (Vincent's disease, trench mouth) causes the most notable halitosis. Adult periodontitis, characterised by gradual plaque related loss of periodontal attachment, can cause variable degrees of oral malodour.2 Aggressive periodontitis, typified by rapid loss of periodontal bone and resultant tooth mobility, can cause intense oral malodour.
Lack of oral cleansing because of xerostomia (dryness of the mouth) also has the potential to cause or enhance malodour,w3 and some evidence indicates that wearing dentures may sometimes cause oral malodour, possibly by virtue of increased tongue coat deposits.w4
Mild transient oral malodour often arises after sleep and is sometimes termed “morning halitosis.” This may be more likely in people with nasal obstruction—for example, due to upper respiratory tract infection—or when people sleep in a hot, dry atmosphere. Transient oral malodour can also arise after someone has eaten volatile foods such as garlic, onions, or spices (durian is reputed to …
The aim of this study was to investigate the incidence and long-term outcome of halitosis before and after eradication therapy in patients with functional dyspepsia and Helicobacter pylori infection.
Halitosis and dyspepsia-related symptoms were investigated by way of a questionnaire. Only patients with functional dyspepsia, H. pylori infection and no histological evidence of atrophy were included in the study. A total of 18 patients fulfilled these criteria and completed the study. Four to six weeks after the end of eradication treatment, endoscopy or [(13)C] breath test was performed to check for H. pylori in the gastric mucosa. Halitosis and dyspeptic symptoms were re-evaluated during and at the end of follow-up.
H. pylori infection was eradicated in all patients, in the 14/18 patients (77.8%) with triple drug therapy, and the 4/18 patients (22.2%) with quadruple drug therapy. During the follow-up period (mean 55.8 +/- 21.3 months (range 6-108 months)) resolution of halitosis was observed in 16/18 patients (88.9%), while 2 patients (11.1%) (p < 0.001) continued to present with halitosis. Also, eradication therapy resulted in statistically significant relief of all dyspeptic symptoms, except bloating.
Eradication of H. pylori in patients with functional dyspepsia and halitosis results in sustained resolution of halitosis during long-term follow-up in the majority of cases. This finding supports the existence of a link between H. pylori infection and halitosis and suggests that H. pylori eradication might be considered in patients with halitosis.
The exact pathophysiological mechanism of halitosis is not clear, and in many patients the etiology is an enigma. We followed three couples in which one member or both had halitosis. All the subjects had evidence of Helicobacter pylori infection. All received a treatment course of colloidal bismuth subcitrate four times a day and 250 mg metronidazole three times a day. There was impressive improvement in their symptoms, the halitosis disappearing along with eradication of the organism. We call the attention of physicians to the possible connection between halitosis, H. pylori infection, and familial occurrence. Further studies to confirm this surprising association are in order.
The relationship between gastrointestinal conditions and halitosis is discussed. Few reports have suggested that gastrointestinal diseases may cause halitosis. H. pylori infection, which causes gastric ulcers, is considered as a possible cause for halitosis. Intensity of malodour of mouth air was found to be higher in H. pylori-positive patients than in negative patients. The levels of hydrogen sulphide and dimethyl sulphide in mouth air were also significantly higher in the positive patients than in the negative patients (P<0.05). When odour strength in exhaled breath was compared between the two groups, no significant difference was found. Hence, H. pylori infection might not cause a systemic condition producing breath odour. Although there were no significant differences in periodontal parameters or tongue coating between the positive and negative groups, H. pylori may be a frequent contributor to the production of malodour even though its role had not been suspected before. Further study would be necessary to clarify the reason for the increase of volatile sulphur compounds (VSCs) level in H. pylori infection.
This review deals with the different forms of halitosis. Halitosis can be subdivided according to its original location. At present, halitosis of oral origin is quite well understood and some excellent reviews have already appeared in the literature. Special attention is given here to extra-oral halitosis. Extra-oral halitosis can be subdivided into: halitosis from the upper respiratory tract including the nose; halitosis from the lower respiratory tract; blood-borne halitosis. In blood-borne halitosis, malodourant compounds in the bloodstream are carried to the lungs where they volatilise and enter the breath. Potential sources of blood-borne halitosis are some systemic diseases, metabolic disorders, medication and certain foods. The methods of analysis of halitosis are critically reviewed. Attention is also given to odour characterisation of various odourants.
BACKGROUND: The aims of this study were to investigate the frequency of halitosis before and after eradication therapy and to determine whether halitosis is a valid indication for eradication therapy in patients with Helicobacter pylori (H. pylori)-positive non-ulcer dyspepsia. METHODS: Dyspepsia, related symptoms, and halitosis were investigated by way of a questionnaire. Only H. pylori-positive patients who showed no organic lesions on endoscopic examination and no atrophy histopathologically were included. A total of 148 patients fulfilled the above criteria and completed the study. Four weeks after the end of eradication treatment, the symptoms were re-evaluated and repeat endoscopy was done to check for H. pylori in the gastric mucosa. Results: H. pylori eradication was successful in 109 patients (73.6%). Prior to treatment, bloating was the most frequent symptom (74.3%), followed by diurnal pain (62.2%) and halitosis (61.5%). The most successfully resolved symptoms in the group as a whole, regardless of eradication status, were halitosis, diurnal pain, and hunger-like pain, respectively. In the patients with confirmed H. pylori eradication, the most successfully resolved symptoms were halitosis and hunger-like pain, respectively. CONCLUSION: Halitosis is a frequent, but treatable, symptom of H. pylori-positive non-ulcer dyspepsia and may be a valid indication for eradication therapy.
Haemorrhagic shock (60 min) in the anaesthetized rat resulted in a prolonged fall in the mean arterial blood pressure (MAP) and heart rate (HR).
Pre-treatment (30 min before shock) or post-treatment (60 min after shock) with inhibitors of cystathionine γ lyase (CSE; converts cysteine into hydrogen sulphide (H2S)), dl-propargylglycine or β-cyanoalanine (50 mg kg−1, i.v.), or glibenclamide (40 mg kg−1, i.p.), produced a rapid, partial restoration in MAP and HR. Neither saline nor DMSO affected MAP or HR.
Plasma H2S concentration was elevated 60 min after blood withdrawal (37.5±1.3 μm, n=18 c.f. 28.9±1.4 μm, n=15, P<0.05).
The conversion of cysteine to H2S by liver (but not kidney) homogenates prepared from animals killed 60 min after withdrawal of blood was significantly increased (52.1±1.6 c.f. 39.8±4.1 nmol mg protein−1, n=8, P<0.05), as was liver CSE mRNA (2.7 ×). Both PAG (IC50, 55.0±3.2 μm) and BCA (IC50, 6.5±1.2 μm) inhibited liver H2S synthesizing activity in vitro.
Pre-treatment of animals with PAG or BCA (50 mg kg−1, i.p.) but not glibenclamide (40 mg kg−1, i.p., KATP channel inhibitor) abolished the rise in plasma H2S in animals exposed to 60 min haemorrhagic shock and prevented the augmented biosynthesis of H2S from cysteine in liver.
These results demonstrate that H2S plays a role in haemorrhagic shock in the rat. CSE inhibitors may provide a novel approach to the treatment of haemorrhagic shock.
British Journal of Pharmacology (2004) 143, 881–889. doi:10.1038/sj.bjp.0706014
Halitosis, or bad breath, is caused by mainly volatile sulfur compounds (VSC) as a result of bacterial breakdown of protein and can be quantitatively and qualitatively measured in the expired oral breath. In eight to ninety percent of cases, halitosis originates in the mouth due to inadequate plaque control, periodontal disease, dry mouth, faulty restorations, and in particular due to excessive bacterial growth on the posterior third of the dorsal surface of the tongue. In the remaining ten to twenty percent of cases, bad breath is caused by systemic disorders such as hepatic, pancreatic and nephritic insufficiencies, trimethylaminuria, upper and lower respiratory tract infection, medication and cases where gastric content may generate oral malodour. The methods of detecting or diagnosing halitosis are organoleptic or human sense of smell, sulfide monitoring and gas chromatography. All of these methods have limitations and disadvantages. A more accurate, analytical system which will be able to precisely detect the volatile compounds in the expired air and correlate the results to a specific cause is not yet available. Dental professionals require a good knowledge on the subject of bad breath in order to feel secure about counseling and managing patients suffering from this condition. The management of halitosis involves maintenance of plaque control, elimination of active periodontal disease and cleaning the tongue on a routine basis. Oral rinsing with a mouthwash could be indicated in some instances, as a temporary measure.
Helicobacter pylori has been known to provoke gastric inflammation, ulceration, and DNA damage, based on which WHO defined H. pylori as a class I carcinogen. Although ginseng, the root of Panax ginseng C.A. Meyer, has been reported to possess antiadhesion or antimicrobial activity against H. pylori, in this study, we examined the protective effect of red ginseng extracts (RGE) against H. pylori-induced cytotoxicity and DNA damage. RGE significantly attenuated both H. pylori-induced DNA damage assessed by comet assay and apoptosis measured by DNA fragmentation.
Inactivation of ERK1/2 signaling and attenuation of caspase-3 activation and PARP cleavage were revealed with RGE against H. pylori infection. RGE decreased H. pylori-stimulated IL-8 gene expression, which resulted from the transcriptional regression of NF-κB. In conclusion, RGE showed significant gastroprotective effects against H. pylori-associated gastric mucosal cell damage, suggesting that red ginseng could be used as a medicinal phytonutrient against H. pylori infection.
Quality of life (QOL) in patients with functional dyspepsia in South Korea has never been studied, mostly due to the lack of a psychometrically validated disease-specific instrument for measuring the QOL. The aim of the present study was to develop and validate a QOL scale for patients with functional dyspepsia.
A Functional Dyspepsia-Related QOL (FD-QOL) scale was developed and validated as follows: item generation, pilot test, and psychometric test. Patients with functional dyspepsia (n = 220) were recruited from seven university hospitals. The participants were asked to complete the preliminary item-generated FD-QOL, the Short Form-36 (SF-36), and the Index of Dyspepsia Symptoms-Korean (IDS-K). The data were analyzed using factor analysis, correlation, anova, and Cronbach's alpha.
Twenty-three items were generated based upon content validity. Factor analysis extracted a four-factor solution, and two items were deleted because they were not loaded significantly on any factor. The FD-QOL was correlated with the SF-36 subscales, of which scores were differentiated according to the levels of dyspepsia symptoms. Cronbach's alpha of the FD-QOL was 0.94.
The FD-QOL scale is a rapid and easily applicable instrument with excellent psychometric properties of content, factorial, convergent, and known-groups validity, and internal consistency reliability in Korean patients with functional dyspepsia.
To assess the volatile sulfur compounds produced by three strains of Helicobacter pylori in broth cultures mixed with sulfur-containing amino acids.
Halitosis has been reported in H. pylori-positive patients, and volatile sulfur compounds such as hydrogen sulfide and methyl mercaptan are known to be responsible for inducing oral malodor. Whether H. pylori produces these volatile sulfur compounds has yet to be established.
Three strains of H. pylori (ATCC 43504, SS 1, DSM 4867) were cultured with 5 mM cysteine and methionine. After 72 hours of incubation, the headspace air was aspirated and injected directly into a gas chromatograph. The concentrations of hydrogen sulfide and methyl mercaptan were analyzed and compared between experimental and control cultures
In broth containing 5 mM cysteine, hydrogen sulfide was increased by ATCC 43504 (P < 0.01) and SS 1 (P < 0.05), while methyl mercaptan was elevated only by SS 1 (P < 0.05). In broth containing 5 mM methionine, methyl mercaptan increases were significant for SS 1 (P < 0.05) and DSM 4867 (P < 0.05). In broth containing 5 mM cysteine and 5 mM methionine, the concentration of hydrogen sulfide was higher than in controls for all three strains (P < 0.01); that of methyl mercaptan was higher only for SS 1 (P < 0.01). Cysteine addition to cultures containing methionine increased hydrogen sulfide and methyl mercaptan for ATCC 43504 (P < 0.05) and SS 1 (P < 0.05). Conversely, addition of methionine to cultures containing cysteine increased methyl mercaptan only for DSM 4867 (P < 0.01).
The production of volatile sulfur compounds by H. pylori is not only very complicated but also strain-specific. Nevertheless, H. pylori was shown to produce hydrogen sulfide and methyl mercaptan, which suggests that this microorganism can contribute to the development of halitosis.
Oral malodor or halitosis is any unpleasant odor emerging from the mouth that is detected by others. Many patients experience extreme discomfort and embarrassment and therefore seek help for this problem. Oral causes, such as poor oral hygiene, periodontal disease, tongue coating, food impaction, unclean dentures, faulty restorations, and dry mouth, are far more common than nonoral causes of malodor. Management may include simple measures such as scaling and root planing, instructions in oral hygiene, tongue cleaning, and mouth rinsing. This paper reviews the current knowledge, etiology, diagnosis, and possible treatment strategies for oral malodor. Emphasis is placed on the recognition of the dental hygienist as a specialist in aspects of patient care and instruction, which relate to the prevention and control of oral malodor.
Halitosis can be a crippling social problem, and standard dental treatments and mouthwashes often provide only temporary relief. The mouth is home to hundreds of bacterial species that produce several fetid substances as a result of protein degradation. Volatile sulfur compound (VSC)-producing bacteria colonizing the lingual dorsum have recently been implicated in the generation of halitosis. Detection of VSCs, such as methylmercaptan and hydrogen sulfite, via organoleptic and objective methods, can aid in the identification of their source. Following comprehensive evaluation for possible causes, most halitosis in patients seen in an ENT practice can be localized to the tongue. We review methods of diagnosis and treatment of oral malodor from the overgrowth of proteolytic, anaerobic, gram-negative bacteria on the crevices of the lingual dorsum. Bacteriologic analysis of biofilm and scraped specimens obtained from the lingual dorsum and other oral sites, primarily gingival pockets and tonsillar crypts, can identify VSC-producing bacteria. Porphyromonas, Prevotella, Actinobacillus, and Fusobacterium species are the most common organisms identified. Halitosis is an oral phenomenon, with almost no cases originating distal to the tonsils. Halitosis arising from the lingual dorsum secondary to overpopulated VSC-producing bacteria can be successfully managed with a combination of mechanical cleansing using tongue brushes or scrapes and chemical solutions containing essential oils, zinc chloride, and cetylpyridinium chloride.
Hydrogen sulfide (H(2)S) has been suggested as a novel gasomediator. We explored its unknown neuromodulatory role in human and guinea-pig colon.
We used immunohistochemistry to detect H(2)S-producing enzymes cystathionine gamma-lyase (CSE) and cystathionine beta-synthase (CBS) in enteric neurons, Ussing chambers to measure mucosal ion secretion, and neuroimaging with voltage- and Ca(++)-sensitive dyes to record H(2)S effects on guinea-pig and human enteric neurons.
More than 90% of guinea-pig and human submucous and myenteric neurons were colabeled for CSE and CBS. Myenteric interstitial cells of Cajal were CSE-immunoreactive. The exogenous H(2)S donor NaHS (0.2-2.5 mmol/L) concentration-dependently increased chloride secretion in human and guinea-pig submucosa/mucosa preparations, but not in the colonic epithelial cell line T84. The secretory response was reduced significantly by tetrodotoxin (0.5 micromol/L), capsaicin desensitization (10 micromol/L), and the transient receptor potentials vanilloid receptor 1 antagonist capsazepine (10 micromol/L). The endogenous H(2)S donor L-cysteine also induced secretion that was diminished significantly by capsaicin desensitization, the CBS inhibitor amino-oxyacetic acid, and the CSE inhibitor propargylglycine. NaHS increased spike discharge in 23% of guinea-pig and 36% of human submucous neurons, but had no effect on Ca(++) mobilization in cultured guinea-pig enteric neurons. This excitatory response was reduced significantly by capsaicin desensitization and capsazepine, but not by glibenclamide (10 micromol/L).
The presence of H(2)S-producing enzymes in human and guinea-pig enteric neurons, the excitatory action on enteric neurons, and the prosecretory effects of NaHS suggest H(2)S as a novel gut-signaling molecule. Its action mainly involves transient receptor potentials vanilloid receptor 1 receptors on extrinsic afferent terminals, which in turn activate enteric neurons.
Isolation of the gastric spiral bacterium Helicobacter pylori totally reversed the false dogma that the stomach was sterile. In addition to its causal role in peptic ulceration, the newly identified bacterium has now been implicated in other gastric and even extragastric diseases, including chronic atrophic gastritis, gastric MALT lymphoma, gastric cancer, functional dyspepsia, idiopathic thrombocytopenic purpura (ITP), iron deficiency anemia, chronic urticaria, ischemic heart disease, and others. The majority of the reports are anecdotal, epidemiologic, or eradication studies, but there are also relevant in vitro studies. ITP represents one disease showing a strong link with H pylori infection. There are also accumulating data on the role of H pylori infection in iron deficiency anemia and ischemic heart disease. In summary, the association between H pylori infection and other extragut diseases is still controversial but worthy of further investigation.
The purpose of this study was to evaluate the relationship between total salivary protein and VSC levels.
A patient group comprised 67 patients from the Fresh Breath Clinic of the Dental Hospital, Tokyo Medical and Dental University, with 18 healthy subjects as a control group. Gas chromatography was used to measure concentrations of VSCs in mouth air. After collecting resting saliva, flow rate, pH, and the amount of total protein in saliva were measured. Salivary protein patterns were analyzed by polyacrylamide gel electrophoresis (PAGE).
In the patient group, the amounts of total salivary protein were significantly correlated with CH3SH levels measured by GC, CH3SH/H2S ratio, and organoleptic score. In addition, a significant correlation between flow rate of salivary protein and CH3SH/H2S ratio and the higher levels of salivary proteins from PAGE analyses were found.
Total salivary protein was considered to be involved in the formation of oral malodor as one of the nutrient sources. The total salivary protein could be changed both quantitatively and qualitatively in subjects with malodor.
To develop and apply a detailed clinical protocol for screening and assessing subjects with a complaint of halitosis.
Cross-sectional.
Several methods were used to recruit subjects with a complaint of halitosis, including a newspaper advertisement. A definition of halitosis arising from within the oral cavity, which is not related to generalized chronic gingivitis, chronic periodontitis or pathology of the oral mucosa was used. An extensive list of exclusion criteria was applied at the initial visit. Eligible subjects were asked to follow strict instructions and complete a questionnaire prior to their second visit for data collection. The clinical examination consisted of an organoleptic assessment, Halimeter reading and periodontal examination.
The best method of recruiting subjects was advertising. Of 66 individuals recruited, four failed to attend the screening visit and 25 were excluded. The main reasons for exclusion were poor oral hygiene and existing periodontal disease. Thirty-seven completed the full protocol, resulting in identification of 18 with halitosis and 19 controls.
Application of the exclusion criteria resulted in significant attrition of eligible participants. Our results suggest that organoleptic assessment should be regarded as a useful standard for defining subjects with halitosis.
Our recent studies documented that red ginseng extract (RGE, isolates from steamed and dried Panax ginseng, C.A. Meyer) can inhibit Helicobacter pylori-induced mitogen-activated protein kinase (MAPK) signaling with repressing either nuclear factor (NF)-kappaB-DNA binding activity or releases of IL-8 and COX-2 in gastric epithelial cells (Dig Dis Sci 50:1218-1227, 2005). We extended the experiment to prove whether RGE influences 5-lipoxygenase (5-LOX) pathway, thereby suppressing the biosynthesis of 5(S)-HETE. The 5-LOX enzyme activities were measured by thin layer chromatography using (14)C-labeled arachidonic acid (AA) and quantified by reverse phase-high performance liquid chromatography in human gastric adenocarcinoma (AGS) cells cocultured with H pylori (ATCC 43504 strain) with or without pretreatment of RGE. Western blotting analyses for MAPK signaling and 5-LOX, reverse transcriptase polymerase chain reaction for interleukin-8, and electrophoretic mobility shift assay for NF-kappaB-DNA binding were done, respectively. H pylori infection increased exclusively 5-LOX enzyme activity and RGE inhibited H pylori-stimulated 5-LOX activity, resulting in suppression of 5(S)-HETE generations from AA. RGE inactivated c-jun phosphorylation and repressed redox-sensitive transcriptional activation, led to reduced expression of IL-8 and 5-LOX mRNA in gastric mucosal cells, of which action was very similar to known LOX inhibitor, 200 mumol of geraniin. RGE could be phytoceutical against H pylori infection-associated gastric inflammation through its LOX-inhibiting actions, inhibitory 5-LOX enzyme activity, and attenuating its expression.
Nitric oxide (NO) and carbon monoxide (CO) synthesized from L-arginine by NO synthase and from heme by heme oxygenase, respectively, are the well-known neurotransmitters and are also involved in the regulation of vascular tone. Recent studies suggest that hydrogen sulfide (H(2)S) is the third gaseous mediator in mammals. H(2)S is synthesized from L-cysteine by either cystathionine beta-synthase (CBS) or cystathionine gamma-lyase (CSE), both using pyridoxal 5'-phosphate (vitamin B(6)) as a cofactor. H(2)S stimulates ATP-sensitive potassium channels (K(ATP)) in the vascular smooth muscle cells, neurons, cardiomyocytes and pancreatic beta-cells. In addition, H(2)S may react with reactive oxygen and/or nitrogen species limiting their toxic effects but also, attenuating their physiological functions, like nitric oxide does. In contrast to NO and CO, H(2)S does not stimulate soluble guanylate cyclase. H(2)S is involved in the regulation of vascular tone, myocardial contractility, neurotransmission, and insulin secretion. H(2)S deficiency was observed in various animal models of arterial and pulmonary hypertension, Alzheimer's disease, gastric mucosal injury and liver cirrhosis. Exogenous H(2)S ameliorates myocardial dysfunction associated with the ischemia/reperfusion injury and reduces the damage of gastric mucosa induced by anti-inflammatory drugs. On the other hand, excessive production of H(2)S may contribute to the pathogenesis of inflammatory diseases, septic shock, cerebral stroke and mental retardation in patients with Down syndrome, and reduction of its production may be of potential therapeutic value in these states.
Hydrogen sulphide (H(2)S) is synthesized from L-cysteine via the action of cystathionine-gamma-lyase (CSE) and cystathionine-beta-synthase (CBS). We have earlier shown that H(2)S acts as a mediator of inflammation. However the mechanism remains unclear. In this study, we investigated the presence of H(2)S and the expression of H(2)S synthesizing enzymes, CSE and CBS, in isolated mouse pancreatic acini. Pancreatic acinar cells from mice were incubated with or without caerulein (10(-7) M for 30 and 60 min). Caerulein increased the levels of H(2)S and CSE mRNA expression while CBS mRNA expression was decreased. In addition, cells pre-treated with DL-propargylglycine (PAG, 3 mM), a CSE inhibitor, reduced the formation of H(2)S in caerulein treated cells, suggesting that CSE may be the main enzyme involved in H(2)S formation in mouse acinar cells. Furthermore, substance P (SP) concentration in the acini and expression of SP gene (preprotachykinin-A, PPT-A) and neurokinin-1 receptor (NK-1R), the primary receptor for SP, are increased in secretagogue caerulein-treated acinar cells. Inhibition of endogenous production of H(2)S by PAG significantly suppressed SP concentration, PPT-A expression and NK1-R expression in the acini. To determine whether H(2)S itself provoked inflammation in acinar cells, the cells were treated with H(2)S donor drug, sodium hydrosulphide (NaHS), (10, 50 and 100 muM), that resulted in a significant increase in SP concentration and expression of PPT-A and NK1-R in acinar cells. These results suggest that the pro-inflammatory effect of H(2)S may be mediated by SP-NK-1R related pathway in mouse pancreatic acinar cells.
Previous reports have suggested that gastrointestinal (GI) diseases may cause halitosis. The aim of this study was to evaluate the relationship between upper GI conditions, especially gastroesophageal reflux disease (GERD), and halitosis.
One hundred and thirty two consecutive patients complaining of upper GI symptoms were included in the study. All the patients completed a validated questionnaire that was designed to characterize and measure the severity of their symptoms. The questionnaire also contained questions about awareness and severity of oral bad breath. Following the filling of the questionnaire, the patients were physically examined and subjected to an upper GI endoscopy.
The final diagnosis among the 132 patients (M/F = 70/62, mean age 45.2 years, range 20-87 years) was GERD in 72 patients (55%), Functional dyspepsia in 52 (39%), Peptic ulcer in seven patients (5%) and gastric cancer in one patient (1%). Halitosis was significantly associated with the occurrence and severity of heartburn (P = 0.027), regurgitation (P = 0.002) sour taste (P < 0.001), belching (P = 0.001) and burburigmus (P = 0.006). Halitosis was not associated with upper abdominal pain, bloating, early satiety and chest pain. In relation to the final diagnosis, halitosis was significantly associated only with GERD (P = 0.002) but not with functional dyspepsia (P = 0.855) and peptic ulcer disease (0.765). No correlation was found between Helicobacter pylori infection status and halitosis occurrence and severity (analysis of variance F = 0.001, P = 0.977).
Halitosis is a frequent symptom of GERD and may be considered as an extra-esophageal manifestation of GERD. On the other hand, we did not find an association between functional dyspepsia, peptic ulcer disease and H. pylori infection with halitosis occurrence or severity.