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At least 19 recordsLinked to original sources
PubMed1998

Medically induced gingival hyperplasia.

Gingival hyperplasia or gingival overgrowth is a common occurrence in patients taking phenytoin, cyclosporine, or calcium channel blockers. Speech, mastication, tooth eruption, and aesthetics may be altered. Controlling the inflammatory component through an appropriate oral hygiene program may benefit the patient by limiting the severity of the gingival overgrowth. In patients in whom gingival overgrowth is present or may be anticipated, recognition of this condition and referral to a general dentist or periodontist are appropriate steps to management. The physician's awareness of the potential for development of overgrowth and the dental practitioner's role in attempting to prevent or minimize this problem are important aspects. In this article, we discuss the medications associated with gingival hyperplasia and describe appropriate recommendations.

Anticonvulsants↗
PubMed1992

Nifedipine-induced gingival hyperplasia.

Gingival hyperplasia is an adverse reaction of nifedipine therapy. Oral manifestations of this condition include enlarged and painful gingiva accompanied by spontaneous bleeding. Nifedipine-induced gingival hyperplasia may be reversible once a proper drug substitution is made. Two cases of gingival hyperplasia resulting from nifedipine are described and the drug's possible mode of action is discussed.

Adult↗
PubMed1996

Metabolism of phenytoin by the gingiva of normal humans: the possible role of reactive metabolites of phenytoin in the initiation of gingival hyperplasia.

Gingival hyperplasia is a well-known complication of therapy with cyclosporine, calcium channel blockers, and phenytoin. It is characterized by the presence of inflammation and a marked fibrotic response. The mechanism of this adverse reaction is unknown. We propose that it may be initiated by the metabolic activation of these drugs to form reactive metabolites. These then cause cellular injury and lead to the gingival hyperplasia. To evaluate this hypothesis we examined phenytoin metabolism and the cytochrome P450 contents of gingival tissues from 10 patients undergoing surgery for various periodontal conditions. We found that microsomes obtained from the gingiva show significant phenytoin hydroxylase activity as determined by the production of 5-(4'-hydroxyphenyl)-5-phenylhydantoin (HPPH) (range, 12.8 pmol HPPH/min.mg microsomal protein to 276.9 pmol HPPH/min.mg microsomal protein; rat control, 133.7 +/- 11.5 pmol HPPH/min.mg microsomal protein). We also found that CYP1A1, CYP1A2, CYP2C9, CYP2E1, and CYP3A4 were present in these microsomes. We detected no CYP2B6 or CYP2D6. We believe that these data support our hypothesis that the proliferative inflammation observed with drugs such as phenytoin, nifedipine, and cyclosporine may be initiated by the formation of reactive metabolites and that the formation of these metabolites may be catalyzed by one or more CYPs found in the gingiva. These metabolites may then cause cellular injury and induce a reactive inflammatory response, followed by fibroblastic proliferation. This proliferation leads to the excess collagen deposition observed with gingival hyperplasia.

Adolescent↗
PubMed1976

The effect of oral physiotherapy on dilantin gingival hyperplasia.

Gingival hyperplasia was studied in 13 boys with epilepsy living in a state hospital. Boys were selected on the basis of having gingival hyperplasia, having all teeth between cuspids (upper and lower), having no occlusal abnormality and being cooperative. After gingivectomy, regrowth of gingiva was compared around lateral incisors on one side of the mouth having operator-assisted oral hygiene with that around lateral incisors on the other side of the mouth without operator-assisted oral hygiene. Regrowth of tissue was documented by precise photogrammetry. Oral hygiene, gingival inflammation and crevicular fluid were monitored. Less inflammation, less crevicular fluid and less regrowth of gingival tissues occurred around teeth subjected to good oral hygiene. Precise periodic photographic documentation of the clinical status of patients during studies such as this is considered very valuable.

Adolescent↗
PubMed2003

Amlodipine-induced gingival hyperplasia.

Gingival hyperplasia can occur during use of drugs such as diphenylhydantoin, cyclosporine and nifedipine. We report, three cases of gingival hyperplasia induced by amlodipine, a second generation calcium channel blocker. Exact cause of induction of thehyperplasia is not known. Individual variation in metabolism of the drug may be a factor.

Adolescent↗
PubMedDate not supplied

Nifedipine-induced gingival hyperplasia.

Gingival hyperplasia, a condition characterized by increased amounts of gingival connective tissue, has most commonly been observed in patients receiving phenytoin, but has also been noted in patients receiving cyclosporine and, as in this case report, nifedipine. Patients receiving nifedipine should be advised to practice good oral hygiene to lessen the possibility of hyperplasia occurring. If gingival hyperplasia develops in a patient taking nifedipine, the drug should be suspected as being responsible and discontinued. Limited data suggest verapamil can be substituted for nifedipine in these patients with improvement of the hyperplasia.

Gingival Hyperplasia↗
PubMed1994

Nifedipine aggravates cyclosporine A-induced gingival hyperplasia.

Gingival hyperplasia is a common side-effect of immunosuppression with cyclosporine A. Nifedipine is often used to control hypertension in kidney graft recipients. Analysis of gingival status in 106 children transplanted at our centre, and treated either with azathioprine, cyclosporine A or both, revealed significantly higher degrees of gingival overgrowth in those children receiving a combination of cyclosporine A and nifedipine compared with those children treated with cyclosporine A or nifedipine alone. Seven children undergoing gingivectomy at our centre over the past few years had received this combination. After a change in the antihypertensive regimen, avoiding long-term nifedipine medication, and improved dental care with chlorhexidine gel, we noted a reduction in the degree of gingival hyperplasia. In the majority of patients, nifedipine could be replaced by a single drug, usually hydralazine. We therefore recommend avoiding calcium channel blockers in the long-term management of hypertension in patients receiving cyclosporine.

Adolescent↗
PubMed1997

Fibroblasts derived from tissue explants of dilantin-induced gingival hyperplasia and idiopathic gingival fibromatosis show distinct disparity in proliferative responsiveness to epidermal growth factor.

Human gingival fibroblasts derived from tissue explants of two patients with dilantin-induced gingival hyperplasia (DGH) and one patient with idiopathic gingival fibromatosis (GF) were studied with respect to the effect of epidermal growth factor (EGF) on the proliferative characteristics of these cells. Immunohistochemical staining showed that there were more EGF receptor-positive cells among DGH fibroblasts than among either normal gingival fibroblasts (NG) or GF cells. Furthermore, EGF binding studies showed that, in spite of there being no disparity in binding affinity among all these cells, DGH fibroblasts possessed approximately two-fold more EGF receptors than either NG or GF cells. In addition, the growth-promoting effect of exogenously added EGF was concentration-dependent in DGH fibroblasts but was not in either NG or GF cells. All of the above findings clearly demonstrate that DGH and GF fibroblasts exhibit distinct disparity in proliferative responsiveness to EGF and suggest that different mechanisms may be involved in the pathogenesis of these two forms of gingival hyperplasia. These observations also suggest a possible therapeutic approach for blocking EGF-induced cell proliferation in DGH.

Anticonvulsants↗
PubMed1999

Clinical effects of periodontal therapy on the severity of cyclosporin A-induced gingival hyperplasia.

BACKGROUND: Gingival hyperplasia (GH) is a major side effect associated with cyclosporin A (CsA) therapy. The condition is further augmented due to the gingival inflammation. In this study, the effects of initial periodontal therapy and gingival curettage are analyzed in a group of patients with clinically significant (>30%) CsA-induced gingival hyperplasia. METHODS: The test group of 15 patients received oral hygiene instructions, supra- and subgingival scaling, polishing, and gingival curettage only oral hygiene instructions were given to 16 control subjects. Plaque index (PI), gingival index (GI), calculus index (CI), periodontal probing depth (PD), and gingival hyperplasia were recorded at baseline and repeated 8 weeks after treatment. Current doses of immunosuppressive agents, serum concentrations of CsA, and duration of CsA therapy were recorded as the pharmacological parameters. RESULTS: Statistical evaluation revealed that all clinical variables showed statistical decreases compared to baseline in the treated patients, while none of the parameters changed significantly in the control group. Initial GH scores of 53.63% in controls and 53.40% in the treated patients were 52.83% and 32.13% following treatment, respectively. A difference of 21.27% in the severity of treated GH was accompanied by a 0.56 decrease in GI scores in the test group. CONCLUSIONS: Compared to the initial observations, the results suggested that nearly 60% of the condition could be of fibrotic origin. Initial periodontal therapy and curettage resulted in the resolution of the inflammation in CsA-induced GH. Further investigation of the treated patients has shown that 7 out of 15 patients (47%) in the test group responded well and their GH scores decreased below 30% at the end of the study. The treatment in this study was effective in eliminating the necessity of more extensive surgical modes of treatment, such as gingivectomy, in 47% of cases.

Adult↗
PubMed1998

Analysis of peripheral blood leukocytes in patients with cyclosporine A-induced gingival hyperplasia.

BACKGROUND: Gingival overgrowth is one of the major adverse effects of the immunosuppressive drug cyclosporine A (CsA). Although several studies have attempted to determine the immunological mechanisms of gingival hyperplasia (GO) due to CsA therapy, the pathogenesis remains unclear. In this study, the distribution of the peripheral blood leukocytes in a group of renal transplant patients undergoing CsA therapy was analyzed and possible correlations of periodontal and pharmacological variables to lymphocyte subpopulations, natural killer cells, and monocytes investigated. METHODS: Thirty-six patients were classified into 2 groups of 18 each according to the degree of gingival overgrowth. The periodontal evaluation included plaque index (PI), gingival index (GI), gingival overgrowth (GO), calculus index (CI), and probing depth (PD). The pharmacological variables of current doses of the therapeutic serum levels of CsA were investigated. The peripheral blood leukocytes were studied by 2-color flow cytometric analysis using anti-human CD2, CD3, CD4, CD8, CD11b, CD11c, CD16, CD19, HLA-DR, and CD3+HLA-DR+ monoclonal antibodies. RESULTS: Statistical evaluation revealed that none of the pharmacological variables varied between the 2 groups. Responders (GO >30%) had significantly higher GI, PD, and GO scores compared to nonresponders (GO < or =30%). Of the immunological parameters studied, only CD2 was higher in the responder group. None of the clinical parameters correlated to the immunological values. CONCLUSIONS: The results of this study may be useful in explaining the underlying mechanisms of drug-induced gingival overgrowth. Several previously unsuspected cells and accessory activation mechanisms for T lymphocytes could play a role in the pathogenesis.

Adult↗
PubMed1993

The potential use of CO2-laser gingivectomy for phenytoin-induced gingival hyperplasia in mentally retarded patients.

Patients with hyperplastic states of the gingiva, i.e., phenytoin hyperplasia, nifedipine hyperplasia, cyclosporin hyperplasia, gingival fibromatosis and others may be treated by laser gingivectomy as no bone surgery is involved in these cases. Patients who are mentally retarded may represent special care problems postoperatively after conventional surgical gingivectomy i.e., unintentional removal of surgical dressing, postoperative bleeding etc. Therefore, the potential use of CO2-laser gingivectomy for mentally retarded persons was evaluated in a prospective study comprising 15 patients with fenytoin hyperplasia of the gingiva. No intra- or postoperative bleeding occurred and no surgical dressing was applied. The majority of the patients did not need any analgesics postoperatively. Healing was uncomplicated and the time needed for healing was of the same order of magnitude as after surgical gingivectomy.

Adolescent↗
PubMed1997

Treatment of cyclosporin-induced gingival hyperplasia with azithromycin.

BACKGROUND: Gingival hyperplasia is a known complication of cyclosporin therapy. Although plaque control has been shown to be of benefit, gingival surgery is occasionally necessary. The aim of this study was to review the effect of a short-course therapy with azithromycin in renal transplant patients with cyclosporin-induced gingival hyperplasia. METHODS: Thirty-eight patients received 500 mg/day of azithromycin for 3 consecutive days. The degree of gingival hyperplasia was classified as: 0, no gingival overgrowth; 1, mild overgrowth; 2, moderate overgrowth, and 3, severe overgrowth. Gingival bleeding and evolution of gingival hyperplasia were determined at 0 (pretreatment), 7, 30, 90 and 180 days. Cyclosporin, serum creatinine and ALT levels were simultaneously determined on the same days. RESULTS: Seven patients were excluded, leaving a total of 31 included in the trial. Eleven had a score of 3, 17 a score of 2, and 3 a score of 1. The degree of gingival hyperplasia was unrelated to the dose and levels of cyclosporin. Gingival hyperplasia improved in all patients (P < 0.001, Friedman test). The degree of improvement was better when the degree of hyperplasia was lower. In 27 patients gingival hyperplasia remained absent 6 months later, 3 patients required a second course of treatment, and another required gingival surgery. Gingival bleeding, present in 28 patients when diagnosed, disappeared in all cases in 2.2 +/- 1.2 (1-7) days. No adverse effects were observed. Cyclosporin, serum creatinine, and ALT levels were not affected by treatment. CONCLUSIONS: Azithromycin improves cyclosporin-associated gingival hyperplasia, especially when administered early in the process.

Adult↗
PubMed1986

Clinical and pharmacologic correlations in cyclosporine-induced gingival hyperplasia.

Cyclosporine-induced gingival hyperplasia was investigated in a clinical study of 100 patients over a period of 2 1/2 years. Seventy percent of the patients exhibited at least mild gingival hyperplasia. For doses within the therapeutic range, no direct correlation was found between the oral dose or the serum trough concentration of cyclosporine and the severity of gingival hyperplasia. The presence of dental plaque was found to be related to the presence of gingival hyperplasia, but only a weak correlation existed between the abundance of plaque and the severity of gingival hyperplasia. Children and especially adolescents had a greater risk of developing cyclosporine-induced gingival hyperplasia than adults had. In 21 patients followed for 1 to 18 months after cessation of cyclosporine therapy, induced gingival hyperplasia was found to be clinically reversible.

Adolescent↗
PubMed1997

Oral metronidazole does not improve cyclosporine A-induced gingival hyperplasia.

Recently, resolution of cyclosporine A (CSA)-induced gingival hyperplasia was reported with antibiotic treatment. We therefore assessed the oral status of 45 children on CSA after renal transplantation and evaluated the effects of metronidazole treatment in children with high-grade gingival hyperplasia. Gingival hyperplasia was absent in 19 (42%), mild in 5 (11%), moderate in 13 (29%), and severe in 8 (18%) children. There was no significantly different incidence in high-grade gingival hyperplasia (moderate and severe) between children with (16 of 30) or without (5 of 15) concomitant treatment with calcium channel blockers. The mean trough level of CSA was not different between children with varying severities of gingival hyperplasia. We treated 13 children with high-grade CSA-induced gingival hyperplasia (9 boys, 4 girls, mean age 14.2 +/- 3.4 years) with 750 mg metronidazole in three divided doses (10-25 mg/kg) for a total of 7 days. All 13 children were concomitantly treated with calcium channel blockers for hypertension; their mean monoclonal CSA trough level was 246 +/- 34 ng/ml. Oral examination and photographic documentation were performed by the same examiner on all patients before and 1 and 3 months after metronidazole treatment. We found no changes in gingival hyperplasia; gingival inflammation improved in 5 children (P = ns). We conclude that synergistic effects of calcium channel blockers and high concentrations of CSA in our population may outweigh beneficial effects of metronidazole treatment of CSA-induced gingival hyperplasia after renal transplantation.

Adolescent↗
PubMedDate not supplied

The measured effect of phenytoin withdrawal on gingival hyperplasia in children.

Gingival enlargement was studied and measured in ten patients before, and for 18 months after discontinuation of phenytoin therapy. A clinically evident decrease in gingival hyperplasia occurred after discontinuing phenytoin in all subjects; all subjects, however, had mild hyperplasia after 18 months. These results may encourage increased use of alternative antiseizure drugs.

Adolescent↗
PubMed1997

[Nicardipine-induced gingival hyperplasia].

Drug-induced gingival hyperplasia is usually associated with the administration of hydantoin in individuals with epilepsy. The same side effect has also been reported, however, after administration of cyclosporin and some calcium channel blockers such as nifedipine, verapamil, diltiazem and nitrendipine in adults generally or in the elderly, as well as after experimental exodipin administration to rats. We report an 8.5-years-old boy who had been receiving nicardipine treatment for cerebral vascular disease since the age of 20 months, with gradually increasing doses and no side effects for 5 years. Gingival hyperplasia then presented and progressed over the next two years after the dose was increased from 40 to 50 mg/day. The patient was not taking and has never taken any other medication. This is the first case of gingival hyperplasia induced by nicardipine described to date.

Calcium Channel Blockers↗
PubMed2004

Effects of azithromycin on cyclosporine-induced gingival hyperplasia in renal transplant patients.

BACKGROUND: Gingival hyperplasia is a well-known complication of cyclosporine therapy, affecting 21% to 35% of renal transplant patients. Metronidazole, clarithromycin, and azithromycin, all azalid antimicrobial agents derived from the macrolide antibiotic erythromycin, have been used for treatment. Marked improvements in gingival hyperplasia have been recorded in particular with azithromycin. The aim of the present study was to investigate histopathological features of cyclosporine-induced gingival hyperplasia and to evaluate the quantitative efficacy of short-term azithromycin therapy. METHODS: Eighteen renal transplant patients with cyclosporine-induced gingival hyperplasia were included in the study. All patients received azithromycin with a dose of 500 mg/d for 3 consecutive days. Changes in gingival hyperplasia were evaluated by measuring the gingival sulcus depth to the cementum-enamel junction of every tooth in each of the four quadrants on days 0, 7, 30, 90, 180. Gum biopsies were obtained on days 0 and 30; the degree of inflammation was classified as "mild," "intermediate," and "severe". RESULTS: Gingival hyperplasia was reduced in all treated patients throughout the study. The degree of improvement was more significant between 0 to 7 and 7 to 30 days than at other times (respectively, P < .0001 and P < .002). Histopathologically, eight patients had severe and one patient moderate chronic inflammation at the beginning of therapy. Three other biopsies were reported as papilloma, mucosal hyperplasia, and normal gingival tissue biopsy. CONCLUSIONS: Azithromycin appears to be useful to treat cyclosporine-induced gingival hyperplasia in renal transplant patients. Treatment is inexpensive and free from known adverse effects.

Adult↗