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Gingival Hyperplasia

Gingival Hyperplasias

Gingival hyperplasia is a disease in which the gum tissues overgrow abnormally. Gingival enlargement or hypertrophy are the two other terms used to describe the condition.


The initial stages of gingival enlargement are often asymptomatic. Symptoms are more pronounced in patients with dental plaques and poor dental hygiene. The major symptoms include bleeding of gums which are tender and swollen. The risk for developing the condition is higher among patients with misplaced teeth and other gum diseases. The severity of disease is directly proportional to the general oral health of the patient.

Phenytoin-induced gingival overgrowth
Individuals with inflamed gums and plaques are predisposed to gingival overgrowth when phenytoin is used. Localized inflammation of gums induced by dental plaques act as a receptacle for phenytoin.

Cyclosporine-induced gingival overgrowth
Patients suffering from gingivitis and dental plaques are more prone to the development of cyclsporine-induced gingival hyperplasia. Treatment regimen comprising of high dose of drug lead to the development of the hyperplasia by the end of first trimester of treatment. However, it should be noted that the condition is temporary and the gums resume to normal state once the treatment is over [14] [15].

The healthy state of gums can be maintained by proactive oral care and plaque control, however this may not help in preventing development of gingival hyperplasia in predisposed patients.

Nifedipine-induced gingival overgrowth

Administration of nifedipine may lead to the aggravation of cyclosporine induced gingival overgrowth.

Calcium antagonist–induced gingival overgrowth
Lack of proper dental care is a predisposing factor for the development of Calcium antagonist - induced gingival overgrowth. The condition can be managed well with rigorous oral hygiene practices.

  • OBJECTIVE: To investigate the occurrence of MDR1 C3435T gene polymorphisms in the Turkish renal transplant patients treated with cyclosporine (CsA), and correlate these findings with prevalence and degree of gingival hyperplasia (GH).[ncbi.nlm.nih.gov]
Dysmorphic Face
  • Congenital generalized hypertrichosis terminalis has been described in association with other features as gingival hyperplasia, osteochondrodysplasia, and a dysmorphic face.[ncbi.nlm.nih.gov]
Renal Artery Stenosis
  • Mourad G, Ribstein J, Argiles A, Mimran A, Mion C (1989) Contrasting effects of acute angiotensin converting enzyme inhibitors and calcium antagonists in transplant renal artery stenosis. Nephrol Dial Transplant 4:66–70 Google Scholar 25.[link.springer.com]
  • The results of blood tests and bone marrow aspiration were compatible with ALL-L3. Remission-induction treatment with BFM-90 ALL chemotherapy protocol was started; however, the patient died 4 weeks after the diagnosis due to neutropenic sepsis.[ncbi.nlm.nih.gov]
Poor Oral Hygiene
  • Delay in the widespread acquisition of skills, epilepsy and poor oral hygiene with gingival enlargement was the main concern to seek medical aid.[ncbi.nlm.nih.gov]
  • The inflammation can be induced by poor oral hygiene or from a dental appliance like orthodontic braces.[colgate.com]
  • 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.[journals.lww.com]
  • oral hygiene Daily oral rinses with Chlorhexidine are recommended to prevent recurrences in patients who have undergone surgery for gingival enlargement.[mddk.com]
  • One can also get inflammatory gingival hyperplasia through poor oral hygiene (gingivitis, excessive plaque build-up, etc.). Other medical conditions Gingival hyperplasia is also linked to a variety of other medical conditions.[guyhisrichdds.com]
Gingival Hypertrophy
  • } {gingival hypertrophy} 0.000023 0.04 183.73 [12] { {gingival hypertrophy} 0.000021 0.03 172.14 [13] {clobazam, phenytoin} {gingival hypertrophy} 0.000016 0.03 153.34 [14] {valproic acid, intellectual disability} {gingival hypertrophy} 0.000023 0.03[jphcs.biomedcentral.com]
  • This medical condition has a few other names associated with it– gingival hypertrophy, gingival overgrowth, and hypertrophic gingivitis. It has shown to be most prevalent in children with epilepsy.[guyhisrichdds.com]
  • From Wikidata Jump to navigation Jump to search Human disease Gingival enlargement (disorder) Gingival enlargement NOS Gingival enlargement NOS (disorder) Gingival enlargement gingival hyperplasia gingival hypertrophy hypertrophic gingivitis edit English[wikidata.org]
  • Gingival overgrowth also called as gingival hyperplasia or gingival hypertrophy or hypertrophic gingivitis. Gingival overgrowth is the enlargement of attached gingiva due to increased number of cells.[dentaltipsforall.com]
  • This condition is also known as gingival overgrowth, hypertrophic gingivitis or gingival hypertrophy.[mddk.com]
Bleeding Gums
  • Gingivitis Associations : Bleeding gums especially with eating, flossing or brushing teeth Pathophysiology : Inflammation involving the mucosal epithelial tissue around the cervical portion of the teeth and alveolar process.[ebmconsult.com]
  • NIH: National Institute of Dental and Craniofacial Research Bleeding gums (Medical Encyclopedia) Gingivitis (Medical Encyclopedia) Gums - swollen (Medical Encyclopedia) Periodontitis (Medical Encyclopedia) Trench mouth (Medical Encyclopedia) [ Read More[icdlist.com]
  • The commonest sign of either gingivitis or periodontitis is bleeding gums, which can be provoked by tooth brushing, flossing, and eating hard foods, but can also be spontaneous. Inflammatory gingival enlargement can be acute or chronic.[periobasics.com]
Muscle Swelling
  • A patient with acute myeloid leukemia (AML M3) developed gingival hyperplasia and muscle swelling and tenderness after starting treatment with all- trans retinoic acid. Microscopic examination showed neutrophilic infiltrate.[ncbi.nlm.nih.gov]
Coarse Face
  • We propose that this type of congenital generalized hypertrichosis terminalis, associated with gingival hyperplasia and a coarse face, is a distinctive new entity.[ncbi.nlm.nih.gov]
Numb Chin Syndrome
  • The similarities of these findings with numb chin syndrome (NCS) and Burkitt's lymphoma (BL) are discussed in this report.[ncbi.nlm.nih.gov]
  • Conclusion Gingival hyperplasia may be triggered by a myriad of factors, but one thing’s for sure– proper oral hygiene is not one to be neglected. Always bear in mind that having good dental habits keeps medical conditions like this one at bay.[guyhisrichdds.com]


Clinical diagnosis of drug related hyperplasia is difficult as there is no diagnostic test available to confirm the condition. There are a number of oral diseases where the lesions resemble hyperplasia. The condition can either be localized (confined to a few locations) or be generalized (lesions present in multiple sites). Gum diseases like periodontal abscess, benign tumors, trauma or by hormone induced tissue overgrowth eg., pregnancy can also result in localized lesions. Studying the clinical history and oral health care history of the concerned patient often helps physicians identify gingival overgrowth that is drug induced.

Generalized hyperplasia also lacks proper diagnostic tests. In some patients, gingival enlargement is difficult to diagnose. Bacterial biofilms are the major culprits for development of gingival hyperplasia. The condition can thus be reversed by performing non-surgical periodontal therapy i.e. deep cleansing of bacterial plaques and biofilms. This should then be diligently followed by a strict oral health care routine to avoid reappearance of plaques. In some cases this may not give a positive result and patients may suffer from persistent lesions even a month after the therapy. Under such circumstances, underlying systemic factors are suspected and warrant a thorough check up. Patients with undiagnosed or poorly managed diabetes often suffer from inflammation, enlargement and substantial desiccation of gums. Acute leukemia, Wegener's granulomatosis and scurvy are some of the other diseases that may result in gingival enlargement.

Swift overgrowth of gums along with haemorrhaging is indicative of conditions like acute myeoblastic leukemia, chronic myeloid leukemia, acute lymphocytic leukemia, or chronic lymphocytic leukemia. Approximately 5% of patients suffering from acute myeloblastic leukemia have gingival enlargement as the index symptoms. In suspected cases the periodontist must direct such patients to appropriate a physician or oncologist for early treatment of cancer to effectively managing the condition [13].

Presence of "strawberry gums" characterized by red and inflamed gums with granular texture is indicative of Wegener's granulomatosis. The condition is usually confirmed by conducting biopsy of the affected gums.

Deficiency of Vitamin C which leads to the condition called scurvy is characterized by inflammation and bleeding of gums along with loose teeth. In such conditions, periodontist usually prescribe vitamin C in very high doses to overcome the deficiency. Other non invasive methods are also used to treat this deficiency induced gingival enlargement.

A very rare hereditary disease known as gingival fibromatosis may also cause gingival enlargement. The condition is usually presented in the form of continuous enlargement of the gums. The disease often necessitates invasive procedure to discard the extra gingival growth. Major drawback of this procedure is the chance of recurrence of the lesions. The condition can easily be differentiated from the commonly reported drug induced overgrowth by examining the the nature of the affected gum tissues and clinical history of the patient and his/her family members.


Substituting the offensive drug is the most effective way to manage gingival enlargement. Clinicians usually substitute common gingival enlargement inducing drugs with diuretics, beta blockers or angiotensin converting enzyme inhibitors with no known side effects on gum tissues.

Phenytoin is usually substituted with ethosuximide, sodium valproate or carbamazepine [16], and cyclosporine A with tacrolimus. When the drug in question cannot be changed or replaced, lesions can be managed non surgically. CCB-induced gingival overgrowth can be managed with root planing or scaling and antimicrobial mouth rinses. However in case of phenytoin induced gingival overgrowth, root planing or scaling is not recommended as presence of collagen in high amounts hinders the shrinkage of gum tissues. Removal of excess gum tissues by surgery helps to reinstate the normal structure and function of gum tissues. Dental laser or electrosurgery is used to perform this procedure.

Relapsing is a common occurrence in gingival overgrowth irrespective of how it was managed (invasive or non invasive). The condition is observed to relapse in about 40% of individuals after the first or second trimester of surgical removal of gum tissues [17]. Poor oral health care practice is the most common reason for the relapse.


The prognosis is often poor and chances of relapsing is high in case of surgical and non surgical intervention of drug-induced gingival hyperplasia. The risk is particularly high when the causative drug is still in use or is removed temporarily. The condition may resurface within 3 to 6 months after surgical remediation, and approximately 40% of the patients will experience a recurrence [13]. Individauls who practice poor dental care and oral hygiene are at a higher risk.


The etiological factors responsible for the pathogenesis of gingival enlargement largely remain unclear. Several mechanisms have been put forth but none have gained enough acceptance from the scientific field.

The major mechanisms that are considered responsible for hyperplasia are as listed below.

  • A drop in collagen degradation by the enzyme - collagenase or a hike in production of extracellular ground substance [5] [6].
  • Presence of a subgroup of gingival fibroblasts which are "genetically more liable" to drug induced hyperplasia [7].
  • The concurring effect of pro-inflammatory cytokines (IL-1b and IL-6) in increasing the collagen production by gingival fibroblasts [8].

Gingival enlargement can be classified into four different groups based on the causation of the condition.

  1. Inflammatory
  2. Drug induced
  3. Hereditary
  4. Systemic conditions induced

Inflammatory Gingival Enlargement

Gingival enlargement can be either localized or generalized and as the name implies is due to the inflammation of gums in response to dental plaques. This type is mainly observed in patients who practice poor dental hygiene. Gums involved are usually red in color, tender and bleed easily. The condition can be reversed by implementing proper dental care including regular tooth brushing and flossing.

Drug-Induced Gingival Enlargement

The gum tissues are firm and pale pink in color. Unlike inflammatory gingival enlargement, gums do not bleed easily. The crown of teeth may get fully covered by gum tissues in most severe forms leading to periodontitis, largely owing to the inability to perform proper teeth brushing and displacement of teeth. The condition however gets resolved once the drug responsible for the condition is discontinued. When this option is not viable, surgical interventions are opted to remove the excess gum tissues. This is not a permanent solution as there is a good chance of recurrence of the condition. As presence of plaques aggravates the condition, practicing good oral hygiene may help in reducing the extent of gingival overgrowth.

Hereditary Gingival Fibromatosis
The condition usually becomes evident in childhood years of life, but in some cases remains unnoticed until adulthood. It is presented as protracted, generalized or sometimes localized non-tender, pale pink, firm overgrowth of the gums. Surgical intervention is required to remove the excess growth to avoid dental displacement and injury. The recurrent nature of disease often requires repeated surgical intervention.

Systemic Causes of Gingival Enlargement
Gingival enlargement (localized or generalized) can be a result of physiologic and systemic disorders. Proper management of underlying conditions often helps the gingival overgrowth to regress spontaneously. Effective oral health care is also required to lower the chance of recurrence/development of the condition.


The United States

Gingival hyperplasia is an infrequent form of disease and therefore no population-based or epidemiological studies are conducted in the United States. Most of the data on incidence is obtained from case-series studies. In most of the cases, patients develop the disease as a side effect towards certain medications used to manage other medical conditions.

Approximately 15 - 50% of patients under phenytoin treatment develop gingival overgrowth. The incidence of hyperplasia in transplant recipient patients under cyclosporine medication is about 27%. About 10-20% of patients under calcium antagonists treatment develop gingival hyperplasia.

High level of caution should be exercised while interpreting these data. Clinical practitioners should always consider the type of population represented within each study (ie, young epileptic patients, recipients of transplants).


The world wide epidemiological prevalence data for gingival overgrowth is not available. In a study conducted in India, about 57% of the children diagnosed with epilepsy (8-13 years) contracted gingival enlargement within 6 months of phenytoin monotherapy.

Sex distribution
Age distribution


The pathophysiological mechanism of gingival hyperplasia is currently not understood [9]. Variations in influx of calcium ions in gingival tissue is observed in case of drug-induced hyperplasia [10]. Testosterone mediated aldosterone synthesis via calcium antagonism is thought to play an important role. Aggravation of gingival hyperplasia was observed in dogs subjected to testosterone injections and administration of oxodipine in castrated dogs resulted in an improvement of hyperplasia [11]. Cyclosporine induced hyperplasia was observed in patients with marked decrease in transglutaminase levels due to non availability of Calcium [12]. Drug (phenytoin) induced gingival enlargement was reported in feline models where stimulation of fibroblast like cells resulted in proliferation of gingival tissue.


The patients should maintain a good oral health care regimen once the condition is diagnosed. It is the single most important way to prevent gums from further enlargement and pathologic inflammation. In addition to that, good oral health will also aid in complimenting the outcome of non invasive medical interventions offered by the physician.


Many factors contribute to gum tissue overgrowth. Drug induced gingival enlargement is the most common. Most of the congenital form of gingival enlargement is either acquired genetically or due to metabolic dysfunctions (eg., fetal valproate syndrome) [1].

First reports on gingival hyperplasia came in 1960s from dental literature. The articles were mainly discussing the side effects of phenytoin (dilantin) as a treatment option for seizures in epileptic children who were institutionalized. Similar side effects were also reported in epileptic adults under phenytoin and phenobarbital drugs [2].

Most of the scientific studies (clinical and epidemiological) conducted so far are retrospective in nature and therefore the etiological factors of the condition largely remain unclear [3]. However, the evidence from current literature points out that an interplay of multiple factors leads to the development of gingival hyperplasia. One of the major disputes regarding the development of drug-induced gingival overgrowth is whether it is due to the hyperplasia of the gingival epithelium or submucosal connective tissue, and/or both. In addition to that, the influence of age and sex of the patient and the treatment regimen (including duration and dosage) in development of drug induced hyperplasia still remains to be understood.

The major risk factors that lead to the development of gingival hyperplasia include:

  1. Gingivitis (inflammation of gums)
  2. Lack of proper oral care
  3. Presence of dental plaques which act as store house for drugs (phenytoin or cyclosporine).
  4. Nickel build up and subsequent proliferation of epithelial cell in orthodontic patients [4].

Patient Information

Gingival over growth (other names: gingival enlargement, gingival hyperplasia and gingival hypertrophy) is a condition in which the gums grow excessively.

Major causes for the condition:

The most common causative factor for gingival overgrowth is intake of certain medications especially that are calcium channel blockers. Some of the other drugs that cause overgrowth include ciclosporin and phenytoin. In rare cases, antibiotics and antidepressant can also cause gingival overgrowth.

Instances like hormonal fluctuations (eg. pregnancy and adolescence) and vitamin/dietary deficiency (eg. Scurvy) in the patient can also trigger gingival overgrowth.

Medical conditions like cancer (eg., acute leukaemia, lymphoma) or systemic conditions (eg. Kaposi sarcomaprimary amyloidosisWegener granulomatosis etc) can also result in overgrowth. Rare congentical abnormalities (eg., Pfeiffer's syndrome, infantile systemic hyalinosis, Cowden's syndromeprimary amyloidosis etc) are another important precursor for development of gingival overgrowth.

Major symptoms

The obvious visual symptom is the overgrowth of gum tissues. Other symptoms include tenderness, difficulty in chewing food and talking or bad breath.

Treatment options

In most of the cases the effective management of underlying conditions that cause gingival overgrowth resolves the disease. In cases where the overgrowth is severe gingivectomy is performed to removed the excessive gum tissue. Other less severe cases are managed by non invasive methods like root planing and scaling.


Maintaining good oral health hygiene can effectively prevent the occurrence and relapse of gingival overgrowth.



  1. Rodriguez-Vazquez M, Carrascosa-Romero MC, Pardal-Fernandez JM, et al. Congenital gingival hyperplasia in a neonate with foetal valproate syndrome. Neuropediatrics. 2007; 38(5):251-252.
  2. Dhingra K, Prakash S. Gingival overgrowth in partially edentulous ridges in an elderly female patient with epilepsy: a case report. Gerodontology. 2012; 29(2):e1201-1206
  3. Moffitt ML, Bencivenni D, Cohen RE. Drug-induced gingival enlargement: an overview. Compend Contin Educ Dent. 2013; 34(5):330-336.
  4. Gursoy UK, Sokucu O, Uitto VJ, et al. The role of nickel accumulation and epithelial cell proliferation in orthodontic treatment-induced gingival overgrowth. Eur J Orthod. 2007; 29(6):555-558.
  5. Barclay S, Thomason JM, Idle JR, et al. The incidence and severity of nifedipineinduced gingival overgrowth. J Clin Periodontol. 1992; 19:311–314.
  6. Lucas RM, Howell LP, Wall BA. Nifedipineinduced gingival hyperplasia. A histochemical and ultrastructural study. J Periodontol. 1985; 56:211–215.
  7. Pernu HE, Knuuttila MLE, Huttenen KRH, et al. Drug-induced gingival overgrowth and class I1 major histocompatibility antigens. Transplantation. 1994; 57:1811-1813.
  8. Johnson RB, Zebrowski EJ, Dai X. Synergistic enhancement of collagenous protein synthesis by human gingival fibroblasts exposed to nifedipine and interleukin-1-beta in vitro. J Oral Pathol Med. 2000; 29:8–12.
  9. Harel-Raviv M, Eckler M, Lalani K, et al. Nifedipine-induced gingival hyperplasia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2002; 79:715-722.
  10. Nyska A, Shemesh M, Tal H, et al. Gingival hyperplasia induced by calcium channel blockers: Mode of action. Med Hypotheses. 1994; 43:115-118.
  11. Dayan D, Kozlovsky A, Tal H, et al.Castration prevents calcium channel blocker-induced gingival hyperplasia in beagle dogs. Hum Exp Toxicol. 1998; 17:396-402.
  12. Nishikawa S, Nagata T, Morisaki I, et al. Pathogenesis of drug-induced gingival overgrowth. A review of studies in the rat model. J Periodontol. 1996; 67:463-471.
  13. Ilgenli T, Atilla G, Baylas H. Effectiveness of periodontal therapy in patients with drug induced gingival overgrowth. Long-term results. J Periodontol. 1999; 70: 967–972.
  14. Daly CG. Resolution of cyclosporin A (CsA)-induced gingival enlargement following reduction in CsA dosage. J Clin Periodontol. 1992; 19(2):143-145.
  15. Fu E, Nieh S, Chang HL, et al. Dose-dependent gingival overgrowth induced by cyclosporin in rats. J Periodontol. 1995l; 66(7):594-8.
  16. Demirer S, Ozdemir H, Sencan M, et al. Gingival hyperplasia as an early diagnostic oral manifestation in acute monocytic leukemia: a case report. Eur J Dent. 2007; 1:111–114.
  17. Wu J, Fantasia JE, Kaplan R. Oral manifestations of acute myelomonocytic leukemia: a case report and review of the classification of leukemias. J Periodontol. 2002; 73:664–668.

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Last updated: 2019-07-11 21:07