scholarly journals Influence of nifedipine on gingiva of Wistar rats

2004 ◽  
Vol 61 (1) ◽  
pp. 5-8 ◽  
Author(s):  
Zlata Brkic
Keyword(s):  
Wistar Rats ◽  
Water Solution ◽  
Channel Blockers ◽  
Gingival Hyperplasia ◽  
Dental Practice ◽  
Gingival Fibroblasts ◽  
Gingival Overgrowth ◽  
Time Period ◽  
Time Periods ◽  
Higher Doses

Noninflammatory hyperplastic growth of gingiva induced by calcium channel blockers, mostly nifedipine, is often seen in everyday dental practice. In order to establish an association of nifedipine and gingival hyperplasia, experimental model was used. Wistar rats were given water solution of nifedipine in different daily doses, using specially designed cannula. At the beginning of the experiment, before the application of nifedipine and in the determined time periods, gingival volume was measured. The volume of lower incisors interdental central papillas, represented multiplied values of vertical hight, mesio-distal width, and bucco-lingual depth, expressed in millimeters. The results indicated that gingival hyperplasia was more excessive in the experimental animals, which were given higher doses of the drug for longer time period. Nifedipine is a drug which induces gingival fibroblasts to produce higher quantity of collagen that causes gingival overgrowth.

scholarly journals Histometric analysis of gingival hyperplasia in Wistar rats during nifedipine administration

2007 ◽  
Vol 64 (1) ◽  
pp. 19-23
Author(s):  
Zlata Brkic
Keyword(s):  
Wistar Rats ◽  
Water Solution ◽  
Control Group ◽  
Channel Blockers ◽  
Gingival Hyperplasia ◽  
Time Intervals ◽  
Tissue Samples ◽  
Experimental Animals ◽  
Periodontal Tissues ◽  
Interdental Papilla

Background/Aim. The use of calcium channel blockers, especially nifedipine, causes gingival hyperplasia which leads to the destruction of the deeper periodontal tissues. During this process, inflammatory changes and the changes of colagen fibers occur. The aim of this study was to metrically compare the extent of proliferation of connective tissue in the deeper periodontal tissue in experimental animals regarding the dose and duration of nifedipine administration. Methods. The study involved 50 Wistar rats to which water solution of nifedipine was given in certain time intervals and doses. Before starting the experiment, i.e. before nifedipine administration, and in the defined time intervals, measuring of the morphology of gingival size was performed including the buccolingual and mesiodistal wideness and vertical altitude of the central interdental papilla. The measurement was performed by the use of a special graduated probe. Histometric analyses of the tissue samples were done on the sagital cross-sections in the direction from the top to the bottom of papilla on five levels. For the statistical analysis of the data, the established values to the extent of the most present changes were used. The mesiodistal and buccolingual diameters for the levels L2 and L3 were quantitively determined and compared. These values were compared to the vertical diameter of gingival growth determined before the onset of patohistologic analyses of the tissue samples. Results. At the beginning of the experiment, the volume of the lower incisive central papilla in the rats was 12 mm3. The central interdental papilla vertical altitude was 6.6 mm in rats which had received a lower dose of nifedipine, 8 mm in rats which had received a higher dose in the defined time intervals while the value for the control group was 3.8 mm. Conclusion. The obtained results showed that the administration of nifedipine led to the extensive gingival hyperplasia in the experimental animals. Gingival hyperplasia correlates with both the dose of nifedipine and the duration of its administration.

Amlodipine Induced Gum Hypertrophy – A Rare Case Report

2021 ◽  
Vol 16 ◽  
Author(s):  
Suryanarayana Challa Reddy ◽  
Naresh Midha ◽  
Vivek Chhabra ◽  
Deepak Kumar ◽  
Gopal Krishna Bohra
Keyword(s):  
Calcium Channel ◽  
Side Effect ◽  
Antihypertensive Drugs ◽  
Case Reports ◽  
Diagnostic Procedures ◽  
Channel Blockers ◽  
Gingival Hyperplasia ◽  
Drug Induced ◽  
Duration Of Action ◽  
Gingival Overgrowth

Background: DIGO or drug-induced gingival overgrowth occurs as a side effect of certain drugs. Until now, the etiology of drug-induced gingival overgrowth is not clearly understood. Among the calcium channel blockers, nifedipine has been shown to be most frequently associated with drug-induced gingival hyperplasia. Amlodipine is a comparatively newer calcium channel blocker that witha longer duration of action and lesser side effects as compared to nifedipine. There are only certain case reports of amlodipine-induced gum hyperplasia. Case presentation: We report a case of amlodipine-induced gum hyperplasia in a 66-year-old hypertensive patient taking amlodipine at a dose of 5 mg once a day. There was significant regression of gum hypertrophy after substitution of amlodipine by Losartan. Conclusion: Amlodipine is one of the commonly prescribed antihypertensive drugs, and gingival hyperplasia is one overlooked side effect in patients taking amlodipine. Awareness of this potential side effect of amlodipine may be helpful to reduce the anxiety of patients and the cost of diagnostic procedures.

scholarly journals Drug-Induced Gingival Overgrowth: A Pilot Study on the Effect of Diphenylhydantoin and Gabapentin on Human Gingival Fibroblasts

2020 ◽  
Vol 17 (21) ◽  
pp. 8229
Author(s):  
Dorina Lauritano ◽  
Giulia Moreo ◽  
Luisa Limongelli ◽  
Elena Tregambi ◽  
Annalisa Palmieri ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Direct Action ◽  
Human Fibroblasts ◽  
Matrix Metalloproteases ◽  
Channel Blockers ◽  
Gingival Hyperplasia ◽  
Drug Induced ◽  
Gingival Overgrowth ◽  
Matrix Deposition ◽  
Extracellular Matrix Deposition

Introduction. The administration of several classes of drugs can lead to the onset of gingival overgrowth: anticonvulsants, immunosuppressants, and calcium channel blockers. Among the anticonvulsants, the main drug associated with gingival overgrowth is diphenylhydantoin. Materials and Methods. In this study, we compared the effects of diphenylhydantoin and gabapentin on 57 genes belonging to the “Extracellular Matrix and Adhesion Molecule” pathway, present in human fibroblasts of healthy volunteers. Results. Both molecules induce the same gene expression profile in fibroblasts as well as a significant upregulation of genes involved in extracellular matrix deposition like COL4A1, ITGA7, and LAMB3. The two treatments also induced a significant downregulation of genes involved in the expression of extracellular matrix metalloproteases like MMP11, MMP15, MMP16, MMP24, and transmembrane receptor ITGB4. Conclusions. Data recorded in our study confirmed the hypothesis of a direct action of these drugs at the periodontium level, inducing an increase in matrix production, a reduction in its degradation, and consequently resulting in gingival hyperplasia.

Drug-Induced Gingival Overgrowth - A Review

1970 ◽  
pp. 26-29
Author(s):  
Mst Fatema Akhter ◽  
Shaheen Lipika Quayum ◽  
Afrin Bintal Ali ◽  
Zia Mamoon
Keyword(s):  
Extracellular Matrix ◽  
Collagen Synthesis ◽  
Immunosuppressive Agents ◽  
Channel Blockers ◽  
Gingival Fibroblasts ◽  
Connective Tissues ◽  
Drug Induced ◽  
Gingival Overgrowth ◽  
Collagen Phagocytosis ◽  
Synthesis And Degradation

Drug-induced gingival overgrowth is a side effect associated with 3 types of drugs: anticonvulsants (phenytoin), immunosuppressive agents (cyclosporine A), and various calcium channel blockers for cardiovascular diseases. Gingival overgrowth is characterized by the accumulation of extracellular matrix in gingival connective tissues, particularly collagenous components with various degrees of inflammation. Although the mechanisms of these disorders have not been elucidated, recent studies suggest that these disorders seem to be induced by the disruption of homeostasis of collagen synthesis and degradation in gingival connective tissue, predominantly through the inhibition of collagen phagocytosis of gingival fibroblasts. In this review, we focus on collagen metabolism in drug-induced gingival overgrowth, focusing on the regulation of collagen phagocytosis in fibroblasts. DOI: 10.3329/bjpp.v25i1.5743Bangladesh J Physiol Pharmacol 2009; 25(1&2) : 26-29

scholarly journals Diphenylhydantoin Induced Severe Gingival Hyperplasia

JMS SKIMS ◽  
2017 ◽  
Vol 20 (1) ◽  
pp. 44-46 ◽  
Author(s):  
Sheikh Saleem ◽  
Sawan Verma ◽  
Irfan Yousuf ◽  
Mushtaq Ahmad Wani ◽  
Ravouf Asmi
Keyword(s):  
Extracellular Matrix ◽  
Unsolved Problem ◽  
Age Groups ◽  
Chronic Administration ◽  
Channel Blockers ◽  
Gingival Hyperplasia ◽  
Gingival Overgrowth ◽  
Younger Age ◽  
Matrix Metabolism

Gingival overgrowth (GO) is a side effect, associated with some distinct classes of drugs, such as anticonvulsants, immunosuppressant, and calcium channel blockers. One of the main drugs associated with GO is the antiepileptic, diphenylhydantoin (DPH)/ phenytoin (1), which affects gingival tissues by altering extracellular matrix metabolism. Phenytoin (DPH)-induced gingival overgrowth (PIGO) due to chronic administration remains an unsolved problem especially in cases where this drug is taken without any supervision due usually to poor follow-up. Younger age groups experience more lesions than adults and in the mentally handicapped the prevalence appears to be highest. The most satisfactory treatment is the replacement of the drug by a safer antiepileptic. Patients who are to be maintained on DPH respond well to a program of meticulous oral hygiene at home along with frequent professional prophylaxes. We present a case of seizure disorder with mental retardation who developed severe gingival overgrowth wherein teeth are almost buried, caused by unsupervised intake of phenytoin. JMS 2017; 20(1):44-46

scholarly journals Phenytoin and gingival mucosa: A molecular investigation

2019 ◽  
Vol 33 ◽  
pp. 205873841982825 ◽  
Author(s):  
Valentina Candotto ◽  
Furio Pezzetti ◽  
Alessandro Baj ◽  
Giada Beltramini ◽  
Dorina Lauritano ◽  
...  
Keyword(s):  
Gene Expression ◽  
Healthy People ◽  
The Other ◽  
Channel Blockers ◽  
Gingival Fibroblasts ◽  
Gingival Overgrowth ◽  
Molecular Investigation ◽  
Matrix Metabolism ◽  
Gingival Mucosa ◽  
Inflammatory Molecules

Several distinct classes of drugs, such as anticonvulsants, immunosuppressants, and calcium channel blockers, caused gingival overgrowth. One of the main drugs associated with the gingival overgrowth is the anti-epileptic such as phenytoin, which affects gingival tissues by altering extracellular matrix metabolism. In our study, we evaluate the effect of phenytoin, a drug whose active substance is phenytoin, on gingival fibroblasts of healthy volunteers. Gene expression of 29 genes was investigated in gingival fibroblasts’ cell culture treated with phenytoin compared with untreated cells. Among the studied genes, only 13 genes (CXCL5, CXCL10, CCR1, CCR3, CCR5, CCR6, IL-1A, IL-1B, IL-5, IL-7, IL-6R, BMP-2, and TNFSF-10) were statistically significant. All but one gene resulted downregulated after 24 h of treatment with phenytoin. BPM2 was the only, although weakly, up-expressed gene. Probably, we have not highlighted overexpression of the other inflammatory molecules because the study was performed on healthy people. Many studies show that phenytoin induces the overexpression of these cytokines but, probably, in our study, the drug does not have the same effect because we used gingival fibroblasts of healthy people.

scholarly journals Drug-induced gingival hyperplasia: An in vitro study using amlodipine and human gingival fibroblasts

2019 ◽  
Vol 33 ◽  
pp. 205873841982774 ◽  
Author(s):  
Dorina Lauritano ◽  
Marcella Martinelli ◽  
Alessandro Baj ◽  
Giada Beltramini ◽  
Valentina Candotto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Responses ◽  
Human Gingival Fibroblasts ◽  
Gingival Tissue ◽  
Gingival Fibroblast ◽  
Gingival Hyperplasia ◽  
Gingival Fibroblasts ◽  
Drug Induced ◽  
Gingival Overgrowth

Gingival overgrowth is a serious side effect that accompanies the use of amlodipine. Several conflicting theories have been proposed to explain the fibroblast’s function in gingival overgrowth. To determine whether amlodipine alters the inflammatory responses, we investigated its effects on gingival fibroblast gene expression as compared with untreated cells. Fragments of gingival tissue of healthy volunteers (11 years old boy, 68 years old woman, and 20 years old men) were collected during operation. Gene expression of 29 genes was investigated in gingival fibroblast cell culture treated with amlodipine, compared with untreated cells. Among the studied genes, only 15 ( CCL1, CCL2D, CCL5, CCL8, CXCL5, CXCL10, CCR1, CCR10, IL1A, IL1B, IL5, IL7, IL8, SPP1, and TNFSF10) were significantly deregulated. In particular, the most evident overexpressed genes in treated cells were CCR10 and IL1A. These results seem to indicate a possible role of amlodipine in the inflammatory response of treated human gingival fibroblasts.

scholarly journals Role of Cyclosporine in Gingival Hyperplasia: An In Vitro Study on Gingival Fibroblasts

2020 ◽  
Vol 21 (2) ◽  
pp. 595 ◽  
Author(s):  
Dorina Lauritano ◽  
Annalisa Palmieri ◽  
Alberta Lucchese ◽  
Dario Di Stasio ◽  
Giulia Moreo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Extracellular Matrix ◽  
Cyclosporine A ◽  
Matrix Metalloproteases ◽  
Gingival Hyperplasia ◽  
Gingival Fibroblasts ◽  
Down Regulation ◽  
Gingival Overgrowth ◽  
Expression Levels

Background: Gingival hyperplasia could occur after the administration of cyclosporine A. Up to 90% of the patients submitted to immunosuppressant drugs have been reported to suffer from this side effect. The role of fibroblasts in gingival hyperplasia has been widely discussed by literature, showing contrasting results. In order to demonstrate the effect of cyclosporine A on the extracellular matrix component of fibroblasts, we investigated the gene expression profile of human fibroblasts after cyclosporine A administration. Materials and methods: Primary gingival fibroblasts were stimulated with 1000 ng/mL cyclosporine A solution for 16 h. Gene expression levels of 57 genes belonging to the “Extracellular Matrix and Adhesion Molecules” pathway were analyzed using real-time PCR in treated cells, compared to untreated cells used as control. Results: Expression levels of different genes were significantly de-regulated. The gene CDH1, which codes for the cell adhesion protein E-cadherin, showed up-regulation. Almost all the extracellular matrix metalloproteases showed down-regulation (MMP8, MMP11, MMP15, MMP16, MMP24, MMP26). The administration of cyclosporine A was followed by down-regulation of other genes: COL7A1, the transmembrane receptors ITGB2 and ITGB4, and the basement membrane constituents LAMA2 and LAMB1. Conclusion: Data collected demonstrate that cyclosporine inhibits the secretion of matrix proteases, contributing to the accumulation of extracellular matrix components in the gingival connective tissue, causing gingival overgrowth. Patients affected by gingival overgrowth caused by cyclosporine A need to be further investigated in order to determine the role of this drug on fibroblasts.

scholarly journals A rare case of accelerated gingival overgrowth with high dose amlodipine therapy

2021 ◽  
Vol 2 (1) ◽  
pp. 39-41
Author(s):  
Rakesh B M ◽  
Sahithi Sharma ◽  
Chandana K H
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blockers ◽  
Rare Case ◽  
Immunosuppressive Drugs ◽  
High Dose ◽  
Channel Blockers ◽  
Gingival Hyperplasia ◽  
Limited Evidence ◽  
Drug Induced ◽  
Gingival Overgrowth

Introduction: Gingival overgrowth represents an over-exuberant response to a variety of local and systemic conditions. Certain anticonvulsants, immunosuppressive drugs, and a number of calcium channel blockers have been shown to produce similar gingival overgrowth in susceptible patients. Case report: We report a case of accelerated drug-induced gingival overgrowth in a 60-year-old hypertensive patient taking amlodipine at a dose of 10 mg. Conclusions: Among the calcium channel blockers, nifedipine is most frequently associated with gingival overgrowth.  Whereas, there is limited evidence of amlodipine-induced gingival hyperplasia.

Treatment Methods Conditioned by the Gravity of Drug-Induced Gingival Hyperplasias

2017 ◽  
Vol 68 (11) ◽  
pp. 2618-2622
Author(s):  
Alina Mihaela Calin ◽  
Mihaela Debita ◽  
Raluca Dragomir ◽  
Ovidiu Mihail Stefanescu ◽  
Cristian Budacu ◽  
...  
Keyword(s):  
Dental Treatment ◽  
Histopathological Examination ◽  
Transplant Rejection ◽  
Surgical Excision ◽  
Channel Blockers ◽  
Gingival Hyperplasia ◽  
Drug Induced ◽  
Treatment Methods ◽  
Systemic Medication ◽  
Bacterial Plaque

The first drug discovered to be involved in the development of gingival hyperplasia is phenytoin, which is indicated in the treatment of epileptic patients. The other drugs are calcium channel blockers with vasodilating effect. The most important one is Nifedipine, while Ciclosporin A, which is used as an immunosuppressant in the prevention of transplant rejection, causes gingival hyperplasia as a secondary effect. Gingival hyperplasia can reach an impressive volume, completely covering the dental crown and affecting the masticatory and physiognomic functions. The elucidation of the mechanism, by which drug-induced gingival hyperplasia occurs, favoring factors and the choice of conservative or surgical treatment methods, emphasizing the prophylactic treatment. The study batch was subject to intraoral and extraoral clinical examinations and the data were included in the dental treatment sheet of each patient, 11 patients aged over 60 years, who came to the Clinic ... in the period 2014-2016. The diagnosis was based on the anamnesis, the clinical aspect of the lesions and the histopathological examination. After the surgical excision of the hyperplasia affected area, recurrence was prevented by dispensarizing the patients and controlling the bacterial plaque through rigorous oral hygiene. Treatment depends on the severity of the lesions, as well as on the physionomic and masticatory functions. Conservative etiological therapy is attempted, by removing the bacterial plaque and local irritant factors, by reducing the dose of drugs, or by changing the systemic medication.

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