Hipertrofia gengival induzida por anlodipina: [revisão] / Amlodipine induced gingival overgrowth: [review]

JUSTIFICATIVA E OBJETIVOS: A hipertrofia gengival (HG) é reconhecidamente um grave efeito adverso a medicamentos, frequentemente encontrado em pacientes em uso de imunossupressores, anticonvulsivantes ou anti-hipertensivos. Nesta última classe, se destaca a nifedipina, porém tem sido crescente o númerode casos secundários ao uso da anlodipina. O objetivo deste estudo foi observar na literatura os dados existentes sobre a epidemiologia, características clínicas e histopatológicas, a prevenção e o tratamento da HG associada a este fármaco. CONTEÚDO: A coleta de dados foi realizada através dos Bancos de Dados BIREME, Pubmed e Medline. As palavras pesquisadas foram: aumento gengival, hipertrofia gengival, hiperplasia gengival, amlodipine induced gingival overgrowth, gingival overgrowth induced by calcium channel blockers, drug induced gingival overgrowth. No bando de dados BIREME foram encontrados 24 artigos referentes ao assunto pesquisado, na Pubmed e Medline foram encontrados 47 artigos pertinentes ao contexto enfocado. Do total, foram utilizados 34 artigos na revisão de literatura. CONCLUSÃO: A anlodipina é um fármaco que comprovadamente atua no tecido gengival causando o seu aumento. Sendo assim, a HG induzida por este fármaco tem aspectos clínicos característicos e é uma reação adversa individualizada devido à influência multifatorial. Em razão do atual aumento do uso deste bloqueador de canal de cálcio, a incidência da HG torna-se cada vez mais crescente. Desta forma, por gerar comprometimento funcional e estético ao indivíduo acometido, é de suma importância o conhecimento desta condição pelos profissionais de saúde para que ocorra a correta identificação do quadro e o estabelecimento precoce de uma conduta terapêutica adequada.

BACKGROUND AND OBJECTIVES: Gingival hyperplasia(GH) is admittedly a severe adverse effect of medications, frequently found in the immunosupressors, anticonvulsivants or antihypertensives users. Among this last class of medications, nifedipine is featured, but adverse effects due amlodipine using have been increasing. The aim of this study was to examine the existing data on the literature about epidemiology, clinical and histopathological features, prevention and treatment of GH due this medication. CONTENTS: The data collection was performed through BIREME, Pubmed and Medline databases. The words searched were: gingival enlargement, gingival hypertrophy, gingival hyperplasia, amlodipine induced gingival overgrowth, gingival overgrowth induced by calcium channel blockers, drug induced gingival overgrowth. In the BIREME databases were found 24 articles concerningon the topic searched, in Pubmed and Medline were found 47 relevant articles focused on the context. Totally, 34 articles ofthe literature review were used. CONCLUSION: Amlodipine is a drug that acts in the gingival tissue inducing its enlargement. Therefore, GH induced by thisdrug has typical clinical features and is an individualized adverse effect by the multifactorial influence. Due to the current increasein the use of calcium channel blocker, the incidence of GH becomes increasingly common. However, by the functional and esthetic commitment of the affected individual, is of high importance the knowledge about this condition by health professionals aiming the correct identification of this case and the early establishment of an appropriate treatment.

Regulation of type I plasminogen activator inhibitor in human gingival fibroblasts with cyclosporine A.

OBJECTIVES: Cyclosporine A (CsA) is used as an immunosuppressive agent and its prominent side effect is the induction of gingival overgrowth. Type I plasminogen activator inhibitor (PAI-1) has shown to play an important role in CsA-induced gingival overgrowth. However, little is known about whether factors can modulate CsA-induced PAI-1 expression. METHODS: Cytotoxicity, reverse transcriptase-polymerase chain reaction, and enzyme-linked immunosorbent assay were used to investigate the effects of Human gingival fibroblasts (HGFs) exposed to CsA. In addition, Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, interlukin-1alpha, tumor necrosis factor-alpha, mitogen-activated protein kinase kinase (MEK) inhibitor U0126, signal-regulated protein kinase (ERK) inhibitor PD98059 and cell-permeable glutathione precursor N-acetyl-L-cysteine (NAC) were added to test how they modulated the effects of CsA-induced PAI-1 expression. RESULTS: The concentration of CsA higher than 500 ng ml(-1) demonstrated cytotoxicity to HGFs (P < 0.05). Periodontal pathogens as well as proinflammatory cytokines were found to increase the CsA-induced PAI-1 mRNA and protein expression (P < 0.05). Pharmacological agents NAC, U0126, and PD98059 were found to decrease the CsA-induced PAI-1 mRNA and protein expression (P < 0.05). CONCLUSIONS: Cyclosporine A (CsA) may predispose to gingival overgrowth under inflammatory environments. The regulation of PAI-1 expression induced by CsA might be critically related with the intracellular glutathione and the ERK-MAPK pathway.

[Risk factors conditioning the incidence and severity of cyclosporine A-induced gingival overgrowth and methods of prevention]. / Fattori condizionanti l'incidenza e la severità dell'ipertrofia gengivale indotta da ciclosporina A e possibilità di prevenzione.

Cyclosporin A (CsA) induced gingival overgrowth is one of the major side-effects conditioning the quality of life of the patient under immunosuppressive therapy. This adverse effect has been first reported in 1983 and affects almost 30% of treated patients. Several papers have been published concerning the cellular/molecular mechanisms by which CsA may induce, at the same time, an immunosuppressive and proliferative action. In this review various factors concerning the patient and his milieu that account for the different prevalence of the severity of gingival overgrowth in clinical studies are analyzed and briefly discussed. In particular, age, sex, pharmacokinetic properties, pharmaceutical preparation, genetic predisposition, association with other drugs and the parodontal conditions before transplantation are considered. In addition, a unique approach to the patients with gingival overgrowth as well as effective methods of prevention and therapy are suggested.