Figure 422

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Pharmacokinetic factors that affect substantivity of rinsing agents.

Mechanisms of Action

Although chlorhexidine affects virtually all bacteria, gram-positive bacteria are more susceptible than are gram-negative organisms. Furthermore, Streptococcus mutans and Antinomies viscosus seem to be particularly sensitive. S. mutans has been associated with the formation of carious lesions in fissures and on interproximal tooth surfaces and has been identified in large numbers in plaque and saliva samples of subjects with high caries activity.

Low concentrations of chlorhexidine are bacterio-static, while high concentrations are bactericidal. Bacteriostasis is the result of chlorhexidine binding to the negatively charged bacterial cell wall (e.g., lipo-polysaccharides), where it interferes with membrane transport systems. Oral streptococci take up sugars via the phosphoenolpyruvate-mediated phosphotrans-ferase (PEP-PTS) system. The PEP-PTS is a carrier-mediated group translocating process in which a number of soluble and membrane-bound enzymes catalyze the transfer of the phosphoryl moiety of PEP to the sugar substrate with the formation of sugar phosphate and pyruvate. Chlorhexidine is known to abolish the activity of the PTS at bactericidal concentrations. High chlor-hexidine concentrations cause intracellular protein precipitation and cell death. Despite its pronounced effect on plaque formation, no detectable changes in resistance of plaque bacteria were found in a 6-month longitudinal study of mouth rinses.

Clinical Uses

The previous routine treatment for cases of severe gingival disease consisted of calculus and plaque removal and oral hygiene instructions. Subsequent resolution of the gingival inflammation was largely dependent on daily plaque control by the patient. However, the use of a 0.1 to 0.2% chlorhexidine mouthwash supplementing daily plaque control will facilitate the patient's effort to fight new plaque formation and to resolve gingivitis. Consequently, use of chlorhexidine is indicated in the following situations: in disinfection of the oral cavity before dental treatment; as an adjunct during initial therapy, especially in cases of local and general aggressive periodontitis; and in handicapped patients.

Adverse Effects and Toxicity

The most conspicuous side effect of chlorhexidine is the development of a yellow to brownish extrinsic stain on the teeth and soft tissues of some patients. The discoloration on tooth surfaces is extremely tenacious, and a professional tooth cleaning using abrasives is necessary to remove it completely. The staining is dose dependent, and variation in severity is pronounced between individuals. This side effect is attributed to the cationic na ture of the antiseptic. Desquamative soft tissue lesions have also been reported with use of drug concentrations exceeding 0.2% or after prolonged application. A frequently observed side effect is impaired taste sensation. It was reported that rinsing with a 0.2% aqueous solution of chlorhexidine digluconate resulted in a significant and selective change in taste perception for salt but not for sweet, bitter, and sour.

In vitro, chlorhexidine can adversely affect gingival fibroblast attachment to root surfaces. Furthermore, protein production in human gingival fibroblasts is reduced at chlorhexidine concentrations that would not affect cell proliferation. Such findings corroborate earlier studies showing delayed wound healing in standardized mucosal wounds after rinsing with 0.5% chlorhexidine solution.

As an oral rinsing agent, to date chlorhexidine has not been reported to produce any toxic systemic effects. Since chlorhexidine is poorly absorbed in the oral cavity and gastrointestinal tract, little if any enters the bloodstream. A summary of chlorhexidine oral rinses is given in Table 42.1.

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