ABSTRACT
Gingival enlargement refers to an increase in the size of the gingival tissue. The etiology varies, and often is multifactorial; however, local and systemic conditions, disease, and idiopathic factors may contribute to gingival enlargement. Tissue consistency can vary from soft and spongy to dense, typically appearing darker in shade compared to the drug-induced gingival enlargement. Treatment modalities usually involve surgical removal of excess tissue, non-surgical debridement, use of chemotherapeutic agents, and/or elimination or mitigation of contributing factors and conditions.
Subject(s)
Gingival Overgrowth/etiology , Diagnosis, Differential , Gingival Diseases/diagnosis , Gingival Neoplasms/diagnosis , Gingival Overgrowth/diagnosis , Gingival Overgrowth/therapy , HumansABSTRACT
BACKGROUND: Nifedipine, a calcium channel-blocking agent, has been associated with gingival enlargement in humans. This enlargement has also been successfully established in animal models. Previous investigators have administered nifedipine through a systemic route, most commonly by oral intake. The aim of the present study was to measure the effects of nifedipine administered directly into rat gingival interproximal papillae. METHODS: Twenty-four adult female rats were assigned to three groups. Each animal received a series of three injections, one week apart; each injection was placed directly into the interdental papilla of the maxillary and mandibular central incisors. Group 1 (control) received only saline. Group 2 received a low (10 microg/ml) concentration of nifedipine, while Group 3 received a higher concentration (500 microg/ml). One week after the last series of injections, gingival specimens were harvested from the injection site and prepared for histological and immunocytochemical analyses. RESULTS: Specimens from Group 3 displayed a significantly greater number of ED2-positive cells compared to the other two groups. Specimens from Group 2 showed a significantly higher mean count of positive cells compared to Group 1. Collectively, our data suggest that repeated local injections of 10 microg/ml and 500 microg/ml nifedipine each elicit an inflammatory response in the gingival connective tissue. CONCLUSIONS: Immunocytochemical analysis revealed dose-dependent increases of resident tissue macrophages in rats receiving nifedipine (p<0.005). An increased inflammatory infiltrate also was observed via routine histology. Gross macroscopic changes consistent with gingival enlargement were not observed.
Subject(s)
Calcium Channel Blockers/administration & dosage , Gingiva/drug effects , Nifedipine/administration & dosage , Animals , Cell Count , Connective Tissue/drug effects , Connective Tissue/pathology , Dose-Response Relationship, Drug , Epithelial Attachment/drug effects , Epithelial Attachment/pathology , Extracellular Matrix/drug effects , Extracellular Matrix/pathology , Female , Fibroblasts/drug effects , Fibroblasts/pathology , Gingiva/pathology , Gingivitis/chemically induced , Gingivitis/pathology , Granulocytes/drug effects , Granulocytes/pathology , Immunohistochemistry , Incisor , Injections , Keratins , Lymphocytes/drug effects , Lymphocytes/pathology , Macrophages/drug effects , Macrophages/pathology , Phagocytes/drug effects , Phagocytes/pathology , Rats , Sodium Chloride , Time FactorsABSTRACT
The first documented case of drug-induced gingival enlargement was reported in 1939. Since that time, specific medications have been associated with this condition. Although the biologic mechanisms responsible for drug-mediated gingival enlargement remain unclear, a multifactorial etiology is considered to be responsible, with contributing factors including age, genetic predisposition, and local conditions. While the role of plaque remains to be completely elucidated, there is abundant clinical evidence demonstrating at least partial resolution of drug-induced gingival enlargement following improved plaque control. Variations in drug kinetics, gingival crevicular fluid concentrations, protein synthesis, and the presence of growth factors also might contribute to the mechanism of gingival overgrowth.