|Year : 2015 | Volume
| Issue : 2 | Page : 146-150
Idiopathic gingival enlargement and its management
Pawan Kumar1, Saindhyatora Sonowal2
1 Unit of Periodontics, Oral Health Science Centre, Post Graduate Institute of Medical Education and Research, Chandigarh, India
2 Department of Periodontics, Regional Dental College, Bhangagarh, Guwahati, Assam, India
|Date of Web Publication||3-Sep-2015|
Dr. Pawan Kumar
Senior Resident, Unit of Periodontics, Oral Health Science Centre, Post Graduate Institute of Medical Education and Research, Chandigarh - 160 012
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Increase in the size of gingiva referred to as "gingival enlargement," usually overfills the interproximal spaces, ballooning out over the teeth and sometimes even protruding into the oral cavity. It may occur as localized enlargement in relation to a single tooth, a group of teeth, or may be generalized involving the entire dentition. It is multifactorial in origin having the influence of bacterial plaque, systemic factors or conditions, genetic predisposition (hereditary or familial), and various medications. Sometimes, it may appear as diffuse enlargement of gingiva without any specific etiologic factor. It is then considered as idiopathic enlargement. In this case report, an idiopathic gingival enlargement was successfully treated using gingivectomy by ledge and wedge procedure. The surgical technique performed yielded functionally as well as esthetically satisfying results. Gingivectomy provides a viable option to manage diffuse enlargement cases. This procedure provides the functional as well as esthetic demands and at the same time, it maintains the integrity of periodontium.
Keywords: Enlargement, gingiva, idiopathic
|How to cite this article:|
Kumar P, Sonowal S. Idiopathic gingival enlargement and its management. J Int Clin Dent Res Organ 2015;7:146-50
| Introduction|| |
Gingival enlargement or overgrowth is a clinical descriptive term for increases in size of gingiva. , It is important for cosmetic and mechanic reasons or possibility of a part of a systemic disease. Complications associated with gingival overgrowth may include retained primary teeth, delayed eruption of permanent teeth, increased distal spacing, drifting of teeth, poor plaque control, poor mastication, affected speech, esthetics, and malocclusion. ,,,, Many cases are iatrogenic, some are inherited while others are idiopathic.  Gingival enlargement can be due to plaque accumulation, poor oral hygiene, inadequate nutrition, or systemic hormonal stimulation.  Gingival enlargements are also seen in several blood dyscrasias, e.g., leukemia, thrombocytopenia, or thrombocytopathy. 
Idiopathic gingival enlargement is a rare type of gingival enlargement (about one in 750,000 individuals)  that has no definite cause and is also known as gingivomatosis  , diffuse fibroma  , idiopathic fibromtosis, hereditary gingival fibromatosis, familial elephantiasis.  Oral manifestations may vary from minimal involvement of only the tuberosity area and the buccal gingiva around the lower molars to generalized enlargement inhibiting eruption of teeth. The hyperplastic gingiva is usually pale pink, firm, leathery in consistency, and presents a characteristic pebbled surface. The condition has been classified into two types. Nodular form characterized by presence of multiple tumors in the dental papillae and other form which is symmetric resulting in uniform enlargement  of gingiva and represents the most common type. There may be a combination of both types. The hyperplastic gingival tissues appear normal at birth but began to enlarge with eruption of primary teeth. Histologically, it is described as a moderate hyperplasia of the epithelium with hyperkeratosis and elongation of rete pegs. The increase in the tissue mass is primarily the result of an increase in thickening of the collagen bundles in the connective tissue stroma.  The cause of gingival overgrowth is unknown.
Here we report an unusual case of a non-syndromic, idiopathic gingival enlargement.
| Case Report|| |
A 12-year-old female patient came to the department of Periodontology with the chief complain of swollen gums. The patient reported that she did not have teeth since her childhood.
The child's mother reported an uncomplicated pregnancy and denied prenatal exposure to tobacco, alcohol, and drug. She also reported no exposure to radiation and no illness during her pregnancy. The birth history was unremarkable with 40-week gestation and normal vaginal delivery. Prenatal history was uneventful with no infection, bleeding, or unusual event.
Patient was referred for genetic and neurologic evaluation. The chromosomal analysis revealed no anomaly.
The patient exhibited no jaundice or cyanosis at birth. There was no family history to suggest birth defects or mental retardation. The affected child had a healthy 6-year-old sibling.
On extraoral examination, it was observed that there was no increase in facial volume. The patient was incapable of closing her mouth because of the volume of the maxillary and mandibular alveolar ridge.
In the intraoral examination, a generalized increase in gingival tissue was observed, involving the maxillary and mandibular arches (Grade 3). The gingiva was pigmented, with a firm, dense consistency. There were no signs of acute inflammation other than strong halitosis [Figure 1] and [Figure 2].
Panoramic examination showed root stump of 46; and 36 was carious broken [Figure 3].
Complete treatment plan with pros and cons were explained to the patient. A written informed consent was taken before carrying out the procedure. Pre-surgical mouth rinse using Chlorhexidine (0.2%) was done prescribed prior to the surgical intervention. The assessment of overgrowth and its severity was correlated using clinical and radiologic parameters. Gingivectomy by ledge wedge procedure using scalpel was done sextant wise on both the arches under local anesthesia (2% lignocaine with 1:80,000 adrenaline) [Figure 4], [Figure 5], [Figure 6]. After each gingivectomy, periodontal dressing was placed. Antibiotics (Amoxicillin 500 mg three times a day (TID) for 5 days) and non-steroidal anti-inflammatory drug (NSAID) was prescribed. Postoperative instructions were given and the patient was recalled after 7 days. After 7 days, periodontal dressing was removed and patient was instructed for proper oral hygiene maintenance. The root stump and carious broken was also extracted during the procedure. The postoperative course was uneventful. Oral hygiene was emphasized to patient and parents.
|Figure 6: Gingivectomy using ledge and wedge procedure in lingual aspect|
Click here to view
Excised tissue was sent for histopathological examination. Microscopic examination revealed a bulbous increase in the amount of connective tissue that is relatively avascular and consists of densely arranged collagen bundles and numerous fibroblasts. The surface epithelium is thickened and acanthotic with elongated rete pegs [Figure 7]. The postoperative course was uneventful. Oral hygiene was emphasized to patient and parents.
The patient was re-evaluated after 1 week, 1, 3, 6, and 12 months and after completion of full mouth gingivectomy. The oral hygiene instructions were reinforced at every visit. It was observed that the patient maintained her oral hygiene properly for this period and the reoccurrence of the growth was not reported at the end of 12 months [Figure 8] and [Figure 9].
| Discussion|| |
Gingival hyperplasia can occur as an isolated form or part of a syndrome and also can be localized or generlized. Several etiologies have been reported including drug-induced (cyclosporine, phenytoin, and nifedipine), hereditary, hormones-related (pregnancy, growth-hormone), inflammation, systemic (leukemia, neurofibromatosis), idiopathic, and syndrome-associated. Depending on the cause, the overgrowth may vary in clinical presentation, severity, onset, and duration. Hereditary gingival hyperplasia is a slowly progressive, generalized, severe gingival enlargement involving maxillary and mandibular arches. The pink firm gingiva is fibrotic and non-hemorrhagic. Severity varies and may cover part/all of the crowns of the erupted teeth. It usually develops around the eruption of permanent teeth and is rarely present at birth. The most common mode of inheritance is autosomal dominant with variable penetrance. ,, The syndrome most commonly associated with gingival hyperplasia is gingival fibromatosis with generalized hypertrichosis, mental retardation, and tonic-clonic seizures. , Isolated cases of gingival fibromatosis associated with amelogenesis imperfecta and aggressive periodontitis have also been reported. , Conditions known to be associated with gingival hyperplasia are I-cell disease (Mucolipidosis II), Ramon syndrome, Juvenile hyaline fibromatosis (Murray-Peretic-Drescher syndrome), Alpha-Mannosidosis, Donohue syndrome (Leprechaunism), Cross syndrome, Hornova-Dluhosova syndrome, Zimmerman-Laband syndrome, Rutherford syndrome, Jones syndrome, and Borrone dermato-cardio-skeletal syndrome.
Gagliano et al.,  suggested that gingival hyperplasia of different etiologies may have different mechanisms of overgrowth. These include an increase in proliferation of resident tissue fibroblasts, a reduced level of metalloproteinase synthesis (matrix metalloproteinases (MMP)-1 and MMP-2), resulting in low levels of extracellular matrix degrading, an increase in collagen type I production, heat-shock protein 47 (hsp47) production, and other extracellular matrix components. 
Though the cause of idiopathic gingival enlargement is unknown, there appears to be a genetic predisposition. The condition may manifest as an autosomal dominant or very rarely as an autosomal recessive mode of inheritance. Autosomal dominant non-syndromic form has been genetically linked to the chromosome 2p21-p22 and 5q13-q22.  It is possible that isolated form may be a result of single gene mutation while syndromic forms may result from alterations of multiple genes or perhaps a gene dosage effect. Recently, a mutation in son of sevenless-1 (SOS-1) has been held responsible for this rare hereditary condition. SOS gene 1 codes for a protein that activates the ras pathway, which signals cell growth. When there is no mutation in this gene there is normal growth of gingiva, otherwise resulting in gingival enlargement. There may be increased collagen deposition as a consequence of post-translational mechanisms. The increase in collagen cross-links renders it less susceptible to MMP degradation leading to gingival enlargement. However, mutations of other genes are also possible.
As the family, medical, prenatal, and drug histories were non-contributory to this case; and the clinical appearance of bilateral uniform enlargement of gingiva led to the diagnosis of a generalized isolated idiopathic gingival enlargement (IGE) in the present case. It is more common in male patients in contrast to the localized form which is more prevalent in female patients. IGE manifests due to congenital/hereditary causes which is not understood accurately. Due to massive gingival enlargement an affected person usually develops abnormal swallowing pattern and experiences difficulty in speech and mastication. The clinical presentation of the gingiva was similar to that of hereditary gingival hyperplasia but did not have a contributory medical or family history that fulfilled any possible syndromes.
General histological findings include normal overlying epithelium, rete pegs extending deep into underlying connective tissues with some areas of hyperplasia, proliferating dense fibrous connective tissue with increased cellularity and coarse collagenous fiber bundles, and hyperkeratosis and acanthosis with elongated papillae.  The cellular and molecular mechanism leading to this condition is not understood. The keratinocytes have an important role in pathogenesis by inducing extracellular matrix accumulation by fibroblasts. This increased proliferation and elevated production of extracellular matrix molecules, type I collagen and fibronectin could lead to the clinically increased bulk of gingiva.
Enlargement usually begins with the eruption of deciduous or permanent teeth; it may rarely present at birth or arise at adulthood. The most extensive enlargement appears to occur at the loss of deciduous teeth or early stage of eruption of permanent teeth. It progresses rapidly with the stage of active eruption and decreases with the end of this stage. The continued recurrence of the enlargement following surgery and a permanent remodelling of tissue after extraction suggests the importance of the presence of teeth and the environment of gingival crevice for the pathogenesis.
Management of gingival hyperplasia depends on the cause of the condition. In general, reinforcement of good home care oral hygiene regimens and periodic professional surgical excision of gingival are the treatments of choice. The treatment performed in this condition was external bevel gingivectomy. Recurrence rate in IGE is very high after surgery and because of this the patient should be followed for considerable period of time and may require repeated surgeries. Appropriate time of the removal of recurrent gingival enlargement varies; Emerson  recommended that the best time is when all the permanent teeth have erupted. Appropriate time for removal of gingival enlargement is at the age of 3, 6, and 12 years to have effective plaque control and to maintain oral hygiene after gingivectomy procedures.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]