Dr. C. Ramu, Dr. T. Padmanabhan, N. Sridhar*, Dr. Vivek Kumar Gupta


Gingival enlargement is usually noted within one to two months after the Initiation of nimodipine therapy. An increasing number of medications are associated with gingival enlargement. Currently, more than 20 prescription medications are associated with gingival enlargement, Rees TD, Levine RA. Systemic drugs as a risk factor for periodontal disease initiation and progression [1]. “Gingival enlargement” or “gingival overgrowth” is the preferred term for all medication-related gingival lesions previously termed “gingival hyperplasia” or “gingival hypertrophy.” These earlier terms did not accurately reflect the histologic composition of the pharmacologically modified gingiva. Drugs associated with gingival enlargement can be broadly divided into three categories: anticonvulsants, calcium channel blockers, and immunosuppressants. Although the pharmacologic effect of each of these drugs is different and directed toward various primary target tissues, all of them seem to act similarly on a secondary target tissue, i.e., the gingival connective tissue, causing common clinical and histopathological findings. The aetiology of nimodipine induced gingival overgrowth is uncertain. The aim of this study was to determine the relationship between plasma and gingival crevice fluid nimodipine concentrations and the degree of gingival overgrowth in patients treated with nimodipine, and also to assess the correlations between clinical and pharmacological variables. Antihypertensive drugs in the calcium channel blocker group are used extensively in elderly patients who have angina or peripheral vascular disease.3,9 The total number of annual prescriptions for this class of agents has continued to rise in recent years [2]. Assessment of enlargement by medical versus dental personnel, differing indices of overgrowth, focus on institutionalized versus outpatient populations, type of systemic condition being treated, age of the patients, other medications administered simultaneously, poorly controlled underlying periodontal conditions, and other factors. Although the prevalence varies greatly in different reports, the gingival enlargement prevalence in phenytoin-treated, non-institutionalized patients is about 50% [3]. The mechanism through which these medications trigger a connective tissue response in the gingiva is still poorly understood. Because only a subset of patients treated with these medications will develop gingival overgrowth, it has been hypothesized that these individuals have fibroblasts with an abnormal susceptibility to the drug. Indeed, it has been shown that fibroblasts from overgrown gingiva in phenytoin-treated patients are characterized by elevated levels of protein synthesis, most of which is collagen [4]. However, results of a study comparing intraoral lesions with the presence of fibrosis at extraoral sites failed to show that the severity of gingival enlargement correlates well with the formation of fibrotic lesions elsewhere in the body.50 Such enlargement cannot be considered a consequence of systemic and/or genetic fibroblast hyperactivity. A limitation of this study was that the conclusions were based on examination of extraoral tissues at the macroscopic level only [5]. Eighteen patients taking nimodipine in regular doses for at least six months participated in the study. Gingival enlargement was evaluated with two indices to score vertical and horizontal overgrowth. Gingival index, plaque index, gingival bleeding time index, probing depth and clinical attachment level were also concentrations were determined by using high performance liquid chromatography.There was no significant difference between responders and non-responders for plaque index, gingival index and gingival bleeding time index. The mean concentration of nimodipine in gingival crevicular fluid was significantly greater than concentration in plasma.No significant difference was observed for gingival crevicular fluid and plasma nimodipine concentration between responders and non-responders.


Nimodipine-induced gingival overgrowth, risk factors, gingival crevicular fluid.

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