Gingival enlargementis an increase in the size of thegingiva(gums). It is a common feature of gingivaldisease.[1]Gingival enlargement can be caused by a number of factors, including inflammatory conditions and the side effects of certain medications. The treatment is based on the cause.[1]A closely related term isepulis,denoting a localizedtumor(i.e. lump) on the gingiva.
| Gingival enlargement | |
|---|---|
| Other names | Gingival overgrowth (GO), hypertrophic gingivitis, gingival hyperplasia, gingival hypertrophy |
 | |
| Gingivitis,a common cause of inflammatory gingival enlargement. | |
| Specialty | Periodontology |
| Symptoms | increase in gum size |
| Causes | inflammatory conditions, Drug-induced, genetic |
Classification
editThe terms gingivalhyperplasiaand gingivalhypertrophyhave been used to describe this topic in the past.[1]These are not precise descriptions of gingival enlargement because these terms are strictlyhistologicdiagnoses,and such diagnoses requiremicroscopicanalysis of a tissue sample. Hyperplasia refers to an increased number ofcells,and hypertrophy refers to an increase in the size of individual cells.[2]As these identifications cannot be performed with a clinical examination and evaluation of the tissue,[3]the termgingival enlargementis more properly applied. Gingival enlargement has been classified according to cause into 5 general groups:[1]
- Inflammatory enlargement
- Drug induced enlargement
- Enlargement associated with systemic diseases or conditions
- Neoplastic enlargement
- False enlargement.
Causes
editInflammatory enlargement
editGingival enlargement has a multitude of causes. The most common ischronicinflammatorygingival enlargement, when thegingivaeare soft and discolored. This is caused by tissueedemaandinfectivecellular infiltrationcaused by prolonged exposure tobacterialplaque, and is treated with conventionalperiodontaltreatment, such asscaling and root planing.[1]
Gingivitisand gingival enlargement are often seen inmouth breathers,[4]as a result of irritation brought on by surface dehydration, but the manner in which it is caused has not been demonstrated.[1]
The accumulation and retention ofplaqueis the chief cause of inflammatory gingival enlargement. Risk factors include poororal hygiene,[5]as well as physical irritation of the gingiva by improperrestorativeandorthodontic appliances.[1]
Drug-induced enlargement
editThis type of gingival enlargement is sometimes termed "drug induced gingival enlargement" or "drug influenced gingival overgrowth",[6]abbreviated to "DIGO".[7]Gingival enlargement may also be associated with the administration of three different classes of drugs, all producing a similar response:[8]Gingival overgrowth is a common side effect of phenytoin, termed "Phenytoin-induced gingival overgrowth" (PIGO).[9]
- anticonvulsants(such asphenytoin,phenobarbital,lamotrigine,vigabatrin,ethosuximide,topiramateandprimidoneNOT common for valproate)[10]
- calcium channel blockers(antihypertensives such asnifedipine,amlodipine,andverapamil). The dihydropyridine derivative isradipidine can replace nifedipine and does not induce gingival overgrowth.[10]
- cyclosporine,animmunosuppressant.[10]
Of all cases of DIGO, about 50% are attributed to phenytoin, 30% to cyclosporins and the remaining 10-20% to calcium channel blockers.
Drug-induced enlargement has been associated with a patient'sgenetic predisposition,[11]and its association with inflammation is debated. Some investigators assert that underlying inflammation is necessary for the development of drug-induced enlargement,[12]while others purport that the existing enlargement induced by the drug effect compounds plaque retention, thus furthering the tissue response.[13]Careful attention to oral hygiene may reduce the severity of gingival hyperplasia.[14]In most cases, discontinuing the culprit drug resolves the hyperplasia.[14]
Enlargement associated with systemic factors
editMany systemic diseases can develop oral manifestations that may include gingival enlargement, some that are related to conditions and others that are related to disease:[15]
- Conditioned enlargement
- pregnancy
- puberty
- vitamin Cdeficiency
- nonspecific, such as apyogenic granuloma
- Systemic disease causing enlargement
- leukemia
- granulolomatous diseases, such asgranulomatosis with polyangiitis,sarcoidosis,ororofacial granulomatosis.[16]
- neoplasm
- benignneoplasms, such asfibromas,papillomasandgiant cell granulomas
- malignantneoplasms, such as acarcinomaormalignant melanoma
- false gingival enlargements, such as when there is an underlyingbonyor dental tissuelesion
Mechanism
editDrug Induced gingival overgrowth:
- Fibrotic type:
- ElevatedCTGF (a.k.a. CCN2)which is a matricellular protein known to be reliable forfibrosis.[17]
- TGF-βincreases drivesCTGF/CCN2(current molecular mechanisms unknown), but supports TGF-β as a therapeutic target.[18]
- CTGF is not down regulated in presence of inflammatory mediators (such asPGE2), unlike other tissues' fibroblasts (such as kidney) which have their CTGF levels down regulated by the samePGE2.
- ElevatedCTGF (a.k.a. CCN2)which is a matricellular protein known to be reliable forfibrosis.[17]
- Inflammatory Type
Management
editThe first line management of gingival overgrowth is improvedoral hygiene,ensuring that the irritative plaque is removed from around the necks of the teeth and gums. Situations in which the chronic inflammatory gingival enlargement include significantfibroticcomponents that do not respond to and undergo shrinkage when exposed to scaling and root planing are treated with surgical removal of the excess tissue, most often with a procedure known asgingivectomy.[1]
In DIGO, improved oral hygiene and plaque control is still important to help reduce any inflammatory component that may be contributing to the overgrowth. Reversing and preventing gingival enlargement caused by drugs is as easy as ceasing drug therapy or substituting to another drug. However, this is not always an option; in such a situation, alternative drug therapy may be employed, if possible, to avoid this deleteriousside effect.In the case of immunosuppression,tacrolimusis an available alternative which results in much less severe gingival overgrowth than cyclosporin, but is similarly asnephrotoxic.[19]The dihydropyridine derivative isradipidine can replace nifedipine for some uses of calcium channel blocking and does not induce gingival overgrowth.[20]
Epidemiology
editThis sectionneeds expansion.You can help byadding to it.(January 2019) |
Gingival enlargement is common.[21]
Other animals
edit
It is commonly seen inBoxer dogsand otherbrachycephalicbreeds,[22]and in theEnglish Springer Spaniel.[23]It usually starts around middle age and progresses. Some areas of the gingiva can become quite large but have only a small attachment to the rest of the gingiva, and it may completely cover the teeth. Infection and inflammation of the gingiva is common with this condition. Under anesthesia, the enlarged areas of gingiva can be cut back with a scalpel blade orCO2laser,but it often recurs.[24]Gingival enlargement is also a potential sequela ofgingivitis.As in humans, it may be seen as a side effect to the use ofciclosporin.[25]
References
edit- ^abcdefghNewman MG, Takei HH, Klokkevold PR, Carranza FA, eds. (2012).Carranza's clinical periodontology(11th ed.). St. Louis, Mo.: Elsevier/Saunders. pp.84–96.ISBN978-1-4377-0416-7.
- ^Merriam-Webster's Medical Desk Dictionary, 2002,ISBN1-4018-1188-4,page 367-368.
- ^Oral Pathology Lecture Series Notes, New Jersey Dental School, 2004–2005, page 24.
- ^Lite, Theodore; Dominic J. DiMaio; Louis R. Burman (1955). "Gingival pathosis in mouth breathers: A clinical and histopathologic study and a method of treatment".Oral Surgery, Oral Medicine, Oral Pathology.8(4): 382–391.doi:10.1016/0030-4220(55)90106-7.ISSN0030-4220.PMID14370764.
- ^Hirschfield, I (1932). "Hypertrophic gingivitis; its clinical aspect".Journal of the American Dental Association(19): 799.
- ^Lindhe J, Lang NP, Karring T, eds. (2008).Clinical periodontology and implant dentistry(5th ed.). Oxford: Blackwell Munksgaard. pp.641.ISBN9781405160995.
- ^Subramani, T; Rathnavelu, V; Yeap, SK; Alitheen, NB (Feb 2013)."Influence of mast cells in drug-induced gingival overgrowth".Mediators of Inflammation.2013:275172.doi:10.1155/2013/275172.PMC3569901.PMID23431239.
- ^Butler RT, Kalkwarf KL (1987). "Drug-induced gingival hyperplasia: phenytoin, cyclosporine, and nifedipine".Journal of the American Dental Association.114(1): 56–60.doi:10.14219/jada.archive.1987.0050.PMID3468168.
- ^Arya, R; Gulati, S (March 2012)."Phenytoin-induced gingival overgrowth".Acta Neurologica Scandinavica.125(3): 149–55.doi:10.1111/j.1600-0404.2011.01535.x.PMID21651505.S2CID6274158.
- ^abcBolognia, Jean L. (2007).Dermatology.St. Louis: Mosby.ISBN978-1-4160-2999-1.
- ^Hassell, T.M.; Burtner, A. Paul; McNeal, Donald; Smith, Robert G. (1994). "Hypertrophic Oral problems and genetic aspects of individuals with epilepsy".Periodontology 2000.6(1): 68–78.doi:10.1111/j.1600-0757.1994.tb00027.x.PMID9673171.
- ^Ciancio, SG (1972). "Gingival hyperplasia and diphenylhydantoin".Journal of Periodontology.43(7): 411–4.doi:10.1902/jop.1972.43.7.411.PMID4504524.
- ^Carranza'a Clinical Periodontology, 9th Ed. W.B. Saunders 1996ISBN0-7216-8331-2,page 282.
- ^abBrian K. Alldredge; et al., eds. (2013).Applied therapeutics: the clinical use of drugs(10th ed.). Baltimore: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 1403.ISBN978-1609137137.
- ^Carranza'a Clinical Periodontology, 9th Ed. W.B. Saunders 1996ISBN0-7216-8331-2,page 285.
- ^Leão, JC; Hodgson, T; Scully, C; Porter, S (Nov 15, 2004)."Review article: orofacial granulomatosis".Alimentary Pharmacology & Therapeutics.20(10): 1019–27.doi:10.1111/j.1365-2036.2004.02205.x.PMID15569103.
- ^Trackman, P.C.; Kantarci, A. (2017-03-22)."Molecular and Clinical Aspects of Drug-induced Gingival Overgrowth".Journal of Dental Research.94(4): 540–546.doi:10.1177/0022034515571265.ISSN0022-0345.PMC4485217.PMID25680368.
- ^Subramani, Tamilselvan; Rathnavelu, Vidhya; Alitheen, Noorjahan Banu (2013)."The Possible Potential Therapeutic Targets For Drug Induced Gingival Overgrowth".Mediators of Inflammation.2013:1–9.doi:10.1155/2013/639468.PMC3652200.PMID23690667.
- ^Spencer, CM; Goa, KL; Gillis, JC (1997). "Tacrolimus: an update of its pharmacology and drug efficacy in the management of organ transplantation".Drugs.54(6): 925–75.doi:10.2165/00003495-199754060-00009.PMID9421697.
- ^Westbrook, P (1997). "Regression of nifedipine-induced gingival hyperplasia following switch to a same class calcium channel blocker, isradipine".Journal of Periodontology.68(7): 645–50.doi:10.1902/jop.1997.68.7.645.PMID9249636.
- ^Livada, R; Shiloah, J (December 2012). "Gummy smile: could it be genetic? Hereditary gingival fibromatosis".The Journal of the Michigan Dental Association.94(12): 40–3.PMID23346694.
- ^"Gingival Fibroma and Epulides".The Merck Veterinary Manual.2006.Retrieved2007-03-08.
- ^Gorrel, Cecilia (2003)."Periodontal Disease".Proceedings of the 28th World Congress of the World Small Animal Veterinary Association.Retrieved2007-03-25.
- ^Bellows, Jan; McMorran, Elizabeth (2017-02-01)."Use CO2 laser on gingival enlargement".Retrieved2017-02-02.
- ^Guaguère E, Steffan J, Olivry T (2004). "Cyclosporin A: a new drug in the field of canine dermatology".Veterinary Dermatology.15(2): 61–74.doi:10.1111/j.1365-3164.2004.00376.x.PMID15030555.