PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “GINGIVAL HYPERPLASIA”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMedDate not supplied

Congenital generalized terminal hypertrichosis with gingival hyperplasia.

Congenital generalized terminal hypertrichosis is a rare disease, especially when associated with gingival hyperplasia. Congenital hypertrichosis can be a clinical feature of several syndromes, so these patients must be studied by a multidisciplinary team that should include a dermatologist, geneticist, psychologist, odontologist, and an endocrinologist. We report a 7-year-old girl with congenital generalized hypertrichosis and gingival hyperplasia, and analyze the clinical approach, differential diagnosis, and treatment.

Child↗
PubMed1995

Proteus syndrome: association with gingival hyperplasia.

A 9-year old Black boy with gigantism of the hands and feet, and recurrent gingival hyperplasia, diagnosed as Proteus syndrome is presented. The oral manifestations of this syndrome are described. To the best of our knowledge, this is the first reported case of gingival hyperplasia associated with Proteus syndrome.

Child↗
PubMedDate not supplied

Reversion of gingival hyperplasia in a heart transplant patient upon interruption of cyclosporine therapy.

A heart transplant patient undergoing a combined cyclosporine and prednisone treatment was monitored during the 18 months following transplantation. A complete oral and dental examination was performed in each of the first six months after transplantation, and then in the 9th, 12th, 15th, and 18th months. The data collected included gingival hyperplasia secondary to cyclosporine use, and clinical and periodontal variables. Histological studies were also conducted on gingival tissue samples in months 1, 3, 9, 15, and 18. Cyclosporine treatment was replaced by azathioprine treatment in month 10 because the patient was experiencing nephrotoxicity. Between months 9 and 18, gingival hyperplasia regressed by 26.5% due to a reduction in the fibrous connective tissue mass, fibroblasts, and inflammatory infiltration. The control group included 13 heart transplant patients subject to equivalent conditions except discontinuance of cyclosporine treatment; seven of the patients had developed hyperplasia by month 9. Average hyperplasia in the control group increased by 2% between months 9 and 18; only one patient showed a 6.2% decrease in hyperplasia. This provides further evidence for the causal relationship between cyclosporine therapy and gingival hyperplasia, and suggests that this side-effect is reversible.

Child↗
PubMed1990

Gingival hyperplasia in rats induced by oxodipine--a calcium channel blocker.

Oxodipine, a new calcium channel blocker, induced gingival hyperplasia in rats. This is the first time that a calcium channel blocker has been documented as resulting in gingival hyperplasia in rats. In contrast to diphenylhydantoin, the hyperplastic changes induced by oxodipine were not precipitated by any prior irritation. The histology consisted of purely fibroblastic proliferation without infiltrate of inflammatory cells.

Animals↗
PubMed2000

Immunolocalizaiton of c-Myc and bcl-2 proto-oncogene products in gingival hyperplasia induced by nifedipine and phenytoin.

BACKGROUND: Hyperplastic gingival tissues show the histopathological characteristics of thick parakeratinized squamous epithelia with acanthosis and rete pegs elongated into the lamina propria. However, the pathogenic factors that contribute to the epithelial morphogenesis of this disease are obscure and remain to be studied. METHODS: We immunohistochemically examined the expression of both c-Myc and bcl-2 oncoprotein, which can exert influence on the epithelial morphogenesis and homeostasis, in 12 hyperplastic gingival tissues induced by nifedipine and phenytoin as well as 5 control tissues using avidin-biotin-peroxidase complex methods. RESULTS: Four specimens out of 5 nifedipine-induced and 5 out of 7 phenytoin-induced hyperplastic gingival tissues revealed the expression of c-Myc oncoprotein, whereas no significant immunostaining of c-Myc oncoprotein was found in 5 control tissues. The c-Myc oncoprotein-positive cells were observed to be localized in the basal and suprabasal cell layers of the hyperplastic gingival epithelia. Although all of the 12 hyperplastic gingival epithelia showed the distribution of bcl-2 oncoprotein in the basal and suprabasal layer cells, in 5 control epithelia the bcl-2 oncoprotein expression was slight and confined to the basal layer cells. CONCLUSIONS: The results of our present study indicate that the synergistic overexpression of c-Myc and bcl-2 oncoprotein may be related to the pathogenesis of gingival hyperplasia induced by nifedipine and phenytoin, especially to the morphogenesis of hyperplastic epithelia.

Adolescent↗
PubMed1998

Felodipine-induced gingival hyperplasia.

Felodipine is a calcium channel blocking agent used in the management of hypertension and angina. We report a case of gingival hyperplasia in a patient with chronic use of this drug. Gingival changes occurred soon after initiation of felodipine and improved upon its discontinuation. The clinical characteristics, inciting agents, proposed pathogenetic mechanisms, as well as prevention and treatment of drug-induced gingival hyperplasia are briefly reviewed.

Aged↗
PubMed1978

Hereditary gingival hyperplasia and physical maturation.

In a family with eight children, six of the children suffered from gingival hyperplasia. Dental age was determined for five of the affected children. In four it was retarded in relation to chronologic age, but within normal limits. The skeletal age of the same five children was retarded by more than 2 standard deviations. The heights of three of these five children were clearly below the 2.5th percentile height curve. The two most retarded children were examined by pediatricians. No hematologic changes or evidence of malabsorption from the alimentary tract could be found. It is suggested that in this family retardation of physical development may be linked with gingival hyperplasia.

Adolescent↗
PubMed1997

Gingival hyperplasia: interaction between cyclosporin A and nifedipine? A case report.

Treatment with either cyclosporin A or nifedipine may induce gingival hyperplasia. A case report is presented which describes a patient medicated simultaneously with both drugs and who subsequently developed extreme hyperplasia. Could such a severe gingival pathology have resulted from an additive interaction between the two drugs?

Calcium Channel Blockers↗
PubMed1983

Multisystem sarcoid presenting with gingival hyperplasia.

A case is reported in which granulomatous gingival hyperplasia was the presenting feature of generalised sarcoidosis. Treatment with oral prednisolone resulted in resolution of both the granulomatous lesion of the gums, and of proteinuria. It is pointed out that although on histological examination sarcoidosis in this site cannot be distinguished from Crohn's disease, the clinical appearance in this patient (and the only similar case in the literature) was quite different from that seen in oral Crohn's disease.

Adolescent↗
PubMed1977

One-sided gingival hyperplasia after treatment with diphenylhydantoin.

After treatment with diphenylhydantoin for 2 years because of post-infarct focal motor epileptic seizures, a 35-year-old woman was admitted to hospital because of symptoms of intoxication. Almost every sign of the previous left-sided paresis and hypaesthesia had disappeared. A pronounced gingival hyperplasia was found almost exclusively in the left side. The concentration of immunoglobulin A in serum was found far below normal. Admitting that she had not been careful brushing her teeth in the left side because of the strange feeling there (dysaesthesia), the patient had actually carried out a controlled trial proving that she, being predispposed to gingival hyperplasia with a low level of immunoglobulin A in serum, could almost prevent the gingival hyperplasia in the right side by brushing her teeth carefully there.

Adult↗
PubMed2005

[X-ray study of alveolar processes of the jaw bones of adult patients with gingival hyperplasia induced by Ca antagonists].

New data are presented about X-ray changes in patients aged 51-78 years with gingival hyperplasia induced by Ca antagonists. The interrelation between bone destruction presence or absence and gingival hyperplasia is disclosed. Orthopantomogram and clinical data showed that the loss of interalveolar bone was closely and significantly approaching the periodontal pockets depth.

Aged↗
PubMed1987

Drug-induced gingival hyperplasia: phenytoin, cyclosporine, and nifedipine.

This article has summarized observations and results of controlled laboratory and clinical studies of drug-induced gingival hyperplasia associated with phenytoin, cyclosporine, and nifedipine use. Furthermore, information regarding the pharmacologic aspects of these medications is presented. More information is needed for a greater understanding of drug-induced gingival hyperplasia. It appears that the primary preventive measure is to maintain a high standard of oral hygiene and the elimination of gingival irritation. As stated by Tyldesley and Rotter, because the structures of the three drugs are different, the gingival changes may result from a metabolic by-product rather than the drugs themselves. Similarly acting metabolites of all the drugs may be involved. Further laboratory investigations and controlled clinical trials are needed for more understanding of this phenomenon.

Adult↗
PubMed1976

[Report of a case of idiopathic gingival hyperplasia].

The clinical and histological picture of a rare gingival disease, i.e. idiopathic gingival hyperplasia, is discussed in detail on the basis of a case of our own Comprehensive diagnostic measures were taken to exclude other possible causes of a hyperplasia of the gingiva. Despite a rapid recurrence after gingivectomy, a "wait and see" attitude is assumed and the next therapeutical procedure is planned only after completion of puberty.

Child↗
PubMed1997

Phenytoin and cyclosporine A specifically regulate macrophage phenotype and expression of platelet-derived growth factor and interleukin-1 in vitro and in vivo: possible molecular mechanism of drug-induced gingival hyperplasia.

Phenytoin (pht) is an anticonvulsant drug commonly used for the prevention of seizures. A common side effect of PHT therapy is gingival hyperplasia, occasionally so severe that it requires surgical intervention. Cyclosporine A (CSA) is a drug widely used for the control of rejection phenomena following solid organ and bone marrow transplantation. A frequent side effect of CSA administration is gingival overgrowth. As yet, the molecular mechanisms of drug-induced gingival hyperplasia are unknown although it has been postulated that certain drugs increase fibroblastic activity through alterations in levels of various growth factors and cytokines. The purpose of this study was to: 1) evaluate monocyte/macrophage platelet-derived growth factor (PDGF) and interleukin (IL)-1 beta production in vitro after exposure to CSA; 2) determine the levels of PDGF-B and IL-1 beta gene expression in minimally inflamed gingival tissues of control patients and PHT-treated patients exhibiting gingival overgrowth as well as patients with severe gingival inflammation; and 3) combine characterization of macrophage phenotype with clinical presentation and expression of PDGF-B and IL-1 beta in gingival tissues from the control and PHT-treated patients. For the in vitro studies, commercial ELISA kits were used to measure PDGF-A/PDGF-B and IL-1 beta levels in conditioned media from rat and human monocyte/macrophage cell cultures. CSA caused a significant elevation of PDGF but did not cause any changes in IL-1 beta levels. For the in vivo studies, quantitative competitive reverse transcription polymerase chain reaction (QC-RTPCR) techniques were utilized to measure PDGF-B and IL-1 beta mRNA levels in experimental groups. PHT-treated patients exhibiting gingival overgrowth demonstrated a significant increase in PDGF-B mRNA compared with minimally inflamed controls. Patients with severe gingival inflammation also demonstrated a significant increase in PDGF-B mRNA however, PHT-induced PDGF-B upregulation is approximately 6 times larger than PDGF-B upregulation produced by inflammation alone. PHT-treated patients exhibiting gingival overgrowth demonstrated no significant increase in IL-1 beta mRNA; however, IL-1 beta mRNA levels in the severely inflamed gingival samples demonstrated a significant increase. Additionally, for the clinical samples, macrophage phenotype was characterized immunohistochemically in adjacent sections using specific monoclonal antibodies for inflammatory and reparative/proliferative phenotypes. There were no significant differences in the numbers of either macrophage phenotype in minimally inflamed gingival tissues; however, in the severely inflamed tissue, there was a significant increase in the inflammatory macrophage phenotype and in the hyperplastic gingival tissue, there was a significant increase in the reparative/proliferative macrophage phenotype. The results of this investigation indicate that the clinical presentation of inflamed and hyperplastic gingival tissues is associated with specific macrophages phenotypes which express the pro-inflammatory cytokine IL-1 beta in inflamed tissues or the essential polypeptide growth factor PDGF-B in PHT-induced hyperplastic tissues.

Adult↗
PubMed1991

Felodipine-induced gingival hyperplasia: a clinical and histologic study.

This paper reports, for the first time, gingival hyperplasia in a patient treated with felodipine, a drug which belongs to the group of calcium ion antagonists. The observed gingival overgrowth was most significant in the area of interdental papillae of the anterior region of the mouth. The described hyperplastic tissue was characterized by a firm and pale appearance, with a normally stippled pattern. Histopathologically, a conspicuous increase of fibrous connective tissue, as well as an inflammatory infiltrate and hyperplasia of the overlying epithelium were observed. Consequently, the present observation adds another drug to the list of substances capable to induce gingival hyperplasia.

Adult↗
PubMed1989

[Clinical study of gingival hyperplasia in epilepsy patient].

Diphenylhydantoin, which was first introduced in clinic by Meritt and Putnam in 1938, has been in wide use for the treatment of epilepsy because of its excellent antispasmodic action. On the other hand, Diphenylhydantoin induced gingival hyperplasia has been examined by many authors in the dental field since gingival hyperplasia was reported by Kimball as its side effect. Recently, we had an opportunity for performing gingivectomy on hypertrophic gingivitis in an epileptic with mental retardation and visual disturbance, on Phenytoin (5,5-Diphenylhydantoin) medication. Some information obtained is reported, together with its therapeutic course.

Adult↗
PubMed1978

The management of drug induced gingival hyperplasia in mentally retarded patients with hemophilia: a report of two cases.

Two cases of hemophilia in severely mentally retarded patients with drug-induced gingival hyperplasia are presented. The method of management in each case is described. A conservative approach is recommended in which tissue removals and only selected extractions are performed. It is also suggested that the sequela of dilantin hyperplasia be considered when dilantin is used in patients with hemophilia or severely mentally retarded patients whose oral hygiene may be difficult to maintain. If feasible, as in the first case reported, discontinuance of the drug should be considered. In case 2 the patient is presently being weaned from dilantin therapy. It should be understood that the authors are concerned with the immediate clinical management of drug-induced gingival hyperplasia in mentally-retarded patients with hemophilia. Although this method of management has proved successful in the hands of the authors, we do not have data to show that it is the best form of treatment for these patients.

Adult↗