The effect of propranolol on salivary gland function and dental caries development in young and aged rats.
Medications commonly used in elderly people cause hyposalivation and are associated with an enhanced prevalence of dental caries. Propranolol (a beta-adrenergic antagonist) is a commonly used antihypertensive agent that is prescribed for long-term use. The purpose of this investigation was to compare the effects of this drug on salivary composition and flow rate, and on caries, in young and aged rats. Forty young (28-day) and 36 aged (20-month) female Sprague-Dawley rats were infected with Streptococcus sobrinus 6715 and fed a cariogenic diet for 28 days. Propranolol was given in high (20 mg/kg/day) and low (10 mg/kg/day) doses via osmotic pumps. Unoperated and desalivated animals served as controls. Smooth-surface caries scores in the young animals receiving propranolol at 20 mg/kg/day were statistically higher than in the young intact rats (p < or = 0.05). Increased smooth-surface and sulcal caries scores were recorded in the aged propranolol-treated animals, but the differences were not statistically significant when compared with those in intact aged animals. Propranolol in aged animals did not affect the amount of alveolar bone loss but increased the risk of development of root caries. Young animals harboured greater populations of Strep. sobrinus and total cultivable flora than did all aged groups except the desalivated group. Salivary flow rates, induced by pilocarpine, were not decreased by the chronic administration of propranolol. Although the total protein concentration in parotid and submandibular saliva from drug-treated animals was reduced, differences were not observed in their SDS-PAGE profile when compared with unoperated animals. The findings demonstrate that chronic use of propranolol reduced the total protein concentration in saliva of all animals, increased caries susceptibility, but did not reduce the stimulated salivary flow rate.
O'Connell
A C
AC
Department of Dental Research, Rochester Caries Research Center, University of Rochester, NY 14642-8611.
Van Wuyckhuyse
B C
BC
Pearson
S K
SK
Bowen
W H
WH
D000375:Aging / Q000502:physiology*; D016301:Alveolar Bone Loss / Q000209:etiology; D000818:Animals; D003731:Dental Caries / Q000209:etiology* / Q000382:microbiology; D003733:Dental Caries Susceptibility; D003773:Dental Plaque / Q000382:microbiology; D004037:Diet, Cariogenic; D005260:Female; D007778:Lactobacillus / Q000302:isolation & purification / Q000502:physiology; D010306:Parotid Gland / Q000378:metabolism; D010862:Pilocarpine / Q000494:pharmacology; D011433:Propranolol / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017213:Root Caries / Q000209:etiology; D012463:Saliva / Q000737:chemistry / Q000378:metabolism; D012469:Salivary Glands / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D012471:Salivary Proteins and Peptides / Q000032:analysis; D012636:Secretory Rate / Q000187:drug effects; D016986:Streptococcus sobrinus / Q000302:isolation & purification / Q000502:physiology; D013363:Submandibular Gland / Q000378:metabolism
D012471:Salivary Proteins and Peptides; D010862:Pilocarpine; D011433:Propranolol