Drs. Mathis and Scheetz raise some interesting questions regarding the dosage form of calcium antagonist and gingival hyperplasia. Because most of our patients received sustained-release preparations of calcium antagonists, we could not do a subgroup analysis with adequate numbers of patients receiving prompt-release dosage forms to do statistical comparisons. We did not assess blood levels or compliance in this prevalence survey; however, previous reports found no relation between the dosage of the calcium antagonist and the development of gingival hyperplasia [1, 2]. We found no statistical differences in age between patients with and without hyperplasia. Our patient population did not allow us to compare prevalence data by race or sex.

Dr. Naylor raises questions about the significance of grade I or II hyperplasia. Most of the patients examined were not aware of the problem before their examination. Gingival hyperplasia, regardless of its severity, causes the formation of pseudopockets, which leads to plaque and bacterial accumulation subgingivally. This increases the risk for periodontal disease and bone loss. The presence of more frequent bleeding with probing in our patients with hyperplasia suggests the presence of inflammation. Evidence with both nifedipine-and phenytoin-associated gingival hyperplasia suggests that early recognition and removal of dental plaque may prevent or slow the progression of hyperplasia [3-5]. Our finding of increased brushing among patients without hyperplasia supports the belief that good oral hygiene is also important for patients treated with calcium antagonists. Finally, in a follow-up to this study, done 5 to 11 months after the initial work, 7 of 22 patients with grade I hyperplasia progressed to grade II gingival hyperplasia. We have also noted gingival regression with discontinuation of therapy with the calcium antagonist. Patients with gingival recession are still at risk for developing gingival hyperplasia. For geriatric patients who might have a loss of manual dexterity and therefore poor oral hygiene, formation of hyperplasia may accelerate periodontal disease. Such patients should be referred to a dentist for more frequent cleanings. It is important to weigh the risk for this complication and its consequences against the relative importance of and treatment alternatives for the calcium antagonists. We strongly believe that patients with teeth who are receiving calcium antagonists be instructed to brush and floss regularly and that regular dental examinations and dental cleaning be done to prevent future periodontal complications.