PubMed · 1075870
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K M Hartlmaier. 1976. [Halitosis].. https://pubmed.ncbi.nlm.nih.gov/1075870/
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Measurement of oral malodor is complicated by a variety of parameters including complexity of gaseous molecular species, sampling difficulties, temporal variations, choice of suitable subject populations, and lack of agreement on reference standards. Since oral malodor is a perceived olfactory stimulus, direct sampling and assessment by human judges may be the most logical measurement approach. However, as with other psychophysical assessments, human malodor measurement by the human nose may vary widely among and between judges, and consequently cannot be confidently reproduced in other laboratories. Such shortcomings have led several investigators to propose quantitative approaches based on measurement of volatile sulfide compounds which are associated with oral malodor. Highly sensitive and discriminatory measurements of volatile sulfides can be made using gas chromatography although for rapid sampling of larger subject populations, portable sulfide monitors may be more appropriate. Future research in this field should consider: 1) improved and simplified instrumentation for more rapid through-put and reliability; 2) development and definition of reference standards for oral malodor assessment; 3) formulation of clinical studies with appropriately sized, well-defined patient populations; and 4) further development of within mouth, site-specific measurements.
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.