Gingival enlargement10615

 Increase in size of gingiva
 Common feature of gingival disease
 Also called Gingival Overgrowth
 “Hypertrophic gingivitis” and “Gingival
hyperplasia” are misnomer and should be
avoided
6/1/2015Dr Saif Khan

I. Inflammatory Enlargement
A. Chronic
B. Acute
II. Drug- induced Enlargement
III. Enlargement associated with Systemic
disease or conditions
A. Conditioned Enlargement
1. Pregnancy
2.Puberty
3. Vitamin C Deficiency

4. Plasma cell ginivitis
5. Nonspecific Conditioned
Enlargement(Pyogenic granuloma)
B.Systemic diseases causing gingival
enlargement
1. Leukemia
2. Granulamatous diseases (eg. Wegener’s
granulomatosis, sarcoidosis)
IV. Neoplastic enlargement
A. Benign
B. Malignant

 Localised: limited to the gingiva adjacent to single
or group of teeth
 Generalised: Involving gingiva throughout the
mouth
 Marginal: Confined to marginal gingiva
 Pappilary: Confined to interdental pappila
 Diffuse: Involving the marginal and attached
gingivae and pappilae.
 Discrete: An isolated sessile or pedunclated,
tumorlike enlargement

 Grade 0: No signs of gingival enlargement.
 Grade I : Enlargement confined to
interdental pappila.
 Grade II: Enlargement involves pappila and
marginal gingiva
 Grade III: Enlargement covers three quarter
or more of the crown

 Result from chronic or acute inflammatory
changes.
 Chronic enlargement are more common
 As secondary complication to any other type
of enlargement creating
‘combined enlargenent”

C/F:
 Slight balooning of interdental pappila or
marginal gingiva
 In early stages; life preserver bulge around
involved tooth
 This bulge can increase in size and cover whole
of the crown
 Localised/generalised or sessile/pedunclated

 Progresses slowly and painlessly unless
complicated by acute infection or trauma
 May undergo spontaneous reduction in size
followed by exacerbation or continued
enlargement.
 Painful ulceration can occur between the
overgrowth and adjacent gingiva

 Chronic inflammatory GE show exudative and
proliferative features of chronic inflammation
 Clinically Deep Red or Bluish Red are soft and
Friable
 Smooth and shiny surface and are
hemorrhagic
 Predominance of inflammatory cells and fluid
with vascular engorgement

 Also associated degenerative changes
are seen
 Lesions that are firm and resilient have
greater fibrotic component with
abundant fibroblasts and collagen
fibres.

 Prolonged exposure to dental plaque
 Factors favouring dental plaque accumulation ;
poor oral hygiene, anatomic abnormalities,
improper restorative or orthodontic appliances
 Gingivitis and gingival enlargement are seen in
mouth breathers
 The maxillary anterior region is common site of
involvement.
 Surface dehydration has been produced as a
possible cause.

Gingival abscess:
Etiology: when a foreign body such as toothbrush
bristle, piece of apple, lobster shell fragment
forcefully implants bacteria into the gingiva
Clinical features
 localised, painful rapidly expanding lesion of sudden
onset
 Limited to marginal gingiva or interdental pappila
 Initially appears as red swelling and smooth, shiny
surface
 Within 24-48 hrs lesion becomes fluctuant and
pointed with surface orifice from which purulent
exudate can be expressed

Histopathology of Gingival A bscess;
Purulent focus of connective tissue surrounded by a
diffuse infiltration of PMNs, edematous tissue and
vascular enlargement
Surface epithelium has varying degree of
intravascular and extravascular edema, leukocyte
invasion and sometimes ulceration

 Side effects of some anticonvulsants,
Immunosuppressant and antihypertensives
 Clinical and microscopic features of the
enlargements caused by different drug are
similar.
 Painless beadlike enlargement of the
interdental pappila is seen which extends to
facial and lingual aspect
 The marginal and pappillary segment unite
ultimately leading to massive fold tissue
covering a considerable portion of crown and
interfering with occlusion

 Lesions are mulberry shaped, firm, pale pink and
resilient with a minutely lobulated surface and
seldom bleed when uncomplicated by inflammation
 Enlargement characteristically projects from
beneath gingival margin from which it is separated
by linear groove
 This enlargement can become secondary inflammed
due plaque accumulation
 Secondary inflammation not only leads to increase
in size of the enlargement but also produces red or
bluish discoloration, obliterate the the lobulated
surface demarcations and increase bleeding
tendency

 The enlargement is usually generalised
throughout the mouth but is more severe in
maxillary and mandibular anterior regions
 Gingival enlargement is seen in the area where
teeth are present and disappears in the area
where teeth are extracted
 Drug-induced gingival enlargement can occur in
mouths with little or no plaque and may be
absent in mouths with abundant deposits
 Suggesting a genetic predisposition to its
occurence

 Pronounced hyperplasia of the connective tisuue and
epithelium is seen
 Acanthosis of the epithelium along with elongated rete
pegs extending deeply into connective tissue
 Densely arranged collagen bundles
 Increase in number of fibroblasts and blood vessel
 Increased Amorphous ground substance
 Structural changes in outer epithelium is seen in outer
epithelial surface in cyclosporine- induced ginigval
enlargements
 Cyclosporine induced gingival enlargements have a
more highly vascularised connective tissue with foci of
chronic inflammation, particularly plasma cells

 First drug induced gingival enlargement
was reported in Phenytoin(Dilantin)
 Other drugs also known to produce GE are
Ethotoin, mephenytoin,Succinimides,
methsuximides and valproic acid
 Gingival enlargement occurs in about 50%
of patients receiving the drug although
incidences range from 3% to 84.5%
 It occurs more often younger patients
 Its occurrence and severity are not related
to dosage after threshold level have been
exceeded

 Tissue-culture experiments have shown that
phenytoin stimulates proliferation of
fibroblast like cells
 Analogs of phenytoin (1-allyl-5-
phenylhydantoinate and 5-methyl-5-
phenylhydantoinate) have similar effects on
fibroblasts like cells
 Fibroblasts from phenytoin induced gingival
overgrowth show increased synthesis of
sulfated glycosaminoglycans in vitro
 Phenytoin may induce decreased collagen
degradation as result of production of
inactive fibroblastic collagenase

 Cyclosporine is a potent immunosuppressive
agent used to prevent organ transport
rejection and to treat autoimmune disease
 It selectively and reversibly inhibits helper T-
cells which play role in humoral and cellular
immunity
 Cyclosporine A is administered IV or PO
 Dosage more than 500mg/day have shown to
induce gingival overgrowth
 GE is more vascularised than that of
phenytoin

 Occurrence varies 25%-75%
 Affects children more frequently
 Magnitude is more related to to plasma concentration
than to periodontal status
 Microscopic finding show many plasma cells and
abundant amorphous extracellular substance
suggesting hypersensitivity reaction to cyclosporine
 Other sideeffects of cyclosporine are nephrotoxicity,
hypertension and hypertrichosis
 Another immunosuppressive drug Tacrolimus also
causes gingival overgrowth

 Treatment of HTN,Angina pectoris,
coronary artery spasm, cardiac arythmias
 Induce direct vasodilation of coronary
arteries and arterioles, improving oxygen
supply to the heart muscles and also reduces
hypertension by dilating peripheral
vasculature
 They are classified
 Dihydropyridine derivatives(amlodipine,
nifedipine)
 Benzothiazine derivative derivatives (diltiazem)
 Phenlylalkylamine (verapamil)

 Nifedipine induces gingival enlargement in
20% of patients
 Diltiazem, Felodipine, nitrendipine, and
verapamil also induces gingival enlargement
 Nifedipine is used with cyclosporin in organ
transplant patients and combined use
produces larger gingival overgrowths

 Also called Gingivamatosis, Idiopathic
fibromatosis, Hereditary gingival
Hyperplasia and Congenital familial
fibromatosis
 Enlargement affects attached as well as
marginal gingiva and interdental pappilae
 Facial and lingual surface of mandible and
maxilla are affected but enlargement can be
limited to either jaw
 GE presents as pink, firm and leathery in
consistency and has characteristic minutely
pebbled surface
 In severe cases the teeth are almost covered
and enlargement projects into oral vestibule

Histopathology:
There is bulbous increase in the amount of
connective tissue which is relatively
avascular and consists of densely arranged
collagen bundles and numerous fibroblasts.
The surface epithelium is thickened and
acanthotic.
Etiology: unknown (idiopathic)
mode of inheritance AR and AD
The enlargement begins with eruption of primary
or secondary dentition and may regress after
extraction suggesting teeth or plaque attached
to it as intiating factor

 Syndrome
characterized by
gingival hyperplasia,
increased growth of
hair, epilepsy and
mental retardation
 Autosomal dominant

 Magnification of an existing inflammation
initiated by dental plaque included in
“Conditioned enlargement”
 Manifestation of the systemic disease
independently of the inflammatory status
of the gingiva

 Occurs when systemic condition exaggerates
or distorts the usual gingival response to
dental plaque
 Bacterial plaque is necessary for the
initiation of this type of enlargement but it is
not the sole determinant of the nature of the
clinical features
 The three types of enlargements are
1. Hormonal (pregnancy, puberty)
2. Nutritional (vitamin C def )
3. Allergic (nonspecific GE)

 In pregnancy there is increase in the level
of progesterone and estrogen and by the
end of third trimester reach 10 and 30
times the levels during menstrual cycle
respectively
 These hormone changes induce changes is
vascular permeablity,leading to gingival
edema and increase inflammatory
response to dental plaque
 There is change in subgingival microbiota
leading to increase in Prevotell intermedia

 Results from aggravation of previous
inflammation
 Enlargement is usually generalised and
tends to be more prominent interproximally
than on facial or lingual surface
 Enlarged gingiva is bright red or magenta
in color, soft and friable and has smooth and
shiny surface.
 Bleeding occurs on slightest provocation

 Also called Pregnancy tumor
 Smooth glistening surface having
numerous deep red pinpoint markings
 Inflammatory response to dental plaque
modified by patient’s condition
 Occurs after 3rd month of pregnancy or
earlier and incidence is 1.8% to 5%

 Lesion appears as discrete, mushroom like
flattened spherical mass that protrudes
from gingival margin or interproximal space
and attached by sessile or pedunclated
base.
 It tends to expand laterally and pressure
from the tongue and cheek gives its
flattened appearance
 lesion is superficial usually and does not
invade underlying bone

 The mass is usually semifirm but has various
degree of softness and friability
 Usually painless unless its shape and size
foster accumulation of debris under its
margin or interfere with occlusion
Histopathology:
Gingival enlargement in pregnancy is
Angiogranuloma

 Involve Marginal and interdental gingivae
and characterized by prominent bulbous
interproximal papilla
 Often facial gingiva are enlarged and
lingual are spared
 Tendency to develop massive recurrence in
the presence of relatively scant plaque
deposits distinguishes pubertal gingival
enlargement from uncomplicated chronic
gingival enlargement

 Acute vitamin C deficiency itself does not
cause gingival inflammation but causes
hemorrhage,collagen destruction and
edema of connective tissue
 Gingival Enlargement in scurvy is marginal,
gingiva is bluish red, soft, and friable and has
smooth shiny surface
 Hemorrhage can occur spontaneously or on
slightest provocation

 Surface necrosis with pseudomembrane
are common feature
 Histopathologically the gingiva has a
chronic inflammatory cellular infiltration
with superficial acute response
 There are scattered areas of hemorrhage and
engorged capillaries
 Marked diffuse edema, collagen
degeneration and scarcity of collagen
fibrils or fibroblasts are striking findings

 Also called atypical gingivitis or plasma cell
gingivitis
 Consists of mild marginal gingival
enlargement that extends to the attached
gingiva
 Gingiva appears red, friable, sometimes
granular and bleeds easily
 There is no loss of attachment
 The lesion is located in the oral aspect of
the attached gingiva and therefore differs
from plaque induced gingivitis

Histopathology:
 Epithelium shows spongiosis and
inflammatory cells inflitration
 Ultrastucturally there is damage in the lower
spinous and basal cell layers
 Connective tissue contains dense infiltrate
of plasma cells which extends to oral
epithelium inducing dissecting type injury
Plasma cell gingivitis is thought to be of
allergic origin caused due to some
ingredients of chewing gum, dentrifices and
diet

 Pyogenic granuloma is tumour like
enlargement which is an exagerrated
conditioned response to minor trauma
 Lesion varies from discrete spherical, tumour
like mass with a pedunclated attachment to a
flattened keloid like enlargement with abroad
base
 Bright red or purple in color, friable or firm
depending on its duration
 In majority of cases it presents with surface
ulceration and purulent exudation

The lesions either involutes spontaneously
or becomes fibroepithelial papilloma and
persists for years
Histopathology:
 Consists of mass of granulation tissue with
chronic inflammatory infiltration
 Endothelial proliferation and formation of
numerous vascular spaces
 Surface epithelium is atrophic in some
areas and hyperplastic in other
 Surface ulceration and exudation are common
feature

 Recurrence rate
;15%.
 Similar in clinical
appearance to the
conditioned
enlargement seen
in pregnancy

1.leukemia:
AML
CML
2.Granulamatous diseases:
Wegener granulomatosis
sarcoidodis

1. Benign tumours
Fibroma
papilloma
peripheral giant cell granuloma
central giant cell granuloma
leukoplakia
Gingival cyst
2. Malignant tumours
Carcinoma
Malignant melanoma

False enlargements are not true enlargements
of gingival tissue but may appear as such as
a result of increase in size of underlying
osseous or dental tissue
Underlying osseous tissue
Eg. Tori and exostoses
Underlying dental tissue
eg: various stages of eruption due to bulge of
crown.

Gingival enlargement10615

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