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Journal articles on the topic 'Drug Induced Gingival Overgrowth, Laser'

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Published: 9 March 2023

Last updated: 10 March 2023

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1

Закиров, Т., T. Zakirov, Е. Бимбас, E. Bimbas, Т. Стати, and T. Stati. "VARIOUS MANIFESTATIONS OF HYPERPLASIA OF PERIODONTAL TISSUES IN CHILDREN." Actual problems in dentistry 9, no. 3 (June 25, 2013): 56–62. http://dx.doi.org/10.18481/2077-7566-2013-0-3-56-62.

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There are many reasons for gingival hyperplasia in children. 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. Gingival overgrowth is characterized by the accumulation of extracellular matrix in gingival connective tissues, particularly collagenous components with various degrees of inflammation. The complex treatment of gingival overgrowth can include conservative therapy and traditional or laser gingivectomy

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2

Muralikrishna, Tupili, Butchibabu Kalakonda, Sumanth Gunupati, and Pradeep Koppolu. "Laser-Assisted Periodontal Management of Drug-Induced Gingival Overgrowth under General Anesthesia: A Viable Option." Case Reports in Dentistry 2013 (2013): 1–4. http://dx.doi.org/10.1155/2013/387453.

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Gingival overgrowth/hyperplasia can be attributed to several causes, but drug-induced gingival overgrowth/hyperplasia arises secondarily to prolonged use of antihypertensive drugs, anticonvulsants and immunosuppressants. The management is complex in nature considering the multitude of factors involved such as substitution of drug strict plaque control along with excision of the tissue to be performed under local anesthesia as outpatient. In the recent times, the patient’s psychological fear of the treatment with the use of surgical blade and multiple visits has developed the concept of single visit treatment under general anesthesia incorporating a laser as viable option. The present case highlights the new method of management of gingival overgrowth.

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3

Fornaini, Carlo, and Jean Paul Rocca. "CO2 LASER TREATMENT OF DRUG-INDUCED GINGIVAL OVERGROWTH." LASER THERAPY 21, no. 1 (2012): 39–42. http://dx.doi.org/10.5978/islsm.12-cr-01.

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4

Hegde, Rashmi, Rahul Kale, and A. Sanjay Jain. "Cyclosporine and Amlodipine Induced Severe Gingival Overgrowth - Etiopathogenesis and Management of a Case with Electrocautery and Carbon-Dioxide(CO2) Laser." Journal of Oral Health and Community Dentistry 6, no. 1 (January 2012): 34–42. http://dx.doi.org/10.5005/johcd-6-1-34.

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ABSTRACT Gingival overgrowth is a well recognized, unwanted side-effect associated with three major drugs/drug groups – phenytoin, cyclosporine and the calcium channel blockers. Cyclosporine is a potent immunosuppressive compound that has been used increasingly in conjunction with kidney, heart and other transplants. Calcium channel blockers are widely used in medical practice for the management of cardiovascular disorders. Due to their wide range of use, gingival overgrowth is now a recognized side-effect associated with them. Here we discuss a case report dealing with severe gingival overgrowth induced by cyclosporine and amlodipine. A 36-year-old man who underwent renal transplant came with a chief complaint of generalized gingival swelling. He had very severe gingival overgrowth in both arches and required thorough scaling and oral hygiene instructions, followed by supportive periodontal therapy for 4 months, after which radical gingivectomy using electrocautery and CO2 laser was performed. The post operative results were excellent and there was no recurrence at 1 year follow-up.

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5

MATTSON, JOHN S., RICHARD BLANKENAU, and JOSEPH J. KEENE. "USE OF AN ARGON LASER TO TREAT DRUG-INDUCED GINGIVAL OVERGROWTH." Journal of the American Dental Association 129, no. 1 (January 1998): 78–83. http://dx.doi.org/10.14219/jada.archive.1998.0024.

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6

Campos, Luana, Marina Gallottini, Débora Pallos, Alyne Simões, and Fabiana Martins. "High-power diode laser on management of drug-induced gingival overgrowth: Report of two cases and long-term follow-up." Journal of Cosmetic and Laser Therapy 20, no. 4 (January 19, 2018): 215–19. http://dx.doi.org/10.1080/14764172.2017.1400165.

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7

Nakib, Nuha, and Seema S. Ashrafi. "Drug-Induced Gingival Overgrowth." Disease-a-Month 57, no. 4 (April 2011): 225–30. http://dx.doi.org/10.1016/j.disamonth.2011.03.010.

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8

Dongari, Anna, Howard T. McDonnell, and Robert P. Langlais. "Drug-induced gingival overgrowth." Oral Surgery, Oral Medicine, Oral Pathology 76, no. 4 (October 1993): 543–48. http://dx.doi.org/10.1016/0030-4220(93)90027-2.

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9

MANAA, R., M. Ben Salem, N. Ben Mahmoud, M. Ben Salah, I. Handous, A. Letaeif, M. Hammouda, S. Aloui, and H. Skhiri. "POS-503 DRUG INDUCED GINGIVAL OVERGROWTH." Kidney International Reports 7, no. 2 (February 2022): S221. http://dx.doi.org/10.1016/j.ekir.2022.01.534.

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10

Aryal, Deepa, Kripa Shahi, and Surendra Man Shrestha. "Amlodipine induced Gingival Overgrowth." Journal of Nepalese Society of Periodontology and Oral Implantology 2, no. 1 (June 4, 2018): 30–32. http://dx.doi.org/10.3126/jnspoi.v2i1.23608.

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Gingival overgrowth caused by drug is a well-documented unwanted side effect and mostly caused by Nifedipine. Newer generation calcium channel blocker, amlodipine, has been used with the increasing frequency to overcome the adverse effect of first and second generation dihydropyridine derivatives of Calcium Chanel Blocker. The pathogenesis of gingival enlargement is uncertain and the treatment is still largely limited to the maintenance of an improved level of oral hygiene and surgical removal of the overgrowth tissue. This article reports the amlodipine induced gingival enlargement and its treatment in a 60 years old hypertensive female patient.

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11

Ogino, M., J. Kido, M. Bando, N. Hayashi, C. Wada, T. Nagata, F. Nishimura, et al. "α2 Integrin +807 Polymorphism in Drug-induced Gingival Overgrowth." Journal of Dental Research 84, no. 12 (December 2005): 1183–86. http://dx.doi.org/10.1177/154405910508401217.

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α2 integrin on fibroblasts is reported to play an important role in the induction of drug-induced gingival overgrowth, which is characterized by excessive accumulation of type I collagen in gingival connective tissue. Silent polymorphism 807 T/C within the α2 integrin gene is associated with high/low α2 integrin expression. The aim of this study was to test the hypothesis that expression of α2 integrin 807 T/C polymorphism correlates with drug-induced gingival overgrowth. A case-control study comparing 136 subjects taking calcium channel blockers (72 with vs. 64 without drug-induced gingival overgrowth) demonstrated that the frequency of the +807 C allele was significantly higher in the case group than in the controls (odds ratio, 3.61; 95% confidence interval, 2.14 – 6.10; P < 0.05). The present findings suggest that the α2 +807 C allele is one of the genetic risk factors for drug-induced gingival overgrowth.

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12

Farook, Fathima Fazrina, Mohamed Nuzaim M. Nizam, and Abdulsalam Alshammari. "An Update on the Mechanisms of Phenytoin Induced Gingival Overgrowth." Open Dentistry Journal 13, no. 1 (December 31, 2019): 430–35. http://dx.doi.org/10.2174/1874210601913010430.

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Background: Phenytoin induced gingival overgrowth, a side effect with multifactorial aetiology, is characterized by an increase in the volume of extracellular tissues, particularly collagenous components, with varying degrees of inflammation. Objective: The aim of this paper is to review the available literature regarding the pathophysiological mechanisms of phenytoin induced gingival overgrowth. Methods: A thorough literature search of the PubMed/ Embase/ Web of science/ Cochrane central database was conducted to identify the mechanisms involved in the process of phenytoin-induced gingival overgrowth using the following keywords: Phenytoin; Anticonvulsant; Gingival Overgrowth; Gingival Enlargement, Gingival Hyperplasia; Drug Induced Gingival Enlargement; Drug Induced Gingival Overgrowth Results: According to the available evidence, several mechanisms have been proposed addressing the pathophysiological mechanism of phenytoin induced gingival overgrowth both at a cellular and molecular level. Evidence suggests that the inflammatory changes in the gingival tissues orchestrate the interaction between phenytoin and fibroblasts particularly resulting in an increase in the extracellular matrix content. Conclusion: However, the mechanism of production of inflammatory mediators is not fully understood. This, together with the high prevalence of Phenytoin induced gingival overgrowth, warrants further research in this area in order to develop treatment and preventive strategies for the management of this condition.

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13

Ramírez-Rámiz, Albert, Lluís Brunet-LLobet, Eduard Lahor-Soler, and Jaume Miranda-Rius. "On the Cellular and Molecular Mechanisms of Drug-Induced Gingival Overgrowth." Open Dentistry Journal 11, no. 1 (July 31, 2017): 420–35. http://dx.doi.org/10.2174/1874210601711010420.

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Introduction: Gingival overgrowth has been linked to multiple factors such as adverse drug effects, inflammation, neoplastic processes, and hereditary gingival fibromatosis. Drug-induced gingival overgrowth is a well-established adverse event. In early stages, this gingival enlargement is usually located in the area of the interdental papilla. Histologically, there is an increase in the different components of the extracellular matrix. Objective: The aim of this manuscript is to describe and analyze the different cellular and molecular agents involved in the pathogenesis of Drug-induced gingival overgrowth. Method: A literature search of the MEDLINE/PubMed database was conducted to identify the mechanisms involved in the process of drug-induced gingival overgrowth, with the assistance of a research librarian. We present several causal hypotheses and discuss the advances in the understanding of the mechanisms that trigger this gingival alteration. Results: In vitro studies have revealed phenotypic cellular changes in keratinocytes and fibroblasts and an increase of the extracellular matrix with collagen and glycosaminoglycans. Drug-induced gingival overgrowth confirms the key role of collagenase and integrins, membrane receptors present in the fibroblasts, due to their involvement in the catabolism of collagen. The three drug categories implicated: calcineuron inhibitors (immunosuppressant drugs), calcium channel blocking agents and anticonvulsant drugs appear to present a multifactorial pathogenesis with a common molecular action: the blockage of the cell membrane in the Ca2+/Na+ ion flow. The alteration of the uptake of cellular folic acid, which depends on the regulated channels of active cationic transport and on passive diffusion, results in a dysfunctional degradation of the connective tissue. Certain intermediate molecules such as cytokines and prostaglandins play a role in this pathological mechanism. The concomitant inflammatory factor encourages the appearance of fibroblasts, which leads to gingival fibrosis. Susceptibility to gingival overgrowth in some fibroblast subpopulations is due to phenotypic variability and genetic polymorphism, as shown by the increase in the synthesis of molecules related to the response of the gingival tissue to inducing drugs. The authors present a diagram depicting various mechanisms involved in the pathogenesis of drug-induced gingival overgrowth. Conclusion: Individual predisposition, tissue inflammation, and molecular changes in response to the inducing drug favor the clinical manifestation of gingival overgrowth.

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14

Charles, Noronha ShyamCurtis, Rahul Chavan, NinadJoshirao Moon, Srinivas Nalla, Jaydeepchandra Mali, and Anchal Prajapati. "Drug-Induced gingival overgrowth: The genetic dimension." North American Journal of Medical Sciences 6, no. 9 (2014): 478. http://dx.doi.org/10.4103/1947-2714.141651.

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15

Bajkovec, Lucija, Anna Mrzljak, Robert Likic, and Ivan Alajbeg. "Drug-induced gingival overgrowth in cardiovascular patients." World Journal of Cardiology 13, no. 4 (April 26, 2021): 68–75. http://dx.doi.org/10.4330/wjc.v13.i4.68.

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16

Seymour, R. A., J. M. Thomason, and J. S. Ellis. "The pathogenesis of drug-induced gingival overgrowth." Journal of Clinical Periodontology 23, no. 3 (March 1996): 165–75. http://dx.doi.org/10.1111/j.1600-051x.1996.tb02072.x.

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17

Mavrogiannis, M., J. S. Ellis, J. M. Thomason, and R. A. Seymour. "The management of drug-induced gingival overgrowth." Journal of Clinical Periodontology 33, no. 6 (June 2006): 434–39. http://dx.doi.org/10.1111/j.1600-051x.2006.00930.x.

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18

Seymour, R. A., J. S. Ellis, and J. M. Thomason. "Risk factors for drug-induced gingival overgrowth." Journal of Clinical Periodontology 27, no. 4 (April 2000): 217–23. http://dx.doi.org/10.1034/j.1600-051x.2000.027004217.x.

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19

Kataoka, Masatoshi, Jun-ichi Kido, Yasuo Shinohara, and Toshihiko Nagata. "Drug-Induced Gingival Overgrowth—a Review." Biological & Pharmaceutical Bulletin 28, no. 10 (2005): 1817–21. http://dx.doi.org/10.1248/bpb.28.1817.

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20

Kendall, Paige, Janelle Vu Pugashetti, and Paul Aronowitz. "Drug-induced gingival overgrowth after renal transplantation." Journal of General Internal Medicine 32, no. 12 (June 27, 2017): 1406. http://dx.doi.org/10.1007/s11606-017-4107-x.

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21

Barot, VarshalJ. "Pills to pearls: Drug-induced gingival overgrowth." Journal of the Practice of Cardiovascular Sciences 4, no. 3 (2018): 235. http://dx.doi.org/10.4103/jpcs.jpcs_60_18.

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22

Subramani, Tamilselvan, Vidhya Rathnavelu, and Noorjahan Banu Alitheen. "The Possible Potential Therapeutic Targets for Drug Induced Gingival Overgrowth." Mediators of Inflammation 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/639468.

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Gingival overgrowth is a side effect of certain medications. The most fibrotic drug-induced lesions develop in response to therapy with phenytoin, the least fibrotic lesions are caused by cyclosporin A, and the intermediate fibrosis occurs in nifedipine-induced gingival overgrowth. Fibrosis is one of the largest groups of diseases for which there is no therapy but is believed to occur because of a persistent tissue repair program. During connective tissue repair, activated gingival fibroblasts synthesize and remodel newly created extracellular matrix. Proteins such as transforming growth factor (TGF), endothelin-1 (ET-1), angiotensin II (Ang II), connective tissue growth factor (CCN2/CTGF), insulin-like growth factor (IGF), and platelet-derived growth factor (PDGF) appear to act in a network that contributes to the development of gingival fibrosis. Since inflammation is the prerequisite for gingival overgrowth, mast cells and its protease enzymes also play a vital role in the pathogenesis of gingival fibrosis. Drugs targeting these proteins are currently under consideration as antifibrotic treatments. This review summarizes recent observations concerning the contribution of TGF-β, CTGF, IGF, PDGF, ET-1, Ang II, and mast cell chymase and tryptase enzymes to fibroblast activation in gingival fibrosis and the potential utility of agents blocking these proteins in affecting the outcome of drug-induced gingival overgrowth.

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23

Sam, George, and Staly Chakkalakkal Sebastian. "Nonsurgical Management of Nifedipine Induced Gingival Overgrowth." Case Reports in Dentistry 2014 (2014): 1–4. http://dx.doi.org/10.1155/2014/741402.

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Drug-induced gingival overgrowth is frequently associated with three particular drugs: phenytoin, cyclosporin, and nifedipine. As gingival enlargement develops, it affects the normal oral hygiene practice and may interfere with masticatory functions. The awareness in the medical community about this possible side effect of nifedipine is less when compared to the effects of phenytoin and cyclosporin. The frequency of gingival enlargement associated with chronic nifedipine therapy remains controversial. Within the group of patients that develop this unwanted effect, there appears to be variability in the extent and severity of the gingival changes. Although gingival inflammation is considered a primary requisite in their development, few cases with minimal or no plaque induced gingival inflammation have also been reported. A case report of gingival overgrowth induced by nifedipine in a patient with good oral hygiene and its nonsurgical management with drug substitution is discussed in this case report.

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Malek, Rayhana, Bouchra El Houari, and Jamila Kissa. "Periodontal Management of Cyclosporin A-Induced Gingival Overgrowth: A Nonsurgical Approach." Case Reports in Dentistry 2019 (April 11, 2019): 1–8. http://dx.doi.org/10.1155/2019/8609547.

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Gingival overgrowth is a major and frequent unwanted effect accompanying the chronic usage of antihypertensive, anticonvulsant, and immunosuppressant drugs. The expression and the severity of this tissue-specific condition are influenced by a variety of factors, mainly drug and periodontal variables. Such increased volume of gingiva may compromise normal oral functions, aesthetics in addition to the patients’ ability to practice optimal oral hygiene. The management of gingival overgrowth includes nonsurgical approach, surgical approach, or both of them for severe cases of gingival overgrowth as well as drug withdrawal. This case report illustrates a successful nonsurgical management of a 21-year-old patient with cyclosporin A-induced gingival overgrowth who experienced a total regression of the gingival enlargement without any surgical procedure or drug substitution. And it highlights therefore the key role of supportive periodontal therapy in maintaining good and stable outcomes over 2 years of follow-up.

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25

Saleem, Sheikh, Sawan Verma, Irfan Yousuf, Mushtaq Ahmad Wani, and Ravouf Asmi. "Diphenylhydantoin Induced Severe Gingival Hyperplasia." JMS SKIMS 20, no. 1 (June 16, 2017): 44–46. http://dx.doi.org/10.33883/jms.v20i1.311.

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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

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26

Ambicki, Miłosz, Robert Brodowski, Marta Mucha, Małgorzata Migut, Adam Malawski-Róg, Wojciech Stopyra, and Bogumił Lewandowski. "Drug–induced gingival overgrowth after cyclosporin A therapy." European Journal of Clinical and Experimental Medicine 15, no. 1 (2017): 82–86. http://dx.doi.org/10.15584/ejcem.2017.1.13.

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27

GORIUC, ANCUTA. "ENDOPLASMIC RETICULUM INVOLVEMENT IN DRUG-INDUCED GINGIVAL OVERGROWTH." FARMACIA 69, no. 6 (December 24, 2021): 1094–100. http://dx.doi.org/10.31925/farmacia.2021.6.11.

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28

Hassell, Thomas M., and Arthur F. Hefti. "Drug-Induced Gingival Overgrowth: Old Problem, New Problem." Critical Reviews in Oral Biology & Medicine 2, no. 1 (January 1991): 103–37. http://dx.doi.org/10.1177/10454411910020010201.

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29

Matsumoto, Hiroko, Reiri Takeuchi, Makiko Ono, Yoshiaki Akimoto, Naomi Kobayashi, and Akira Fujii. "Drug-induced gingival overgrowth and its tentative pharmacotherapy." Japanese Dental Science Review 46, no. 1 (February 2010): 11–16. http://dx.doi.org/10.1016/j.jdsr.2009.09.001.

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30

Rakesh B M, Sahithi Sharma, and Chandana K H. "A rare case of accelerated gingival overgrowth with high dose amlodipine therapy." Journal of Pharmacovigilance and Drug Research 2, no. 1 (March 1, 2021): 39–41. http://dx.doi.org/10.53411/jpadr.2021.2.1.8.

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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.

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31

Subramani, Tamilselvan, Vidhya Rathnavelu, Swee Keong Yeap, and Noorjahan Banu Alitheen. "Influence of Mast Cells in Drug-Induced Gingival Overgrowth." Mediators of Inflammation 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/275172.

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Mast cells (MCs) are multifunctional effector cells that were originally thought to be involved in allergic disorders. Now it is known that they contain an array of mediators with a multitude of effects on many other cells. MCs have become a recent concern in drug-induced gingival overgrowth (DIGO), an unwanted outcome of systemic medication. Most of the studies have confirmed the significant presence of inflammation as a prerequisite for the overgrowth to occur. The inflammatory changes within the gingival tissue appear to influence the interaction between the inducing drug and the fibroblast activity. The development of antibodies to MC-specific enzymes, tryptase and chymase, has facilitated the study of mast cells in DIGO. Many immunohistochemical studies involving MCs have been conducted; as a result, DIGO tissues are found to have increased the number of MCs in the gingiva, especially in the area of fibrosis. At the cellular level, gingival fibrogenesis is initiated by several mediators which induce the recruitment of a large number of inflammatory cells, including MCs. The purpose of this paper is to access the roles played by MCs in gingival overgrowth to hypothesize a relationship between these highly specialized cells in the pathogenesis of DIGO.

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32

Trackman, P. C., and A. Kantarci. "Connective Tissue Metabolism and Gingival Overgrowth." Critical Reviews in Oral Biology & Medicine 15, no. 3 (May 2004): 165–75. http://dx.doi.org/10.1177/154411130401500305.

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Gingival overgrowth occurs mainly as a result of certain anti-seizure, immunosuppressive, or antihypertensive drug therapies. Excess gingival tissues impede oral function and are disfiguring. Effective oral hygiene is compromised in the presence of gingival overgrowth, and it is now recognized that this may have negative implications for the systemic health of affected patients. Recent studies indicate that cytokine balances are abnormal in drug-induced forms of gingival overgrowth. Data supporting molecular and cellular characteristics that distinguish different forms of gingival overgrowth are summarized, and aspects of gingival fibroblast extracellular matrix metabolism that are unique to gingival tissues and cells are reviewed. Abnormal cytokine balances derived principally from lymphocytes and macrophages, and unique aspects of gingival extracellular matrix metabolism, are elements of a working model presented to facilitate our gaining a better understanding of mechanisms and of the tissue specificity of gingival overgrowth.

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Salama, Mohamed Helmy, Abdelraheem R. Algendy, and Saleem Shaikh. "Estimation of Bcl-2 and Ki-67 in Gingival Epithelium of Epileptic Patients." Asian Pacific Journal of Health Sciences 7, no. 3 (August 5, 2020): 53–58. http://dx.doi.org/10.21276/apjhs.2020.7.3.13.

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Abstract Introduction: Gingival overgrowth is one of several oral side effects of phenytoin, a potent antiepileptic drug. Several mechanisms have been elucidated to understand the pathogenesis of drug induced gingival overgrowth. The frequency of gingival overgrowth associated with chronic phenytoin therapy remains controversial. and the possible subclinical effects of this drug on the gingival epithelium should be investigated histopathologically and immunohistochemically. Purpose of the study: To investigate the Bcl-2 for apoptosis rate and Ki-67 for the epithelial proliferative activity in epileptic patients. Materials and methods: Twenty four samples of gingival tissue from epileptic patients treated with phenytoin and in eight samples of gingival tissue from healthy patients who didn’t use phenytoin (control) were evaluated for Bcl-2 and Ki-67 immunohistochemically. Results: The results revealed moreproliferative activity of the overlying epithelium and an increased pattern of Bcl-2 and Ki-67 in phenytoin users compared to controls. Conclusion: These results concluded that the increased epithelial thickness observed in phenytoin induced gingival overgrowth is associated with increased apoptotic rate and mitotic activity , especially in the oral epithelium. Keywords: Gingival overgrowth, Bcl-2, Ki-67, Phenytoin.

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Rijal, Arjun Hari, Bhageshwar Dhami, Nashib Pandey, Deepa Aryal, and Kamana Neupane. "Localised Gingival Overgrowth in Patient taking Amlodipine." Journal of Nepalese Society of Periodontology and Oral Implantology 4, no. 2 (December 31, 2020): 96–99. http://dx.doi.org/10.3126/jnspoi.v4i2.34315.

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Gingival enlargement is an increase in the size of gingiva. It is one of the side effects of systemic administration of antihypertensives, anticonvulsants, and immunosuppressants. Amlodipine, a new third-generation dihydropyridine, very useful in middle-aged to older aged patients for various cardiovascular conditions can cause gingival enlargement. Treatment modalities for drug induced gingival enlargement include removal of local irritating factors, meticulous plaque removal and drug substitution after consultation with a physician. This article reports an amlodipine induced gingival enlargement and its treatment in a 40 years old hypertensive male patient.

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35

Manjunatha, Vinayaka Ambujakshi, Gayathri Gunjiganur Vemanaradhya, and Triveni Mavinakote Gowda. "A clinico-histopathological report on low dose of amlodipine: A third-generation calcium channel blocker-induced gingival overgrowth." Journal of Oral Medicine, Oral Surgery, Oral Pathology and Oral Radiology 7, no. 3 (October 15, 2021): 182–85. http://dx.doi.org/10.18231/j.jooo.2021.054.

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This clinical & histopathological report describes the clinical features, mechanism of action on drugs causing drug-induced gingival overgrowth (DIGO), diagnosis and management of patients with arterial hypertension with the regular usage of amlodipine drug. The report also highlights the importance of an involvement of cardiologist and his/her vital role in the management of amlodipine-induced gingival overgrowth.

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36

Guelmann, Marcio, Leandro Britto, and Joseph Katz. "Cyclosporin-induced gingival overgrowth in a child treated with CO2 laser surgery: a case report." Journal of Clinical Pediatric Dentistry 27, no. 2 (January 1, 2004): 123–26. http://dx.doi.org/10.17796/jcpd.27.2.v70187716x08286q.

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A case of a 10 year-old boy with gingival overgrowth due to cyclosporin therapy after heart transplantation is described. Different treatment approaches are discussed and the surgical effect of CO2 laser is illustrated. The critical role of routine professional cleaning and good oral health maintenance for the healthy status of the gingival tissue is also emphasized in this paper. Replacement of cyclosporin by tacrolimus, another immunosuppressive agent associated with minimal to none gingival overgrowth, might be considered in cases with reported recurrences.

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37

Uzel, M. Ilhan, Alpdogan Kantarci, Hsiang-Hsi Hong, Cem Uygur, Michael C. Sheff, Erhan Firatli, and Philip C. Trackman. "Connective Tissue Growth Factor in Drug-Induced Gingival Overgrowth." Journal of Periodontology 72, no. 7 (July 2001): 921–31. http://dx.doi.org/10.1902/jop.2001.72.7.921.

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38

Bharti, Vipin, and Chhaya Bansal. "Drug-induced gingival overgrowth: The nemesis of gingiva unravelled." Journal of Indian Society of Periodontology 17, no. 2 (2013): 182. http://dx.doi.org/10.4103/0972-124x.113066.

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Ruhl, S., S. Hamberger, R. Betz, T. Sukkar, G. Schmalz, R. A. Seymour, K. A. Hiller, and J. M. Thomason. "Salivary Proteins and Cytokines in Drug-induced Gingival Overgrowth." Journal of Dental Research 83, no. 4 (April 2004): 322–26. http://dx.doi.org/10.1177/154405910408300410.

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Little is known about the involvement of saliva in gingival overgrowth (GO). It was hypothesized that, in this situation, the composition of saliva is altered. Thus, proteins, albumin, cytokines, and growth factors in whole and glandular saliva were investigated. Differences between glandular and gingival contributions to the composition of saliva were explored in patients medicated with cyclosporin who exhibited GO (responders), those without GO (non-responders), and non-medicated subjects (controls). In whole saliva, interleukin-1α (IL-1α), IL-6, IL-8, epidermal growth factor (EGF), nerve growth factor (NGF), and albumin were detected, but in glandular saliva only EGF and NGF were identified. Albumin and IL-6 differed significantly between responders and controls, although the overall profile of salivary proteins remained unchanged. Thus, inflammatory cytokines and albumin are confined to whole saliva and are associated with GO, whereas its content of EGF and NGF appears unaffected by cyclosporin.

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Trackman, P. C., and A. Kantarci. "Molecular and Clinical Aspects of Drug-induced Gingival Overgrowth." Journal of Dental Research 94, no. 4 (February 13, 2015): 540–46. http://dx.doi.org/10.1177/0022034515571265.

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Park, Youn-Jung, Joo-Hee Lee, Young-Gun Kim, Jeong-Seung Kwon, Hyung-Joon Ahn, and Jong-Hoon Choi. "Drug-induced Gingival Overgrowth Related to Sirolimus and Felodipine." Journal of Oral Medicine and Pain 42, no. 1 (March 30, 2017): 20–24. http://dx.doi.org/10.14476/jomp.2017.42.1.20.

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Sharma, Arun, Rinku Joshi, Sweta Rajya Laxmi Rana, Dhan Bahadur Shrestha, Pramod Raj Joshi, and Sitarama Khadka. "Amlodipine induced Gingival Overgrowth in Patients at a Tertiary Level Hospital of Nepal." Journal of Nepalese Society of Periodontology and Oral Implantology 2, no. 1 (June 4, 2018): 2–5. http://dx.doi.org/10.3126/jnspoi.v2i1.23571.

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Background: Amlodipine is a commonly prescribed anti-hypertensive in clinical practice. Gingival overgrowth is a rare side effect of this drug; with a reported prevalence of 1.7-3.3% in literature. Gingival overgrowth can cause aesthetic and functional problems as well as cause hindrance to maintain proper oral hygiene, thereby deteriorating the periodontal condition of the patient. The prevalence of Amlodipine induced gingival overgrowth is poorly defined in our country. Aim: This study aims to assess Amlodipine induced gingival overgrowth in a tertiary level referral hospital of Nepal Army. Materials and Methods: This study was conducted on hypertensive patients with amlodipine therapy under regular follow up in the Department of Internal Medicine of Shree Birendra Hospital from September to December 2017. The data from record keeping was used for the study. Ethical clearance from Institutional Review committee of Nepal Army Institute of Health Sciences was obtained before conducting the study. Results: Out of 507 patients taking amlodipine, 240 were eligible for study and six (2.5%) were found to have amlodipine induced gingival overgrowth. These patients were on a dose of 5-10 mg over six months to 25 years. The gingival overgrowth was correlated with dose and duration which was statistically significant (p<0.05). Conclusion: Low prevalence of amlodipine induced gingival overgrowth and correlation with dose and duration was seen in this short-term study. However further large-scale follow-up studies may be required to assess the severity of the problem.

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Mehta , Dr Vivek. "Dental management of a child patient with phenytoin-induced gingival overgrowth: report of a case with a brief review of literature." Journal of Dental Health, Oral Disorders & Therapy 14, no. 1 (2023): 1–2. http://dx.doi.org/10.15406/jdhodt.2023.14.00585.

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Drug-induced gingival overgrowth is medication-related gingival overgrowth commonly associated with certain systemic medications. Gingival overgrowth is a common adverse effect of phenytoin therapy. The condition is more frequently seen in children as compared to adults, affects both genders equally, and may vary from mild to severe. It may be associated with difficulty in mastication, delayed eruption of teeth, tissue trauma, and secondary inflammation. It can be managed by both surgical and nonsurgical therapies. A case of dental management of phenytoin-induced gingival enlargement in a 7-year-old girl is presented with a brief literature review.

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Lauritano, Dorina, Marcella Martinelli, Alessandro Baj, Giada Beltramini, Valentina Candotto, Francesco Ruggiero, and Annalisa Palmieri. "Drug-induced gingival hyperplasia: An in vitro study using amlodipine and human gingival fibroblasts." International Journal of Immunopathology and Pharmacology 33 (January 2019): 205873841982774. http://dx.doi.org/10.1177/2058738419827746.

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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.

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Corrêa, Jôice Dias, Celso Martins Queiroz-Junior, José Eustáquio Costa, Antônio Lúcio Teixeira, and Tarcilia Aparecida Silva. "Phenytoin-Induced Gingival Overgrowth: A Review of the Molecular, Immune, and Inflammatory Features." ISRN Dentistry 2011 (July 25, 2011): 1–8. http://dx.doi.org/10.5402/2011/497850.

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Gingival overgrowth (GO) is a side effect associated with some distinct classes of drugs, such as anticonvulsants, immunosuppressant, and calcium channel blockers. GO is characterized by the accumulation of extracellular matrix in gingival connective tissues, particularly collagenous components, with varying degrees of inflammation. One of the main drugs associated with GO is the antiepileptic phenytoin, which affects gingival tissues by altering extracellular matrix metabolism. Nevertheless, the pathogenesis of such drug-induced GO remains fulfilled by some contradictory findings. This paper aims to present the most relevant studies regarding the molecular, immune, and inflammatory aspects of phenytoin-induced gingival overgrowth.

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Mahajan, Anushi, and Ritesh Sood. "Oral Contraceptives Induced Gingival Overgrowth – A Clinical Case Report." POJ Dental and Oral Care 1, no. 1 (July 13, 2017): 1–5. http://dx.doi.org/10.32648/2578-8817/1/1/001.

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Aim: The purpose of this article is to report a case of drug induced gingival enlargement due to oral contraceptives, managed by nonsurgical periodontal therapy. Background: Drug-induced gingival overgrowth remains the most widespread unwanted effect of systemic medication on the periodontal tissues. Hormones are specific regulatory molecules that modulate a host of body functions. Oral contraceptives that contain estrogen and/or progesterone are associated with gingival enlargement. Report: A 32-year-old female presented with a complaint of swelling of the gingiva with spontaneous bleeding in the mandibular anterior region for a period of two years. The health history documented the use of contraceptives for two years, and a clinical examination revealed the existence of poor oral hygiene and enlarged painful gingival tissues that bled when touched. Summary: Females on oral contraceptives can be considered as a “risk group” for periodontal diseases. Not all females on oral contraceptives respond in similar way. Plaque control is the most important procedure in periodontal therapy. Although the initial picture presented the possibility of surgical intervention, the clinical problems were resolved with non-surgical treatment. Another factor contributing to response to therapy is patient compliance. The patient followed home care instructions well and was effective in personal oral hygiene measures. Keywords: Gingival enlargement, Sex hormones, Oral contraceptives.

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Suzuki, A. M. M., A. Yoshimura, Y. Ozaki, T. Kaneko, and Y. Hara. "Cyclosporin A and Phenytoin Modulate Inflammatory Responses." Journal of Dental Research 88, no. 12 (November 6, 2009): 1131–36. http://dx.doi.org/10.1177/0022034509350566.

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Gingival overgrowth is a common side-effect of administration of the immunosuppressant cyclosporin A and the anti-epileptic drug phenytoin. While cyclosporin-induced gingival overgrowth is often accompanied by gingival inflammation, phenytoin-induced gingival overgrowth usually forms fibrotic lesions. To determine whether these drugs alter the inflammatory responses of gingival fibroblasts, we investigated the effects of cyclosporin and phenytoin on Toll-like receptor (TLR)-mediated responses to microbial components. In Chinese hamster ovary reporter cell lines, cyclosporin alone triggered signaling, whereas phenytoin down-regulated signaling induced by the TLR2 or TLR4 ligand. In human gingival fibroblasts, cyclosporin alone did not induce evident inflammatory responses, but augmented the expression of CD54 and the production of interleukin (IL)-6 and IL-8 induced by TLR ligands, whereas phenytoin attenuated those responses. Cyclosporin also augmented CD54 expression in gingiva of mice injected with lipopolysaccharide. These results indicated that cyclosporin positively and phenytoin negatively modulated inflammatory responses of human gingival fibroblasts.

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Naruishi, Koji. "Gingival Fibroblasts-mediated Pathophysiology of Periodontal Diseases, Periodontitis and Drug-induced Gingival Overgrowth." Nihon Shishubyo Gakkai Kaishi (Journal of the Japanese Society of Periodontology) 51, no. 1 (2009): 7–18. http://dx.doi.org/10.2329/perio.51.007.

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Walsh, P., L. Häkkinen, H. Pernu, M. Knuuttila, and H. Larjava. "Expression of fibronectin-binding integrins in gingival epithelium in drug-induced gingival overgrowth." Journal of Periodontal Research 42, no. 2 (April 2007): 144–51. http://dx.doi.org/10.1111/j.1600-0765.2006.00927.x.

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Butt, Amara, Kanwal Sohail, and Amber Kiyani. "Amlodipine-Associated Gingival Hyperplasia: A Case Report and Review of Literature." Journal of the Pakistan Dental Association 31, no. 01 (April 10, 2022): 55–58. http://dx.doi.org/10.25301/jpda.311.55.

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Gingival overgrowth can be adverse reaction of calcium channel blockers. Although nifedipine is commonly associated with this process, some case reports have also implicated amlodipine as a possible etiology. Here we present a case of a 59-yearold Pakistani female who developed gingival hyperplasia secondary to amlodipine use. We believe that the knowledge about amlodipine-associated gingival hyperplasia is necessary for dentists, so they can accurately diagnose this condition and provide appropriate management. KEYWORDS: Drug-induced gingival overgrowth (DIGO), gingival hyperplasia, amlodipine

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