Abstract

Clonidine is a widely prescribed, centrally acting antihypertensive with proposed pharmacologic mechanisms of stimulation of central postsynaptic α<sub>2</sub>–adrenergic receptors and agonist activity at presynaptic α<sub>2</sub>–adrenergic receptors, interfering with peripheral regulation of norepinephrine and acetylcholine release. Both of these mechanisms are capable of adversely influencing salivary output and composition, potentially leaving an individual with increased caries risk. The purpose of the present study was to determine the effect of chronic administration of clonidine on saliva, salivary glands, and caries in rats. Sprague–Dawley rat pups were infected with Streptococcus sobrinus, given Diet 2000 and 10% sucrose water ad libitum, and either desalivated, or treated with clonidine HCl (125 or 250 μg/kg administered daily for 28 days by means of osmotic minipumps), or assigned as controls. There were no statistical differences in stimulated parotid or submandibular gland salivary output or sublingual gland weights among the groups. The weight of the submandibular glands as a percent of total body weight was significantly decreased in animals that received clonidine when compared with controls. Sulcal caries scores in both clonidine groups and smooth surface caries scores in the high clonidine group were increased when compared with control animals. Positive control animals (desalivated) had significantly higher caries scores than all other groups. These data show that chronic administration of clonidine significantly decreases submandibular gland weight and increases susceptibility to dental caries.

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