Journal of clinical periodontology · 2000
Effect of an essential oil-containing antiseptic mouthrinse on induction of platelet aggregation by oral bacteria in vitro.
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Whitaker E J, Pham K, Feik D, Rams T E, Barnett M L, Pan P
Аннотация
BACKGROUND: With an increasing body of data suggesting an association between periodontitis and cardiovascular disease, studies have been conducted to elucidate potential mechanisms by which oral bacteria might exert systemic effects. 2 oral bacteria, Streptococcus sanguis and Porphyromonas gingivalis, have been shown to induce platelet aggregation in vitro. This study was conducted to determine the effect of treatment with an essential oil mouthrinse (Listerine Antiseptic) on the platelet-aggregating activity of these organisms.
METHOD: Bacteria were grown under standard culture conditions. S. sanguis ATCC strain 10556 was exposed for 3 min to the essential oil mouthrinse at either full strength or a 1:1 dilution, while P. gingivalis FDC strain 381 was exposed to the essential oil mouthrinse at a 1:10 dilution. Positive control cells were treated with Hanks balanced salt solution (HBSS). Aggregation was measured using a recording platelet aggregometer. The assay of each organism in its respective mouthrinse dilution(s) or HBSS was repeated 5 times.
RESULTS: In all cases, the HBSS-treated organisms induced platelet aggregation, with mean(+/-S.E.) lag times of 12.30 (+/-1.36) min and 11.36 (+/-0.58) min for P. gingivalis and S. sanguis, respectively. In contrast, treatment with the essential oil mouthrinse completely inhibited the platelet aggregating activity of P. gingivalis and of S. sanguis exposed to the 1:1 mouthrinse dilution in all assays; the aggregating activity of S. sanguis treated with full-strength mouthrinse was completely inhibited in 4 of 5 assays, and inhibited by 75% in the 5th, for a mean inhibition of 95 +/- 1.5%.
CONCLUSION: This study provides additional evidence that the essential oil mouthrinse can interfere with bacterial cell surface-associated activities which may have clinical relevance.
METHOD: Bacteria were grown under standard culture conditions. S. sanguis ATCC strain 10556 was exposed for 3 min to the essential oil mouthrinse at either full strength or a 1:1 dilution, while P. gingivalis FDC strain 381 was exposed to the essential oil mouthrinse at a 1:10 dilution. Positive control cells were treated with Hanks balanced salt solution (HBSS). Aggregation was measured using a recording platelet aggregometer. The assay of each organism in its respective mouthrinse dilution(s) or HBSS was repeated 5 times.
RESULTS: In all cases, the HBSS-treated organisms induced platelet aggregation, with mean(+/-S.E.) lag times of 12.30 (+/-1.36) min and 11.36 (+/-0.58) min for P. gingivalis and S. sanguis, respectively. In contrast, treatment with the essential oil mouthrinse completely inhibited the platelet aggregating activity of P. gingivalis and of S. sanguis exposed to the 1:1 mouthrinse dilution in all assays; the aggregating activity of S. sanguis treated with full-strength mouthrinse was completely inhibited in 4 of 5 assays, and inhibited by 75% in the 5th, for a mean inhibition of 95 +/- 1.5%.
CONCLUSION: This study provides additional evidence that the essential oil mouthrinse can interfere with bacterial cell surface-associated activities which may have clinical relevance.