Drug-induced Gingival Hyperplasia Research Articles

Photodynamic therapy for the successful management of cyclosporine-related gum hypertrophy: A novel therapeutic option.

Background:Drug-induced gingival overgrowth is associated with the intake of three classes of drugs: anticonvulsants, immunosuppressants, and calcium channel blockers. It is clinically characterized by hyperplasia of the gingival connective tissue which appears edematous, bloody, and purplish-red in color. In more severe cases, drug-induced gingival hyperplasia negatively affects the patient’s quality of life, making it difficult to eat and practice good oral hygiene. Drug-induced gingival overgrowth therapy is controversial and, in fact, no studies in the literature highlight a well-defined therapeutic protocol. The therapies that are described provide primarily for non-surgical periodontal treatment and second-line surgical treatment. The aim of this work is to highlight a case of drug-induced gingival hyperplasia which was completely resolved thanks to photodynamic therapy which is completely free from side effects.Design and Methods:Photodynamic therapy was performed on an 18 year-old female patient with LEDs at a power of 450–470 nm and 5500 mW/cm2 + 7500 mW/cm2, combined with a Curcuma longa-based photosensitizer. A single session was performed, with applications of approximately 30 s for each interdental papilla.Results:The patient improved markedly after only one cycle of PDT. There was an absence of clinically detectable inflammation, edema, and rubor of the involved dental papillae. At the 4, 6, and 12 week follow-ups there were no recurrences.Conclusions:This case report highlights the first case of drug-induced gingival hypertrophy entirely treated with photodynamic therapy to be described in the literature. Therefore, although it is only a case report, this therapy which is free from side effects should be investigated as an alternative to current therapies.

POS-503 DRUG INDUCED GINGIVAL OVERGROWTH

Drug-influenced gingival hyperplasia is an adverse event noted in patients taking calcium channel blockers, cyclosporine, and anticonvulsants. Overgrowth usually begins within 3–6 months of initiation of therapy. Although mechanisms of action may be different, the clinical and microscopic aspect of drug-induced gingival hyperplasia is similar.

A case of chronic periodontitis with drug-induced gingival hyperplasia who improved with non-surgical periodontal treatment

A case of chronic periodontitis with drug-induced gingival hyperplasia who improved with non-surgical periodontal treatment

Biology of Drug-Induced Gingival Hyperplasia: In Vitro Study of the Effect of Nifedipine on Human Fibroblasts

Background: It has been proven that the antihypertensive agent nifedipine can cause gingival overgrowth as a side effect. The aim of this study was to analyze the effects of pharmacological treatment with nifedipine on human gingival fibroblasts activity, investigating the possible pathogenetic mechanisms that lead to the onset of gingival enlargement. Methods: The expression profile of 57 genes belonging to the “Extracellular Matrix and Adhesion Molecules” pathway, fibroblasts’ viability at different drug concentrations, and E-cadherin levels in treated fibroblasts were assessed using real-time Polymerase Chain Reaction, PrestoBlue™ cell viability test, and an enzyme-linked immunoassay (ELISA), respectively. Results: Metalloproteinase 24 and 8 (MMP24, MMP8) showed significant upregulation in treated cells with respect to the control group, and cell adhesion gene CDH1 (E-cadherin) levels were recorded as increased in treated fibroblasts using both real-time PCR and ELISA. Downregulation was observed for transmembrane receptors ITGA6 and ITGB4, the basement membrane constituent LAMA1 and LAMB1, and the extracellular matrix protease MMP11, MMP16, and MMP26. Conclusions: The obtained data suggested that the pathogenesis of nifedipine-induced gingival overgrowth is characterized by an excessive accumulation of collagen due to the inhibition of collagen intracellular and extracellular degradation pathways.

Amlodipine-induced gingival hyperplasia

Drug-induced gingival hyperplasia is the increased growth of gingival epithelium and submucosa which may cause bleeding and loss of teeth. Certain anticonvulsant, immunosuppressive, and antihypertensive drugs are the underlying cause in most cases. Among them, cases due to amlodipine are very rare. Here, we discuss the topic along with a case of gingival overgrowth induced by amlodipine. A 51-year-old female presented with gingival overgrowth. She was on amlodipine because of primary hypertension. She had gingival hyperplasia increasingly growing in the last few months. Her antihypertensive regimen was changed with cessation of amlodipine. This study suggests that amlodipine may lead to gingival hyperplasia.

GINGIVAL HYPERPLASIA ASSOCIATED WITH THE USE OF CYCLOSPORINE, PHENYTOIN, AND NIFEDIPINE SYSTEMIC ACTION MEDICINES

Objective: To carry out a narrative review of the literature regarding gingival hyperplasia modified by the use of medications, as well as to discuss the clinical characteristics, etiopathogenesis, and recommended therapeutic procedures. Study Design: A narrative review consisting of data collection from the following sources: Medline, Lilacs, and SciELO. Scientific articles and clinical cases that approached the subject of gingival hyperplasia and drugs were selected. The review was done in published articles covering the subject, as well as in academic books on stomatology and oral pathology. Results: Drug-induced gingival hyperplasia is defined as an abnormal growth of gingival tissues due to the use of medications, especially anticonvulsants such as phenytoin, calcium channel blockers such as nifedipine, and cyclosporine, which is an immunosuppressive agent for transplanted patients. Therefore, its prevention is important, as well as its early diagnosis by the dentist. Conclusion: Most of the authors agree that good oral hygiene acts positively on cyclosporine-induced gingival hyperplasia, since it diminishes signs of inflammation, but does not act effectively against gingival growth. Recently, studies have shown that the antibiotic azithromycin is useful in the treatment of gingival hyperplasia.

Review on Differential Diagnosis of Drug-Induced Gingival Hyperplasia and other Oral Lesions

Chronic medication usage is a major component of the medical diagnosis of patients. Nowadays, some of the most common diseases such as cancer, hypertension, diabetes and etc., are treated with drugs which cause a variety of oral side-effects including gingival overgrowth and appearance of lesions on the tissues of the oral cavity. As such, drug-induced oral reactions are an ordinary sight in the dental practice. This review will point out the main therapeutic agents causing gingival hyperplasia and other pathologic lesions in the oral cavity. Some frequently used medications, in particular antihypertensives, nonsteroidal antiinflammatory drugs and even antibiotics, can lead to overgrowth of the gingiva and to the multiple unwanted conditions, namely: lupus erythematosus, erythema multiforme, mucositis, oral lichen planus, pemphigus vulgaris and more.

Review: Differential Diagnosis of Drug-Induced Gingival Hyperplasia and Other Oral Lesions

Chronic medication usage is a major component of the medical diagnosis of patients. Nowadays, some of the most common diseases such as cancer, hypertension, diabetes and etc., are treated with drugs which cause a variety of oral side-effects including gingival over growth and appearance of lesions on the tissues of the oral cavity. As such, drug-induced oral reactions are an ordinary sight in the dental practice. This review will point out the main therapeutic agents causing gingival hyperplasia and other pathologic lesions in the oral cavity.

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

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.

Using Evidence-Based Dentistry in the Clinical Management of Combined Periodontal Conditions

ObjectiveThis report proposes a framework to integrate evidence-based dentistry (EBD) in a systematic approach in the clinical management of a patient diagnosed with drug-induced gingival hyperplasia combined with generalized aggressive periodontitis.This report illustrates the case of a 37-year-old female who presented to the Department of Periodontology at Tufts University School of Dental Medicine with enlarged, tender, bleeding gums, and loose teeth combined with a history of uncontrolled hypertension treated with calcium channel blockers. MethodsIncorporating the EBD process, a new 5-step framework is proposed: ask the clinical question, acquire and appraise the evidence, apply it in the clinical setting, and assess the subjective and objective outcomes. Articles on aggressive periodontitis and/or gingival enlargement were sought using the assistance of an expert librarian. The search was conducted on the PubMed, Embase, and Scopus databases. ResultsInitial literature search identified 34 publications. Articles were reviewed by 2 clinicians, and 31 relevant articles were selected. Twenty-six of the references matched the levels of evidence initially agreed upon. Based on the scientific evidence, patient's chief complaint, and clinical expertise, a decision tree highlighting treatment options was compiled. The outcomes of the clinical management revealed that combined conditions can be successfully treated with nonsurgical therapy before proceeding with surgical therapy. ConclusionWithin the limitations of this study, integrating EBD concepts was a reliable method to treat an atypical case, where 2 severe periodontal conditions were combined: drug-induced gingival enlargement and generalized aggressive periodontitis.

Drug-induced gingival hyperplasia that was difficult to differentially diagnose from malignancy: A case report

Drug-induced gingival hyperplasia that was difficult to differentially diagnose from malignancy: A case report

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

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.

Drug-induced gingival hyperplasia: a retrospective study using spontaneous reporting system databases

BackgroundDrug-induced gingival hyperplasia (DIGH) causes problems with chewing, aesthetics, and pronunciation, and leads to the deterioration of the patient’s quality of life (QOL). Thus, the aim of this study was to evaluate the incidence of DIGH using spontaneous reporting system (SRS) databases.MethodsWe analyzed reports of DIGH from SRS databases and calculated the reporting odds ratios (RORs) of suspected drugs (immunosuppressants, calcium channel blockers, and anticonvulsants). The SRS databases used were the US Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS) and the Japanese Adverse Drug Event Report (JADER) database. With the data, we evaluated the time-to-onset profile and the hazard type using the Weibull shape parameter (WSP). Furthermore, we used the association rule mining technique to discover undetected relationships such as possible risk factors.ResultsThe FAERS contained 5,821,716 reports. The RORs (95% confidence interval: CI) for cyclosporine, everolimus, sirolimus, mycophenolate mofetil, amlodipine, nifedipine, carbamazepine, clobazam, levetiracetam, phenobarbital, phenytoin, primidone, topiramate, and valproic acid, were 39.4 (95% CI: 30.3–51.2), 4.2 (1.7–10.0), 6.6 (2.5–17.7), 13.1 (7.2–23.2), 94.8 (80.0–112.9), 57.9 (35.7–94.0), 15.1 (10.3–22.3), 65.4 (33.8–126.7), 6.5 (3.6–11.8), 19.7 (8.8–44.0), 65.4 (52.4–82.9), 56.5 (21.1–151.7), 2.9 (1.1–7.7), and 17.5 (12.6–24.4), respectively. The JADER database contained 430,587 reports. The median time-to-onset of gingival hyperplasia values for immunosuppressants, calcium channel blockers, and anticonvulsants use were 71, 262, and 37 days, respectively. Furthermore, the 95% CI of the WSP β for anticonvulsants was over and excluded 1, which meant that they were wear-out failure type.ConclusionsOur results suggest that DIGH monitoring of patients administered immunosuppressants, calcium channel blockers, or anticonvulsants is important. We demonstrated the potential risk of DIGH following the long-term use of calcium channel blocker over approximately 260 days. Based on the results of the association rule mining approach, patients with intellectual disability who are administered phenytoin should be monitored carefully. We recommend that patients who experience symptoms related to DIGH should be closely monitored.

Periodontal therapy for a patient with the chronic periodontitis and drug-induced gingival hyperplasia

Periodontal therapy for a patient with the chronic periodontitis and drug-induced gingival hyperplasia

Periodontal Management of Phenytoin-Induced Gingival Overgrowth

Phenytoin can induce excessive gingival overgrowth that hampers oral function and compromises effective oral hygiene and aesthetics. A 39-year-old male was referred for dental treatment with several complaints, especially upper and lower gingival overgrowth that hindered speech and swallowing. Generalized deep probing pocket depths and bone loss were detected. A diagnosis of gingival overgrowth, associated with phenytoin use and chronic periodontitis, was established. The treatment plan consisted of conservative management involving dental education, motivation, and meticulous instruction in oral hygiene, together with scaling and root planning. During the re-evaluation, a marked reduction in the clinical parameters was noted. Surgical therapy was also performed in order to reduce the pocket depths. The histological diagnosis was consistent with drug-induced gingival hyperplasia, and supportive periodontal therapy was proposed. At this writing, the patient was undergoing follow-up projected to continue for a total of 4 years. Phenytoin-induced gingival overgrowth can be managed through the use of periodontal procedures and oral hygiene.

Amlodipine-induced Gingival Hyperplasia - A Case Report and Review.

Anticonvulsants, antihypertensive calcium channel blockers and immunosuppressants are the three main classes of drugs known to cause drug-induced gingival hypertrophy or hyperplasia. Among the calcium channel blockers, nifedipine administration has most frequently been associated with medication-related gingival hyperplasia. The incidence with amlodipine, which has a mode of action pharmacodynamically comparable to nifedipine, has rarely been reported. Here, we present a rare case of amlodipine-induced gingival hyperplasia in a hypertensive patient.

Inflammatory environment induces gingival tissue‐specific mesenchymal stem cells to differentiate towards a pro‐fibrotic phenotype

Human gingival tissues are prone to hyperplasia under inflammatory stimuli. We have identified gingival tissue-specific mesenchymal stem cells (GMSCs) and found their functional change being correlated with drug-induced gingival hyperplasia. However, whether these cells exhibit characteristics of pro-fibrotic phenotype under inflammatory condition remains unknown. GMSCs isolated from human normal gingival tissues (N-GMSC) and inflammatory gingival tissues (I-GMSC) were cultured in vitro, representative cytokines were added to simulate the in vivo inflammatory environment. Under the influence of the inflammatory cytokines, GMSCs exhibited higher rate of proliferation than those under normal condition, while their potential for osteogenic and adipogenic differentiation was suppressed. The expression of matrix metalloproteinases (MMP)-1, MMP-2, IL-1, IL-6, TNF-α and type 1 collagen was significantly higher in I-GMSCs than in N-GMSCs. Furthermore, compared with dental pulp stem cells, GMSCs showed different pattern of gene expression and extracellular matrix formation in inflammatory environment. Inflammatory microenvironment induces GMSCs to differentiate towards a pro-fibrotic phenotype, which could underlie the hyperplastic appearance of inflammatory gingiva.

Azithromycin Treatment of Drug-Induced Gingival Hyperplasia in Renal Transplant Patients

Azithromycin Treatment of Drug-Induced Gingival Hyperplasia in Renal Transplant Patients

Drug-Induced Gingival Hyperplasia

ImageA 37-year-old Spanish-speaking man presented with a complaint of tender, bleeding, and swollen gums. He had had an orthotopic heart transplant in 1997. His current mediations include Cyclosporine 125 mg bid and amlodipine 5 mg qd as well as CellCept, aspirin, and allopurinol for gout. Gingival overgrowth, also known as gingival hyperplasia, has been well described in the literature. The most recognized cause is drug-induced gingival enlargement from phenytoin (Dilantin), which is commonly used to treat patients with epileptic seizures. Less known drugs that contribute to this phenomenon are Cyclosporine, a potent immunosuppressant used in organ transplant recipients, and calcium channel blocker agents. The interaction of these medications with epithelial keratinocytes, fibroblasts, and collagen can lead to an overgrowth of gingival tissue, particularly in patients with poor oral hygiene, periodontal disease, and malpositioned teeth. Treatment for gingival hyperplasia includes discontinuing the drug or reducing its dose. In those for whom this is not possible, good oral hygiene and referral for surgical gingivectomy remain the only treatment. Gingival hyperplasia should be considered when treating organ transplant recipients on immunosuppressant therapy. Dr. McGregor is an assistant professor of emergency medicine at the Warren Alpert Medical School of Brown University and an attending at Rhode Island Hospital and the Miriam Hospital. Dr. Hsu-Hung is a resident in emergency medicine at the Warren Alpert Medical School of Brown University.

Drug-induced gingival hyperplasia and scaffolds: They may be valuable for horizontal food impaction

Food impaction is a severe clinical trouble that bothers most people especially middle aged and old people. It is reported that the rate of food impaction is 92.2%. The incidence of 40-59 years old is 98.9%. It is a disease of high prevalence in population. It has influenced people's social intercourse and everyday life because it may cause halitosis, gingivalitis, periodontitis, gingival abscess, alveolar bone absorption, root caries, eventually lead to severe results from teeth loose to deletion and so on. Several reasons are involved with food impaction such as gingival recession, periodontal disease, caries, age, excessive attrition, etc. Food impaction can be divided into two kinds: vertical and horizontal food impaction. At present, there are some clinical methods such as crown or dental filling for vertical one, but horizontal food impaction is still difficult to deal with. Though some methods are being adopted like making crowns and removable obstructers, the problems have never been settled effectively for the injury to teeth and inconvenience of these treatments. Here we put forward a hypothesis that periodontal tissues can regenerate much the same as normal situation by way of using drug to induce gingiva hyperplasia initiatively and implanting scaffolds. Then horizontal food impaction will be cured when the interproximal clearance is filled with periodontal tissues. It will bring the patient hope.