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TRANSCRIPT
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GINGIVAL
ENLARGEMENT
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CONTENTS
INTRODUCTION
CLASSIFICATION
ETIOLOGY
CLINICAL FEATURES
DIFFERENTIAL DIAGNOSIS
MANAGEMENT
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INTRODUCTION GINGIVA:-
It is defined as that part of oral
mucous membrane that covers the alveolar
bone and surrounds the necks of all the
teeth.
gingiva can be divided into
1.marginal
2.interdental .
3.attached
NORMAL CHARACTERISTICS OF HEALTHY
GINGIVA
1.colour:-colour is coral pink and may vary as
darker in people with darker complexions.
2.contour/shape:-shape of free gingiva is knife
edged &closely adapted to tooth surface.
3.consistency:-firm in consistency.
4.Surface texture:-free gingiva is smooth in
texture. Attached gingiva exhibits surface
stippling.
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5.size:-free gingiva is flat& fits snugly around
the teeth.
GINGIVAL ENLARGEMENT
DEFINITION:-
It is defined as increase in size of gingiva so
that soft tissue overfills the interproximal
spaces, balloons out over the teeth
&protrudes into the oral cavity.
CAUSES:-
1.poor oral hygiene.
2.food impaction.
3.mouth breathing.
4.harmonal changes.
5.drug therapy.
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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
3). Vitamin C4). Plasma cell gingivitis
5). Nonspecific conditioned enlargement
B). Systemic diseases causing gingival
enlargement
1). Leukemia
2). Granulomatous diseases (Wegeners
granulomatosis, sarcodiosis)
IV) Neoplastic enlargement
A). Benign tumors
B). Malignant tumors
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a se en argemen
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 thecanine region
B). Generalized involving the gingiva
throughout the mouth.
C). Diffuse; Involving the marginal and attached
gingiva and papillae
D). Papillary: Confined to the interdental papilla
E).Marginal: confined to marginal papilla.
f).Discrete: an isolated tumour like enlargement
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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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
Clinical features :
y
Site - interdental, marginal, attachedgingiva
y Shape - slight ballooning to life
preserver shaped bulge
y slow progressing and painless
y painful ulceration sometimes
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cu e n amma ory en argemen -
Gingival abscess
Etiology:
y Bacteria carried deep into the tissues
by toothbrush bristles, piece of apple
coat etc.
Clinical features:
y site - marginal and interdental gingiva
y localized, painful, rapidly expanding.
y Within 24 to 28 hrs lesion becomesfluctuant & purulent exudate
expressed as surface orifice &
rupture spontaneously
DRUG INDUCED GINGIVAL
ENLARGEMENT.
Anticonvulsants
Immunosuppressant's
Calcium channel blockers
affects the speech, mastication, tooth
eruption, and aesthetics problems
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General clinical features:
y site - interdental papilla, facial and lingual
gingival margins
y Starts as a bead massive tissue fold
covering the crown.
y mulberry shaped , firm , pale pink,
resilient.
y no tendency to bleed.
yappears to project frombeneaththe
gingivalmarginseparated by alinear
groove.
y Plaque control becomes difficult.
secondary inflammation .
y red, bluish colored lobulated
demarcations, increased bleeding.
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1).Anticonvulsants
y First gingival enlargement reported
y Introduced by Merritt and Putnam in
1938.
y Drugs used for the treatment of
epilepsyy Phenytoin, ethotoin, mephenytoin,
succinimides etc.
y 50% of the patients
y younger patients more prone
y appears in saliva
y
in systemic administration acceleratesthe healing of gingival wounds in non-
epileptic humans.
MECHANISM
PHENYTOINstimulates fibroblast production of an
proliferation inactive fibroblastic
collagenase
gingival overgrowth
increase in the sulfated decrease in the
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g ycosam nog ycans n co agen egra a on
vitro.
2). Immunosuppressants
y Cyclosporine's used to prevent organ
transplant rejection & to treat
autoimmune origin
y if dosage > 500mg/day reported to
induce gingival enlargement.
y 30% patient.
y More vascularised
y associated with nephrotoxicity,
hypersensitivity, hypertension,
hyperthricosis.
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3).Calcium channel blockers
y used for CVS disorders, hypertension,
angina pectoris, coronary artery spasm
& cardiac arrhythmia.
y Drugs like nifedipine,diltiazem,
felodipine, nitrendipine and verapamil.
y Nifidipine induces enlargement in 20%
cases
y Nifidipine + cyclosporine (for kidney
transplant)
y larger overgrowth
y dose dependent growth
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Idiopathic gingival enlargement
y termed as gingivostomatitis,
elephantiasis, idiopathic fibromatosis,hereditary gingivalhyperplasia &
congenitalfamilialfibromatosis.
Etiology:-
y unknown
y
hereditary basis (autosomal dominant orrecessive)
y begins with primary & secondary
dentition eruption.
Clinical features:
y Site - attached gingiva, gingival margin,
and interdental papilla
y pink, firm and leathery with pebbled
appearance
y Severe cases jaw appears distorted due
to bulbous enlargement
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ENLARGEMENT ASSOCIATED WITH
SYSTEMIC DISEASES
y Many systemic diseases can develop
oral manifestations that may affect 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
secondary inflammation
2). Manifestation of systemic disease
independent of the inflammatory status of
the gingiva. This group described as
Systemic diseases causing gingivalenlargement
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Conditioned enlargement
y 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
A) Enlargement in pregnancyMarginal and generalized
y Etiology-
y increase in progesterone and
estrogen till 3rd trimester
y increased vascular permeability and
gingival edema.
Marginal enlargement
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n ca ea ures :-
y generalized and interproximal
y bright red, soft friable and
bleeds spontaneously.
B) Enlargement in Puberty
y In both male & female adolescents
y Clinical features :
y -marginal & interdental
y
-chronic gingival diseasey -reduces after puberty
y -Capnocytophagasp.. & P. intermedia
C)enlargementinVitaminCdeficiency
Clinical features :
y Marginal gingivitis
y hemorrhage on slight provocation
and surface necrosis with
pseudomembrane formation
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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
Non specific conditioned
enlargement (pyogenic
granuloma)
Tumor like gingival enlargement
conditioned response to minor trauma
Clinical features:
y discrete spherical tumor like mass
y pedunculated, keloid like
y red friable with ulceration
yfibro epithelial papilloma
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Systemic diseases causing
gingival enlargement :-
LeukemiaClinical features:y -diffuse or marginal
y localized or generalized tumor like
mass in interproximal spaces
y red, friable, firm and hemorrhagic
y
painful necrotizingy ulcerative inflammation
Granulomatous diseases :-
Wegeners granulomatosisEtiology: cause unknown (immunologically
mediated tissue injury)
y Characterized by acute granulomatous
necrotizing lesion of respiratory tract
involving the orofacial region
Clinical features:
y reddish purple bleeds easily.
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arco os s :-
Etiology:-
y unknown
y red, smooth, painless enlargement
NEOPLASTIC ENLARGEMENT (GINGIVALTUMORS) :-
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
y slow growing, firm, nodular, soft,
vascular, pedunculated.
2). Papilloma:
y proliferation of surface
epithelium associated with
human papilloma virus(HPV)
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y cau ower e pro u erances
broad, hard.
Human Papilloma Virus(HPV) :-
Histopathology:
y Finger like projections of stratified
squamous epithelium, often
hyperkeratotic.
yfibrovascular core.
3)Peripheral giant cell granuloma
Clinical features
y interdentally, gingival marginy pedunculated, smooth,
multilobulated,ulcerations
y painless, firm , spongy
locally invasive destroys underlying
bone
Central giant cell granuloma :-
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y w n e aw an pro uce cen ra
cavitations.
Leukoplakia
y
Defined as a white plaque that cannotbe 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.
Gingival cyst :-
y Localized, marginal& attached
mandibular canine & premolar areas
painless& erodes the bone
y Cyst developers from odontogenic
epithelium
2).Malignant tumors
Carcinomas
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y 3% of all malignant tumors in the body.
y squamous cell carcinoma- common.
clinical features :-
y Exophytic, irregular growth, ulcerative,
flat, erosive lesions.y symptomless initially then painful
invades the bone .
Malignant melanoma
y site - hard palate& maxillary gingiva
localized pigmentation
yflat or nodular
y rapid growth with early metastasisy arises from melanocytes from the
gingiva
Sarcoma
Fibrosarcoma, lymphosarcoma& reticulumcell sarcoma of gingiva
Kaposis sarcoma.
False enlargement :-
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Appear as a result of increase in size of
underlying osseous or dental tissues.
A.UNDERLYING OSSEOUS LESIONS:-
y
Enlargement of bone subjacent tothe gingival area occurs, most
often in tori & exostosis & can also
occur in pagets disease, fibrous-
dysplasia,cherubism,osteoma,ost
eos-arcoma.
B. Underlying dental tissues
y during stages of eruption
particularly primary dentition.
y labial gingiva may show a bulbousmarginal distortion.
This enlargement is called developmental
enlargement.
Syndromes associated with
gingival enlargement :-
1.Cross syndrome:- gingival enlargement,
hypopigmentation,
microopthalmos,
athetosis,
oligophrenia
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. u er or syn rome:- g ng va
enlargement ,corneal dystrophy.
3.Robinow syndrome:- gingival
enlargement, foetal face.
4.Sturge-webersyndrome:- gingival
angiomas , Enchephalofacial angoimatosis.
5.Cowdens syndrome:-generalized
papillomatosis.
6.Murray-Puretic- Dresher syndrome:-gingival fibromatosis with multiple fibromas.
DIFFERENTIAL DIAGNOSIS:-
1.Fibrotic gingival enlargement tissue is
firm,hard,fibrous in consistency.do not bled
readily.
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. umour e g ng va en argemen :- es ons ar
discrete mushroom like spherical masses with
deep red pinpoint margins.
3.Inflammatory gingival enlargement :- involved
tissues are glossy,smoth, oedematous and
bleed readily.
4.Idiopathic gingival enlargement :- gingiva is
pink ,firm,leatherywith pebbled appearance.
5.enlargement in pregnancy :-gingiva is bright
red,soft friable& bleeds spontaneously.
6.Enlargement in vitamin c deficiency :-gingivais bluish red,soft, shiny surface.
7.Non specific condiotioned enlargement:-
discrete spherical ,tumour like masseswith
pedunculated attachment.
8.Leukaemia :- lesions are red,friable,firm&necrotizing.
9.Wegners granulomatosis :-reddish purple
lesion.
10.Sarcoidosis :- lesion is smooth,red ,painless.
MANAGEMENT
1). CHRONIC INFLAMMATORY ENLARGEMENT
Enlargements which are soft ,discolored are
treated by scaling and root planning.
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n argemen s w c are rous are rea e y
surgical removal.
Surgical removal involves 2 techniques
1.GINGIVECTOMY.
2.FLAP OPERATION.
2).TUMORLIKE INFLAMMATORY
ENLARGEMENT :-
These are treated by gingivectomy as follows,
Local anaesthesia is given to the patient and
tooth surfaces beneath the mass arescaled toremove calculus and debris.
Lesion is separated from the mucosa at its
base with a number 12 bard parker blade.
The involved tooth surfaces are scaled &the
area is cleansed with warm water.
A periodontal pack is applied and removed
after a week.
3). PERIODONTAL ABSCESSES :-
These are treated by following steps,
1.Drianage through pocket retraction or
incision.
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.sca ng an roo p ann ng.
3.Periodontal surgery.
4.Systemic antibiotics.
5.Tooth removal.
4).GINGIVAL ABSCESSES :-
y Scaling and root planning leads to removal
of microbial deposits.
y In acute situations,flctuant area is incised
with a 15 scalpel blade,exudates isexpressed by gentle pressure.
y The area is irrigated with warm water and
covered with moist gauze
5).DRUG ASSOCIATED GINGIVALENLARGEMENT :-
y Primary consideration should be possibility
of discontinuing the drug or changing
medication.
ANTICONVULSANT ALTERNATIVE DRUG
Phenytoin Carbamazepine
Valproic acid
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CALCIUM CHANNEL ALTERNATIVE DRUG
BLOCKERS
Nifedipine Diltiazem
Verapamil
IMMUNOSUPPRESANTS ALTERNATIVE DRUG
Cyclosporine Tacrolimus
y Secondarily plaque control is emphasized.
y Tertiarily persisting gingival enlargements
are treated with gingivectomy and flap
surgery
y Recurrence of drug induced enlargement isseen in surgically treated cases.
y Chlorhexidine gluconate rinses,professional
cleanings can decrease the speed & degree
of recurrence.
LEUKAM IC GINGIVAL ENLARGEMENT :-
y Scaling and root planning under local
anesthesia.
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y n a rea men cons s s o remov ng a
loose accumulations with cotton pellets,
performing superficial scaling
y Progressively deeper scaling is carried
out at subsequent levels.
y
Antibiotics are administeredsystemically the evening before and for
48 hrs after each treatment to reduce
risk of infection.
GINGIVAL ENLARGEMENT IN
PREGNANCY:-
y Elimination of all local irritants.
y
Marginal and interdental gingivalenlargement are treated by scaling
and curettage.
y Good preventive dental programme
consisting of nutritional
counseling,plaque control measures.
y
Lesions should be removed surgicallyduring pregnancy only if they
interfere with mastication or it is
unaesthetic.
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GINGIVAL ENLARGEMENTS IN
PUBERTY :-
y Scaling and curettage.
y Removal of al sources of irritation
and controlling plaque.
y Anti microbial mouth
washes,antibiotic therapy in
severe cases.
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REFERENCE BOOKS
*BURKITTS ORAL MEDICINE
*CARRANZA-TEXTBOOK OF
PERIODONTOLOGY
*SHAFFERS ORAL PATHOLOGY
*CRISPY AND SCULLY
*INTERNET