Organoleptic studies indicate that the oral cavity is usually the principal source of physiologic malodor associated with the early morning halitosis. In all individuals, regardless of the age or health status of the oral tissues, the most intense oral malodor is exhibited after prolonged periods of reduced saliva flow and abstinence from food and liquid. This results from normal metabolic activity in the oral cavity and is accentuated in cases with periodontal involvement. Physiologic oral malodor is transient in duration as it can be controlled to varying degrees in most individuals by oral hygiene measures, such as tooth brushing, dental prophylaxis, tongue scraping and rinsing with antiseptic mouth washes. Experimental evidence strongly suggests that putrefaction of sulphur-containing proteinaceous substrates by predominantly gram-negative oral microorganisms is the primary cause of oral malodor. Optimum putrefactive activity occurs in low carbohydrate environment, physiological pH, and anaerobic conditions. Salivary sediment containing the exfoliated epithelial cells is the primary source of substrate which exists in a disulphide state. Proteolysis and reduction of disulphide bonds precedes the formation of odor. The odor intensity of putrescent saliva and plaque head-space vapor has been correlated with the concentration of volatile sulphur compounds consisting of hydrogen sulphide, methyl mercaptan, dimethyl sulphide and dimethyl disulphide. Except for dimethyl disulphide, the same sulphur-containing compounds have been found in mouth air of all tested individuals. Hydrogen sulphide and methyl mercaptan emanate an offensive putrid odor and account for approxiamtely 90% of the total sulphur content of mouth air. In half of the population tested, methyl mercaptan and hydrogen sulphide content of early morning mouth air is sufficiently high to account for the oral malodor. Brushing studies indicate that both plaque and tongue are important sources of malodor with most of the odor emanating from the dorso-posterior surface of the tongue. None of the gas chromatographic or mass spectrometric analyses have detected the presence of amines, indole, or skatole in the head-space, mouth air, or breath vapor samples.

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Hydrogen sulfide (H2S) and methyl mercaptan (CH3SH) are the volatile sulfur compounds (VSC) that were investigated for a possible role in the etiology of periodontal disease. The results show that the permeability of porcine non-keratinized sublingual mucosa is increased by up to 75% or 103% following exposure to H2S and CH3SH, respectively. The effect may be attributed to VSC reaction with tissue components resulting in alteration in the integrity of the tissue barrier. The increase in permeability of the mucosa to [35S]-Na2SO4 was dependent on both the time of exposure and concentration of VSC in the head-space. The [35S]-H2S was retained by the mucosal tissue and was able to penetrate the intact layers consisting of non-keratinized epithelium, basal membrane, and connective tissue. Treatment of the mucosa with 0.22% ZnCl2, either prior to or after exposure to CH3SH, nullified the effect of CH3SH and restored the permeability to a state similar to that observed in control 95% air/5% CO2 systems.

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