[Biochemical study of diphenylhydantoin gingival hyperplasia--effect of DPH on rat gingival glycosaminoglycan synthesis from succinate-1,4-14C].
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Animals↗
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Results for “GINGIVAL HYPERPLASIA”
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Diphenylhydantoin-induced gingival hyperplasia: its response to changes in drug dosage.
Changes in gingival hyperplasia were studied in 48 patients treated for epilepsy with diphenylhydantoin (DPH) over a two-year period. During this time changes in the dose of DPH were made in some patients in order to increase control of seizures or decrease side-effects: in 27 patients the dose was increased, in nine it was decreased and in 12 the dose remained unchanged. It was found that the severity of gingival hyperplasia varied directly with both the dose and serum level of the drug.
Adolescent↗
Phenytoin as a risk factor in gingival hyperplasia.
Fifty-four out-patients with epilepsy who had been taking phenytoin for more than one year were examined for gingival hyperplasia. Approximately 76% of patients showed either mild or no gingival hyperplasia. Lesion severity was then compared statistically to phenytoin dosage and drug concentrations as well as to other clinical and laboratory parameters. There was a tendency for gingival hypertrophy to be associated with both increasing dosage of phenytoin per unit of body weight and the duration of phenytoin administration. All patients followed had a statistically significant progressive trend to increasing gingival hyperplasia with higher total and free phenytoin concentration.
Adult↗
[Congenital idiopathic gingival hyperplasia observed in a 6-year-old child].
Congenital diffuse gingival hyperplasia is a rare entity. A case is presented for the first time in Senegal, the etiology of the affection being undetermined. The various pathogenic hypotheses for this lesion include: diffuse gingival fibroma, congenital, hereditary or idiopathic gingival fibromatosis, familial gingival elephantiasis and idiopathic or hereditary gingival hyperplasia.
Adult↗
The gingival hyperplasia resulting from diphenylhydantoin in children and adults.
The incidence of gingival hyperplasia resulting diphenylhydantoin was studied in two hundred and nineteen patients of epilepsy from children to adults. The children group below puberty showed unexpectedly low incidence of gingival hyperplasia among the side effects of it comparing with other age groups.
Adolescent↗
Gingival hyperplasia associated with nifedipine therapy. Report of a case.
A case of gingival hyperplasia associated with the administration of nifedipine is reported. Clinically and histologically, the tissue resembled that seen in hyperplasia induced by phenytoin (Dilantin). We believe this to be the first reported case of gingival hyperplasia associated with this drug.
Female↗
Keratinocyte growth factor receptor is up-regulated in cyclosporin A-induced gingival hyperplasia.
Keratinocyte growth factor stimulates the growth and activity of epithelial cells via the keratinocyte growth factor receptor. We have recently shown that the growth factor is markedly elevated in cyclosporin A-induced gingival hyperplasia tissue in vivo, but the effects of cyclosporin A on the receptor are not yet known. The present study was therefore carried out to determine whether expression of the keratinocyte growth factor receptor is up-regulated in gingival hyperplasia compared with normal gingiva. Using immunohistochemistry and the reverse-transcribed polymerase chain-reaction, we obtained results which showed that receptor antigen and gene transcript levels were both elevated in gingival hyperplasia tissue. In addition, flow cytometry and the reverse-transcribed polymerase chain-reaction showed that the receptor and mRNA were also higher in gingival epithelial cells following incubation with cyclosporin A in vitro. These findings suggest that the keratinocyte growth factor-receptor pathway of mesenchymal-epithelial interaction could play an important part in the molecular pathogenesis of gingival hyperplasia.
Adolescent↗
Surgical treatment of nifedipine-induced gingival hyperplasia. A case report.
A surgical technique for treating nifedipine-induced gingival hyperplasia is described. A brief overview of nifedipine (trade name Procardia) is given, along with its use in the treatment of hypertension and its side effects, particularly as they relate to the induction of gingival hyperplasia. A detailed description and rationale for the surgical excision of the hyperplastic gingival tissue with a flap approach is given. A case is presented to illustrate the technique and post treatment results.
Angina Pectoris↗
Nifedipine-induced gingival hyperplasia. A comprehensive review and analysis.
A comprehensive review of the literature and analysis of the clinical history, mechanisms, pathogenesis, histology, and management of nifedipine-induced gingival hyperplasia is reported. A correlation to age, gender, drug, dosage, duration of drug therapy, location, and mode of treatment is discussed. The case report presented provides a model for management of nifedipine-induced gingival hyperplasia and other drug-induced gingival hyperplasia.
Calcium↗
Light and electron microscopic study of cyclosporin A-induced gingival hyperplasia.
Four transplant (3 kidney, 1 bone marrow) patients with cyclosporin A (CyA)-induced gingival hyperplasia are described. Light and electron microscopic findings of gingival biopsies showed in all patients that, in addition to an increase of collagen, CyA induced in the subepithelial space an enormous infiltration of morphologically normal plasma cells in different stages of maturation. These data, together with the reversibility of the lesion upon discontinuation of the drug, suggest that individual hypersensitivity is probably the most acceptable explanation of CyA-induced gingival hyperplasia. This hypothesis is also discussed in relation to the CyA-suppression of the functions of some T-lymphocyte subsets.
Adult↗
The effect of conversion from cyclosporine to tacrolimus on gingival hyperplasia, hirsutism and cholesterol.
UNLABELLED: The use of cyclosporine for immunosuppression in renal transplantation allograft recipients is associated with hypertrichosis, gingival hyperplasia, and hypercholesterolemia. Conversion of patients to tacrolimus may lead to an improvement in these effects with minimal risk of rejection or allograft dysfunction. METHODS: Sixteen renal transplant recipients were prospectively converted from CsA to tacrolimus and followed for 1 year. Gingival hyperplasia index, total cholesterol, and blood pressure were recorded at the outset, 4-, 8-, and 12-month intervals. Glomerular filtration rate was checked before conversion and 1 year later. Photographs documenting hypertrichosis were taken before conversion and 1 year later. Adverse effects from tacrolimus were recorded at 4, 8, and 12 months. RESULTS: Twelve patients with hypertrichosis noted rapid improvement. Mean gingival hyperplasia index decreased from 24 to 6; mean total cholesterol decreased from 237 to 195. Glomerular filtration rate was essentially unchanged (56 to 54). One episode of rejection occurred, three patients developed diarrhea, three noted headaches, and one had a tremor. CONCLUSION: If carefully monitored, patients suffering adverse effects secondary to cyclosporine may be converted to tacrolimus with minimal risk of allograft dysfunction or rejection.
Adolescent↗
[Gingival hyperplasia during treatment with nifedipine].
INTRODUCTION: Nifedipine is a relatively new and increasingly used medication for treatment of all kinds of angina pectoris and arterial hypertension. The principal action of nifedipine is to inhibit the influx of extracellular calcium ions across the membranes of cardiac and vascular smooth muscle cells, without changing serum calcium concentration (1). One of the side effects of this drug is gingival hyperplasia which was first described in 1984 by Lederman (2). He noted that gingival hyperplasia is mostly marked on the labial gingiva of the upper and lower anterior teeth and appeared 1 to 2 months after nifedipine therapy began at a dose of 90 mg per day, and never occurs in edentulous areas. This paper reports gingival hyperplasia in a patient treated with nifedipine. CASE REPORT: A 73-year-old man referred to the dental clinic for evaluation of gingival enlargement in the maxillar left quadrant which he had noticed about 3 months after starting the nifedipine therapy. Clinical examination showed gingival enlargement around the teeth 22, 23, 24 and 27, but with normal edentulous area (Fig. 1). The enlarged gingiva was red, smooth and shiny, with no pain on touch, and bled easily on probing. There were metal crowns with overhanging margins and pseudopockets--6 mm with dental plaque and calculus. Radiographs showed moderate alveolar bone resorption of horizontal type. The patient's maxillar left first premolar exhibited severe bone loss, resulting in a hopeless prognosis. This tooth was extracted under local anesthesia. The dental treatment included replacement of the ill-fitting metal crowns, scaling and root planning, and instructions on appropriate method for brushing teeth. 6 weeks later, the hyperplastic tissues were removed surgically. In a 1-year follow-up period, the patient was recalled at regular intervals for control, and no signs of recurrence of gingival hyperplasia have been observed in spite of continued nifedipine treatment. Biopsies taken from the gingivectomy specimens were handled with standard histological method. Histological examination showed a thick epithelium with parakeratosis and acanthosis, and irregular elongation of the rete peg. The underlying connective tissues contained dense fibers with inflammatory cell infiltrate mainly composed of plasma cells. DISCUSSION: The exact mechanism of action of nifedipine in causing gingival enlargement is unknown at present. There is also no answer to the question why gingival enlargement appears in some patients treated with nifedipine, but in others not. The clinical findings (3, 4, 5, 6, 7) and results of in vitro study (8) and this case report showed that hyperplastic change of gingiva started only in areas displaying signs of inflammation, but not in healthy and edentulous areas. These observations suggest that local factors and associated inflammation is essential for onset of the nifedipine-induced gingival hyperplasa. Moreover, it was suggested that duration of nifedipine therapy (more than 2 months) and drug dosage (90 mg per day) could be important (1,2,3). This case report also demonstrates that no signs of recurrence of hyperplasia were observed after elimination of the local inflammatory factors: extensive dental pluque control and surgical removal of the hyperplastic gingival tissue even though administration of nifedipine was continued. CONCLUSION: It was concluded that gingival enlargement occurs in patients with nifedipine therapy only in the areas where local inflammatory factors are present.
Aged↗
Therapeutic alternatives in phenytoin-induced gingival hyperplasia. A case report and discussion.
The problem of phenytoin-induced gingival hyperplasia is dicussed within the context of consultative planning between oral care practitioners and the physician managing the epilepsy. The reluctance of the neurologist or of the patient to change an ongoing anti-convulsant program is often a response to a long history of tedious steps in medication adjustments to establish a level of seizure control without sacrificing alertness and mood control. Realistic indicators for discontinuing phenytoin are enumerated and therapeutic alternatives in treating phenytoin hyperplasia are discussed. A complicated case of seziure control is offered as an example of requirements in the medical control of epilepsy and the context in which periodontal therapy can be planned in conjunction with these medication adjustments. The mechanism of phenytoin induction of gingival hyperplasia is briefly discussed. Phenytoin (Dilantin) and a newer agent, valproic acid (Depakene), are compared as alternatives in seizure control.
Adolescent↗
Upper airway obstruction due to massive gingival hyperplasia. A case report and description of a new surgical treatment.
Drug-induced gingival hyperplasia is a frequent complication of phenytoin anticonvulsant therapy. In severe cases, gingival hyperplasia can cause marked cosmetic deformity, phonatory abnormalities and significant occlusal changes which severely restrict masticatory function. Airway obstruction has not been previously reported with this condition. We describe a unique case of massive phenytoin-induced gingival overgrowth causing glossoptosis and subsequent upper airway obstruction. Possible medical and surgical treatment options, including laser wedge resection of the base of the tongue, are discussed.
Airway Obstruction↗
Cytomegalovirus-induced gingival hyperplasia.
We report a rare presentation of gingival hyperplasia associated with cytomegalovirus infection in a 33-year-old human immunodeficiency virus-infected man.
AIDS-Related Opportunistic Infections↗
Prevalence and risk factors associated with leukoplakia, hairy leukoplakia, erythematous candidiasis, and gingival hyperplasia in renal transplant recipients.
The aims of this study were to determine the prevalence of intraoral lesions in renal transplant recipients and to identify possible risk factors. The oral mucosa of 159 renal transplant recipients and 160 control patients was examined. The most common lesion in renal transplant recipients was cyclosporin-induced gingival hyperplasia (prevalence 22%) and patients with gingival hyperplasia were found to be taking significantly more cyclosporin-A than those without (p < 0.001). The prevalence of hairy leukoplakia and leukoplakia in renal transplant recipients was 11.3% and 10.7%, respectively, compared with 0% and 5.6% in the controls. Oral candidiasis was observed in 9.4% of renal transplant recipients compared with 2.5% of the controls; 3.8% of renal transplant recipients exhibited erythematous candidiasis, but this was not seen in the controls. Renal transplant recipients had a significantly increased risk of developing gingival hyperplasia (p < 0.0001), oral candidiasis (p < 0.0005), and two other conditions that have a well-established association with the immune suppression accompanying HIV infection, hairy leukoplakia (p < 0.0001) and erythematous candidiasis (p < 0.01).
Alcohol Drinking↗
Cyclosporine A-induced gingival hyperplasia pemphigus vulgaris: literature review and report of a case.
Gingival hyperplasia appears in 8% to 85% of patients treated with cyclosporine. Most studies show an association between oral hygiene status and the prevalence and severity of this gingival overgrowth. Thus, besides attempting to substitute this drug with another whenever possible, treatment usually involves maintenance of strict oral hygiene coupled with scaling and root planing and removal of iatrogenic factors. Sometimes a second treatment phase involving periodontal surgery is necessary. Cyclosporine-induced gingival overgrowth has been mainly described in post-organ transplant patients. The present case describes, for the first time, a severe form of cyclosporine-induced gingival overgrowth arising in a 15 year-old male with pemphigus vulgaris. Periodontal treatment included oral hygiene and scaling and root planing under local anesthesia. There was a significant reduction in gingival enlargement, as well as a reduction in plaque levels and inflammation. Cessation of drug administration, combined with continuous periodontal treatment, brought further improvement. This successful conservative treatment of cyclosporine-induced gingival overgrowth in a pemphigus vulgaris patient suggests that early diagnosis and comprehensive treatment of these lesions may yield good response and reduce the need for periodontal surgery.
Adolescent↗
Focal gingival hyperplasia in a horse.
A diagnosis of gingival hyperplasia in a 22-year-old Quarter Horse gelding was confirmed by histologic examination. Clinical signs included difficulty eating hay, and a large, intraoral soft tissue mass measuring 13 x 8 x 4.5 cm. The mass was located in the mucosa on the lingual aspect of the caudal left portion of the mandible, ventral to the base of the tongue, and covered the second and third lower molars, extending rostrally along the buccal mucosa to the premolars. The left maxillary second and third molars were overgrown with sharp edges. Lateral radiography of the mandible revealed absence of the left third molar, with associated bony irregularity and sclerosis. The horse was positioned in right lateral recumbency under general anesthesia, and the entire mass was resected. It was speculated that the lesion developed secondary to chronic irritation from opposing teeth and food-packing after loss of the lower third molar; this would not be an unexpected development in a species with continuously advancing molars.
Animals↗