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Results for “GINGIVAL HYPERPLASIA”

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PubMed2003

The subgingival microflora in phenytoin-induced gingival hyperplasia.

OBJECTIVES: Microbial flora and gingival conditions were compared between a group of patients with phenytoin-induced gingival hyperplasia as a test group, a control group of patients who were administered phenytoin without gingival hyperplasia and a blank group who took no phenytoin and no gingival hyperplasia in mentally retarded patients. MATERIALS AND METHODS: Subgingival plaque samples were collected from a PHT-induced overgrown gingival pocket and microbiological experiments were performed by culture and PCR methods. RESULTS: The predominant genera in total cultivable bacteria from subgingival plaque samples were streptococcus and actinomyces with recovery ranges of 37.6-42.1% and 23.4-25.5% of total bacteria, respectively, in all groups. The test group showed a significantly higher level of obligate Gram-negative rods than the control and blank groups. Black-pigmented obligate anaerobic Gram-negative rods were detected in 10.3% of total cultivable bacteria in the test group. The black-pigmented rods were predominantly Prevotella intermedia in the test group and Prevotella nigrescens in the control and blank groups. Porphyromonas gingivalis and Porphyromonas endodontalis were also detected in the test group with small values. CONCLUSIONS: These results suggested that black-pigmented rods, particularly P. intermedia, could be habitable in the environment of gingival hyperplasia.

Adolescent↗

PubMed1998

Pre-transplant gingival hyperplasia predicts severe cyclosporin-induced gingival overgrowth in renal transplant patients.

The relationship between the pre-transplant periodontal status and the development of post-transplant gingival overgrowth was investigated in a longitudinal study. The periodontal condition of 35 patients was examined on 2 occasions while they were on the transplant waiting list and then at 4-6, 10-12, 16 and 20 weeks post-transplant. At each visit the plaque index, the bleeding index and a pocket index (CPITN) were measured. Dental impressions were taken of the pre- and post-transplant gingival condition and used to make stone models which were used to score the gingival overgrowth index (GOI). The patients divided into 3 distinct groups having severe (n=13), mild (n=16) or no post-transplant gingival overgrowth (n=6). Only 1 of the patients had taken cyclosporin prior to inclusion into the study. All the patients who developed severe overgrowth had evidence of gingival hyperplasia before the transplant. There was no difference in the serum cyclosporin levels between the three groups (chi2<2.28, p>0.319). Furthermore, there was no statistical difference for any of the periodontal indices. This study indicates that the hyperplastic gingival inflammatory response of some individuals appears to be potentiated by cyclosporin resulting in severe post-transplant overgrowth. In other patients the same reaction may allow the fibroblastic activity to occur to an extent where it produces a mild clinically apparent overgrowth.

Chi-Square Distribution↗

PubMed1989

Nifedipine-induced gingival hyperplasia.

Nifedipine-induced gingival hyperplasia was first reported in 1984. Nifedipine is a relatively new drug used in the treatment of ventricular arrhythmias and angina. This article reports a case of gingival hyperplasia induced by the drug and reviews the cases reported so far in the literature.

Coronary Disease↗

PubMed2002

Drug-induced gingival hyperplasia in transplant recipients.

Gingival hyperplasia is a common occurrence in transplant recipients who are taking cyclosporine. This condition can be complicated when calcium channel blockers or phenytoin are added to the armamentarium of medications; it can be painful and may interfere with eating, speech, and appearance. Multiple mechanisms exist for gingival overgrowth. Prevention with appropriate oral hygiene appears important in controlling the inflammatory component and decreasing the severity of the overgrowth. Patients must be aware of the potential for the development of gingival hyperplasia and must follow up with regular professional cleanings. If the overgrowth persists, treatment options should be discussed between patients and their physician. Conversion from cyclosporine to tacrolimus, treatment with antibiotic therapy, and surgical excision or laser therapy are all potential therapies to consider.

Cyclosporine↗

PubMed1985

Nifedipine-induced gingival hyperplasia. A histochemical and ultrastructural study.

Gingival hyperplasia induced by nifedipine (Procardia), a calcium channel-blocking agent used as an anti-anginal drug, was studied. In recent months, the role of nifedipine in the etiology of gingival hyperplasia has attracted interest. The purpose of this study was to determine the causal relationship and compare nifedipine to other drug-induced (phenytoin) and nondrug-induced gingival hyperplasias. Histochemical studies revealed increased numbers of fibroblasts containing strongly sulfated mucopolysaccharides in the nifedipine- and phenytoin- (Dilantin) induced gingival hyperplasias as compared to the nondrug-induced cases. Numerous secretory granules were also noted in the fibroblast cytoplasm in the nifedipine-treated case studied by electron microscopy. These results imply that there is an increase in acid mucopolysaccharide production in the nifedipine- and phenytoin-induced gingival hyperplasias. The potential significance and comparisons of the drugs' effects at the cellular level are discussed.

Acid Phosphatase↗

PubMed2006

Amlodipine-induced gingival hyperplasia.

Drug-induced gingival hyperplasia is a serious concern both for the patient and the clinician. A 45 year-old Caucasian male patient with hypertension, who received amlodipine (10 mg/day, single dose orally) for two months, sought medical attention because of the new-onset gingival enlargement. On clinical examination a generalized and firm overgrowth of the gingival throughout the maxilla and the mandible were evident. The lack of gingival inflammation and purulent discharge were other features of the clinical scenario. Histological assessment of the biopsy specimen revealed the hyperplasia of connective tissue, epithelial acanthosis, and elongated rete ridges along with few inflammatory cells. The histological and the clinical evidences were consistent with amlodipine-induced gingival hyperplasia. We believe that the present report indicates the most rapidly developed case of amlodipine-induced gingival hyperplasia reported to date. The related literature is reviewed and the underlying pathogenic mechanisms of this rare side-effect are discussed here.

Amlodipine↗

PubMed1995

Prevalence of nifedipine-induced gingival hyperplasia.

This study investigated the prevalence of gingival hyperplasia in subjects who were undergoing treatment with a calcium channel blocker, nifedipine, in dentate and edentulous subjects. In addition, the relationship between gingival hyperplasia and 5 other variables (duration of nifedipine intake, dose, age, oral hygiene index, and number of teeth) was investigated. Results of statistical analyses showed overwhelming evidence that the percent of nifedipine subjects with gingival hyperplasia was greater than that of the control subjects (P < 0.05) and that, across treatment group, the percent of dentate subjects with hyperplasia was significantly higher than that for edentulous subjects (P < 0.05). The chi2 test showed a strong univariate relationship between gingival hyperplasia and, separately, oral hygiene and number of teeth. For 24% of the subjects with gingival hyperplasia index (GHI) values of 2 or 3, gingivectomy was performed, and the tissues were prepared for histological examination. Microscopic examination of the biopsy material showed findings similar to those from previously reported cases of nifedipine- or phenytoin-induced hyperplasia.

Age Factors↗

PubMed1994

Cystinosis and gingival hyperplasia: demonstration of cystine crystals in gingival tissue and unusual aspects of management.

A patient with nephropathic cystinosis developed gingival hyperplasia secondary to cyclosporine-A therapy for his renal allograft. The typical crystals described on electron microscopic examination of other organs of patients with cystinosis were seen in the resected gingiva of this patient. These crystals have not been previously described in this location. Unusual aspects of the management of this patient are discussed.

Adult↗

PubMed1991

The administration of folic acid to institutionalized epileptic adults with phenytoin-induced gingival hyperplasia. A double-blind, randomized, placebo-controlled, parallel study.

Twenty severely retarded institutionalized epileptic adults with phenytoin-induced gingival hyperplasia were divided into two groups and received a daily 3 mg capsule of either folic acid or lactose for 16 weeks in a randomized, double-blind, parallel study. Serum folate and phenytoin levels were recorded at baseline and on completion of the study. Twelve areas of the gingiva on each patient were graded at 4-week intervals for 16 weeks with respect to the three indexes: hyperplasia, gingival health, and plaque index. There were no significant differences between treatment groups for any of the three indexes over time. The poststudy serum folate levels were three times baseline levels for the active drug group (p less than 0.001) but unchanged in the placebo group. Phenytoin blood levels that began within the therapeutic window (10 to 20 micrograms/ml) tended to remain within the therapeutic window for both groups, with no reported seizure activity. A single daily oral 3 mg capsule of folic acid did not show efficacy as the sole therapeutic agent in the reduction of phenytoin-induced gingival hyperplasia.

Adult↗

PubMed2000

Relationship between gingival hyperplasia and class II histocompatibility antigens in renal transplant recipients.

Gingival hyperplasia, a well-known side effect of ciclosporin A (CS-A), is much more prominent when CS-A is used in combination with calcium channel blockers, especially dihydropyridines. On the other hand, it is interesting to note that this complication is not observed in all patients using this drug combination. This study was conducted in order to investigate the relationship (if any) between major histocompatibility complex antigens and gingival hyperplasia. Seventy-six renal transplantation patients were evaluated by an experienced dentist for gingival hyperplasia. The patients were then divided into two groups according to the presence (group 1, n = 18) or absence (group 2, n = 58) of gingival hyperplasia. There was no significant difference between the two groups regarding age, sex, transplant age, donor type, antihypertensive and immunosuppressive therapy protocols, and CS-A levels. HLA-DR2 antigen was present in 63% of the patients with gingival hyperplasia and in 34% of the patients without gingival hyperplasia. However, the HLA-DR1 antigen frequencies were found to be 11 and 22% in group 1 and group 2, respectively. In patients receiving nifedipine as an antihypertensive therapy, gingival hyperplasia developed more often than in patients receiving verapamil or diltiazem. As a result, in renal allograft recipients with HLA-DR1 antigen, gingival hyperplasia was seen less frequently than in HLA-DR2-positive patients. It is believed that the presence of these antigens regulates the response of the patients to either CS-A and/or calcium channel blockers.

Adult↗

PubMed2005

Non-Hodgkin's lymphoma manifest as gingival hyperplasia in a renal transplant recipient.

Gingival hyperplasia is a frequent complication in transplant patients who receive cyclosporine or calcium channel blockers. We studied an unusual case involving a renal transplant recipient with post-transplant non-Hodgkin's lymphoma that manifested as gingival hyperplasia. We initially consider that it was a side effect of cyclosporine and nifedipine. The lesion did not respond to dose reductions or the withdrawal of cyclosporine and nifedipine, and the gingival hyperplasia progressed in a localized fashion, becoming ulcerated and bleeding easily. Histological examination revealed the presence of malignant lymphoma.

Adult↗

PubMed1990

[Cyclosporine-induced gingival hyperplasia in renal transplant patients].

Cyclosporine-induced gingival hyperplasia was investigated in a clinical study of 80 renal transplant patients. 34% of the patients exhibited at least mild gingival hyperplasia in the anterior, and 9% presented this finding also in the posterior region. No direct correlation was found between the oral dose or the whole blood concentration of cyclosporine and the presence of gingival overgrowth. Young and female patients were at a significantly greater risk of developing cyclosporine-induced gingival hyperplasia than the other patients. The presence of dental plaque or gingival inflammation was not found to be related to the incidence of gingival hyperplasia.

Adolescent↗

PubMed2003

Recurrent recalcitrant gingival hyperplasia and plasminogen deficiency: a case report.

BACKGROUND: Recurrent gingival hyperplasia due to plasminogen deficiency is a rare condition due to fibrin deposition in the connective tissue. Only eight cases have previously been reported in the English literature, and all cases were diagnosed before the age of 35 years. This paper presents an older patient with recurrent gingival hyperplasia due to plasminogen deficiency (hypoplasminogenemia). METHODS: A 59-year-old woman presented with recurrent gingival swelling of 6 years' duration. Multiple biopsies performed at various time periods were histologically reported to be gingival hyperplasia with chronic inflammation. Routine hematoxylin and eosin (H & E) staining and direct immunofluorescence were performed. RESULTS: H & E-stained sections showed subepithelial, eosinophilic, amorphous, acellular deposits. Direct immunofluorescence showed positive staining for fibrin, immunoglobulin (Ig) G, IgA, and IgM. Functional plasminogen and plasminogen activator inhibitor-1 assays were done and found to be deficient. A diagnosis of gingival hyperplasia due to plasminogen deficiency (hypoplasminogenemia) was rendered. CONCLUSIONS: Recurrent gingival hyperplasia due to plasminogen deficiency (hypoplasminogenemia) is a newly recognized and rare condition. H & E staining, direct immunofluorescence, and assessment of functional plasminogen levels are essential to differentiate this condition from other conditions in which subepithelial, eosinophilic, amorphous materials are deposited.

Deficiency Diseases↗

PubMed1997

Prevalence of amlodipine-related gingival hyperplasia.

Calcium channel blockers are known to contribute to gingival hyperplasia. The vast majority of reports discuss patients taking the drug nifedipine. During the past few years a newer calcium channel blocker, amlodipine, has been used with increasing frequency. To date, six cases have been published indicating that amlodipine may also promote gingival hyperplasia; however, no data have been reported regarding the prevalence of this phenomenon. The purpose of this study was to examine a large group of patients taking amlodipine and determine the prevalence of gingival hyperplasia. One hundred fifty dentate patients who had been taking amlodipine, 5 mg per day for at least 6 months, volunteered to undergo a screening examination for gingival hyperplasia. Mild hyperplasia (< 1/3 clinical crown) was found in five patients-a prevalence of 3.3%. This is significantly less (P < .001) than rates reported for patients taking nifedipine, and not significantly different from rates previously reported in control groups of cardiac patients not taking calcium channel blockers. The results from this group of patients indicated that amlodipine, 5 mg per day, did not induce gingival hyperplasia.

Adult↗

PubMed1997

[Gingival hyperplasia associated with amlodipine].

Drug-induced gingival hyperplasia is a well documented unwanted side effect within the literature. It has been associated with the use of three different types of pharmaceutical agents, including phenytoin, cyclosporine and calcium channel blocking agents. Amlodipine belongs to the dihydropyridine-derived calcium blocking agents that may cause the side effect of drug-induced gingival hyperplasia. In the present study the possible pathogenic mechanisms, clinical and histologic presentation and therapeutic indications of amlodipine-induced gingival hyperplasia are discussed.

Aged↗

PubMed1994

Calcium channel blocker-induced gingival hyperplasia: case report and review of this iatrogenic disease.

Gingival hyperplasia is a common disorder associated with phenytoin and cyclosporine therapy. However, induction of this condition by calcium channel blockers is less well known. Inflammation of the gingival tissue from bacterial plaque and the subsequent development of gingival crevicular fluid may allow sequestration of the calcium channel blocker, thus predisposing the tissue to a localized toxic effect and the development of gingival hyperplasia. Calcium channel blockers have cellular effects similar to those of phenytoin and cyclosporine, including the production of a localized folic acid deficiency. All of the available calcium channel blockers have been reported to cause gingival hyperplasia. Treatment options include meticulous plaque control, and in severe cases, gingivectomy. Gingival hyperplasia can be prevented with meticulous plaque control or avoidance of the offending medication.

Aged↗

PubMed1998

Efficacy of azithromycin in the treatment of cyclosporine-induced gingival hyperplasia in renal transplant recipients.

BACKGROUND: Gingival hyperplasia (GH) is a common side effect of cyclosporine . Azithromycin (Zithromax; AZI) is a macrolide antibiotic reported in case studies to reduce cyclosporine-induced gingival hyperplasia (CIGH) in renal transplant recipients (RTR). METHODS: The efficacy of AZI to treat CIGH in RTR was examined in a double-blind, randomized crossover trial. Patients (n=17) with CIGH were randomized to receive AZI and a matching placebo in alternate order for 5 days, separated by a 2-week washout period. Follow-up visits were conducted at week 6 and week 12. Changes in GH were evaluated by measuring the clinical gingival sulcus depths, tooth length, and the length of the interdental papillae to the cementum-enamel junction of two teeth in each of the four quadrants. RESULTS: Significant improvements were observed in all three types of periodontal measurements, representing reductions of gingival tissue above the medial aspect of the tooth, of the gingival sulcus depth, and of the length of the interdental papillae. Patients reported an improvement in gum bleeding. AZI was well tolerated, and 67% of the patients reported that the treatment was at least somewhat useful. CONCLUSIONS: AZI should be considered for RTR with CIGH.

Adult↗

PubMed1994

Clinical assessment of gingival hyperplasia in patients treated with nifedipine.

Gingival hyperplasia caused by the use of nifedipine has been extensively reported. In this paper, the gingiva of 18 patients suffering from cardiopathy and treated with nifedipine were compared with those of 10 patients with cardiac disorders who had not been treated with calcium antagonists and with a no-treatment group of 12 patients. Nifedipine produced gingival hyperplasia, although patients who had not been treated with calcium antagonists also had mild hyperplasia. Hyperplasia first appeared in the interproximal areas, an observation which may be important for early detection. There was a direct correlation between the degree of hyperplasia and the bacterial plaque score. When we studied the influence of administration time and dose of nifedipine with the degree of hyperplasia, no statistically significant differences were found.

Dental Plaque Index↗