Gingival hyperplasia
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Gingival hyperplasia or Gingival enlargement, the currently accepted terminology for an increase in the size of the gingiva, is a common feature of gingival disease.[1] This is strictly a clinical description of the condition and avoids the erroneous pathologic connotations of terms used in the past such as hypertrophic gingivitis or gingival hyperplasia. Gingival enlargement can be caused by a number of various stimuli, and "treatment is based on an understanding of the cause and underlying pathologic changes."[2]
Imprecise use of terminology
The terms hyperplasia and hypertropy 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,[3] and hypertrophy refers to an increase in the size of individual cells.[4] Because these identifications obviously cannot be performed with a clinical examination and evaluation of the tissue,[5] the term gingival enlargement is more properly applied.
Etiology
Inflammatory enlargement
As previously mentioned, gingival enlargement may be caused by a multitude of causes. The most common is chronic inflammatory gingival enlargement, when the gingiva presents clinically as soft and discolored. This is caused by tissue edema and infective cellular infiltration caused by prolonged exposure tobacterial plaque, and is treated with conventional periodontal treatment, such as scaling and root planing.[6] 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.[7]
Gingivitis and gingival enlargement are often seen in mouth breathers,[8] as a result of irritation brought on by surface dehydration, but the manner in which it is caused has not been demonstrated.[9]
Drug-induced enlargement
Gingival enlargement may also be associated with the administration of three different classes of drugs, all producing a similar response:.[10]
- anticonvulsants, such as phenytoin, succinimides and valproic acid
- calcium channel blockers, such as nifedipine and verapamil.the dihydropyridine derivative isradipidine can replace nifedipine and does not induce gingival overgrowth.
- cyclosporin, an imunosuppresant.
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:[11]
- Conditioned enlargement
- pregnancy
- puberty
- vitamin C deficiency
- nonspecific, such as a pyogenic granuloma
- Systemic disease causing enlargement
- leukemia
- granulolomatous diseases, such as Wegener's granulomatosis and sarcoidosis
- neoplasm
- benign neoplasms, such as fibromas, papillomas and giant cell granulomas
- malignant neoplasms, such as a carcinoma or malignant melanoma
- false gingival enlargements, such as when there is an underlying bony or dental tissue lesion
Risk factors and prevention
Inflammatory enlargement
The accumulation and retention of plaque is the chief cause of inflammatory gingival enlargement. Risk factors include poor oral hygiene,[12] as well as physical irritation of the gingiva by improper restorative and orthodontic appliances.[13]
Drug-induced enlargement
Drug-induced enlargement has been associated with a patient's genetic predisposition,[14] and its association with inflammation is debated. Some investigators assert that underlying inflammation is necessary for the development of drug-induced enlargement,[15] while others purport that the existing enlargement induced by the drug effect compounds plaque retention, thus furthering the tissue response.[16]
In drug-induced disease, reversing and preventing gingival enlargement is as easy as ceasing drug therapy. 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 immunosupression, tacrolimus is an available alternative which results in much less severe gingival overgrowth than cyclosporin, but is similarly as nephrotoxic.[17] The dihydropyridine derivative isradipidine can replace nifedipine for some uses of calcium channel blocking and does not induce gingival overgrowth.[18]
In non-humans
It is commonly seen in Boxer dogs and other brachycephalic breeds,[19] and in the Springer Spaniel.[20] 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, but it usually recurs. Gingival enlargement is also a potential sequela of gingivitis. As in humans, it may be seen as a side effect to the use of cyclosporin.[21]
References
- ↑ Carranza'a Clinical Periodontology, 9th Ed. W.B. Saunders 1996 ISBN 0-7216-8331-2, page 279.
- ↑ Carranza'a Clinical Periodontology, 9th Ed. W.B. Saunders 1996 ISBN 0-7216-8331-2, page 754.
- ↑ Merriam-Webster's Medical Desk Dictionary, 2002, ISBN 1-40181-188-4, page 367.
- ↑ Merriam-Webster's Medical Desk Dictionary, 2002, ISBN 1-40181-188-4, page 368.
- ↑ Oral Pathology Lecture Series Notes, New Jersey Dental School, 2004-2005, page 24.
- ↑ Carranza'a Clinical Periodontology, 9th Ed. W.B. Saunders 1996 ISBN 0-7216-8331-2, page 754.
- ↑ Carranza'a Clinical Periodontology, 9th Ed. W.B. Saunders 1996 ISBN 0-7216-8331-2, page 754.
- ↑ Lite, T, Dimaio, DJ (1955). "Gingival patterns in mouth breathers: a clinical and histopathologic study and a method of treatment". Oral Surg (8): 382.
- ↑ Carranza'a Clinical Periodontology, 9th Ed. W.B. Saunders 1996 ISBN 0-7216-8331-2, page 280.
- ↑ Butler, RT, Kalkwarf KL (1987). "Drug-induced gingival hyperplasia: phenytoin, cyclosporin and nifedipine". JADA (114): 56.
- ↑ Carranza'a Clinical Periodontology, 9th Ed. W.B. Saunders 1996 ISBN 0-7216-8331-2, page 285.
- ↑ Hirschfield, I (1932). "Hypertrophic gingivitis; its clinical aspect". JADA (19): 799.
- ↑ Carranza'a Clinical Periodontology, 9th Ed. W.B. Saunders 1996 ISBN 0-7216-8331-2, page 280.
- ↑ Hassell, TM (1994). "Hypertrophic Oral problems and genetic aspects of individuals with epilepsy". Periodontology 2000 (6): 68.
- ↑ Ciancio, SG (1972). "Gingival hyperplasia and diphenylhydantoin". J Perio (43): 411.
- ↑ Carranza'a Clinical Periodontology, 9th Ed. W.B. Saunders 1996 ISBN 0-7216-8331-2, page 282.
- ↑ Spencer, CM (1997). "Tacrolimus: an update of its pharmacology and drug efficacy in the management of organ transplantation". Drugs (54): 925.
- ↑ Westbrook, P (1997). "Regression of nifedipine-induced gingival hyperplasia following switch to a same class calcium channel blocker, isradipine". J Perio (68): 645.
- ↑ "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.
- ↑ Guaguère E, Steffan J, Olivry T (2004). "Cyclosporin A: a new drug in the field of canine dermatology". Vet Dermatol. 15 (2): 61–74. PMID 15030555.