Forty-one subjects with bad breath were assessed for oral malodor and periodontal status on three occasions, at intervals of approximately one week. Oral malodor was assessed by measurement of peak and steady-state volatile sulphide levels with a portable sulphide monitor and by organoleptic measurement of whole-mouth, tongue dorsum, and interproximal dental odors by two independent judges. Reproducibility of measurements, assessed by paired t tests and Kappa testing, demonstrated no significant differences between any of the test results from the first and second appointments. Steady-state sulphide levels were the most reproducible of all tests. The ability of the tests to detect an expected reduction of malodor following a 0.2% chlorhexidine mouthrinse regimen was investigated by comparison of test values between the second and third appointments. Following the mouthrinsing treatment, 43% reductions of peak, 47% reductions of steady-state volatile sulphide levels, and 15-58% reductions in all other measurement categories were observed. The majority of the participants (22/41) had no pockets greater than 5 mm and exhibited both moderate gingival inflammation (Mean Gingival Index = 1.17) and moderate plaque accumulation (Mean Plaque Index = 1.84). Plaque Index and presence of pockets greater than 7 mm were weakly related to sulphide measurements. Whereas assessment of steady-state sulphide levels by the sulphide monitor does not constitute a direct measure of oral malodor, its relation to organoleptic measurement, superior reproducibility, objectivity, and sensitivity support the use of the sulphide monitor in clinical studies.

AsSOCIA11ONS BETWEEN ORAL MALODOR, measures of periodontal disease, and trypsinlike activity of periodontal pathogens on tongue and teeth were examined in 127 subjects. Volatile sulphur compound (VSC) measurements were made with a portable sulphide monitor; oral malodor was also estimated by organoleptic methods. Measurements repeated one week apart indicated that steady-state VSC levels (r = 0.72; P = 0.0001) and peak VSC levels (r = 0.63; P = 0.0001) were reproducible but these r values were not significantly different (P >0.1). There was a significant correlation between tongue odor and peak VSC levels (r = 0.40; P = 0.0001) and between tongue odor and whole mouth organoleptic measures (r = 0.55; P = 0.0001). To study the effect of reducing microbial colonization on oral malodor, chlorhexidine gluconate (0.2%) rinsing was prescribed for 7 days. Reductions of VSC levels were significant for both peak (37%) and steady-state (41%) data (P = 0.0001). Anaerobic periodontal pathogens on the tongue estimated by the proportions of positive BANA tests were reduced 19% (P = 0.001) and this was concomitant with a 40% (P = 0.0001) decrease in organoleptic measurement of the tongue dorsum. Mean pH measurements of the tongue dorsum showed large reductions from 6.9 initially to 6.3 post-treatment (P = 0.0001). Subjects were divided into periodontitis/no periodontitis based on periodontal inflammation and probing depth (;?5 mm). Of the 37 subjects with periodontitis, 23 had oral malodor whereas 52 out of 90 periodontally healthy subjects exhibited malodor. Chi square analysis comparing halitosis in subjects with and without periodontitis showed no statistically significant association (X2 = 0.208; P 0.65) between these two factors although the intensity of malodor as based on VSC concentration in periodontally healthy subjects was 19% less (mean = 111 ppb) than in subjects with periodontitis (mean = 136 ppb). The odds ratio was 1.2, indicating that oral malodor was not associated with periodontitis. These data indicate that a large proportion of individuals with oral malodor are periodontally healthy and that the mucosal surface of the tongue is a major site of oral malodor production. J PeriodontoI1994;65: 37-46.

No abstract

Restriction endonuclease analysis (REA) was performed on the total cellular DNA from each of 396 strains of mutans streptococci (1) to determine its potential usefulness for the study of transmission of the organism and (2) to document the proportions and variety of strains harbored by members of a small group of families. The DNA was digested with restriction enzyme EcoRI andlor HindIII, electrophoresed on agarose gels, and the resulting patterns compared. The strains examined included fresh isolates from 58 subjects, including 19 strains from each member offive families. The sensitivity and reproducibility of REA patterns from the mutans streptococci seemed ideal for studies of their epidemiology and transmission. The pattern of each isolate from humans was unique, except for isolates from the same individual or from the same family. REA types from subjects from different families were always heterogeneous. A high frequency of multiple REA types (up to 5) was observed in many subjects. While evidence for intra-familial transmission was obtained, including transmission between spouses, there was also strong evidence offrequent sources of infection outside of the family. Mutations of strains to streptomycin resistance or to lactate dehydrogenase deficiency caused no detectable change in the REA patterns. The lack of plasmids in any of the 57 fresh isolates that were examined for them suggested that they may have contributed little to the heterogeneity of the patterns seen.