Volatile sulfur compounds (VSC) in mouth air were estimated by gas chromatography. The amount of VSC and the methyl mercaptan/hydrogen sulfide ratio were significantly increased in patients with periodontal disease. These two parameters also increased in proportion to the bleeding index and probing depth. A study was also done on the effect of removal of tongue coating on VSC concentrations in mouth air from patients with periodontal involvement. VSC and the methyl mercaptan/hydrogen sulfide ratio were reduced to 49% and 35%, respectively, by removal of the tongue coating. The average amount of tongue coating removed from patients with periodontal disease was significantly higher than from controls (90.1 mg vs. 14.6 mg, p less than 0.01). Estimated production of VSC from tongue coating was 4 times higher than the control value, and the methyl mercaptan/hydrogen sulfide ratio was also markedly increased. However, a saliva putrefaction study suggested that saliva does not contribute to the elevated ratio of methyl mercaptan in mouth air. These results strongly suggest that, in addition to periodontal pockets, tongue coating has an important role in VSC production, in particular leading to an elevated concentration of methyl mercaptan, which is more pathogenic than hydrogen sulfide.

The amounts of volatile sulfur compounds (VSC) and methyl mercaptan/hydrogen sulfide ratio in mouth air from patients with periodontal involvement were 8 times greater than those of control subjects. Our studies demonstrated that, in patients with periodontal disease: 1) the concentration of disulfide, which is converted to VSC, increased in proportion to the total pocket depth; 2) 60% of the VSC was produced from the tongue surface; 3) the amount of tongue coating was 4 times greater than in control subjects; and 4) VSC production and the methyl mercaptan/hydrogen sulfide ratio of the tongue coating were increased. 2‐Ketobutyrate, which is a byproduct of the metabolism of methionine to methyl mercaptan, was higher in the saliva of patients with periodontal disease. This implies that metabolism of methionine to methyl mercaptan increases in the oral cavity of patients with periodontal pockets. Since free L‐methionine, rather than protein, is the main source for methyl mercaptan, we estimated the methionine supply from the gingival fluid into the oral cavity of patients with periodontal involvement. The results showed that the ratio of methionine to whole free amino acids was significantly higher than that of cysteine. Our studies suggest that not only microorganisms, but also the tongue coating and gingival fluid are factors which enhance VSC production in patients with periodontal disease. J Periodontol 1992; 63:783–789.

Tongue coating score, modified sulcus bleeding index and calculus index were factors significantly related to oral malodor in this study.

In this paper, the classification of halitosis and the examination procedures used in diagnosing halitosis are outlined. Halitosis is classified into categories of genuine halitosis, pseudo-halitosis and halitophobia. Genuine halitosis is subclassified into physiologic halitosis and pathologic halitosis. Pathologic halitosis itself is subdivided into oral and extraoral halitosis. Patients diagnosed with pseudo-halitosis and halitophobia usually complain about having oral malodour that does not really exist. Pseudohalitosis can be treated by dental practitioners, but halitophobic patients must be referred to psychological specialists. Oral malodour can be measured using an organoleptic measurement or a gas chromatography analysis. The organoleptic measurement is the most practical procedure with which one can evaluate oral malodour. Gas chromatography (GC) analysis using a flame photometric detector has been shown to be the gold standard for measuring oral malodour, owing its reputation to its objectivity and reproducibility. Moreover, GC is specific for volatile sulphur compounds (VSC), which are the main causes of oral malodour. It has been demonstrated that there is a high correlation between the intensity of oral malodour and the VSC concentration as measured by GC.

Clinical investigations on patients suffering from halitosis clearly reveal that in the vast majority of cases the source for an offensive breath odor can be found within the oral cavity (90%). Based on these studies, the main sources for intra-oral halitosis where tongue coating, gingivitis/periodontitis or a combination of the two. Thus, it is perfectly logical that general dental practitioners (GDPs) should be able to manage intra-oral halitosis under the conditions found in a normal dental practice. However, GDPs who are interested in diagnosing and treating halitosis are challenged to incorporate scientifically based strategies for use in their clinics. Therefore, the present paper summarizes the results of a consensus workshop of international authorities held with the aim to reach a consensus on general guidelines on how to assess and diagnose patients' breath odor concerns and general guidelines on regimens for the treatment of halitosis.

Many elderly people under long-term care suffer from malnutrition caused by dysphagia, frequently leading to sarcopenia. Our hypothesis is that sarcopenia may compromise oral function, resulting in dysphagia. The objectives of this study were to evaluate sarcopenia of the lingual muscles by measuring the tongue thickness, and elucidate its relationship with nutritional status. We examined 104 elderly subjects (mean age = 80.3 ± 7.9 years). Anthropometric data, such as triceps skinfold thickness and midarm muscle area (AMA), were obtained. The tongue thickness of the central part was determined using ultrasonography. Measurement was performed twice and the mean value was obtained. The relationship between tongue thickness and nutritional status was analyzed by Pearson’s correlation coefficient and Spearman’s rank correlation coefficient. AMA and age were identified by multiple-regression analysis as factors influencing tongue thickness. The results of this study suggest that malnutrition may induce sarcopenia not only in the skeletal muscles but also in the tongue.

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Hydrogen sulfide caused apoptosis and DNA damage in human gingival fibroblasts. An increased level of reactive oxygen species stimulated by hydrogen sulfide may induce apoptosis and DNA strand breaks.