Halitosis management by the general dental practitioner--results of an international consensus workshop.

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.

Halitosis and Helicobacter pylori infection.

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.

Appropriate sample bags and syringes for preserving breath samples in breath odor research: a technical note.

It is now generally accepted that the volatile sulfur compounds (VSCs) hydrogen sulfide, methyl mercaptan and dimethyl sulfide are the main contributors to halitosis when of oropharyngeal origin. The VSCs hydrogen sulfide and methyl mercaptan are the major causes of bad breath in oral malodour whereas dimethyl sulfide is generally the major cause of bad breath in extra-oral halitosis. To facilitate research in the field of halitosis, it is highly advantageous to be able to preserve breath samples for longer periods of time before measurement of the VSCs, e.g. for sampling patients at home or when studying a large cohort of patients where an immediate measurement of the VSCs is not possible. After testing numerous sample bags, ultimately the foil balloons, coated inside with the synthetic polymer polyethylene, were the preferred ones. All the VSCs in breath remained quite stable for at least 3 days in these balloons. Besides the sampling bags, the use of an appropriate syringe for sampling mouth air and for injecting samples in e.g. a gas chromatograph is also of great importance. Usually, syringes with a rubber barrel seal are used. However, some rubbers quickly adsorb the VSCs in breath. When preserving breath samples for longer periods, the rubber also releases VSCs, especially methyl mercaptan. It was also found that these syringes release a compound which interferes with dimethyl sulfide, when using gas chromatographic measurements with the OralChroma. We now use all-plastic syringes (B/Braun Injekt), made of polypropylene and polyethylene, in which the VSCs in breath remain quite stable for at least 9 h.

New methods for the release of volatile sulfur compounds from human serum: its determination by Tenax trapping and gas chromatography and its application in liver diseases.

New methods are described for the release of sulfur volatiles from human serum or whole blood and for its determination by Tenax trapping and gas chromatography by use of a specific sulfur detector. Methanethiol (MT) is covalently bound in serum in at least two different ways. One fraction of MT is released by addition of acid and is covalently bound to a compound with a mol wt less than 500, probably as methyl-beta-D-thioglucuronide. Another fraction of MT is released by reaction with dithiothreitol and is covalently bound to proteins in a disulfide linkage. No significant differences were observed in the protein-bound MT fraction between normal individuals and patients with cirrhosis. In contrast, the acid-hydrolyzable MT fraction was significantly elevated (P less than 0.0001) in the group with cirrhosis (0.41 +/- 0.19 mumol/L, mean +/- SD, n = 39) compared with the normal group (0.22 +/- 0.04 mumol/L, n = 21). The acid-hydrolyzable MT fraction is excreted in the urine. The concentration in normal persons amounted to 9 to 37 mumol/L. Dimethylsulfide (DMS) was measured in whole blood. There was a close correlation between venous blood DMS concentration and its concentration in breath. Dimethyldisulfide was not present in detectable amounts in the blood of normal individuals. Ethanethiol was absent in the serum and blood of all studied subjects.

Effect of bile salt binding or protease inactivation on plasma cholecystokinin and gallbladder responses to bombesin.

BACKGROUND/AIMS: Bombesin-stimulated plasma cholecystokinin levels decrease after an initial increase despite continuous infusion of bombesin. The aim of this study was to determine if a feedback mechanism, mediated by bile salts or proteolytic enzymes, is responsible for this decline. METHODS: Bombesin (1.0 ng.kg-1.min-1) was infused into volunteers for 180 minutes on separate occasions. Cholestyramine, colestipol, camostate, or saline were perfused intraduodenally during the second hour of the tests. Cholestyramine was also administered without infusion of bombesin. RESULTS: Colestipol and cholestyramine, dependent on their bile salt-binding capacity, markedly enhanced (P < 0.05) bombesin-stimulated plasma cholecystokinin from 2.1 +/- 0.5 pmol/L to 6.4 +/- 2.2 pmol/L and 12.1 +/- 3.3 pmol/L (P < 0.05 vs. colestipol), respectively, and further decreased gallbladder volume (P < 0.05) from 9.4 +/- 1.6 mL to 2.0 +/- 0.4 mL and 2.2 +/- 0.5 mL, respectively. The protease inhibitor camostate had no effect. Bile salt precipitation also enhanced plasma pancreatic polypeptide responses (P < 0.01) but did not alter gastrin responses. Plasma cholecystokinin responses to cholestyramine without bombesin infusion varied considerably, but increments were highly correlated to decreases in gallbladder volume (r = 0.91; P < 0.005). CONCLUSIONS: Bile salt sequestration but not protease inactivation enhances plasma cholecystokinin and gallbladder responses to bombesin infusion in humans.