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Results for “GINGIVAL HYPERPLASIA”

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At least 163 records · Page 9Linked to original sources
PubMed1976

[Prospects of surgical treatment in hydantoin-induced gingival hyperplasia].

During the past 20 years, gingivectomies were carried out in 100 out-patients of the maxillo-facial clinic of the Heidelberg university hospitals because of intensive gingival hyperplasia. 57% of the patients were epileptics who had been hydantoin-containing preparations. Follow-ups were made in 41 patients. The group of epileptics was critically compared with that of non-epileptics. In addition to the rate of recurrences, especially oral hygiene, existing bite abnormalities and the degree of mental retardation were considered. It was surprising that the number of recurrences did not drop when the hydantoin containing preparation was postoperatively discontinued. Even in edentulous regions of the jaws of two patients, recurrences of considerable size were found.

Adolescent↗
PubMed1994

A 15-year follow-up of phenytoin-induced unilateral gingival hyperplasia: a case report.

INTRODUCTION-The aim of this case report is to present a 15-year follow-up of a patient with phenytoin (PHT) intoxication with unilateral gingival hyperplasia (GH). MATERIAL AND METHODS-A 50-year-old woman was followed-up for 15 years clinically and paraclinically after a heavy PHT intoxication. Her immunoglobulins in serum were checked on PHT and after 15 years treatment with carbamazepine. RESULTS-A gross mass of hyperplasia tissue found primarily in the left side of her mouth had disappeared and serum IgA which was subnormal at the first visit had normalized. CONCLUSION-It is possible to prevent GH from PHT treatment by intensive dental care, correct mouth hygiene and by change of treatment of carbamazepine.

Adult↗
PubMed2003

[Ciclosporine A-induced gingival hyperplasia].

The increasing use of cyclosporine A (CSA) in organ transplants and in the treatment of autoimmune diseases has increased the incidence of cyclosporine A-related adverse effects, including gingival hyperplasia (GH). GH causes esthetic, speech, mastication and tooth growth problems in the affected patients. The prevalence of cyclosporine-induced GH varies in different studies and may be as high as 85%, depending on the diagnostic criteria. This review approaches etiological, histological and clinical issues, as well as the prevention and treatment of this important injury.

Cyclosporine↗
PubMed1988

[Gingival hyperplasia and serous papules due to cyclosporin treatment].

After 3 months of immunosuppressive treatment with cyclosporin because of a focal segmental glomerulosclerosis, a 13-year-old female developed marked gingival hyperplasia, hypertrichosis of the arms and papulo-vesicular skin lesions on the left leg. Histological and immunohistological examinations of the gingivae showed hyperplasia of the mucosa with perivascular infiltrates of plasma and B cells in the submucosa. The lesions on the leg revealed signs of cutaneous vascular inflammation with eosinophils, but there was no evidence of leucocytoclastic vasculitis. Ten months after discontinuation of cyclosporin, the lesions had nearly regressed. The patient's renal function deteriorated progressively to the point of terminal insufficiency.

Adolescent↗
PubMed1993

Gingival hyperplasia in renal allograft recipients receiving cyclosporin-A and calcium antagonists.

Although it is established that the immunosuppressant cyclosporin-A (CsA) and calcium antagonists [Nifedipine (Nif) and Diltiazem (Dz)] can independently induce gingival enlargement, little has been documented on the significance of the salivary CsA levels and the combined effect of CsA and a calcium antagonist upon gingival tissues. In the present cross-sectional investigation, clinical periodontal parameters and the pharmacologic profiles of CsA, Nif, and Dz were determined for 66 renal transplant recipients. Subjects were divided into the following groups: Group (Gp) 1: CsA [n = 18]; Gp 2: CsA + Nif [n = 15]; Gp 3: CsA + Dz [n = 12] and a negative Control Gp 4: azathioprine [n = 21]. A gingival enlargement score was assessed for each patient from study models using a hyperplastic index (HI). Pharmacologic profiles included CsA whole blood and whole saliva levels as measured by fluorescence polarization immunoassay. The HI scores between Gp 1, 2 and 3 were not significantly different. However, when compared with controls (Gp 4), there was a significant difference in HI and all individual groups (Gp 1, 2, 3) (p < 0.05). Gingival hyperplasia was only weakly related to plaque and calculus but was unrelated to CsA dose (mg/kg/day), duration of CsA therapy (months), CsA blood or saliva levels (ng/ml), or the concurrent administration of a Nif or Dz. Gingival enlargement was found to occur in 49% of subjects who were either on CsA or CsA and a calcium antagonist. It is concluded that CsA alone or in combination with a calcium antagonist caused a significant increase in gingival enlargement compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Gingival hyperplasia in dogs induced by oxodipine, a calcium channel blocking agent.

Subchronic oral exposure of dogs to Oxodipine, a new calcium channel blocker of the dihydropyridine-type, resulted in dose-related gingival hyperplastic changes. The doses at which an effect was elicited were 24 and 73 times the intended therapeutic dose for man. The effects were first noted after 7 weeks of treatment, and were limited to the high and intermediate dose groups of both sexes. Macroscopically, a generalized enlargement of the maxillary and mandibular facial and lingual gingivae were noted. The histological changes were similar to those described in man for Nifedipine and hydantoin-related drugs. An increase in the activity of alkaline phosphatase and a decrease in alanine aminotransferase was demonstrated. This article is the first to describe gingival hyperplasia in dogs induced in a dose-dependent manner by a calcium channel blocker.

Alanine Transaminase↗
PubMed1981

Persistent purple plaques of the face caused by gingival hyperplasia.

Persistent plaques that develop primarily on the face may be caused by a variety of conditions, but rarely is purely intraoral infection the primary cause. A case report is presented in which massive prolonged gingival hyperplasia resulted in a persistent and peculiar purple facial lymphedema. The condition resolved only after the intraoral disease had been successfully treated.

Facial Dermatoses↗
PubMed1990

[Gingival hyperplasia and hyper IgE syndrome].

The hyperimmunoglobulin E recurrent-infection syndrome is considered a primary immunodeficiency syndrome characterized by recurrent staphylococcal infections both cutaneous and pulmonary, chronic dermatitis, otitis and sinusitis. Our case report can be interesting for the age of the patient (39 years old), for the absence of visceral lesion and for the development of a peculiar gingival hyperplasia. The review of literature has shown that this kind of gingivitis is not usual but not extraordinary.

Adult↗
PubMed1990

Effect of cell donor age on the synthetic properties of fibroblasts obtained from phenytoin-induced gingival hyperplasia.

Diploid fibroblasts obtained from explants of human gingiva and maintained in vitro undergo a several-fold decrease in protein and collagen synthesis as a function of increasing donor age. Using drug-induced gingival hyperplasia as a model, we performed experiments to learn whether fibroblasts derived from hyperplastic tissue behave in a similar manner. Fibroblast strains were established from explants of hyperplastic gingiva obtained from 10 patients chronically ingesting phenytoin and ranging in age from 9 to 45 years. Protein production and degradation were compared to previously reported data similarly obtained from periodontally normal donors ranging in age from 12 to 68 yr. The total quantity of protein and collagen produced by the phenytoin cells was significantly greater than previously reported for cells from normal gingiva. No donor age-related decrease in protein and collagen production nor in the proportion of cell synthetic activity committed to collagen production was observed for cultures of phenytoin cells. The gross pattern of proteins produced, as assessed by 2-dimensional gel electrophoresis, was unrelated to donor age in both normal and phenytoin cells, but three polypeptides ranging in size from about 20 kD to 40 kD that were not found in the cultures of normal cells were produced by five of seven phenytoin cells strains. The observations demonstrate that the phenytoin cells do not undergo the donor age-dependent decrease in synthesis observed for normal cells. This abnormality may account in part for the phenytoin-induced hyperplasia. The phenytoin cells appear to be a unique phenotype.

Adolescent↗
PubMed1994

Multimodal treatment of drug-induced gingival hyperplasia in a kidney transplant patient.

Medical advances for treating organ diseases have resulted in thousands of organ transplants being performed each year. Every patient receiving a transplanted organ will also be placed on drugs that may induce gingival hyperplasia as a side effect. This article discusses the multiphasic approach to treating the disfiguring hyperplasia through chemical and mechanical plaque control, surgical removal of the tissue by lasers, and postsurgical rinses with folate.

Adult↗
PubMedDate not supplied

Chlorhexidine as an oral hygiene adjunct for cyclosporine-induced gingival hyperplasia.

Recent advances in surgical technique and chemotherapeutic procedures have greatly increased the survival rates of organ transplantation patients. Of dental importance is the widespread use of the immunosuppressive agent cyclosporine in this special-patient population, a drug that has the potential to cause severe gingival hyperplasia as a side effect. A case is presented illustrating the use of the plaque-inhibitor chlorhexidine as a therapeutic adjunct in possibly arresting this gingival condition.

Child, Preschool↗
PubMed1992

Nifedipine-induced gingival hyperplasia.

Gingial hyperplasia is a complication which may be seen in a significant number of patients taking nifedipine (Procardia, Pfizer) a commonly used medication for cardiac vessel dilitation. This is a report of gingival changes in a 43-year-old hypertensive male who began using the calcium channel blocking agent during his active dental treatment. Gingival hyperplasia developed which was severe enough to alter the course of his dental treatment and prompt his changing to other medications to control his blood pressure. The recognition that the drug was responsible for the hyperplasia led to prompt and effective methods to resolve this problem.

Gingival Hyperplasia↗
PubMed1990

[Cyclosporin A-induced gingival hyperplasias: cross-sectional study of young organ transplantation patients].

In this study 137 patients (30 adolescence, 2-21 years, 107 adults, 22-68 years), which had been treated with Cyclosporine-A, between 17 to 2461 days after organ transplantation, were examinated by gingival status. The severity of gingival hyperplasia increases in both groups with mean transplantations period, independent of mean daily doses of CsA and Azathioprin and independent of mean plasma concentration. Adolescence and adults differ significantly, in relation of each severity group frequency. The adolescence group includes 66.7% of the cases with gingival enlargement of severity degree 3. In both groups increases the mean value of PGI-Index with the severity degree.

Adolescent↗
PubMed1979

Gingival hyperplasia induced by diphenylhydantoin in a gorilla.

An adult male lowland gorilla had been treated with diphenylhydantoin for 6 months following several acute convulsive episodes. The gorilla remained clinically normal during that period. Then, for no apparent reason, it refused its usual diet. Physical examination revealed acute inflammatory gingival hyperplasia. Full mouth gingivectomy and antibiotic and analgesic therapy resolved the oral inflammation and the anorexia.

Animals↗
PubMed1976

Phenytoin-induced depression of salivary IgA and gingival hyperplasia.

IgA concentrations were determined in saliva from epileptic patients taking phenytoin and in saliva from healthy controls, by single radial immunodiffusion technique. Mean salivary IgA in epileptic children was 7.23 mg/ml; in healthy children, 16.44 mg/ml. Corresponding values for adults were 13.53 and 19.48 mg/ml, respectively. In 14 out of 84 samples, salivary IgA levels were too low for quantitative analysis. Salivary IgA levels were normal in untreated patients and fell during treatment with phenytoin. Gingival inflammation was commonly accompanied by an increase of salivary IgG and serum-derived IgA, whereas compensatory increase of IgM was infrequent. Phenytoin-induced deficiency of salivary IgA can result in increased susceptibility to gingival inflammation, which is considered one of the predisposing factors for subsequent development of gingival hyperplasia.

Adolescent↗