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DEFINITION
Increase in the size of the gingiva is termed as gingival
enlargement or gingival overgrowth.

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CLASSIFICATION
According to the etiologic factors and pathologic
changes.
I) Inflammatory enlargement
a). Chronic
b). Acute
II) Drug induced enlargement
III) Enlargements associated with systemic diseases
A). Conditioned enlargement
1). Pregnancy
2). Puberty

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 3). Vitamin C
4). Plasma cell gingivitis
5). Nonspecific conditioned enlargement
B). Systemic diseases causing gingival
enlargement
1). Leukemia
2). Granulomatous diseases (Wegener’s
granulomatosis, sarcodiosis)
IV) Neoplastic enlargement
A). Benign tumors
B). Malignanttumors
V) False enlargement
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On the basis of location and distribution

A). Localized:Limited to the gingiva adjacent

to a single tooth or group of tooth.
eg. The gingival enlargement localized in the
canine region

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B). Generalized involving the
gingiva throughout the mouth.
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D). Papillary: Confined to the interdental papilla

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E). Discrete: An isolated sessile or
pendunculated tumor like enlargement

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F). Diffuse; Involving the marginal and
attached gingivae and papillae

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Scoring of gingival enlargement

Grade 0: No signs of gingival enlargement

Grade I: Enlargement confined to interdental
papilla
Grade II: Enlargement involves papilla and
marginal gingiva.
Grade III: Enlargement covers three
quarters or more of the crown

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Grade 0 Grade I

Grade II Grade III

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INFLAMATORY ENLARGEMENT
Gingival enlargement may result from chronic
or acute changes.

Chronic inflammatory enlargement

Etiology:
 Prolonged exposure to dental plaque
 poor oral hygiene
 irritation by anatomic abnormalities
 improper restorative & orthodontic
appliances.
 Mouth breathing habit
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 Clinical features :
 Site - interdental, marginal, attached
gingiva
 may be localized or generalised.
 Shape - slight ballooning to life preserver
shaped bulge
 slow progressing and painless
 painful ulceration sometimes

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Chronic inflammatory enlargement in a 27
year old woman

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 Chronic inflammation associated with
mouth breathing in a 16 year old child

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Histology :
 chronic inflammatory cells (Lymphocytes,
macrophages, plasma cells etc.)
 lesions deep red, soft, friable, smooth
 bleeds easily due to vascular engorgement
 abundant fibroblasts & collagen fibers

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Acute inflammatory enlargement
Gingival abscess
Etiology:
Bacteria carried deep into the tissues by
toothbrush bristles, piece of apple coat
etc.
Clinical features:
 site - marginal and interdental gingiva
 localized, painful, rapidly expanding.
 Within 24 to 28 hrs lesion becomes
fluctuant & purulent exudate expressed as
surface orifice & rupture spontaneously.
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Gingival enlargement in the case of acute
necrotising gingivitis

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Gingival abscess

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Histopathology:
 epithelium - varying degree of intra&
extracellular oedema.
Leukocytic invasion & ulceration
 connective tissue- purulent focus
surrounded by PMNs.
 edematous tissue
 vascular engorgement.

Periodontal abscess:
involves the supporting periodontal tissues.

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 DRUG INDUCED GINGIVAL
ENLARGEMENT.
 Anticonvulsants
 Immunosuppressants
 Calcium channel blockers
affects th speech, mastication, tooth
eruption, and aesthetics problems
General clinical features:
 site - interdental papilla, facial and
lingual gingival margins
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 Starts as a bead massive tissue fold
covering the crown
 mulberry shaped , firm , pale pink, resilient
 no tendency to bleed
 appears to project from beneath the gingival
margin separated by a linear groove.
 Plaque control becomes difficult

secondary inflammation

red, bluish colored lobulated demarcations,

increased bleeding

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 Regress spontaneously within few months
after discontinuation of the drug.
Histopathology:
 Epithelium - acanthosis, elongated rete pegs
 conn. Tissue - densely arranged collagen
bundles, fibroblasts, neovascularisation
 abundance of amorphous ground substance
 cyclosporins - Highly vascularised & foci of
chronic inflammatory cells
 phenytoin - fibroblast to collagen ratio
normal, oxytalan fibers are numerous

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1).Anticonvulsants
 First gingival enlargement reported
 Introduced by Merritt and Putnam in 1938.
 Drugs used for the treatment of epilepsy
 Phenytoin, ethotoin, mephenytoin,
succinimides etc.
 50% of the patients
 younger patients more prone
 appears in saliva
 in systemic administration accelerates the
healing of gingival wounds in non- epileptic
humans.
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Mechanism: PHENYTOIN

stimulates fibroblast production of an

proliferation inactive fibroblastic
collagenase
gingival overgrowth

increase in the sulfated decrease in the

glycosaminoglycans in collagen degradation
vitro.

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 Phenytoin gingival
enlargement
on the facial surface

Phenytoin gingival
enlargement on the
occlusal surface

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 Phenytoin enlargement
in the posterior region

Phenytoin gingival
enlargement -
close-up view of
anteriors.
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2). Immunosuppressants
 Cyclosporines used to prevent
organ transplant rejection & to
treat autoimmune origin
 if dosage > 500mg/day reported
to induce gingival enlargement.
 30% patient.
 More vascularised
 associated with nephrotoxicity,
hypersensitivity, hypertension,
hyperthricosis.

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 Cyclosporine induced
gingival
enlargement
in a 14yr old boy

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3).Calcium channel blockers
 used for CVS disorders, hypertension,
angina pectoris, coronary artery spasm &
cardiac arrhythmia.
 Drugs like nifedipine,diltiazem, felodipine,
nitrendipine and verapamil.
 Nifidipine induces enlargement in 20%
cases
 Nifidepine + cyclosporines (for kidney
transplant)
larger overgrowth
 dose dependent growth
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Nifedipine induced gingival enlargement

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Idiopathic gingival enlargement
 termed as gingivostomatitis, elephantiasis,
idiopathicfibromatosis, hereditary gingival
hyperplasia & congenital familial
fibromatosis.
Etiology:
 unknown
 hereditary basis (autosomal dominant or
recessive)
 begins with primary & secondary dentition
eruption.

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Clinical features:
 Site - attached
gingiva, gingival
margin, and
interdental papilla
 pink,firm and leathery
with pebbled
appearance
 Severe cases jaw
appears distorted due
to bulbous enlargement
 secondary inflammation

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Histopathology:
 epithelium -thickened & acanthosis
elongated rete pegs.
 Conn. Tissue- highly vascular, densely
arranged collagen bundles & numerous
fibroblasts

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ENLARGEMENT ASSOCIATED WITH
SYSTEMIC DISEASES
Many systemic diseases can develop oral
manifestations that mayaffect the
periodontium by two different mechanisms
1). Magnification of existing inflammation
initiated by dental plaque “Conditioned
enlargement”
a). Hormonal conditions(pregnancy &
puberty)
b). Nutritional (vitamin C deficiency)
c). Non- specific conditioned enlargement
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2). Manifestation of systemic disease
independent of the inflammatory status of
the gingiva.This group described as
“Systemic diseases causing gingival
enlargement”.

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Conditioned enlargement
systematic condition of the patient
exaggerates the usual gingival
response to dental plaque
bacterial plaque is necessary for its
initiation
3 types
a) Enlargement in pregnancy
b) Enlargement in puberty
c) Enlargement in vitamin C deficiency
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 A) Enlargement in pregnancy
Marginal and generalized
Etiology- increase in progesterone and estrogen
till 3rd trimester
- increased vascular permeability
and gingival edema.
Marginal enlargement
Clinical features
-generalized and interproximal
- bright red, soft friable and bleeds
spontaneously.

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Tumor like gingival enlargement
Also called pregnancy tumor
inflammatory response to
bacterial plaque
clinical features
-lesions are discrete, mushroom
like, flattened spherical
masses
-sessile, pedunclated
-exibits deep red pin point
margins.
-Painful ulcerations

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- histopathology:
- called angiogranuloma.
- central mass of connective tissue
- neovascularisation lined by cuboidal
endothelial cells.
-varying degree of edema & chronic
inflammatory infiltrate
- epithelium thickened, prominent retepegs.
Preventable by removal of plaque & calculus.

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B) Enlargement in Puberty
In both male & female
adolescents
Clinical features :
-marginal & interdental
-chronic gingival disease
-reduces after puberty
-Capnocytophaga sp.. & P.
intermedia
Histopathology
-chronic inflammation with
edema

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C) enlargement in Vitamin C deficiency
Clinical features :
- Marginal gingivitis
- hemorrhage on slight provocation and suface
necrosis with pseudomembrane formation
Histopathology:
- chronic inflammatory cellular infiltrate with
superficial acute response
- scattered hemorrhage
- diffuse edema, collagen degeneration &
scarcity of collagen

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Gingival englargement with ulceration
due to severe deficiency of vit C
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 Plasma cell gingivitis
Referred to as atypical
gingivitis and plasma
cell gingivostomatitis
site- marginal and
attached gingiva
Clinical features :
-red, friable, bleeds
easily
-oral aspect of
attached gingiva

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Histopathology:
-epithelium- spongiosis and infiltrated with
chronic inflammatory cells.
-lower spinous layer and basal layer damaged
-plasma cells infiltrate

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Non specific conditioned enlargement
(pyogenic granuloma)
Tumor like gingival enlargement
conditioned response to minor
trauma
Clinical features:
-discrete spherical tumor like
mass
-pedunclated, keloid like
-red friable with ulceration
-fibroepithelial papilloma

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Histopathology:
-chronic inflammation with granulation tissue
-vascular spaces & epithelial atrophy
Treatment - removal of lesion and local irritating factors

gingival mass at the mass regress 3 time of pregnancy months after pregnancy

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Systemic diseases causing gingival
enlargement
Leukemia
Clinical features:
-diffuse or marginal
-localized or generalized tumor like mass in
interproximal spaces
-red, friable, firm and hemorrhagic
-painful necrotising
-ulcerative inflammation

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Leukaemic gingival enlargement

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Histopathology:
 Epithelium - varying degree of leukocytic
infiltration & edema
 Psuedomembranous meshwork of fibrins,
necrotic epithelial cells, PMNS & bacteria.
 Conn.. Tissue - infiltrated with a dense
mass of immature & proliferating
leukocytes
 engorged capillaries

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Granulomatous diseases
Wegener’s granulomatosis
Etiology: cause unknown (immunologically
mediated tissue injury)
Characterized by acute granulomatous
necrotising lesion of respiratory tract
involving the orofacial region
Clinical features:
 reddish purple bleeds easily
Histopathology:
 chronic inflammatory giant cells & foci of
acute inflammation, microabscesses
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Red hemorrhagic mass surrounding
gingiva

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Sarcoidiosis

Etiology unknown
red, smooth, painless enlargement

histopathology discrete, noncaseating whorls

of epitheloid cells &
multinucleated
foreign-body-type giant cells

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NEOPLASTIC ENLARGEMENT
(GINGIVAL TUMORS)
A).Benign tumors of gingiva
Epulis all discrete tumors & tumor like
masses of gingiva
considered inflammatory
growth of gingiva & hard palate
1)Fibroma - arises from connective
tissue or PDL
slow growing, firm, nodular, soft,
vascular, pedunculated.
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Histopathology:
Bundles of well formed collagen fibers.
Multinucleated fibroblasts in Giant cell
fibroma

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2). Papilloma:
 proliferation of
surface
epithelium
associated with
human papilloma
virus(HPV)
 cauliflower like
protuberances
 broad, hard

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Human Pappilloma
Virus(HPV)

histopathology:
 Finger like projections
of stratified squamous
epithelium, often
hyperkeratotic
 fibrovascular core
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3)Peripheral giant cell granuloma
Clinical features
 interdentally, gingival margin
 pedunclated, smooth, multilobulated,
ulcerations
 painless, firm , spongy
 locally invasive destroys underlying bone
Histopathology:
 Numerous foci of multinucleated giant cells &
hemosiderin particles
 chronic infiltration

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Peripheral giant cell
granuloma

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 Hyperplastic epithelium
 ulceration

Central giant cell granuloma

within the jaw and produce central cavitation.
Leukoplakia
Defined as “a white plaque that cannot be
diagnosed as any other etiology other than
that associated with tobacco chewing”.
Etiology- C, albicans, HPV-16, trauma
Clinical features - white, flattened, scaly,
thick keratinous plaque
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Histopathology
 hyperkeratosis acanthosis
 premalignant cahnges with atypical
epithelium
 dysplastic changes
 carcinoma in situ
 inflammatory infiltration

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Gingival cyst
 Localized, marginal& attached
 mandibular canine & premolar areas
 painless& erodes the bone
 Cyst developers from odontogenic epithelium
Histopathology
 flattened, localized thickening of epithelium
 Other benign tumors- Nevus, Myoblastoma,
hemangioma, neurilemmoma, neurofibroma,
ameloblastoma

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2).Malignant tumors

Carcinomas
 3% of all malignant tumors in the body.
 squamous cell carcinoma- common
 clinical features
 Exophytic, irregular growth, ulcerative,
flat, erosive lesions
 symptomless initially then painful
 invades the bone

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Malignant melanoma
 site - hard palate& maxillary gingiva
 localized pigmentation
 flat or nodular
 rapid growth with early metastasis
 arises from melanocytes from the gingiva
Sarcoma
Fibrosarcoma, lymphosarcoma&
reticulum cell sarcoma of gingiva
Kaposi’s sarcoma.
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FALSE ENLARGEMENT
Not true enlargement but appear as an
increase in size of underlying osseous or
dental tissues.
A). Underlying osseous lesions
Enlargement of bone - exostosis or tori
paget’s disease, fibrous dysplasia,
cherubism, central giant cell granuloma,
ameloblastoma osteoma, osteosarcoma.

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B). Underlying dental tissues
during stages of eruption particularly
primary dentition
 labial gingiva- bulbous marginal distortion
 Enlargement called developmental
enlargement
 & persists until junctional epithelium has
migrated enamel to CEJ
 Physiologic
 complicated by marginal inflammation

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