gingival enlargements / dental implant courses

Gingival
Enlargement
 INDIAN DENTALACADEMY
 Leader in continuing Dental Education
www.indiandentalacademy.com

CONTENTS
 Classification
 Etiology
 Clinical Features
 Histopathology
 Treatment

Gingiva is the part of oral mucosa that covers
the alveolar process of the jaws and surrounds
the necks of the teeth.
 The gingiva is divided anatomically into 3
areas:
1. Marginal
2. Attached
3. Interdental

 Gingival enlargement - increase in size of the
gingiva-common feature of gingival disease
 Previously called - hypertrophic gingivitis or
gingival hyperplasia
 Current accepted terminology for this condition
is gingival enlargement or gingival overgrowth.

 The degree of gingival enlargement can be scored :
 Grade O : No signs of enlargement.
 Grade I :Enlargement confined to interdental papilla.
 Grade II : Involves papilla & marginal gingiva.
 Grade III : Covers three quarters / more of crown.
Bökenkamp A, et al (1994)

Classification
Inflammatory Enlargement
 Chronic
 Acute
Hyperplastic Reactive Lesions
Drug-induced Enlargement

Enlargements associated with
systemic diseases or conditions
A. Conditioned Enlargement
1.Pregnancy
2.Puberty
3.Vitamin C deficiency
4.Plasma cell gingivitis
B. Systemic diseases causing gingival
enlargement
1. Leukemia
2.Granulomatous disease

Neoplastic enlargements
 Benign tumors
 Malignant tumors
False enlargement

Inflammatory Enlargement

Chronic Inflammatory Enlargement
Etiology:
 Caused by prolonged exposure to dental plaque.
 Poor oral hygiene, irritation by anatomical
abnormalities and improper restorative &
orthodontic appliances may favor plaque
accumulation and retention.
Hirschfeld I (1932)

Clinical Features
 It originates as a slight ballooning of the interdental
papilla and marginal gingiva.
 In the early stages it produces a life preserver
shaped bulge around the involved teeth.
 This bulge can increase in size until it covers part of
the crowns.
 The enlargement may be localized / generalized &
progress slowly & painlessly, unless complicated by
acute infection / trauma.

 Occasionally occurs as a
discrete sessile/ pedunculated
mass resembling a tumor.
 It may be interproximal / marginal /attached
gingiva.
 The lesions are slowly growing masses and usually
painless.
 They may undergo spontaneous reduction in size,
followed by exacerbation & continued
enlargement.

Histopathology
 Have a preponderance of inflammatory cells &
fluid, with vascular engorgement, new capillary
formation, & associated degenerative changes.

Treatment
 Treated - scaling & root planning
 When a significant fibrotic component that does not
undergo shrinkage after scaling and root planing,
surgical removal is the choice of treatment.
 Two techniques
1. Gingivectomy
2. Flap Surgery

 Selection of the appropriate technique depends
on the size of the enlargement and character of
the tissue.
 When the enlarged gingiva remains soft and
friable even after scaling and root planing -
gingivectomy is done
 Tumor like inflammatory enlargements are
treated by gingivectomy.

 Root planing done under LA
 The lesion is separated from the mucosa at its base,
if the lesions extends interproximally, the interdental
gingiva is included in the incision to ensure exposure
of irritating root deposits
 After lesion is removed involved root surfaces are
scaled and planed & the area is cleaned with warm
water
 A periodontal pack is applied and removed after one
week.

Mouth Breathing
 Gingivitis and gingival enlargement are often seen in
mouth breathers.
Lite T, Dimaio DJ, Burman LR (1955)
 Gingiva appears red and edematous, with a diffuse
surface shininess of the exposed area.
 Maxillary anterior region is common site.
 Altered gingiva clearly demarcated from the adjacent
unexposed normal gingiva.

 The exact manner in which mouth breathing
affects gingival changes has not been
demonstrated.
 Its harmful effect is generally attributed to
irritation from surface dehydration.
 However, comparable changes could not be
produced by air-drying the
experimental animals.
Klingsberg J, et al (1961)

Hyperplastic Reactive
Lesions

Peripheral Giant Cell Granuloma
 In the past, giant cell lesions of the gingiva called as
“peripheral reparative giant cell tumors”.
 These lesions, however, are essentially responses to
local injury & are not neoplasms; and their reparative
nature has not been proved, they are now referred to
as peripheral giant cell granulomas.
 It is a hyperplastic reaction of the gingival connective
tissue in which their histiocytic & endothelial
components are predominant.

Clinical Features
 It is found in all age groups , slightly peak in adults
around 30 years & in children in mixed dention stage.
 More common in females , equally distributed in
mandible & maxilla.
 It can occur in both anterior & posterior region ,most
often found anterior to the molars.
 Occasionally found on the edentulous areas of
alveolar ridge.

 Giant cell lesions of the gingiva arise
interdentally / from gingival margin, occur most
frequently on the labial surface, & may be sessile /
pedunculated.
 They vary in appearance from smooth, regularly
outlined masses to irregularly shaped,
multilobulated protuberance with surface
indentations.
 The lesions are painless, vary
in size & may cover many teeth

 In some cases the giant cell granulomas of
the gingiva is locally invasive and causes
destruction of the underlying bone, complete
removal leads to uneventful recovery.

Pyogenic Granuloma
 It is fast-growing reactive proliferation of endothelial
cell commonly on the gingiva and usually in response
to chronic irritation.
 The exact nature of the systemic conditioning factor
has not been identified.
Kerr DA (1951)
 The lesion varies from a discrete spherical, tumorlike
mass with a pedunculated attachment to a flattened,
keloid like enlargement with a broad base.

 Trauma / introduction of foreign material into the
gingival sulcus may provide the stimulus for this
proliferative hyperplasia.
 Most often seen in the interdental papilla region.
 This lesion may extend from the buccal to the
lingual / palatal region ; most often limited to
either the buccal / facial surfaces.

 It is extremely vascular, appears as fiery red & will
show gray pseudomembrane over the surface,
secondary to ulceration of the overlying
epithelium
 Other locations like tongue, lips, & buccal
mucosa.

Histopathology
 It appears as a mass of granulation tissue with chronic
inflammatory cellular infiltration.
 Endothelial proliferation and the formation of
numerous vascular spaces are the prominent features.
 The surface epithelium is atrophic in some areas and
hyperplastic in others.
 Surface ulceration and exudation are common
features.

Treatment
 Consists of removal of the lesion plus the elimination of
irritating local factors.
 It is reactive hyperplasias , relatively high rate of
recurrence after simple excision.
 After surgical excision underlying tissue should be
thoroughly curetted & root planing should be done
 The recurrence rate is about 15%.
Bhaskar SN, Jacoway JR. (1966)

DRUG-INDUCED GINGIVAL
ENLARGEMENT

 Gingival enlargement is a well known
consequence of the administration of some
anticonvulsants, immuno-suppressants and
calcium channel blockers
 May create speech, mastication, tooth eruption
and aesthetic problems.

General Features
 The growth starts as a painless beadlike enlargement
of the interdental papilla and extends to the facial and
lingual margins.
 As the condition progresses, the marginal and papillary
enlargements unite; they may develop into a massive
tissue fold covering considerable portion of the crowns,
and they may interfere with occlusion.
 When uncomplicated by inflammation, the lesion is
mulberry shaped, firm, pale pink, and resilient, with a
minutely lobulated surface and no tendency to bleed.

 The enlargement characteristically appears to
project from beneath from the gingival margin,
from which it is separated by a linear groove.
 Presence of enlargement makes plaque control
difficult.
 The resultant enlargement then becomes a
combination of the increase in size caused by the
drug and the complicating inflammation caused
by the bacteria.

 Secondary inflammatory changes not only add to
the size of the lesion caused by drug, but also
produce a red / bluish red discoloration, obliterate
the lobulated surface demarcations, and increase
bleeding tendency.
 The enlargement is usually generalized
throughout the mouth but is more severe in the
maxillary & mandibular anterior regions.
 It occurs in areas in which teeth are present, but
not in edentulous spaces, and the enlargement
disappear in areas from where teeth are extracted.

 Drug-induced enlargement may occur in mouths
little or no plaque and may be absent in mouths
with abundant deposits.
 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.

Anticonvulsants
 First drug-induced enlargements reported with
Phenytoin (Dilantin).
 Dilantin is hydantoin introduced in 1938 by Merritt
and Putnam for the treatment of all forms of
epilepsy, except petit mal.
 Other hydantoins known to induce gingival
enlargement are ethotoin and mephenytoin.

 Other anticonvulsants that have same side effect
succinimides [Zerontin, Celontin], and valproic
acid [Enpil-CR,Valporil]
Hallmon WW, Rossmann JA(1999)
 Some evidence links it to a direct effect on specific,
genetically predetermined subpopulations of
fibroblast, inactivation of collagenase, and plaque-
induced inflammation.

 Gingival enlargement occurs in about 50% patients
receiving the drug.
 Its occurrence & severity are not necessarily related
to the dosage after a threshold level exceeded.
Seymour RA, et al (1996)

 The mature phenytoin enlargement has a
fibroblast/collagen ratio equal to that of normal
gingiva from normal individuals; Some point in the
development of the lesion, fibroblast proliferation
must have been abnormally high.
Hassell TM, et al (1994)
 Oxytalan fibers are numerous beneath the
epithelium and in areas of inflammation.
 Phenytoin may induce decrease in collagen
degradation as a result of the product of an inactive
fibroblastic collagenase.

 Photo 23-9

Immunosuppressants
 Cyclosporine [ Sandimmun, Imusporin] is a potent
immunosuppressive agent used to prevent organ
transplant rejection & to treat autoimmune diseases.
 Its exact mechanism of action is not known, but it
appears to selectively and reversibly inhibit helperT
cells, which play a role in cellular and humoral
immune responses.
 Cyclosporine A is administered IV or by mouth
dosages >500mg/day have been reported to induce
gingival overgrowth.
Daley TD Wysocki GP, Day C (1986)

 Cyclosporine-induced gingival enlargement is more
vascularized than phenytoin enlargement.
 Children more frequently affected.
 Its magnitude appears to be relate more to the
plasma concentrations than to the patient’s
periodontal status.
 Gingival enlargement is greater in patients who are
medicated with both cyclosporine & calcium channel
blockers.
Slavin J, et al (1996)

 Photo 23-11
Mild involvement
Advanced generalized
enlargement

 The microscopic finding is many plasma cells plus
presence of an abundant amorphous extracellular
substance is suggested that enlargement is
hypersensitivity response to the cyclosporine.
Mariani G, et al (1993)

Calcium Channel Blockers
 Calcium channel blockers are developed for the
treatment of cardiovascular conditions such as
hypertension, angina pectoris, coronary artery spasms,
and cardiac arrhythmias.
 They inhibit calcium ion influx across the cell
membrane of heart and smooth muscle cells, blocking
intracellular mobilization of calcium.
 This includes direct dilatation of coronary arteries &
arterioles, improving oxygen supply to the heart
muscle: also reduces hypertension by dilating
peripheral vasculature.

 Drugs are Dihydropyridine derivatives;
Amlodipine [Amlibon,Amlip,Amlostat ],
Felodipine [Plendil, Felogard, Renedil],
Nicardipine [Cardene],
Nifedipine [Cardif, Nitrepin ]
 Benzothiazine derivates; diltiazem [Dilgem].
 Phenylalkylamine derivatives verapamil [Calaptin].
Hallmon WW, Rossmann JA (1999)

Amlodipine induced enlargement

Treatment Options
 First, consideration should be given to the possibility of
discontinuation of the drug / changing medication.
 Simple discontuation of the offending drug is usually
not practical, but its substitution with another
medication might be an option.
 If any drug substitution is attempted, it is important to
allow for a 6 to 12 month period to elapse between
discontuation of the offending drug and the possible
resolution of gingival enlargement before a decision to
implement surgical treatment is made.www.indiandentalacademy.com

 Alternative medications to the anticonvulsant
phenytoin include carbamzepine and valproic acid,
both have a lesser effect in inducing gingival
enlargement.
Dahilof G, et al (1993)
 Drug substitutions for cyclosporine are more limited.
 Cyclosporine -induced gingival enlargement can
spontaneously resolve if tacrolimus is substituted.
Hernandez G, et al (2000)

 For patients taking nifedipine prevalence of
gingival enlargement up to 44% other calcium
channel blockers such as diltiazem or verapamil
induce gingival enlargements 20% & 4%
respectively.
Fattore L, et al (1991)
 Use of another class of antihypertensive
medications rather than calcium channel
blockers, none of which known to induce gingival
enlargement.

 Second, the clinician should emphasize plaque
control as first step.
 The exact role played by bacterial plaque is not
well understood.
 Good oral hygiene & frequent professional
removal of plaque decrease the degree of gingival
enlargement and improves overall gingival health.
Dongari A, et al (1993)

 Third, gingival enlargement persists after careful
consideration of the previous approaches,
surgery may require, either gingivectomy or
periodontal flap.

 Surgery can be done in 2 methods
1. Gingivectomy
2. Flap Surgery
 Gingivectomy can be effectively perform for
small areas ( up to six teeth) with no evidence of
attachment loss.
 Flap surgery can be perform larger areas (>6teeth)
/ areas where attachment loss & osseous defects
are present.

 Other drugs potentially to cause gingival
enlargement.
1. Co-trimaxazole
2. Erythromycin
3. Ketoconazole
4. Lamotrigine
5. Lithium
6. Primidone
7. Sertraline
8. Topiramate
9. Vigabatrin

Idiopathic Gingival Enlargement
 It is rare disease of undetermined cause.
 It has been designated by such terms as
gingivomatosis, elephantiasis, idiopathic
fibromatosis, hereditary gingival hyperplasia, and
congenital familial fibromatosis.

Etiology
 The cause is unknown, thus the condition is
designated as “idiopathic”.
 Some cases have a hereditary basis. But genetic
mechanism involved are not well understand.
 Several families found the mode of inheritance to be
autosomal recessive in some cases autosomal
dominant.
Jorgenson RJ, et al (1974)

Clinical Features
 The enlargement effects the attached gingiva, as
well as the gingival margin and interdental papilla.
 The facial and lingual surfaces of the mandible &
maxilla are generally affected, but the
involvement may be limited
to either jaw.
 The enlarged gingiva is pink,
firm & almost leathery in
consistency & characteristic
minutely pebbled surface.

 In severe cases the teeth are
almost completely covered &
enlargement projects into the oral vestibule.
 The jaws appear distorted because of the bulbous
enlargement of gingiva.
 Secondary inflammatory changes are common at
the gingival margin.
 The enlargement usually begins with eruption of
primary or secondary dentition.www.indiandentalacademy.com

Histopathology
 It shows a bulbous increase in the amount of
connective tissue that is relatively avascular &
consists of densely arranged collagen bundles &
numerous fibroblasts.
 The surface epithelium is thickened & acanthotic
with elongated rete pegs.

Treatment
 Removal of local irritants if present.
 The enlargement may regress after extraction .

Enlargements associated with
systemic diseases or
conditions

Conditioned Enlargement
 Conditioned enlargement occurs when the systemic
condition of the patient exaggerates or distorts the
usual gingival response to dental plaque.
 Bacterial plaque is necessary for the initiation of this
type of enlargement, however, plaque is not the sole
determinant of the nature of the clinical features.
 The 3 types of conditioned gingival enlargement are
hormonal (pregnancy, puberty), nutritional
( associated with vit C) , & allergic.
 Nonspecific conditioned enlargement is also seen

Enlargement in Pregnancy
 Enlargement may be marginal & generalized or may
occur as single or multiple tumor-like masses.
 During pregnancy there is an increase in levels of both
progesterone & estrogen, which, by the end of third
trimester reach levels 10 & 30 times the levels during
the menstrual cycle, respectively.
Amar S, Chung KM (1994)
 These hormonal changes include changes in vascular
permeability, leading to gingival edema & an
increased inflammatory response to plaque.

 The sub-gingival microbiota may also undergo
changes, including an increase in Prevotella
intermedia.
Kornman KS, et al (1980)
 Marginal gingival enlargement during pregnancy
results from the aggravation of previous
inflammation.
 The gingival enlargement does not occur without
presence of bacterial plaque.

 Enlargement usually generalized & tend to be
more prominent interproximally than on the
facial and lingual surfaces.
 The enlarged gingiva is bright red or magenta,
soft, & friable and has a smooth, shiny surface.
 Bleeding occurs spontaneously or on slight
provocation.

 Tumor like gingival enlargement ( Pregnancy tumor)
is an inflammatory response to bacterial plaque and
is modified by the patient condition. It usually
appears after the third month of pregnancy, reported
incidence is 1.8% to 5%
Maier AW, Orban B (1949)
 The lesion appears as a discrete, mushroom like
flatted spherical mass that protrudes from the
gingival margin or more often interproximal space &
is attached by a sessile or pedunculated base.

 It tends to expand laterally, & pressure from tongue
and the cheek perpetuates its flattened
appearance.
 Generally dusky red or magenta, it has a smooth
glistering surface that often exhibits numerous
deep-red pinpoint markings.
 It is a superficial lesion and usually does not invade
the underlying bone.
 It is usually painless, unless accumulation of debris
or interfere with occlusion.

Histopathology
 Gingival enlargement in pregnancy is called
angiogranuloma.
 Both marginal and tumor like enlargements
consist of a centrally mass of connective tissue,
with numerous diffusely arranged, newly formed,
and engorged capillaries lined by cuboid
endothelial cells.

 As well as a moderately fibrous stroma with varying
degrees of edema and chronic inflammatory
infiltrate.
 The stratified squamous epithelium is thickened,
with prominent rete pegs some degree of intra &
extra cellular bridges, leukocytic infiltration.

Timing ofTreatment and Indications
 Gingival lesions in pregnancy should be treated as
soon as they are detected, although not
necessarily by surgical means.
 Gingival enlargement do shrink after pregnancy,
but they usually not disappear.
 After pregnancy the entire mouth should be
reevaluated, a full set of radiographs taken and
the necessary treatment undertaken.

 Lesions should be removed surgically during
pregnancy only if they interfere with mastication
or produce an esthetic disfigurement that the
patient wants removed.
 Every pregnant patient should be scheduled for
periodic dental visits.
 It requires elimination of all local irritants.

 Elimination of local irritants early in pregnancy is
preventive measure against gingival disease.
 Marginal and interdental gingival inflammation
and enlargement are treated by scaling and
curettage.
 Tumor like enlargement can be treated by surgical
excision and scaling and planing of the tooth
surface.

Enlargement in Puberty
 Enlargement of the gingiva is sometimes seen
during puberty.
 It occurs in both male and female adolescents &
appears in areas of plaque accumulation.
 It is marginal and interdental and it is
characterized by prominent bulbous
interproximal papillae

 Often, only the facial gingiva are enlarged, &
lingual surfaces are unaltered.
 Gingival enlargement during puberty has all
clinical features generally associated with chronic
inflammatory gingival disease.
 It is the degree of enlargement and the tendency
to develop massive recurrence in presence of
relatively scant plaque deposits that distinguish
pubertal gingival enlargement from
uncomplicated chronic inflammatory gingival
enlargement.

 After puberty the enlargement undergoes
spontaneous reduction but does not disappear until
plaque and calculus are removed.
 A study of 127 children 11 to 17 years of age showed a
high initial prevalence of gingival enlargement that
tend to decline with age.
Sutcliffe P (1972)

 A study of sub-gingival microbiota of children
between ages 11 & 14 and their associated clinical
parameters has implicated Capnocytophaga species
in initiation of pubertal gingivitis.
Mombelli A, et al (1990)
 Other studies have reported that hormonal changes
coincided with an increase in the proportion of
Prevotella intermedia and Prevotella nigrescens.
Nakagawa, et al (1994)

 Photo 23-16

Histopathology
 The microscopic appearance of gingival
enlargement in puberty is chronic inflammation
with prominent edema and associated
degenerative changes.

Treatment
 Gingival enlargement in puberty is treated by
performing scaling and curettage, removing all
sources of irritation, and controlling plaque.
 Surgical removal may be required in severe cases.
 The problem in these patients is recurrence caused
by poor oral hygiene.

Enlargement inVit C deficiency
 Enlargement of the gingiva is generally included
in classic descriptions of scurvy.
 Acute vit C deficiency itself does not cause
gingival inflammation, but it does cause
hemorrhage, collagen degeneration, and edema
of the gingival connective tissue.

 These changes modify the response of the gingiva to the
plaque to the extent that the normal defensive delimiting
reaction is inhibited, & the extent of the inflammation is
exaggerated, resulting in the massive gingival
enlargement seen in scurvy.
Glickman I (1948)
 Enlargement in vit C deficiency is marginal; the gingiva is
bluish red, soft, and friable and has a smooth, shiny
surface.
 Hemorrhage, occurring either
spontaneously or on slight
provocation, and surface
necrosis with pseudomembrane
formation are common. www.indiandentalacademy.com

Histopathology
 Gingiva has a chronic inflammatory cellular
infiltration with a superficial acute response.
 These are scattered areas of hemorrhage, with
engorged capillaries.
 Marked diffuse edema, collagen degeneration,
and scarcity of collagen fibrils or fibroblats are
striking findings.

Treatment
 It includes improvement of oral hygiene and
administration of vitamin C
 Normal dose will be 50mg/ day
 In scurvy patients dose will be 100-500mg/day.
 Available Tab. Chewcee
Tab. Limcee
Tab. Sukcee

Plasma Cell Gingivitis
 Also called as atypical gingivitis and plasma cell
gingivostomatitis.
 It consists of mild marginal gingival enlargement that
extends to attached gingiva. A localized lesion
referred as plasma cell granuloma.
Bhaskar SN, et al (1988)
 The gingiva appears red, friable, and sometimes
granular and bleeds easily; usually it does not a loss of
attachment.

 The lesion is located in attached gingiva & differs from
plaque-induced gingivitis.
 It is thought to be allergic in origin, possibly related to
components of chewing in origin gum, dentifrices, or
various diet components.

Histopathology
 Oral epithelium shows spongiosis and infiltration
with inflammatory cells.
 Ultra structurally, there are signs of damage in the
lower spinous layers and the basal layers.
 The underlying connective tissue contains a dense
infiltrate of plasma cells that also extends to the
oral epithelium, inducing a dissecting type of
injury.

Treatment
 Cessation of exposure to allergen brings
resolution of the lesion

Systemic Diseases Causing
Gingival enlargement

Leukemia
 It is characterized by the progressive overproduction
of white blood cells usually appears in the
circulating blood in an immature form.
Based type of cell involved :
1. Myeloid – involving the granulocyte series
2. Lymphoid– involving the lymphocytic series
3. Monocytic– involving the monocyte series

 Based on duration :
1. Acute
2. Sub-acute
3. Chronic
 Gingival enlargement & oral ulcerations seen in
acute myelogenous leukemia.
 Generally in chronic leukemias there wont be any
gingival enlargement seen.

Clinical Features
 It may be diffuse or marginal and localized or
generalized.
 It may appear as a diffuse enlargement, or discrete
tumorlike interproximal mass.
 In leukemic enlargement the gingiva is bluish red and
has a shiny surface.
 The consistency is moderately firm, but there is
tendency toward friability & hemorrhage, occurring
spontaneously or slight irritation.

Histopathology
 Mature leukocytes & areas of connective tissue are
infiltrated with a dense mass of immature &
proliferating leukocytes, the specific nature of which
varies with the type of leukemia.
 Engorged capillaries, edematous & degenerated
connective tissue, & epithelium with various degree of
leukocytic infiltration & edema found.
 Isolated surface areas of acute necrotizing
inflammation with a pseudomembraneous meshwork
of fibrin, necrotic epithelial cells, PMN’s, & bacteria
are often seen

Treatment
 The patient’s bleeding and clotting times and platelet
count should be checked and hematologist consulted
before periodontal treatment is instituted.
 After acute symptoms subside, attention is directed
to correction of the gingival enlargement.
 The rationale is to remove the local irritating factors
to control the inflammatory component of the
enlargement.

 The enlargement is treated by scaling and root
planing carried out in stages under L A.
 The initial treatment consists of gently removing all
loose accumulations with cotton pellets, performing
superficial scaling.
 Instruct the patient in oral hygiene for plaque control,
which include, at least initially, daily use of
chlorhexidine mouthwashes.
 Oral hygiene procedures are extremely important in
these patients and should be performed by the nurse
if necessary.

 Progressively deeper scaling is carried out at
subsequent visits.
 Treatments are confined to a small area of the
mouth to facilitate control of bleeding.
 Antibiotics are administered systemically the
evening before & 48 hours after each treatment
to reduce the risk of infection.

Granulomatous Diseases
Wegener’s Granulomatsis
 It is an uncommon disease consisting of an
inflammatory granulomatous process , characterized
by severe vasculitis and necrosis involving the upper &
lower respiratory system & kidneys.
 The cause is unknown, but the condition is considered
an immunologically mediated tissue injury.
Cortan RS, Kumar V, Robbins SL (1989)

 The initial manifestations include oral mucosal
ulceration, gingival enlargement, abnormal tooth
mobility, exfoliation of teeth, and delayed healing
response.
Buckely DJ, et al (1987)
 The granulomatous papillary enlargement is reddish
purple and bleeds easily on
stimulation.
 It is also called as
strawberry gingivitis

Histopathology
 Chronic inflammation occurs, with scattered giant
cells and foci of acute inflammation and
microabscesses covered by a thin, acanthotic
epithelium.
 Vascular changes have not been described with
gingival enlargement inWegener’s granulomatosis,
probably because of small sine of the gingival blood
vessels.
Israelson H, Binnie WH, Hurt WC. (1981)

Sarcoidosis
 It is chronic disease affecting the skin , mucosa ,
salivary glands , lungs ,& other organs; consisting
of multiple noncaseating epitheliod granulomas &
fibrosis of adjacent tissues.
 It starts in individuals in their 20’s / 30’s,
predominantly affects blacks, and can involve
almost any organ, including gingiva, where a red
smooth, painless enlargement may appear.

Histopathology
 It consists of discrete, noncaseating whorls of
epitheliod cells and multinucleated, foreign body-
type giant cells with peripheral mononuclear cells.
Rees TD (1999)
 Multiple nuclei of the giant cells are often arranged in
a ring around the periphery & may additionally
contain some stellate-shaped structures called
asteroid bodies.

Treatment
 Can be done by surgical excision.
 Removal must be include all the giant cell tissue ,
because recurrence is common.
 In dentuluous patients usually requires removal
of one / more teeth & curettage of the socket.

Neoplastic Enlargement
BenignTumors of the Gingiva

Fibroma
 These are arising from gingival connective tissue or
from the periodontal ligament.
 They are slow growing, spherical tumors that tend to
be firm and nodular but may be soft & vascular
 Fibromas are usually pedunculated.
 Hard fibromas of the gingiva are rare; most of the
lesions diagnosed clinically as ‘fibromas’ are
inflammatory enlargements.
Schneider LC, Weisinger E (1978)

Histopathology
 Fibromas are composed of bundles of well-formed
collagen fibers with a scattering of fibrocytes and a
variable vascularity.

Papilloma
 They are benign proliferations of surface epithelium
associated with the human papillomavirus.
 Viral subtypes HPV-6 and HPV-11 have been found in
most cases of oral papillomas.
 Gingival papillomas appear as solitary, warlike or
cauliflower-like protuberances.
 They may be small & discrete or broad, hard elevation
with minutely irregularly surfaces.

Histopathology
 It has numerous foci of multinuclear giant cells and
hemisederin particles in a connective tissue stroma.
 Areas of chronic inflammation are scattered
throughout the lesion, with acute involvement
occurring at the surface.
 The overlying epithelium is usually hyperplastic, with
ulceration at the base.
 Bone formation occurs within the lesion.

Malignant Tumors of the Gingiva

Carcinoma
 Squamous cell carcinoma is the most common
malignant tumor if the gingiva.
 It may be exophytic, presenting as an irregular
outgrowth, or ulcerative, appearing as flat,
erosive lesions.
 It is often symptom free, going unnoticed until
complicated by inflammatory changes that may
mask the neoplasm but cause pain; sometimes it
becomes evident after tooth extraction.

 These masses are locally invasive, involving the
underlying bone and periodontal ligament of
adjoining teeth and the adjacent mucosa
 Metastasis is usually confined to the region above
the clavicle; however more extensive involvement
may include the lung, liver, or bone

Buccal view
Occusal view

Malignant Melanoma
 It is rare oral tumor that tends to occur in the hard
palate and maxillary gingiva of older persons.
Neville BW, Damm DD, et al (1995)
 It is usually darkly pigmented & is often preceded by
localized pigmentation.
Chaudry AP, Hampel A, Gorlin RJ. (1958)

 It may be flat or nodular and is characterized by
rapid growth & early metastasis.
 It arises from melanoblasts in the gingiva, cheek
or palate.
 Infiltration into the underlying bone and
metastasis to cervical and axillary lymphnodes
are common

Metastasis
 Tumor metastasis to the gingiva occurs
infrequently.
 Metastasis reported with adenocarcinomas of
the colon, lung carcinoma, primary hepatocellular
carcinoma, renal cell carcinoma,
chondrosarcoma, and testicular tumor.
Buchner , et al (1980)

False Enlargement
 These are not true enlargements of the gingival
tissues but may appear as such as a result of
increases in size 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
 Enlargement of the bone subjacent to the gingival
area occurs most often in tori and exostoses,
but it can also occur in Paget’s disease fibrous
dysplasia, central giant cell granuloma
ameloblastoma osteoma and osteosarcoma.
 The gingival tissue can appear normal or may
have unrelated inflammatory changes.

Underlying DentalTissues
 Particularly eruption of primary dentition, the
labial mucosa may show a bulbous marginal
distortion caused by superimposition of the bulk of
the gingiva on the normal prominence of the
enamel in the gingival half of the crown; this is
termed developmental enlargement.
 In strict sence, developmental
gingival enlargements are
physiologic and usually
presents no problem. www.indiandentalacademy.com

Syndromes Associated
With Diffuse Gingival
Enlargement

Autosomal Dominant Inhertance
Rutherford Syndrome:
 Characteristic features are: Congenital enlarged
gingiva, delayed tooth eruption, “ curtain like ”
superior corneal opacities.
 Associated mental retardation aggressive
behavior, dentigerous cysts.

Zimmerman-Laband Syndrome:
 Main features gingival fibromatosis with defects
of ears, nose, bones, nails, & terminal phalanges
( “froglike” fingers & toes) .
 And also hyperextensible joints and
hepatospenomegaly.

Goltz-Gorlin Syndrome:
 Gingival & other mucosal papillomatosis , lip
and tooth defects, piikiloderma , dermal fat
herniation, adactyl & syndactyl seen over 90%
female .
 Microdontia with enamel hypoplasia is common
finding.
 Cleft lips / palate seen in several cases

Cowden’s Syndrome:
 Papillomatosis of lips, gingiva, palate, pharynx,
and fauces, pebbly fissured tongue.
 Lichenoid & papillomatous lesions of perioral,
perinasal, & periorbital, ear & neck.
 Hamartomas of skin, GIT, breast & thyroid.
 Neoplasams principally affects ovaries, colon, ear
canal & various soft and hard tissues.

Tuberous Sclerosis:
 Single or multiple fibromas of gingiva, oral
mucosa, and skin.
 Epilepsy , mental retardation, and
hamartomas of brain, heart & kidney.
 Cranial defects, adenoma sebaceum,
astrocytoma & glioblastoma.

Autosomal Recessive Inheritance
Murray- Puretic –Drescher Syndrome:
 Gingival fibromatosis with multiple juvenile PAS +ve
hyaline fibromas of head (“ turban tumors ”) , trunk
& extrimities.
 Suppurative lesions of skin and mucosa flexion
contractures, mental retardation, elevated urinary
hyaluronic acid & dermatan sulfate.

Cross Syndrome:
 Typical features are gingival and alveolar
enlargement, micropthalmia, cloudy corneas,
hypo pigmentations .
 And also white hair, blond skin, decreased
melanocytes with reduced tyrosine activity ;
mental retardation is rare

Ramon Syndrome:
 Gingival fibromatosis, hypertrichosis,
cherubism, mental retardation, & epilepsy:
characteristic perivascular fibrosis in gingival
biopsy specimens.
Lysosomal Storage Diseases:
 Neonatal / childhood gingival enlargement,
widened alveolar ridges & widely spaced teeth.
 Specific enzymatic deficiencies; generalized
viseralomegaly .

Sporadic or Unknown Pattern of Inhertance
Sturge-Weber Syndrome:
 Orofacial & meningeal angiomatosis with secondary
mental deficiency, seizures, & hemiplegia; ipsilateral
nevus flammeus & mild to severe gingival
enlargement.
 Along with hyperplastic vascular gingiva blanch with
pressure; bony hemangiomas and delayed tooth
eruption.

Acanthosis Negricans:
 Gingival papillomatosis associated with
periorofacial, mucosal, & skin ( pigmented )
lesions, gastric adenocarcinoma.
Epidermal Nevus:
 Cutaneous nevi that can extend to oral mucous
membrane & gingiva, with localized warty
papillomatosis, mental deficiency, skeletal
abnormalities, and hypoplasti teeth.

References
1. CARRANZA’S Clinical Periodontology: 10th
Edition.
2. BURKIT’S Oral Medicine Diagnosis &Treatment:
10th Edition.
3. SHAFER’STextbook of Oral Pathology: 4th Edition
4. Contemporary Oral & Maxillo-facial Pathology: 2nd
Edition

TH
AN
K
YO
U

gingival enlargements / dental implant courses

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (20)

Similar to gingival enlargements / dental implant courses

Similar to gingival enlargements / dental implant courses (20)

More from Indian dental academy

More from Indian dental academy (20)

Recently uploaded

Recently uploaded (20)

gingival enlargements / dental implant courses