[Biochemical study of diphenylhydantoin gingival hyperplasia--effect of diphenylhydantoin on gingival C14-1,4-succinate metabolism].
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Animals↗
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Results for “GINGIVAL HYPERPLASIA”
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Chronic fibrous gingival hyperplasia, hypertrophic fibrous chronic gingivitis.
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Gingivitis↗
Gingival hyperplasia induced by calcium channel blockers: mode of action.
Gingival hyperplasia is a known side effect in patients treated with diphenylhydantoin, cyclosporin and the calcium channel antagonists. The present study proposes a mechanism by which calcium channel antagonists may induce gingival hyperplasia. The calcium antagonist induces blockage of the aldosterone synthesis in zona glomerulosa of the adrenal cortex since this pathway is calcium-dependent, cyclic nucleotide-independent. This may produce a feedback stimulation of an increase in pituitary secretion of ACTH which affects zona glomerulosa hyperplasia. This hyperplasia is merely related by accumulation of steroid intermediate products (androgens) that are transformed to testosterone because of an increase in 17-alpha-hydroxylase enzyme activity. Elevated levels of testosterone may act on the gingival cells and matrix to produce gingival hyperplasia.
Adrenocorticotropic Hormone↗
Nifedipine-induced gingival hyperplasia: a clinical and in vitro study.
Two cases of gingival hyperplasia associated with long-term administration of nifedipine, a drug that dilates coronary arteries, are reported. The clinical and histopathological features of the gingival hyperplasia induced by nifedipine were similar to those induced by phenytoin, an anticonvulsant drug. In the present cases, gingival inflammation had developed before drug administration. In one case, extensive dental plaque control in addition to surgical removal of the overgrown gingival tissues resulted in satisfactory progress without the need to discontinue drug administration, suggesting that the preexisting gingival inflammation was involved in the development of this periodontal disease. In the other case, change from nifedipine to another drug resulted in spontaneous recovery, strongly suggesting that the drug had induced the gingival hyperplasia. Nifedipine had no direct effects in vitro on proliferation or collagen synthesis of gingival fibroblastic cells from one of the patients. Study of these two cases suggests that both local inflammatory factors and long-term administration of nifedipine were responsible for the gingival hyperplastic changes observed.
Cell Division↗
Nitrendipine-induced gingival hyperplasia. First case report.
Drug-induced gingival hyperplasia is well documented within the literature. It has been associated with phenytoin, cyclosporine, and calcium channel blocking agents. Nitrendipine is an experimental calcium channel blocking agent that also appears to cause the side effect of drug-induced gingival hyperplasia. The clinical and histologic presentation of this side effect and possible biochemical mechanisms of pathogenesis are discussed.
Aged↗
Mast cells are not involved in the development of cyclosporin A-induced gingival hyperplasia: a study with mast cell-deficient mice.
BACKGROUND: A previous study suggested that mast cells (MC) are involved in the development of cyclosporin A-induced gingival hyperplasia, since an increased number of MC were observed in the tissue sections of enlarged gingiva. To determine the role of MC in gingival hyperplasia, an MC-deficient mouse model was used in the current study. METHODS: MC-deficient mice (WBB6F1xW/Wv) and their littermates (+/+) were fed sucrose-containing diets supplemented with or without varying concentrations (300, 400, 500, 600 mg) of cyclosporin A/kg of diet. After 30 days, the mice were sacrificed and the degree of gingival hyperplasia was evaluated by the appearance of the gingiva. Tissue MC were stained with toluidine blue to confirm the presence or absence of MC in the enlarged gingiva. RESULTS: Both W/Wv and +/+ mice, when fed with 600 mg cyclosporin A/kg diet for 30 days, exhibited a similar degree of gingival hyperplasia, while other test mice or control mice did not. Toluidine blue staining of the tissue sections confirmed the presence of MC in the enlarged gingiva of the +/+ mice, but not the W/Wv mice. CONCLUSIONS: These results indicate that mast cells are not necessary in the development of cyclosporin A-induced gingival hyperplasia, and that the increased number of MC observed in the enlarged gingiva may be a secondary effect of gingival hyperplasia. We also conclude that a study of mice lacking certain molecules or cells would be quite useful in determining the molecules or cell types responsible for the pathogenesis of drug-induced gingival hyperplasia.
Animals↗
On the relation of nitric oxide to nifedipine-induced gingival hyperplasia and impaired submandibular glands function in rats in vivo.
Calcium-channel blockers such as nifedipine could be associated with gingival overgrowth. The aim of this study was to examine the role of nitric oxide (NO) on nifedipine-induced gingival hyperplasia along with submandibular secretory function in rats. Animals in divided groups received nifedipine (250 mg/kg diet) alone and in combination with L-arginine (2.25% w/v) or N(omega)-nitro-L-arginine methyl ester (L-NAME) (0.7% w/v) in drinking water for 20 days. Controls received only tap water. Pure submandibular saliva was collected intraorally by micropolyethylene cannula and the mandibular gingiva was examined by means of dissecting microscope for signs of redness, thickness, inflammation and exuda. Twenty-day nifedipine treatment induced gingival hyperplasia accompanied with reduced salivary flow rate and concentrations of total protein, epidermal growth factor (EGF) and calcium in comparison with controls. Co-treatment of animals with nifedipine and L-arginine protected from gingival hyperplasia and retained flow rate, and concentrations of total protein, EGF and calcium in normal levels. Co-treatment of animals with nifedipine and L-NAME potentiated nifedipine-induced gingival hyperplasia and reductions in flow rate and concentrations of total protein, EGF, and calcium. It is concluded that nifedipine-induced gingival hyperplasia is associated with salivary dysfunction. Activation of cGMP-dependent positive signal-transduction mechanisms in salivary glands might be the mechanism for protective effects of NO against nifedipine-induced gingival hyperplasia.
Animals↗
Immunohistochemical localization of transforming growth factor beta, basic fibroblast growth factor and heparan sulphate glycosaminoglycan in gingival hyperplasia induced by nifedipine and phenytoin.
Although drug-induced gingival hyperplasia has been extensively studied, the pathogenesis of this disorder has not been clarified to date. Transforming growth factor beta (TGF beta) and basic fibroblast growth factor (bFGF) have been shown to be implicated in diverse fibrotic and hyperplastic diseases. Heparan sulphate proteoglycan (HSPG), which is composed of heparan sulphate glycosaminoglycan (HSGAG), has also been shown to play an important role in the pathogenesis of tissue overgrowth by enhancing the functions of bFGF. However, the possible implication of these growth factors in gingival hyperplasia has not been studied. Immunohistochemical localization of TGF beta, bFGF, their receptors and HSGAG was studied in 4 nifedipine-induced and 5 phenytoin-induced hyperplastic gingival tissues, and 5 non-hyperplastic control gingival tissues to elucidate the pathogenesis of this disease. Significant immunostaining against TGF beta, bFGF, the receptors of these two growth factors and HSGAG was observed in the lamina propria of hyperplastic gingival tissues while less immunostaining was observed in the controls. The mean numbers of immunostained cells against TGF beta, bFGF, their receptors in a square unit (0.1 x 0.1 mm) of the lamina propria, which were counted to 10 units of each hyperplastic gingival tissue, were significantly higher than those of the controls. The results suggest that the increased synthesis of TGF beta, bFGF, their receptors and HSGAG may be related to the pathogenesis of drug-induced gingival hyperplasia.
Adolescent↗
Prosthodontic treatment for a patient with advanced hydantoin-associated gingival hyperplasia: a case report.
A patient in whom gingival hyperplasia was caused by prolonged use of an anticonvulsant drug (hydantoin) is described. Advanced gingival hyperplasia and significant displacement of the remaining teeth caused severe damage, especially to the patient's appearance. It was not possible to cure the problems completely with routine periodontal treatment. It was decided to extract all the remaining teeth and restore function and esthetics early with complete dentures. Cephalometric analysis was used to determine the degree to which the teeth had drifted. During fabrication of the dentures, the analysis was very useful in deciding the position of the anterior teeth and checking the vertical dimension of occlusion.
Adult↗
Idiopathic gingival hyperplasia and orthodontic treatment: a case report.
There are many reasons for gingival hyperplasia. Mostly, proper oral hygiene is sufficient to achieve normal healthy gingiva. In some situations, however, gingival hyperplasia is drug-induced or can be a manifestation of a genetic disorder. In the latter, it may exist as an isolated abnormality or as part of a syndrome. If orthodontic treatment is needed in patients with gingival hyperplasia, both orthodontic and periodontal aspects need to be considered. Extreme hereditary gingival fibromatosis was periodontally treated, by removal of all gingival excess using flaps and gingivectomies. After a follow-up period, the orthodontic treatment started with fixed appliances. Monthly periodontal check-ups (scaling and polishing) were scheduled to control the gingival inflammation. After the orthodontic treatment, permanent retention was applied, once more followed by a complete gingivectomy in both maxilla and mandible. One of the most important keys to successful treatment of hyperplasia patients is the cooperation between the periodontist and the orthodontist.
Adolescent↗
Partial regression of advanced cyclosporin-induced gingival hyperplasia after treatment with azithromycin. A case report.
Gingival hyperplasia is a well recognised complication of cyclosporin A therapy. Although its pathogenesis is still debated in several recent reports a second generation macrolide antibiotic-azithromycin induced partial or even complete regression of hyperplasia. We present a patient after kidney transplantation treated with cyclosporin who developed very advanced gigival overgrowth (stage 3+). The patient received a 3-day treatment with azithromycin which was repeated after 3 months. The first course of the drug caused a partial regression of gingival hyperplasia during following months but the repeated treatment did not provide a further regression of the changes.
Adult↗
New developments in understanding phenytoin-induced gingival hyperplasia.
In approximately half of the patients taking phenytoin, gingival fibroblasts proliferate, causing tissue overgrowth and gingival hyperplasia. Recent clinical and basic research is reviewed, describing the conditions associated with phenytoin therapy and gingival hyperplasia.
Gingival Hyperplasia↗
Cyclosporin, nifedipine and gingival hyperplasia: a randomized controlled study.
Nifedipine increases the frequency and severity of gingival hyperplasia associated with CyA therapy in renal transplant recipients and this effect appears to be independent of whole-blood CyA levels. De novo malignancies have been reported arising in areas of gingival hyperplasia, in a group already at high risk of malignancy. Patients receiving CyA and nifedipine should receive advice regarding the need for strict oral hygiene to control the initial development of gingival hyperplasia, with severe cases being promptly referred for gingivectomy and histological examination.
Calcium Channel Blockers↗
[Gingival hyperplasia caused by nifedipine].
In a 66-year-old patient a relationship between the development of gingival hyperplasia and nifedipine treatment was suggested. The hyperplasia was clinically and histologically similar to the gingival hyperplasia induced by diphenylhydantoin. The nifedipine-induced gingival hyperplasia may be probably caused by alterations in calcium metabolism. The withdrawal of the drug results in a complete remission of the disease.
Aged↗
Is oral azithromycin effective for the treatment of cyclosporine-induced gingival hyperplasia in cardiac transplant recipients?
Anecdotal evidence suggests that azithromycin is effective for the treatment of cyclosporine-induced gingival hyperplasia in solid-organ transplant recipients. We present the cases of two heart transplant patients who insidiously developed gingival hyperplasia, likely because of immunosuppression with cyclosporine, which was treated with azithromycin. Evidence supporting the efficacy of azithromycin in the treatment of cyclosporine-induced gingival hyperplasia in solid organ transplant recipients was searched for, identified, and then critically assessed. While no data were found specifically evaluating azithromycin in cardiac transplant patients, there were nine pertinent papers identified that evaluated the clinical question of interest in the renal transplant population [Wahlstrom et al. (1995) The New England Journal of Medicine 332, 753; Boran et al. (1996) Transplantation Proceedings 28, 2316; Gomez et al. (1997) Nephrology Dialysis Transplantation 12, 2694; Ljutic (1997) Dialysis & Transplantation 26, 787; Puig et al. (1997) Transplantation Proceedings 29, 2379; Nash et al. (1998) Transplantation 65, 1611; Nowicki et al. (1998) Annals of Transplantation 3, 25; Wirnsberger et al. (1998) Transplantation Proceedings 30, 2117; Citterio et al. (2001) Transplantation Proceedings 33, 2134]. These studies and case reports are summarized. While more evidence is required to support routine use of azithromycin for the treatment of cyclosporine-induced gingival hyperplasia in cardiac transplant recipients, preliminary published evidence from renal transplant patients is certainly favourable.
Administration, Oral↗
Expression of p53 protein and Ki-67 antigen in gingival hyperplasia induced by nifedipine and phenytoin.
BACKGROUND: Although it has been thought that drug-induced gingival hyperplasia is not related to tumorigenesis, recent case reports have shown that squamous cell carcinomas may arise in gingival hyperplasia induced by cyclosporin and phenytoin. The possible implications between the pathogenesis of this disease and tumorigenesis have not been elucidated and remain to be studied. METHODS: We immunohistochemically examined the expression of tumor-related markers such as p53 protein and Ki-67 antigen in 11 hyperplastic gingival tissues induced by nifedipine and phenytoin, as well as 5 control tissues using an avidin-biotin-peroxidase complex method. RESULTS: Two specimens out of 4 nifedipine-induced and 4 out of 7 phenytoin-induced hyperplastic gingival tissues revealed the expression of p53 protein in the nuclei of epithelial cells, while no expression of p53 protein was observed in the epithelia of the 5 non-hyperplastic control tissues. The immunoreactions against p53 protein showed sporadic distribution in the suprabasal layers of hyperplastic epithelia. The mean percentage of epithelial cells expressing Ki-67 antigen in the hyperplastic gingival tissues was more than 10% higher than that in the controls. The expression of Ki-67 antigen was suppressed in the typical rete pegs deeply elongated into lamina propria of hyperplastic gingival tissues. Intense immunostaining of Ki-67 antigen was found in fibroblasts of hyperplastic gingival tissues, while that of the control tissues was negligible. CONCLUSIONS: The expression of p53 protein in gingival hyperplasia suggests that the pathogenesis of this disease is involved with impaired DNA, while the growth arrest observed in the hyperplastic epithelia with typically elongated rete pegs as expressed with Ki-67 antigen may prevent the invasive expansion of epithelial cells undergoing DNA damage within gingival tissues and may consequently suppress tumorigenic progression.
Adolescent↗
Nifedipine-induced gingival hyperplasia: case reports and literature review.
Nifedipine-induced gingival hyperplasia is a newly reported but relatively unknown side effect. We describe three cases of severe nifedipine-induced gingival hyperplasia that required dental extraction.
Gingival Hyperplasia↗
Cyclosporine-induced gingival hyperplasia: case report and literature review.
A case of gingival hyperplasia was related to the use of cyclosporine for the prevention of renal allograft rejection. With the increasing use of cyclosporine to protect allograft organ transplants, general dentists and dental specialists increasingly will be called on to diagnose and treat gingival hyperplasia.
Adult↗