Gingival Enlargement

Dr . Dhwanit Thakore

Hi Doc, I am Julia

Introduction

Hyperplasia.
Hypertrophy.

Overgrowth.
Enlargement

Classification

I. Inflammatory enlargement
A. Chronic
B. Acute
II. Drug-induced enlargement
III. Enlargements associated with systemic diseases
A. Conditioned enlargement
1. Pregnancy
2. Puberty
3. Vitamin C deficiency
4. Plasma cell gingivitis
5.
Nonspecific
conditioned
enlargement
(granuloma
pyogenicum)

B. Systemic diseases causing gingival enlargement

1. Leukemia
2.Granulomatous diseases (Wegener's granulomatosis,
sarcoidosis, and so on)
IV. Neoplastic enlargement (gingival tumors)
A. Benign tumors
B. Malignant tumors
V. False enlargement

Shaefers classification
Inflammatory gingival hyperplasia
Non inflammatory (fibrous) gingival hyperplasia
Combination of inflammatory and fibrous hyperplasia

Based on location and distribution

Localized
Generalized
Marginal
Papillary
Diffuse
Discrete

Scoring
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

Photographic analysis Ellis &

Seymour
Criteria for assessing gingival encroachment/overgrowth
on adjacent tooth surfaces for a gingival unit (where a
discrepancy exists between adjacent teeth, the highest
score is awarded).
0=no encroachment of interdental papilla onto tooth
surface.
1=mild encroachment of interdental papilla, producing a
blunted appearance to papilla tip.
2=moderate encroachment, involving lateral spread of
papilla across buccal tooth surface of less than one
quarter tooth width.
3=marked encroachment of papilla, i.e., more than 1/4
tooth width. Loss of normal papilla form.

Inflammatory Enlargement

Inflammatory Enlargement

Chronic

Acute

More Common .
Secondary Complication..
Etiology
Prolonged exposure to dental plaque
-Poor oral hygiene

-Overhanging margins

-Malocclusion

-Irritation from clasps & denture

-Hypofunction

-Nasal Obstructions..

-Cervical cavities

-Mouth breathing

Chronic Inflammatory Enlargement

Clinical Features

Originates as a slight ballooning of the interdental papilla

and/or the marginal gingiva.
Early stages it produces a life preserver-shaped bulge around
the involved teeth

 Slow and Painless.. Acute Infection , Trauma

Discrete Sessile or Pedunculated mass resembling a tumor
May undergo spontaneous reduction in size with followed by
exacerbation, ulceration

Histopathology
Exudative and proliferative features of chronic inflammation

Clinically deep red or bluish

red are soft and friable with a
smooth, shiny surface, and they

Lesions that are relatively

bleed
easilyInflammatory
firm,
resilient,
pink
cells
fluid& collagen
with
vascular
fibroblasts
fibers
engorgement,
formation,

capillary
and associated

degenerative changes

Gingival enlargement in Mouth

Breathing
Red and edematous with a
diffuse surface shininess of the
exposed area
Maxillary anterior region is the
common site of involvement
Altered
gingiva
clearly
demarcated from the adjacent
unexposed normal gingiva
Exact manner.not known
Harmful
affect
surface dehydration

attributed

Klingsberg 1961.Rodent

Acute Inflammatory Enlargement

Gingival Abscess
Localized, Painful, Rapidly expanding lesion Sudden onset
Early lesion shows red swelling with smooth shiny surface
fluctuant.pointed on surface bursts.
Sometimes adjacent teeth also sensitive
Etiology
Foreign substance
Toothbrush bristle,
A piece of apple core,
A lobster shell fragment
Histologically : Purulent Focus surrounded by inflammatory
cells.

Drug-induced gingival enlargement

Anti epileptics:
Phenytoin (Kimball 1939).
Vigabatrin
Immunosupressants
Cyclosporine.
Tacrolimus
Dihydropyridines:
Nifedipine, Verapamil, Diltiazem, Nitrendipine,

nicardipine, amlodipine, felodipine, etc.

NSAIDS.
Hormones:
Oral contraceptive drugs.
Miscellaneous:
Sodium valproate, erythromycin,etc.

Drugs associated with Gingival Overgrowth

3 Classes of drugs

1. Anticonvulsants
2. Immunosuppressants
3. Calcium channel
blockers
Drugs modify the inflammatory
responses of the host to plaque.

and

immunologic

Goldman

 First reported in 1939 by Kimball associated with chronic

usage of the anti-epileptic drug Phenytoin.
Clinically and histologically, gingival overgrowth induced
by different drugs, are virtually indistinguishable.

Wysocki et al. 1983, Tyldesley & Rotter 1984),

Prevalence rate differs:

50% of patients medicated with phenytoin
30% for cyclosporin
20% for Nifedipine
(Angeiopoulous & Goaz 1972, Seymour et al. 1987, Barclay et ai.
1992)

 Children and adolescents >>> Adults

Anterior >>> Posterior gingival tissues.

ShowsIntra-patient variation,
May reach a "STATE OF EQUILIBRITIM" often within the
first year of commencing medication.
Systemic illness drug dosage

General features of DIGO

Starts
as
a
painless,
beadlike enlargement of
the interdental papilla
As
the
condition
progresses, the marginal
and papillary enlargements
unite
and
results
in
massive
tissue
fold
covering most part of the
crowns.
When uncomplicated by
inflammation, the lesion is
mulberry
shaped,
firm,
pale pink, and resilient,
with a minutely lobulated
surface and no tendency to
bleed

Usually generalized more

severe in the maxillary and
mandibular anterior regions.
A genetic predisposition is a
suspected
factor
in
determining
whether
a
person
treated
with
phenytoin
will
develop
gingival enlargement or not

(Hassell T.M. et al)

The enlargement is chronic

and slowly increases in size
When surgically removed, it
recurs
Spontaneous disappearance
occurs within a few months
after discontinuation of the
drug

Histologic features
Pronounced hyperplasia of the
connective tissue and epithelium
Acanthosis of the epithelium, and
elongated rete pegs extend deep
into the connective tissue
Densely arranged collagen bundles
Increase
in
the
number
of
fibroblasts, new blood vessels
Abundance of amorphous ground
substance (Mariani et al)
The enlargement begins as a
hyperplasia of the connective tissue
core of the marginal gingiva and
increases by its proliferation and
expansion beyond the crest of the
gingival margin

 In cyclosporine enlargements, the connective tissue

appears highly vascular with foci of chronic inflammatory
cells, particularly plasma cells

(Lucas R.M., Howell L.P. et al)

The Mature" phenytoin enlargement has a fibroblast to

collagen ratio equal to that of normal gingiva from normal
individuals.
Oxytalan fibers are numerous beneath the epithelium and
in areas of inflammation (Baratieri A. 1967)

Recurrence

Anticonvulsants

 Merritt and Putnam (1938.

PHENYTOIN
Effectiveness
Low cost
Availability
Partial seizure

Over 60 years

- Phenytoin
- Carbamazapine
- Phenobarbital

Generalised seizures

- Phenytoin
- Carbamazapine

- Valproic acid

- Phenobarbital
Generalised absence seizures- Ethosuxamide + Valproic acid

 Incidence Rate :
0% to 84.5% . Average 50% (Angelopoulos et al.)
Children and institutionalized.. prevalence

(Dahllof &

Modeer)

Progression
One month
12-18 months.. Max severity
Decreased rate in the second year.
Severity
Daily dose
Blood levels
Duration of use

Addy et al (1982) & Kapuar et al. (1973)

Dahllof & Modeer (1986) &Hassell et al. (1991)

 Trough or a minimum threshold level..

Rees TD (1993)

Usual therapeutic plasma level of phenytoin 10-20g

Classification of gingival hyperplasia caused by

Dilantin
James R. Babocks( 1974)
Grade-I Minimal:

No hyperplasia

Grade-II Moderate: Definite hyperplasia of gingiva, with

encroachment on the clinical crown of the
teeth, but no
interference of function.
Grade-III Severe:
Interference with function due to
overgrowth
of tissue

Histological Classification [Barak (1987)]

Grade I Normal Gingiva - Width of epithelium - 0.3-0.5 mm.
Grade II Slight Overgrowth - Width of epithelium 0.5-1.5
mm.
Grade III-

Moderate Overgrowth Width of epithelium 1.5-3

mm.
Grade IV Severe Overgrowth- Width of epithelium 3- 4 mm.

Seymour, Smith and Turnbill 1985

The degree of gingival thickening on both labial

and lingual aspects was graded as follows:
0 = normal;
1 = thickening from the normal up to2 mm;
2 = thickening from the normal greater than
2 mm

The extent of encroachment of

the gingival tissues onto the
adjacent crowns was also
graded 0, 1, 2 and 3 on the
labial and lingual surfaces are
also graded

The 2 scores (thickening and gingival encroachment were

added, thus giving a hyperplasia score for each gingival unit.

1ST THEORY
(Hassell 1981)
Different subpopulations of fibroblasts
Some of which are capable of high protein and
collagen synthesis
In presence of Phenytoin, the High activity fibroblasts
react and produce a significant increase in collagen
production
Higher concentration than peripheral or systemic
circulation

This theory has not been widely accepted

2nd THEORY
(Sorrell et al 1971)
Long-term
phenytoin
..
immunosuppression.
Tissues more susceptible to inflammation
But other anti-epileptic drugs though they have
immunosupressive action dont
cause gingival
overgrowth

Hence, this theory also has not been widely accepted

3rd THEORY
Staple 1951,1952
Phenytoin therapy is reported to cause an alteration in the
metabolism of adrenal gland secretions
Supression of ACTH and alteration in pituitary gland
activity
Reduced glucocorticoid synthesis and this has been
suggested a an explanation for the gingival overgrowth

Much consideration has been given to this hypothesis

4th THEORY
Waxman (1970)
Patients on phenytoin have low serum level of folic
acid
Drug may reduce the absorption from GIT or block its
transport across intestinal epithelium
Also inhibit folate reductase
A deficiency results in impaired maturation of
epithelium, rendering C.T. more susceptible to
inflammation
However, it has not been concluded that folic acid
supplements reduces or eliminates gingival overgrowth in
epileptics taking phenytoin

Immunosuppressants
Cyclosporin

 First isolated in Switzerland 1970 (Jean Borel)

Used first by Calne et al. A renal Transplant
Widely used now for prevention of graft rejection
Primary ..or in com with Steroids
Various diseases:
IDDM, Behcets disease. Rheumatic and psoriatic arthritis,
bullous pemphigoid and pemphigus, Crohns diseaseetc
Suppress some humoral immunity ( B lymphocytes) and to a
much greater extent, cell-mediated immunity (T lymphocyes)
such as allograft rejection, delayed hypersensitivity.
Inhibits IL-2 synthesis and release.
Dosages : 10-20mg/kg BW/day.Serum concentration of
100-400ng/ml

 Adverse effects :
Dose dependent & Frequently reversible
Gingival overgrowth
Nephrotoxicit & weight gain
Hyperension , Hyperuricaemia, Mild anaemia,
Neurotoxicity visual disturbances .. Hypertrichosis.
Tacrolimus adv effects to lesser extent
(Graffenreid and Krupp;1986)

Incidence
25% of renal transplant cases
38% cardiac transplants
37%... Liver transplants

 First casesof CIGORateitschak-Pluss (1983)

50 RT cases..developed GE in 4-6 weeks
1984 : Tyldesley & Rotter
36 RT cases
1986 : Friskopp & Klintmalm restricted to keratinised
gingiva..but could extend coronally
Absence in edentulous areas
More Hyperaemic than PIGO
1986 : Rostock et alspontaneous repositioning of
migrated teeth
1987 : Seymour et al..24 RT patients on Cyclosporin A &
Azathioprine
Significant growth in 3-6 months..
1988, 1994( Hefti et al.) 400ng/ml
Synergistic effects have been reported .+ calcium
channel blockers.
Slavin and Taylor 1987

Calcium Channel blockers

 Management of cardiovascular conditions ..1978

Hypertension , Angina, : coronary artery spasm, cardiac
arrythemias
Inhibit Ca ion across the cell membrane of cardiac &
smooth muscles
Dilatation of coronary arteries
Decreased mycardial contractility & oxygen demand
1984..first reported caseNIFEDIPINE
Amlodipine, Felodipine, Diltiazem, Nitrendipine and
Verapamil
Dose dependency
Rat model (800ng/ml).. Nishikawa et al. 1995
Human studies..not supportedtrough or threshold
should precede

 Ellis & Seymour 1993 :

Nifedipine in GCF.. Respondersand Non responders.
Incidence: 15% - 84%...42.5%
Not found in edentulous areas
around implants??..Silverstein et al 1995

Dissimilar drugs similar effects??

MOA at the cellular level
Influence the Ca and Na influx

(Mesing 1985, Gelfand 1987).

This regulates the rate of fibroblast proliferation.

The action of various drugs on the Ca and Na influx may
provide a unifying hypothesis linking the three dissimilar
drugs to a common unwanted effect.

SEX HORMONES AND ORAL CONTRACEPTIVES

Most widely used.
Mostly a combined preparation of estrogen and progesterone.
Resolves when drug is withdrawn.
Appears to be a secondary reaction to the presence of local
factors.
Estrogen increases the keratinization of already keratinized
tissues.
Mucosal tissues are thickened

 Tendency to overgrowth and inc activity of epithelial cells.

In non-epi tissue, inc in mucopolysaccharide content is
observed.
Progesterone increases the permeability of the gingival
vasculature.
Exacerbate the response, thus optimal plaque control is
imperative.

The Factors Playing A Role In The Pathogenesis O

1. Age.
2. Genetic predisposition.
3. Pharmacokinetic variables.
4. Drug induced alterations in Ging C.T.
homeostasis.
5. Drug induced action on growth factors.

Age
Children and adolescents more susceptible.
Fibroblasts obtained from both Cyclosporin and phenytoininduced gingival overgrowth cases failed to show an agedependent decrease in protein synthesis and collagen
production
Unique fibroblast phenotype
Influence of androgen metabolism.
"Target" sub-populations of gingival fibroblasts and cause
either an increase in collagen synthesis and/or a decrease
in collagenase activity.

Genetic predisposition
Not all Patients manifest Gingival overgrowth
Responders and non-responders
Gingival fibroblasts exhibit functional Heterogeneity
There exists diff subpopulations of fibroblasts
A genetic predisposition :
Metabolism of the 3 drugs Hepatic cytochrome
P450.
Phenytoin CYP 2C9
Dihydropyridines & Cyclosporin CYP3A4
Cyt P 450 exhibits considerable polymorphism

 Human Lymphocyte Antigen (HLA)

Relationship between HLA expression and incidence of
DIGO (Cebecci 1996a, Margiotta 1996, Pernu 1994, Thomasson
1996).

HLA-DR1 and HLA-DR2.

HLA-DR1 afforded some degree of protection against
gingival overgrowth
HLA-DR2 may increase the development of this
unwanted effect.

Pharmacokinetic variables
Its a Contentious issue .
Threshold level.. activate fibroblasts
Salivary concentration both positive and negative
correlation
Conflicting results because dental plaque could
act as a reservoir for the drug which is released by the
washing effect of the salivary flow.
GCF
Nifedipine and amlodipine has shown significant
sequestration in GCF in pts with DIGO (Ellis 1992, Seymour
1994).

Concomitant Medication
Polypharmacy has been studied with phenytoin and
cyclosporin Induced GO
Incidence, Severity and Recurrence rate is higher..
(Bokenkamp 1994, Margiotta 1996)

Prednisolone and Azathioprine generally given in such pts

could influence the expression of overgrowth

Drug induced alterations in gingival

CT. Homeostasis
Increase in CT essential feature of all
Collagen production / Collagen metabolism
Collagen production controlled by co-ordination of
transcripted and post transplantation collagen regulatory
mechanisms,
Intracellular degradation.
Controlled by synthesis and release of MMPs and TIMPs
Histometric analysis
Increase in the normal growth,
(ratio
remaining
unaltered
unlike
hyperplasia
or
hypertrophy).
Increases the level of translatable collagen RNA.
Overproduction of collagen involves increased steady state level
of mRNA and not a decrease in collagen degradation

 Cell culture studies have shown that the

ECM from PIGO fibroblasts facilitates FIBROBLAST
SPREADING. prostanoid in origin.
Both Nifedipine and Phenytoin alter the expression of Type
I and IV collagen genes.
CsA induced GO is related to an increase in Type I
procollagen mRNA, indicating increased secretion
A membrane receptor or CYCLOPHILIN, a cytosolic
protein which has been identified as a cellular receptor
for Cyclosporin

Non-Collagenous Matrix
Prolonged
phenytoin
show
increased
levels
of
Hexosamine, uronic acid and total protein per wet weight
of tissue
Increased amounts
( Hassel 1983)

to

sulphated

glycosaminoglycans

Alterations in CT. Metabolism

1980 Goultch & Shoskan :
PIGO was because of lack of collagen breakdown
inactive collagenase
1998 Zebrowski :
Proved them wrong as the drugs show variable action
against all 3 drugs in different patients.
Collagenase activity was increased by nifedipine,
decreased by phenytoin and unaltered by cyclosporin
2000 Tipton and Dabbous:
Concluded that the drugs regulate TIMP production
which is probably more significant than a decrease in
collagenase activity

Role of Cytokines
IL-1, IL-6 may play a role in the fibrogenic responses of
the gingiva to these medications
IL-6 appears to target connective tissue cells such as
fibroblasts both by enhancing proliferation and by exerting
a positive regulation on collagen and glycosaminoglycan
synthesis.

Role of MMP Synthesis & Function

Human gingival fibroblasts treated with clinically relevant
CsA doses exhibit significantly reduced levels of MMP-1
and MMP-3 secretion;
These reduced levels may contribute to the accumulation
of extracellular matrix components

Drug induced action on Growth

Factors
EGF and PDGF have gained significance. ..

Modeer 1990

Phenytoin may cause increase in number of cell surface

receptors of EGF,
May cause an alteration of Ging connective tissue
homeostasis, mediated by the action of drug on intra
cellular Ca accumulations
Values for PDGF were significantly higher for phenytoin
exposed cells

TGF beta1
TGF Beta 1 most prominent cytokine in mammals. TGF stimulates ECM deposition, by
Promoting Matrix synthesis, and
Inhibiting
enzymatic
degradation
of
matrix
macromolecules.
TGF - has been implicated in a variety of diseases like
pulmonary fibrosis, renal fibrosis and ore recently Gingival
fibromatosis
Endothelin is amplified by CsA .. synthesis and
activation of TGF - 1.

Other Postulates..
Jyoti Das (2001)
Dramatic increase in the keratinocyte growth factor
(KGF) among the epithelial cells in all types of DIGO
thus suggesting the role of KGF in the pathogenesis
Pernu 2002
Points that the drug starts to accumulate in the
keratinocyte which then increases the mitotic activity .
Modeer 1992
Phenytoin results in up regulation of PgE2 which could
cause an increase in GAG synthesis.

Enlargements associated with

Systemic Diseases

Mechanisms
1. Magnification of an existing inflammation..
Conditioned Enlargements
2. Manifestation of systemic disease independent of the
gingival inflammatory status
Systemic disease causing gingival enlargement
Neoplastic enlargements

Conditioned Enlargements
Exaggeration or Distortion of gingival response to plaque
Bacterial Plaque is necessary for initiation.not sole
determinant
3 types
Hormonal
Pregnancy
Puberty
Nutritional
Vitamin c deficiency

Enlargement in Pregnancy
May
be
marginal
and
generalized, Single or multiple
tumor-like masses
Progesterone and Estrogen
These hormonal changes induce
changes in vascular permeability
leading to gingival edema and an
increased inflammatory response
to dental plaque
The subgingival microbiota may
also undergo changes, including an
increase in Prevotella intermedia

(Kornmann K.S. 1980)

Marginal enlargement in pregnancy

Aggravation of previous inflammation
Incidence has been reported as 10% and 70%

(Barclay S. 1992).

Clinical Picture
Varies considerably
Generalized and more prominent interproximally than
on the facial and lingual surfaces
Enlarged gingiva is bright red or magenta, soft, and
friable and has a smooth, shiny surface.
Bleeding occurs spontaneously or on slight provocation

Tumor like gingival enlargement

Not a Neoplasm; it is an inflammatory response to
bacterial plaque
Modified by the patient's condition
Usually appears after the third month of pregnancy
Reported incidence is 1.8% to 5%.

(Maier AW 1949)

Lesion appears as a
Discrete
Mushroom like,
Flattened spherical mass
Protrudes from the gingival margin or more
commonly from the interproximal space and is
attached by a sessile or pedunculated base

 Generally dusky red or magenta, it has a smooth,

glistening surface that often exhibits numerous deep
red, pinpoint markings
Superficial lesion
Consistency varies; the mass is usually semi firm
Usually painless

Histopathology
Central mass of connective tissue,
Newly formed, and engorged capillaries lined by
cuboid endothelial cells
With varying degrees of edema and chronic
inflammatory infiltrate
Stratified
squamous
epithelium is thickened,
with prominent rete pegs
degree
of
Some
intracellular
and
extracellular
edema,
prominent
intercellular
bridges, and leukocytic
infiltration

Enlargement in Puberty
Both male and female adolescents
Appears in areas of plaque accumulation
Often only the facial gingivae are enlarged with lingual
surfaces are relatively unaltered becausemechanical
action of tongue
Similar to chronic inflam..degree.recurrences.
After puberty, the enlargement undergoes spontaneous
reduction but does not disappear until plaque and calculus
are removed

 Sutcliffe P. 1972Mean no. of sites time ..max sites

Oral hygiene.. A pubertal peak in gingival
inflammation that was unrelated to oral hygiene factors
occurred.

Mobelli 1990 . Capnocytophaga sp. in the initiation

of pubertal gingivitis
Other studies.. Hormonal changes
Increase in the proportion of Prevotella intermedia
and Prevotella nigrescens.

Enlargement in Vitamin C
Deficiency
Classic description of scurvy
Such enlargement is essentially a conditioned response
to bacterial plaque
Acute vitamin C deficiency
Causes hemorrhage, collagen degeneration, and
edema of the gingival connective tissue
Modify the response of the gingiva to plaque :
Normal defensive delimiting reaction is inhibited,
Extent of the inflammation is exaggerated
(Glickman 1948).

Possible etiologies..
1. Low levels of vitamin C influence the metabolism of collagen
within the gingiva and periodontium affecting tissue to
regenerative and repair.
2. Deficiency increases permeability of the oral mucosa to
bacterial endotoxin, inulin, dextran.epithelial barrier
function sub-optimum.
3. Optimal levels are needed to maintain integrity of periodontal
microvasculature and vascular response to bacterial irritation.
4. Depletion interfers
pathogenecity.

with

microbial

ecologyincreases

Clinical features
Marginal Gingival enlargement
The gingiva is bluish red, soft, and friable and has a
smooth, shiny surface
Hemorrhage occurring spontaneously or on slight provocation

Histologic features
Surface necrosis with pseudomembrane
Chronic inflammatory cellular infiltration and scattered areas
of hemorrhage, with engorged capillaries
Marked diffuse edema, collagen degeneration,
Scarcity of collagen fibrils or fibroblasts are striking findings

Plasma cell Gingivitis

Atypical gingivitis & Plasma cell gingivostomatitis
Consists of a mild marginal gingival enlargement that
extends to the attached gingiva
Allergic in origin
Plasma cell granulomaLocalised lesion (Baskar 1988)

Clinical features
Gingiva appears red, friable, and sometimes granular and
bleeds easily
No attachment loss usually
Located in the oral aspect of the attached gingiva..
An associated cheilitis and glossitis have been reported
Plasma cell gingivitis is thought to be allergic in origin.

 Spongiosis and infiltration with inflamm cells

Dense infiltrate of plasma cells in CT extending upto oral
epithelium

Nonspecific Conditioned Enlargement

Pyogenic Granuloma
Tumor-like gingival enlargement that is considered an
exaggerated conditioned response to minor trauma
The exact nature of the systemic conditioning factor has
not been identified
Clinical Features
Discrete
spherical,
tumor-like
mass
with
a
pedunculated attachment to a flattened, keloid-like
enlargement with a broad base
It involutes spontaneously to become a fibroepithelial
papilloma or persists relatively unchanged for years
Treatment consists of removal of the lesions plus the
elimination of irritating local factors
The recurrence rate is about 15%.

 Histologic features
Mass of granulation tissue with chronic inflammatory
cellular infiltrate
Endothelial proliferation
Formation of numerous vascular spaces

Inherited Gingival Overgrowth

Elephantiasis gingivae,
Hereditary gingival hyperplasia,
Idiopathic fibromatosis and
Hypertrophied

Rare (1 in 750,000) hereditary condition characterized by

slow, progressive enlargement of the gingivae.
Inheritance mode Autosomal Dominant

 May occur alone

abnormalities,

or

in

conjunction

with

other

As part of a syndrome,
Hypertrichosis and epilepsy,
With or without mental retardation.

Studies have found that gingival fibroblasts cultured from affected

individuals generally produce higher levels of TGF-b1, have higher rates of
proliferation, and respond to TGF-beta1 by making increased levels of
extracellular matrix.

Systemic Diseases Causing Gingival

Enlargement

Leukaemia
Diffuse or marginal, localized or generalized
An oversized extension of the marginal gingiva or Discrete
tumor like inter-proximal mass
Generally bluish red and has a shiny surface
Moderately firm, but there is a tendency toward
friability and hemorrhage
Occurring either spontaneously or on slight irritation
Associated chronic inflammation
True leukemic enlargement occurs commonly in acute
lukemia but may also be seen in subacute leukemia

Histologic features
Varying degree of chronic inflammation + mature
leukocytes
Areas of CT infiltrated with immature and proliferating
leukocytes
Engorged capillaries edematous and degenerated CT.

Granulomatous Disease

Wegener's Granulomatosis
Rare disease characterized by acute granulomatous
necrotizing lesions of the respiratory Tact, including
nasal and oral defects
Cause .. Not knownimmunologically mediated tissue
injury.
Clinical features
Reddish purple and bleeds easily on stimulation

Sarcoidosis
Granulomatous disease of unknown etiology
Starts in individuals in their twenties or thirties
Affects predominantly blacks and can involve almost any
organ
In gingiva - red, smooth, painless enlargement may appear
Discrete , noncaseating whorls of epithelioid cells and
multinucleated giant cells.

Neoplastic enlargement
Gingival Tumors
Benign
Fibroma
Papilloma
Peripheral Giant Cell Granuloma
Central Giant Cell Granuloma
Other
Nevus
Myoblastoma
Hemangioma
Neurilemoma
Neurofibroma
Mucoceles
Ameloblastoma

 Malignant Tumors of the Gingiva

Carcinoma
Squamous cell carcinoma
Malignant Melanoma
Sarcoma
Fibrosarcoma
Lymphosarcoma
Reticulum cell sarcoma
Kaposis sarcoma

False Enlargements
Not true enlargements of the gingival tissues
Appear as such as a result of increases in size of the
underlying osseous or dental tissues.
The gingiva usually presents with no abnormal clinical
features except the massive increase in size of the
area.
Underlying Osseous Lesions
Examples - Tori and exostoses, Paget's disease, Fibrous
dysplasia, Cherubism, Ameloblastoma
Underlying Dental Tissues
Examples - Developmental
primary dentition

enlargements

seen

in

TREATMENT
Treatment of gingival enlargement based on
understanding of the cause and underlying pathology
changes.

Chronic Inflammatory enlargement

Scaling and root planing

Fibrotic component that does not

undergoes shrinkage after scaling and
root planing
Surgical removal is the treatment of choice.

Two techniques available Gingivectomy

Flap operation

Soft and friable even after

SRP gingivectomy is the
treatment of choice.
If
all attached gingiva
creating
mucogingival
problem flap operation is
indicated

Abscesses
Acute Periodontal Abscess
Patients general systemic response should be evaluated
Rise in temperature fever and feeling of malaise should be
noted and proper antibiotic regime started
Drainage established through the pocket or through
external incision

Gingival Abscess
Drainage
Warm saline gargles
If residual size too great remove surgically.

Treatment of chronic periodontal abscess

Adequate drainage, antibiotic treatment

Drug associated gingival enlargement

First, consideration should be given to the possibility of
discontinuing the drug or changing the medication
Substitution with suitable alternative
1 to 8 weeks for resolution of gingival lesions.
Unfortunately, not all patients respond to this mode of
treatment, especially those with longstanding gingival
lesions.
Phenytoin: lomatrigine, gabapentin, sulthiame, and topiramate
Nifedipine: vasodilators, isradipine,
CsA : Tacrolimus (FK506)

 Second, the clinical should emphasize plaque control as

the first step in the treatment of drug induce enlargement
Third, if gingival enlargement persists after consideration
of the above mentioned approaches, the cases need to be
treated by surgery i.e., gingivectomy or periodontal
flap.

3 modes of surgical approach

Conventional technique
Gingivectomy Knives
Scalpel
Electrosurgery
Lasers

Treatment of leukemic gingival

enlargement
Mostly with Acute / Subacute cases rarely with chronic
Consultation with patients Physician and Hematologist
Superficial Scaling in localized area under topical
anaesthesia management of bleeding
Progressive deeper scaling is done in subsequent visits.
Systemic antibiotic coverage

Treatment of gingival enlargement in

pregnancy
Elimination of all local irritants.
Marginal and interdental inflammation are treated by
scaling and curettage
Treatment of tumor like gingival enlargement consists
of surgical excision and SRP.
Lesion should be removed surgical during pregnancy only
if they interfere with mastication or produce aesthetic
disfigurement that the patient wishes removed.

Recurrence of gingival enlargement

Most common problem in the management of gingival
enlargement.
Residual local irritation, systemic or hereditary or
causative factors for recurrence
Recurrence during healing period is manifested as red bead
like granulomatus masses that bleed on slight provocation
Condition is corrected by removing the granulation tissue
and SRP.
Familial or hereditary gingival enlargement recurs even if
all local factors have been removed.

Hi Doc, Remember me ??

Summary & Conclusion

References
Textbook of Clinical Periodontology- Fermin A. Carranza: 8 th-9th
edition
Textbook of Clinical Periodontology and Implantology Jan.Lindhe 4th edition
Contemporary Periodontics - Genco, Goldman, Cohen.
Informational Paper Drug -Associated Gingival enlargement JP
2004
Connective tissue metabolism and Gingival overgrowth :
Trackman 2004
Risk factors associated with Gingival overgrowth-JCP 2000
The role of drugs in pathogenesis of gingival overgrowth ; A
collective review of current concepts: Perio 2000 1999
A clinical review of drug-induced overgrowths : Bartold M 1999
Pathogenesis of Drug Induced Gingival Overgrowth- JCP 1996.