Plaque bacteria counts and vitality during chlorhexidine, Meridol and Listerine mouthrinses

The aim of this double-blind study was to enumerate the total number of living and dead bacteria on defined tooth areas during the application of antibacterial mouthrinses. After prophylaxis, 40 students refrained from all oral hygiene measures for 3 d, during which they rinsed with a phenolic compound (Listerine), an amine fluoride/stannous fluoride solution (Meridol), 0.2% chlorhexidine (CHX) or a control solution (0.02% quinine-hydrochloride). The plaque index (PII) was recorded at the start and the end of the investigation. Total bacterial counts (BC) and colony-forming units (CPU) of 1d-, 2d- and 3d-old dentogingival plaque were determined. The plating efficiency (PE) was calculated as a percentage of CFU/BC and the portion of vital microflora estimated by a vital fluorescence technique (VF). All groups started with a P1I approximating 0.1. On day 3, the P1J values were 1.21 in the control group and 0.51, 0.37 and 0.14 after Listerine, Meridol and CHX use, respectively. A tremendous variation existed between the numbers of viable bacteria found per mm- on the enamel surface on day 3 (CHX: 0.2: Meridol: 300; Listerine: 6×10⁴; control: 2×10⁶). while higher total numbers of bacteria were concomitantly present (CHX and Meridol: 1–2×10⁴; Listerine: 2×10⁵: control: 2×10⁶). Both vitality parameters PE and VF reached 92% in the control group at day 3, but only 7% after CHX use. With Meridol and Listerine, the corresponding PE values were 3% and 43%, respectively, while the VF values reached 48% and 54%. The P1I, BC, CFU and PE values of the CHX and the Meridol groups differed significantly from those of the control group. In contrast, Listerine showed no difference as compared to the control rinse. Due to the strong antibacterial action of CHX and Meridol during their use, almost only dead or non-proliferating bacteria were found on the tooth surfaces. Thus, only a thin plaque could develop. As a clinical consequence, both substances showed retardation of plaque development as reflected by significantly reduced plaque indices.