Gingival EnlargementDefinition

Increase in size of gingiva. Often a feature of gingival and periodontal disease.It is also called gingival overgrowth.

Classification Inflammatory enlargement

o Chronico Acute

Drug induced enlargement Idiopathic enlargement Enlargement associated with systemic diseases

o Conditioned Enlargemento Systemic diseases causing gingival enlargement

Neoplastic enlargemento Benign tumorso Malignant tumors

False enlargement

Based on location and distribution

Localized and generalized. Also Marginal ,Papillary ,Diffuse and Discrete

Score for gingival enlargement (Bokenkamp & bornhost 1994)

Grade 0-No sign of GE

Grade 1-E confined to interdental papillae

Grade 2-E involving papilla and marginal gingival

Grade 3-E covers three quarters or more of crown

Inflammatory Enlargement

Clinical features

a) Chronic Inflammatory Enlargement

Originates as a slight ballooning of interdental papilla and/or marginal gingival

Early stage – creates life preserver shape bulge Can increase till it covers part of crown Localized/generalized Progresses slowly and painless unless complicated by acute

infection or trauma Occasionally seen as sessile/pedunculated resembling tumor Interproximal/Marginal/Attached gingiva May undergo spontaneous reduction in size Followed by exacerbation and continued enlargement Sometimes painful ulceration

Histopathology Exudative and proliferative features of chronic inflammation Inflammatory cells & fluid, vascular engorgement New capillary formation Associated degenerative changes

(clinically deep red or bluish red soft and friable, smooth shiny surface, bleed easily)

Sometimes, relatively gingival may appear firm resilent and pink because of greater fibrotic component with an abundant of fibroblasts & collagen fibres.(in case of low grade inflammation for long duration and better immunity of patient)

ETIOLOGY Prolonged exposure to dental plaque. Factors that favor plaque accumulation and retention. Anatomic contributing factors. Restorative contributing factors. Orthodontic contributing factors. Habits as contributing factors.

Gingival changes in Mouth breathing

Gingivitis & GE seen often Red and edematous with diffuse surface shininess of exposed area Maxillary anterior-common site Often altered gingiva is clearly demarcated from adjacent

unexposed normal gingiva Irritation from surface dehydration

b) Acute inflammatory enlargement

Gingival abscess

Localized, painful swelling confined to gingiva Limited to marginal/interdental with purulent exudates

Early stage-red,shiny. Turns fluctuant within 24-48 hrs. If progress, ruptures.

Adjacent teeth would be sensitive to percussion Causes-Bristle, apple core, lobster shell

2. Drug Induced Gingival Enlargement General information

Some drugs such as anticonvulasants, immunosuppresants and calcium channel blockers.

Enlargement may appears within 1 to 3 months after initiation of treatment with these.

Usually enlargement would be fibrotic confined to the attached gingiva

May create speech, mastication, tooth eruption and aesthetic problems.

Clinical features Starts at painless BEADLIKE enlargement of

interdental papilla Extends to the facial and lingual gingival margins As the condition progresses, marginal and papillary

enlargements unite May develop into a massive tissue fold covering

considerable portion of crown May interfere with occlusion

When uncomplicated by inflammation

Lesion is usually MULBERRY SHAPED

Firm, Pale pink, Resilient, Minutely lobed surface No tendency to bleed Projects from beneath the gingival margin from which it

is separated by a linear groove When complicated by secondary inflammatory

Obliterates the lobulated surface Increase bleeding tendency Usually generalized throughout the month More severe in anterior regions-both arch Occurs in areas where teeth are present, not in

edentulous areas GE disappears when teeth extracted…rarely remains DIGE may occur in mouths with little or no plaque And may be absent in mouth with abundant deposits Proper oral hygiene toothbrush & CHX reduces

inflammation but does not lessen or prevent gingival overgrowth.

a) Anticonvulsants

First DIGE by Kimball 1939--PHENYTOIN

Average seen in 50% cases, More often in younger patients

Mephenytoin, succinimides and valproic acid also may cause DIGE

GE is chronic and slowly increases in size. When surgically removed , it recurs Spontaneous disappearance within few months after

discontinuation Phenytoin appears in saliva but not clear whether

severity of overgrowth related to the levels of levels in saliva or plasma.

Mechanisms of Gingival Enlargement 1. In non-inflamed/normal gingiva, fibroblasts are LESS

ACTIVE OR INACTIVE and do not respond to circulating phenytoin…

Whereas fibroblasts within inflamed tissue are in ACTIVE state…(due to the influence of inflammatory mediators and endogeneous growth factors present in inflammation)

2. Genetic predeposition is a suspected factor(GE may result from the genetically determined ability or inability of host to deal effectively with prolonged administration of phenytoin)

3. Increased synthesis of sulfated glycosaminoglycans(GAG)Fibroblasts from a phenytoin induced gingival overgrowth

4. Presence of inactive fibroblastic collagenase-which causes decreased collagen degradation and thus results in GE

c)Immunosuppressants Cyclosporine-to prevent organ transplant rejection

and to treat several diseases of autoimmune origin Acts by inhibit helper T cells(Selectively and

reversibly) Given iv or orally Dosages greater than 500mg/day have reported GE This type of GE is more vascularized than phenytoin

induced. Seen in 25-70% people using it Affects children more frequently Microscopic finding-Many plasma cells and

abundant amorphous extracellular substance (Suggested that this GE is a hypersensitivity

response to cyclosporine) Other side effects-

Nephrotoxocity,Hypertension,Hypertrichosis Substitute-TACROLIMUS(less severe GE and

Hypertension, Hypertrichosis

Calcium channel blockers

Used for the treatment of Hytpertension, Angina, Coronary artery spasms, Cardiac arrhythmias

Inhibit calcium ion influx across the cell membrane of heart and smooth muscle cell,

Thus blocking intracellular mobilization of calcium. Nifedipine, one of the most commonly used drug

induced GE in about 20% cases Diltiazem,felodipine, verpamil also-GE ISRADIPINE can replace nifedipine in some cases

and doesn’t induce gingival overgrowth Nifedipine is also used with cyclosporine in kidney

transplant reciepients

3. IDIOPATHIC GINGIVAL ENLARGEMENT

Rare condition of undetermined cause Also known as Gingivomatosis, Idiopathic

fibromatosis, Elephantiasis, Hereditary gingival hyperplasia, Congenital familial fibromatosis

Clinical Features

Affects attached gingival as well as gingival margin and interdental papillae

Facial and lingual surfaces of mandible and maxillae are generally affected but involvement may be limited either jaw.

Enlargement is pink, firm and leathery in consistency Characteristic MINUTELY PEBBLED SURFACE In severe cases, teeth almost completely covered and

GE projects into the vestibule Secondary inflammation common Cause unknown Autosomal recessive/dominant In some families, GE may be linked to impairment of

physical development GE starts usually begins with eruptions of primary or

secondary dentition and may regress after extraction Suggest that the teeth or plaque may be initiating

factors Presence of bacterial plaque is a complicating factor

4. Enlargements Associated With Systematic Diseases Systematic diseases can develop oral manifestations

and affect periodontitum including GE by two mechanisms---1. Manifestation of an existing inflammation

initiated by plaque(conditioned)2. Manifestation of systematic disease may be

independent of the inflammatory status of gingival(systematic diseases causing GE)

a) Conditioned enlargement

Occurs when systematic condition of patient exaggerates or distorts the usual gingival response

Bacterial plaque is necessary for initiation However plaque is not the sole determinant of nature

of the clinical features3 types

o Hormonalo Nutritionalo Allergic

Hormonal – Gingival Enlargement in pregnancy

Seen as single or multiple tumor like masses Increase in progesterone & estrogen By 3rd trimester, 10-30 times the normal level Cause changes in vascular permeability leading to

gingival edema Increase in inflammatory response to plaque Seen in 10-70%, does not occur without plaque

Generally GE more prominent interproximally seen as bright red or magenta, soft, friable, smooth shiny surface

Bleeds on probing or spontaneous Tumorlike GE-Pregnancy tumor (not a neoplasm)

which is an inflammatory response to bacterial plaque. It is modified by patient’s condition

Usually after 3rd month of pregnancy, but may be seen earlier also

Lesion appears as a discrete mushroom like flattened spherical mass that protudes from gingival margin or more often from Interproximal spaces

Sessile/pedunculated Tends to extend laterally….Pressure from cheek

and tongue—flattened appearance Doesn’t generally invade bone and is usually

painless May interfere with occlusion and cause painful

ulceration

Histopathathology Central mass of Connective Tumor – numerous

newly formed diffusely arranged engorged capillaries

Most gingival diseases during pregnancy PREVENTED by removal of plaque & calculus

Fastidious oral hygiene at the outset Recurs if local irritants not completely removed

Hormonal – Enlargement in Puberty

Occurs in areas of plaque accumulation Size of GE greatly exceeds that usually seen in

association with comparable local factors Has all clinical features of chronic inflammation

gingival disease Degree of E and tendency to develop massive

recurrence in the presence of relatively scant plaque deposits

Spontaneous reduction after puberty but doesn’t completely disappear until plaque and calculus removed.

Some studies- - - Capnocytophaga sp. In intiation of pubertal gingivitis

Nutritional – Enlargement in Vitamin C Deficieancy

Scurvy Modify the response of gingiva to plaque to the

extend that normal defensive reactions are inhibited.

Extend of inflammation is exaggerated resulting in massive GE seen in scurvy

GE is gen marginal, bluish red soft and friable has smooth shiny

Surface necrosis with pseudomembrane formation are common features

Histopathology

Marked diffusive edema, collagen degradation and scarcity fibrils/fibroblasts

Plasma cell gingivitis-Also called a typical gingivitis Often, mild marginal enlargement, extends to

attached gingival Gingiva appears red, friable and granular, bleeds

easily, Located in the oral aspect of attached gingival(differs

from plaque induced gingivitis)

Nonspecific conditioned GE

Pyogenic granuloma – tumorlike GE Exaggerated conditioned response to minor trauma,

Exact mechanism not clear Predunculated/sessile Treatment – removal of irritants Similar to pregnancy tumor – distinguish based on

patient history

b) Systematic enlargement that causes GE

Leukemia

o Often in acute leukemia, may be seen in subacute

Granulomatous diseaseso Wegener’s granulomatosis

5. NEOPLASTIC GE (GINGIVAL TUMORS)

Benign tumors – epuliso Fibroma, papilloma, peripheral giant cell

granuloma, central giant cell granulomao Leukoplakia, gingival cyst, others

Malignanto Carcinomao Malignant melanoma

6. False Enlargement

Underlying osseous lesionso Tori, Exostoses, Paget’s, Fibrous dysplasia,

Cherubism ,Ameloblastoma, Osteoma Underlying dental tissue

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