Inhibition of malodorous gas formation by oral bacteria with cetylpyridinium and zinc chloride

Publication date: December 2017
Source:Archives of Oral Biology, Volume 84
Author(s): Jeong Hyun Kang, Dae Jeong Kim, Bong Kyu Choi, Ji Woon Park
ObjectiveThe antimicrobial efficacy of zinc- (ZnCl2) and cetylpyridinium-chloride (CPC) and their inhibition capacity on volatile sulfur compound (VSC) production by oral bacterial strains were investigated.DesignMinimum inhibitory concentrations (MIC) and growth curves were determined for ZnCl2, CPC, and CPC with ZnCl2 solutions against eight oral microorganisms (Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum, Porphyromonas gingivalis, Prevotella intermedia, Treponema denticola, Tannerella forsythia, Staphylococcus aureus and Streptococcus mutans) known to be involved in the pathophysiology of both halitosis and periodontal disease. Gas chromatography was applied to measure VSCs (H2S, CH3SH, (CH3)2S) production levels of each strains following exposure to the solutions.ResultsZnCl2 and CPC effectively inhibited growth of all eight strains. ZnCl2 was generally more effective than CPC in suppressing bacterial growth excluding A. actinomycetemcomitans, P. intermedia, and T. forsythia. Synergism between CPC and ZnCl2 was shown in A. actinomycetemcomitans. The MIC for CPC was significantly lower than ZnCl2. VSC production was detected in five bacterial strains (A. actinomycetemcomitans, F. nucleatum, P. gingivalis, T. denticola, and T. forsythia). Each bacterial strain showed unique VSCs production profiles. H2S was produced by F. nucleatum, P. gingivalis, and T. denticola, CH3SH by all five strains and (CH3)2S by A. actinomycetemcomitans, F. nucleatum, P. gingivalis, and T. denticola. Production of CH3SH, the most malodorous component among the three major VSCs from mouth air was evident in F. nucleatum and T. forsythia.ConclusionBoth ZnCl2 and CPC effectively inhibit bacterial growth causative of halitosis and periodontal disease, resulting in a direct decrease of bacterial VSCs production.



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