This narrative review summarized the latest findings on halitosis in patients living with chronic kidney disease (CKD), including its epidemiology, etiology, classification, contributing compounds, diagnosis and treatment. Halitosis is present in 30-57% of patients living CKD in most reports. Accumulated metabolites in the blood circulation and multiple oral changes secondary to CKD are its main causes. It consists of intra-oral halitosis and extra-oral halitosis according to etiology. Ammonia, dimethylamine, trimethylamine, hydrogen sulfide, methyl mercaptan and dimethyl sulfide are its main contributing compounds. A combination of the subjective organoleptic test and the objective OralChroma breath test is essential for its diagnosis. Also, it is recommended that the organoleptic test and OralChroma breath test be performed for both mouth and nose breath. By comparing these two sets of results, clinicians can identify which subtype of halitosis is predominant in an individual patient. Kidney replacement therapies and antibiotics appear to be effective to treat this condition through reducing accumulated metabolites in the blood circulation.

Background: Halitosis in elderly dental patients is rarely attributable to a single etiology; tongue coating, periodontal inflammation, denture biofilm, and reduced salivary flow may coexist and modify treatment response. We compared three procedure pathways and examined whether tongue-coating reduction mediates procedure-related improvement. Methods: A prospective cohort of 94 patients aged 65 years or older was assigned by dominant indication to periodontal debridement with tongue cleaning (PDT, n = 33), denture biofilm management (DBM, n = 31), or restorative/prosthetic maintenance (RPM, n = 30). This was a single-center, nonrandomized prospective cohort study; assignment followed the dominant clinical indication rather than randomization. All clinical assessments were made by a single examiner who was masked to the formal procedure-group assignment; masking was partial because the clinical picture at follow-up could sometimes reveal the care delivered. The primary outcome was percentage reduction in volatile sulfur compound (VSC) concentration at 8 weeks. Secondary outcomes included organoleptic score, HALT, OHIP-14, tongue-coating index, denture plaque index, and a composite clinical response (≥30% VSC reduction plus ≥ 1-point organoleptic improvement plus ≥ 8-point HALT improvement). Linear mixed-effects, multivariable regression, and bootstrap mediation analyses were performed. Results: All three procedures reduced VSC at 8 weeks, but PDT produced the largest absolute reduction (-102.6 ± 20.2 ppb) and the highest composite response rate (57.6%), versus 9.7% in DBM and 3.3% in RPM (p < 0.001). Adjusted analyses showed PDT improved VSC reduction by 22.8 percentage points and DBM by 11.7 percentage points relative to RPM. Tongue-coating reduction mediated 29.5% of the PDT effect and 35.6% of the DBM effect. Xerostomia and reduced salivary flow attenuated the response in DBM and RPM but not in PDT. Conclusions: Periodontal debridement with tongue cleaning was the most effective procedure pathway for elderly halitosis. Tongue-coating reduction was a meaningful, though statistically rather than experimentally established, mediator of treatment benefit, supporting an oral-ecological framework for managing geriatric oral malodor that warrants confirmation in randomized studies.

Supportive periodontal care is essential for maintaining periodontal stability after active therapy, yet adherence to periodontal maintenance remains difficult. Once bleeding, halitosis or other presenting concerns improve, some patients may interpret the disease as resolved and the maintenance visit as "just a clean." This Perspective uses the intention-behaviour gap to examine behavioural, financial and health-literacy barriers to continued supportive care. It then considers a narrower, testable hypothesis: artificial intelligence (AI) might assist clinicians in organising clinician-verified periodontal information and presenting it through personalised visual summaries or prompts. Evidence that AI improves periodontal recall attendance is currently sparse; most dental AI research concerns image interpretation or classification, and the only directly relevant periodontal adherence study is proof-of-concept. Proposed risk projections are therefore presented as a distant research concept rather than a clinically validated tool. AI should not replace clinical judgement, and any future system would require validation, transparent uncertainty, consent, governance, equity safeguards and comparison with simpler non-AI interventions.

Halitosis affects a substantial proportion of adults worldwide, yet the compositional and functional basis of the oral microbiome in halitosis remains incompletely understood, particularly in East Asian populations. We performed 16S rRNA gene amplicon sequencing of oral gargle samples from 45 individuals with halitosis and 45 healthy controls in South Korea, generating approximately 4,600 amplicon sequence variants. Beta diversity analysis revealed significant community-level separation (PERMANOVA, P = 0.001) and an elevated Firmicutes/Bacteroidota ratio in halitosis, although alpha diversity did not differ between groups. Because the halitosis group was significantly older than controls, age-adjusted PERMANOVA and age-matched sensitivity analyses confirmed that separation persisted independent of age (age-adjusted R[2] = 0.030, P = 0.003). Halitosis-associated microbiomes were enriched for Prevotella melaninogenica and Peptostreptococcus stomatis, whereas healthy microbiomes were distinguished by Haemophilus parainfluenzae and Veillonella rogosae (LEfSe). Functional profiling using PICRUSt2 revealed a counterintuitive, predicted suppression of sulfur metabolism in halitosis: pathways for sulfate assimilation, cysteine, and methionine biosynthesis were predicted to be significantly reduced relative to healthy controls. This predicted shift was significantly inversely correlated with directly measured volatile sulfur compounds (H2S and methyl mercaptan; Spearman ρ = -0.54 and -0.64, both P < 0.0001), providing phenotypic support for the predicted signature. These findings suggest healthy oral microbiomes efficiently channel sulfur into anabolic pathways, whereas dysbiotic microbiomes may lose this capacity, allowing volatile sulfur compounds to accumulate. Our study provides a species-resolved, functionally annotated reference framework for halitosis-associated oral dysbiosis in a Korean cohort, and identifies candidate targets for diagnosis and intervention.IMPORTANCEHalitosis (bad breath) affects up to 30% of adults worldwide and is caused by volatile sulfur compounds (VSCs) produced by oral bacteria, yet the underlying microbial mechanisms remain poorly understood. Our study of 90 Korean adults reveals that halitosis is associated not only with an overgrowth of Prevotella species but also with a predicted, paradoxical suppression of the microbial community's capacity to assimilate sulfur into anabolic biosynthetic pathways. This predicted "sulfur assimilation failure" was associated with elevated VSC accumulation, supporting a reframing of halitosis as a community-level metabolic dysfunction rather than simple bacterial overproduction. These findings have direct clinical implications: the identified Prevotella-dominated dysbiosis and associated sulfur pathway signatures represent candidate biomarkers for objective halitosis diagnosis, and the restoration of microbial sulfur-channeling capacity offers a rational target for probiotic and prebiotic interventions. This work also contributes a well-characterized oral microbiome reference data set from an underrepresented East Asian population.

Esophagitis dissecans superficialis (EDS), also known as sloughing esophagitis, is a rare and frequently underrecognized esophageal disorder characterized by superficial sloughing of the esophageal mucosa. Its variable clinical presentation and overlap with structural esophageal abnormalities may result in misdiagnosis and unnecessary diagnostic or therapeutic interventions. We report a case of a 25-year-old woman with no history of chronic degenerative, autoimmune, or atopic disease who presented with abrupt retrosternal chest pain, recurrent vomiting, progressive esophageal dysphagia, halitosis, hematemesis, and marked unintentional weight loss. Initial evaluation showed a double-lumen appearance on barium esophagography and an upper endoscopic appearance initially interpreted as a large pharyngoesophageal diverticulum. Repeat endoscopy subsequently revealed extensive longitudinal sloughing and detachment of the esophageal mucosa, supporting the diagnosis of EDS. Histopathologic evaluation demonstrated a submucosal blistering lesion infiltrated by eosinophils, without evidence of malignancy or dysplasia. These findings raised suspicion for esophageal bullous pemphigoid; however, direct immunofluorescence was unavailable, and an autoimmune bullous disorder could not be definitively confirmed. Additional computed tomography imaging showed no evidence of esophageal disruption, mediastinal collection, pneumomediastinum, malignancy, or another structural abnormality. Severe oral intolerance, recurrent vomiting, persistent dysphagia, and marked nutritional compromise led the nutrition support team to select temporary total parenteral nutrition as an individualized strategy pending clinical and endoscopic reassessment. The severe mucosal involvement and suspected autoimmune bullous component prompted empiric treatment with intravenous corticosteroids. The patient achieved clinical stabilization, and outpatient endoscopic reassessment was scheduled. In the absence of follow-up endoscopic findings, no conclusions regarding mucosal healing or treatment efficacy could be drawn. This case highlights the importance of careful clinical, endoscopic, radiologic, and histopathologic correlation in severe or atypical presentations of EDS, particularly when the findings mimic a structural esophageal disorder.

Intraoral halitosis is predominantly caused by anaerobic microbes within the tongue biofilm that break down sulfur-containing amino acids, especially cysteine and methionine, to volatile sulfur compounds (VSCs). In addition to microbial activity, there is growing evidence to suggest that dietary factors are able to influence VSC formation by affecting substrate availability, redox equilibrium, and oral ecological stability and that some of these effects are due to extraoral metabolic activity. This review integrates food chemistry, microbial ecology, and oral health to explain how dietary exposures can interact with the oral microbiome to trigger and maintain halitosis. We synthesize current evidence on tongue biofilm ecology, key microbial taxa and metabolic pathways, and the modifying roles of salivary flow, periodontal inflammation, and common beverages and condiments. Diagnostic approaches are discussed with a mechanistic viewpoint, which has focused on combined organoleptic, gas specific analysis, tongue biofilm imaging, and selective provocation testing. Comprehensively, halitosis is presented as a diet modifiable, ecology-driven disease, the diagnostics of which should be guided by phenotype, and the intervention based on microbiomes and tailored care plans should be sustainable so that evidence-based functional foods and personalized care plans can be developed.

Background: Chewing gum may reduce oral malodor through salivary stimulation and may also serve as a carrier for oral probiotics. Evidence on Heyndrickxia coagulans in this setting is lacking. Methods: This exploratory secondary analysis used data from a randomized, blinded, placebo-controlled study in which 52 healthy adults were assigned to a sugar-free gum with H. coagulans SNZ1969[®] or to a matched placebo gum for four weeks. Hydrogen sulphide (H2S) and methyl mercaptan (CH3SH) were measured by OralChroma™ at baseline (T0), during intervention (T1-T2), and one week after gum discontinuation (T3). Dental plaque 16S rRNA profiles from the parent trial were re-analysed in relation to VSC values. Results: Forty-four participants completed follow-up. H2S and CH3SH concentrations did not differ between probiotic and placebo groups at any visit, and changes from baseline were also similar between arms. In the probiotic group, H2S was lower than baseline at T2 (p = 0.008) and T3 (p = 0.031), but this within-arm decrease was not greater than the change seen with placebo. Taxon-level analyses suggested nominal associations with taxa plausibly linked to sulphur metabolism, mainly for H2S, but no association survived false-discovery-rate correction. Conclusions: The probiotic gum did not show a statistically significant additional effect on VSC concentrations compared with the placebo gum. The within-arm H2S decrease and microbiome signals are exploratory and require confirmation in trials designed for participants with clinically established halitosis.