Gingival enlargement
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 |
Gingival enlargement is an increase in the size of the
Classification
The terms gingival hyperplasia and gingival hypertrophy have been used to describe this topic in the past.[1] These are not precise descriptions of gingival enlargement because these terms are strictly histologic diagnoses, and such diagnoses require microscopic analysis of a tissue sample. Hyperplasia refers to an increased number of cells, 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 term gingival enlargement is 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
Inflammatory enlargement
Gingival enlargement has a multitude of causes. The most common is
Gingivitis and gingival enlargement are often seen in mouth 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 of
Drug-induced enlargement
This 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 as phenytoin, phenobarbital, lamotrigine, vigabatrin, ethosuximide, topiramate and primidone NOT common for valproate)[10]
- calcium channel blockers (antihypertensives such as nifedipine, amlodipine, and verapamil). The dihydropyridine derivative isradipidine can replace nifedipine and does not induce gingival overgrowth.[10]
- cyclosporine, an immunosuppressant.[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's genetic 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
Many 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 C deficiency
- nonspecific, such as a pyogenic granuloma
- Systemic disease causing enlargement
- leukemia
- granulolomatous diseases, such as granulomatosis with polyangiitis, sarcoidosis, or orofacial granulomatosis.[16]
- neoplasm
- malignant melanoma
- false gingival enlargements, such as when there is an underlying bony or dental tissue lesion
Mechanism
Drug Induced gingival overgrowth:
- Fibrotic type:
- Elevated CTGF (a.k.a. CCN2) which is a matricellular protein known to be reliable for fibrosis.[17]
- TGF-β increases drives CTGF/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 as PGE2), unlike other tissues' fibroblasts (such as kidney) which have their CTGF levels down regulated by the same PGE2.
- Elevated CTGF (a.k.a. CCN2) which is a matricellular protein known to be reliable for fibrosis.[17]
- Inflammatory Type
Management
The first line management of gingival overgrowth is improved oral 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 significant fibrotic components 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 as gingivectomy.[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 deleterious side effect. In the case of immunosuppression, tacrolimus is an available alternative which results in much less severe gingival overgrowth than cyclosporin, but is similarly as nephrotoxic.[19] The dihydropyridine derivative isradipidine can replace nifedipine for some uses of calcium channel blocking and does not induce gingival overgrowth.[20]
Epidemiology
This section needs expansion. You can help by adding to it. (January 2019) |
Gingival enlargement is common.[21]
Other animals
It is commonly seen in
Gingival enlargement is an autosomal recessive disease with predominance in males, and is correlated with selection for superior fur quality in European farmed foxes[26]
References
- ^ ISBN 978-1-4377-0416-7.
- ISBN 1-4018-1188-4, page 367-368.
- ^ Oral Pathology Lecture Series Notes, New Jersey Dental School, 2004-2005, page 24.
- PMID 14370764.
- ^ Hirschfield, I (1932). "Hypertrophic gingivitis; its clinical aspect". Journal of the American Dental Association (19): 799.
- ISBN 9781405160995.
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- ^ ISBN 978-1-4160-2999-1.
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- ISBN 0-7216-8331-2, page 282.
- ^ ISBN 978-1609137137.
- ISBN 0-7216-8331-2, page 285.
- PMID 15569103.
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- ^ "Gingival Fibroma and Epulides". The Merck Veterinary Manual. 2006. Retrieved 2007-03-08.
- ^ Gorrel, Cecilia (2003). "Periodontal Disease". Proceedings of the 28th World Congress of the World Small Animal Veterinary Association. Retrieved 2007-03-25.
- ^ Bellows, Jan; McMorran, Elizabeth (2017-02-01). "Use CO2 laser on gingival enlargement". Retrieved 2017-02-02.
- PMID 15030555.
- PMID 25829563.