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 73 records · Page 4Linked to original sources
PubMed1999

[Clinical experience with the treatment of gingival hyperplasia induced by calcium channel blocking agents].

The prevalence of the nifedipine-induced gingival hyperplasia is ranging from 0.5-83% in the dental literature. The pathomechanism of the nifedipine-induced gingival hyperplasia is not clearly understood. Evaluating the dental history and the course of disease of 34 patients treated and followed up at the Department of Periodontology the following answers were raised: What sort of local and systemic factors are enhancing the recurrence of the gingival overgrowth and how this can be anticipated in patients on continuous Ca channel blocking medication. Eight out of the 34 patients participating in the clinical trial did not remember the onset of their gingival overgrowth. 10 cases developed three years and three cases after less then one year of the onset of the drug administrations. 27 out of the 34 cases required gingival surgery and seven showed good clinical improvement after the hygienic phase of the comprehensive periodontal treatment. 70% of the gingival hyperplasia cases presented no clinical sign of recurrence one year after the completion of the active phase of the treatment. A positive correlation was found between the oral hygiene and the recurrence rate of gingival overgrowth. Oral hygiene seems to play a decisive role in the development of gingival enlargement. The present findings and substantial evidences from the dental literature indicate that the gingival enlargement can be successfully controlled even under the continuous nifedipine administration by meticulous professional and individual oral hygiene.

Calcium Channel Blockers↗
PubMed1991

Gingival hyperplasia induced by nifedipine.

We describe 4 cases of gingival hyperplasia induced by nifedipine, together with clinical and histological findings. Hyperplasia of the interdental papillae was observed in all cases. Histologic examination showed multilayered epithelial parakeratosis with variations in the width, proliferation, reticulation and elongation of the rete pegs. Substitution of another drug and improvement of oral hygiene led to reduction of the gingival overgrowth without gingivectomy. These treatments are essential for gingival hyperplasia induced by nifedipine.

Aged↗
PubMed2003

Hypertrichosis terminalis, gingival hyperplasia, and a characteristic face: a new distinct entity.

Congenital generalized hypertrichosis terminalis has been described in association with other features as gingival hyperplasia, osteochondrodysplasia, and a dysmorphic face. Bondeson and Miles [1993: Am J Med Genet 47:198-212] described a woman with universal congenital hypertrichosis terminalis associated with gingival hyperplasia; the face of this patient was coarse and different from other forms of hypertrichosis described before. We present an 11-year, 6-month-old girl with universal congenital hypertrichosis terminalis, gingival hyperplasia, and a characteristic coarse face resembling the patient described by Bondeson and Miles [1993: Am J Med Genet 47:198-212]. We propose that this type of congenital generalized hypertrichosis terminalis, associated with gingival hyperplasia and a coarse face, is a distinctive new entity.

Abnormalities, Multiple↗
PubMed1990

Langerhans cells in human chronic gingivitis and phenytoin-induced gingival hyperplasia.

Langerhans cell numbers in oral epithelium increase as dental plaque accumulates. The anti-convulsant drug phenytoin predisposes to gingival hyperplasia in certain patients who take this medication for epilepsy and who also have poor oral hygiene. In this study 7 patients with phenytoin-induced gingival hyperplasia were compared with 5 subjects with chronic marginal gingivitis. On initial examination and on completion of the hygiene phase of periodontal therapy (a period ranging from 3.0 to 4.25 months), clinical indices of plaque and gingivitis were recorded and biopsies were taken from the lower anterior labial gingiva. Frozen sections were stained by an immunoperoxidase technique using the monoclonal antibody OKT6, and the number of Langerhans cells in a defined cross-sectional area was counted. In phenytoin-induced gingival hyperplasia there was a marked increase in Langerhans cells (13.8 +/- 0.45) when compared with chronic gingivitis (7.7 +/- 0.31; p less than 0.05). Both groups showed marked reductions in their plaque and gingival indices and numbers of Langerhans cells once treatment had been completed. However, levels of Langerhans cells in the drug-induced hyperplasia remained significantly higher (3.5 +/- 0.26) than in chronic gingivitis (1.5 +/- 0.22; p less than 0.05).

Adult↗
PubMed1983

Risk factors in phenytoin-induced gingival hyperplasia.

A survey was carried out into the degree of gingival hyperplasia in 68 patients receiving phenytoin in a hospital for the mentally handicapped. Comparisons of degree of gingival hyperplasia exhibited by the patients were made with a range of parameters by analysis of variance and Chi square tests. The severity of the hyperplasia increased with increasing dose, increasing dose per unit body weight and serum levels of phenytoin and also with decreasing age and weight of the patients. No significant relationship (P less than 0.2) was found between serum folate levels and degree of hyperplasia. Poor oral hygiene predisposed patients to hyperplasia.

Adolescent↗
PubMedDate not supplied

Generalized gingival hyperplasia occurring during pregnancy.

In this report, we present a case of generalized gingival hyperplasia related to pregnancy causing chewing, speaking, breathing and cosmetic problems. The patient was a 26-year-old woman in the fourth month of her second pregnancy, with generalized gingival hyperplasia affecting both buccal and lingual aspects of the maxilla and mandible. The hyperplastic tissues, together with mobile teeth, were excised completely; no recurrence was observed for the remainder of the pregnancy. Hormonal changes occurring during pregnancy have long been known to be associated with generalized gingival hyperplasia. Pregnancy does not cause the condition, but altered tissue metabolism in pregnancy accentuates the response to local irritants. This case was of clinical interest because of the extent of tissue proliferation, with the teeth in both the upper and lower jaw completely submerged.

Adult↗
PubMed1985

Gingival hyperplasia induced by nifedipine, an arterial vasodilating drug.

In a 32-year-old patient a relationship was suggested between the development of gingival hyperplasia and the vasodilating drug nifedipine (Adalat). The hyperplasia was clinically and histologically similar to the gingival hyperplasia previously noticed with diphenylhydantoin. The nifedipine-induced gingival hyperplasia may be caused by alterations in calcium metabolism.

Adult↗
PubMed1989

Folate treatment of diphenylhydantoin-induced gingival hyperplasia.

It has recently been reported that folic acid supplementation reduced DPH-induced gingival hyperplasia in cat and in a pilot study also in man. The present study was performed to further evaluate this therapy in man. Twenty-three children with DPH-treatment for more than 1 yr, and eight children with short-time DPH-treatment were randomly assigned to groups with and without daily supplementation of folic acid (5 mg Folacin) for 1 yr. Although the DPH-levels were in many cases below the lower reference value, the seizure control of the children was good before and during the year of study. The plasma and red cell folate levels were within or above the given reference values in all but one child. There were no significant changes in the size of the gingival hyperplasias after 1 yr of folate supplementation. Nine severely mentally retarded DPH-treated adults were also given supplementation with folic acid. Their serum DPH-levels were above the higher reference values both at the start and during the study. Their plasma and red cell folic acid levels were below the reference value at the start of the study, but as a consequence of the Folacin supplementation these values rose. The size of the gingival hyperplasias was significantly reduced. Seizure control was unchanged. Folate levels should be checked and supplementation with folic acid considered in patients on long-term anticonvulsive multipharmacy therapy.

Adolescent↗
PubMed1984

Gingival hyperplasia caused by nifedipine--a preliminary report.

We observed marked gingival hyperplasia, similar clinically and histologically to the hyperplasia caused by 5:5 sodium diphenylhydantoin (Dilantin) during the last 18 months in five patients treated by nifedipine. Histologically, marked epithelial hyperplasia-acanthosis, with moderate inflammatory reaction in the lamina propria, was observed in all the biopsy specimens. Evidence points to a strong relationship between the gingival hyperplasia and the administration of nifedipine.

Aged↗
PubMedDate not supplied

Laser treatment of orthodontically induced gingival hyperplasia.

Several studies have shown that gingivitis is common in children and adolescents. Introduction of orthodontic devices may exacerbate the gingival inflammation. Orthodontically induced gingival hyperplasia in adolescents, its etiology, and treatment alternatives are discussed. Three instances in which laser therapy was used are described.

Adolescent↗
PubMed1998

Castration prevents calcium channel blocker-induced gingival hyperplasia in beagle dogs.

1. The purpose of this study was to investigate testosterone's role on the calcium channel antagonist oxodipine-inducing gingival hyperplasia in a dog model. 2. Two experiments were conducted using castrated and intact male dogs. Oxodipine was administered orally for 90 days, at a dose of 24 mg/kg/day. In the first experiment, the occurrence of gingival hyperplasia was evaluated. In the second, the gingival index (GI) and gingival hyperplasia index (GHI) were recorded and correlated with serum levels of testosterone. 3. A significant positive correlation between GI, GHI and plasma testosterone was noted. Castrated dogs were injected with testosterone, 4 months after the start of oxodipine treatment, while in the non-castrated dogs, administration of oxodipine was stopped. Castration correlated with lack of GH, while testosterone injection to the same dogs was associated with an increase of GI and GHI. 4. Since it is known that testosterone receptors are present in the gingiva, it is proposed that oxodipine-induced gingival hyperplasia could be mediated by the calcium channel blocker on plasma testosterone levels.

Animals↗
PubMed2006

MDR1 gene polymorphisms and risk of gingival hyperplasia induced by calcium antagonists.

BACKGROUND: Gingival overgrowth is a common side effect of calcium antagonists. Although the pathogenesis is unknown, several lines of evidence point to a modulation of inflammatory processes. Because the calcium antagonists, albeit to a variable degree, act as inhibitors of P-glycoprotein (P-gp), the gene product of multidrug resistance 1 (MDR1), and inflammation may modify P-gp expression, we analyzed the MDR1 polymorphisms as risk factors for gingival overgrowth induced by calcium antagonists. METHODS: Clinical, laboratory, and anamnestic data including periodontal parameters and use of calcium antagonists were assessed in a cross-sectional epidemiologic investigation (N = 1484). MDR1 polymorphisms in exon 21 G2677T/A and exon 26 C3435T were determined. P-gp expression was detected in gingival tissues. In a matched-pair analysis, 93 subjects using calcium antagonists and 186 not using them were compared. RESULTS: P-gp is expressed in the endothelial layers of blood vessels obtained from healthy or inflamed gingiva. Subjects treated with calcium antagonists had significantly deeper gingival pockets than their drug-free counterparts (P <.0001). This drug-related side effect was associated with the MDR1 2677G/G or G/TA genotype (P <.001) but not with the variant genotype T/TA. This drug effect was proved by multiple regression analysis with adjustment for the risk factors of periodontitis (age, sex, smoking, and education) (P <.0001) and was associated with elevated C-reactive protein levels. The association of probing depth with the MDR1 polymorphism was confirmed in the matched-pair analysis (P <.0001). CONCLUSION: Treatment with calcium antagonists leads to gingival hyperplasia, which is associated with the MDR1 G2677T/A polymorphism. The MDR1 genotype may modify the inflammatory response to the drugs.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1989

[Cyclosporin and gingival hyperplasia: apropos of three clinical cases].

Three cases of extensive gingival hyperplasia associated with long-term cyclosporine therapy are presented. Following periodontal therapy, the patients have been maintained well for 15 months. The authors attempt to explain the etio-pathology of gingival hyperplasia following the use of immunosuppressant drugs. They stress the need for better understanding of this phenomenon among physicians who prescribe cyclosporine.

Adolescent↗
PubMed1979

[Ultrastructure of the connective corium in hereditary gingival hyperplasia].

The ultrastructural study of the gingival lamina propria of 4 patients from the same family with hereditary gingival hyperplasia showed a density increase of the collagen fibres, a decrease in their mean diameter and the dissociation in sub-units of certain fibres whereas their periodicity was not altered. This study showed also the presence of elastic and oxytalan fibres in greater amounts than in normal gingiva, whereas the number of fibroblasts did not seem to increase. However these fibroblasts seemed to undergo modifications in relation to age and to secrete a large quantity of amyloid substance in the extracellular spaces. The glycoproteins and the glycosaminoglycans more abundant than in normal gingiva were not influenced by the age of the tissue.

Adolescent↗
PubMed1987

Ultrastructure of fibroblasts in cyclosporin A-induced gingival hyperplasia.

Specimens from 2 cases of gingival hyperplasia resulting from the treatment with the immunosuppressant cyclosporin A (CSGH) and 4 cases of inflamed gingiva (non-CSGH) were examined by electron microscopy with particular interest in the fibroblasts. In general, the fibroblasts in CSGH revealed the ultrastructural characteristics of active protein synthesis and secretion and less cytotoxic or degenerative changes. Some fibroblasts in the CSGH (23.8%) displayed cytological modifications comparable to so-called myofibroblasts, i.e., microfilament bands with semi-periodic dense nodes, nuclear indentations, and basal-lamina associated, cell-to-stromal junctions. Conversely, 5.9% of the fibroblasts in the non-CSGH showed these modifications. The modified fibroblasts were found most predominantly in the transitional area between inflamed and fibrous connective tissues. From these findings, it is suggested that the myofibroblastic modification in CSGH is regarded as a common morphological sign in actively proliferating fibrous tissue and may participate in the host-tissue response to the plaque-associated irritants.

Adult↗
PubMedDate not supplied

[Gingival hyperplasia due to nifedipine: case report].

This article reports a case of gingival hyperplasia induced by nifedipine. It is a relatively new drug used in the treatment of hypertension, ventricular arrhythmias and angina. Both clinical and histological conditions and also treatment resemble other drug-induced gingival hyperplasia.

Gingival Hyperplasia↗
PubMed1999

Incidence of gingival hyperplasia caused by calcium antagonists in continuous ambulatory peritoneal dialysis patients.

Calcium antagonists are widely used for the treatment of cardiovascular diseases in patients receiving dialysis therapy. The incidence of gingival hyperplasia has been reported as 10%-20% in patients treated with calcium antagonists in the general population. However, precise reports examining the incidence or pathogenesis of gingival hyperplasia in continuous ambulatory peritoneal dialysis (CAPD) patients are lacking. We recruited 54 CAPD patients. Three patients treated with long-acting nifedipine and one patient treated with felodipine were reported by a periodontist to have gingival hyperplasia. No patients were taking amlodipine and other calcium antagonists. After discontinuation of calcium antagonists, gingival hyperplasia disappeared within 1 month. Based on these results, we suggest that it is important to examine whether the gingiva is overgrown in CAPD patients taking calcium antagonists.

Adult↗