GIANT CELL LESIONS

OF THE
JAWS
Dr Syeda Noureen Iqbal
 DEFINITION

Giant cells are very large, multinucleate, modified

macrophages which may be formed by
coalescence of mononuclear cells or by nuclear
division without cytoplasmic division of
monocytes, particularly in response to the
presence of a foreign body.
 ORIGIN
Giant cells are derived from the cells of
mononuclear

phagocyte system.

Originate from precursor cell in the bone marrow and

also closely related cells of bone marrow origin.

They are transported inblood as monocytes, which are

pool of immature cells.

Monocytes invade areas of damage & inflammation,
where

they differentiate into macrophages.

When the macrophages fail to deal with particles to be

removed they fuse together to form multinucleated giant

cells.
 CLASSIFICATION OF GIANT
CELL LESION
Metaboli
Inflammatory /
c:
Reactive:  Hyperparathyroidism
•
• Peripheral Giant
•Cherubism Histiocytosis
Cell Granuloma Neoplastic:
•
• Central Giant
 Central Giant Cell Tumor
Cell Granuloma
 •Osteoid osteoma /
• Aneurysmal Bone
Cyst •Osteoblastoma
• Traumatic Bone
Cyst
 CENTRAL GIANT CELL
GRANULOMA
• Was 1st described in jaws by Jaffe
(1953).
• Designated as Giant Cell Reparative
Granuloma.
• Waldron & Shafer
(1966)
• Classified on the basis of biologic
behavior as:
Non-aggressive &
Aggressive.

Etiology:

• Reactive lesion

• Trauma

• Origin from odontoclasts

Clinical Features:
• Male : female ratio of 1:2

• Age: 11-30yrs

• Present almost exclusively in jaws

• Mandible > maxilla

• Frequent site in mandible is the ant. region not

crossing midline.
• Non-aggressive
type:
Asymptomatic, slow

expansion of the

affected bone.

• Aggressive
type:
Painful,
rapid growth,
root

resorption, perforation of
Radiographic
Features:
• Solitary unicystic
radiolucency, as it grows it
becomes multilocular with
soap-bubble appearance.
• Multilocular > unilocular
• Root displacement / resorption
• Loss of lamina dura
• Expansion of cortical plate
Histologic Features:
• Proliferation of spindle cells in collagenous
stroma.
• Numerous small vascular channels.
• Giant cells with 15-20 nuclei present throughout
the stroma, adjacent to capillaries.
Treatment:
Intralesional steroids:
• Triamcinolone – 20 mg/cc once per wk for 6 wks

•Suppresses inflammatory component of lesion

Calcitonin – s.c. inj.:

• Dose – 20 IU O.D.

• Antagonizes bone resorption by inhibiting

Giant cells.

JOMS 61:649-53,2003
CASE REPORT
(JOMS 61:649-
53,2003)
α-Interferon – s.c. inj.:

• Dose – 30 lac IU O.D.

• Suppresses angiogenic component of

lesion.

Surgical:

• Curettage

• Enucleati
on
 Surgical
(JOMS 60:756-
technique
61;2002 )
• Incisions placed (1cm away from
radiographic extent of the lesion)
• mucoperiosteal flap raised
• Buccal bone overlying lesion removed
• Through curettage is done
• Peripheral ostectomy may be done
 Doesn’t spread via perineural spread so
preserve neurovascular bundle
 Through debribment of bony cavity
• Control of hemorrhage
• Flap repositioned & sutured
Preserve teeth in area of lesion
 With good prognosis
(adequate bone
support)
 Treat endodontically
before surgery

Extract teeth in area of

lesion
 With poor prognosis
(poor bone support)
 Recurrenc
e
• Varies from 10 – 50
• %
Higher for Locally aggressive
• lesion
Recurrent lesion respond well to further curettage,
lesions may require more radical surgery for
aggressive
• cure.
Incomplete
removal
 GIANT CELL TUMOR
• Very rarely found in jaws.
• Aggressive –
low grade osteosarcoma
variant of
• H/F: similar to
except
CGCG,that the giant cells
are larger with more
nuclei and are more
evenly spread.
• Treatment:
(Resection
high recurrence
rate)
 PERIPHERAL GIANT CELL
GRANULOMA
• Common tumor like growth in the oral
cavity.
• Does not represent a true neoplasm but a reactive
lesion.
• Arising from periosteum or PDL
membrane.
• Often called as peripheral giant cell reparative
granuloma.
C/
F
• :Age: 5ht0r 6htdecade of life.
• Common in
females.
• Mandible is affected more
often.
• Occurs exclusively on
gingiva, edentulous
alveolar
ridg
e.
• Reddish or bluish
nodule, most
lesions
2cm in diameter
smaller
.
• than
May be due
to
ulcerated trauma.
 H/F:
• Fibroblast are the basic element.
• Giant cells are scattered throughout the stroma.
• Foci of hemorrhage, liberation of hemosiderin
pigment.
R/
• May or may not be present
F:
• Larger lesion may exhibit superficial erosion of
the cortical bone
• May demonstrate widening of adjacent PDL
spaces

Treatment:
Local surgical excision down to the underlying
bone
Differential diagnosis
• CGCG
• Pyogenic
granuloma
 ANEURYSMAL BONE
CYST
• First described by Jaffe & Lichtenstein in
1942.
• First case in jaw was reported by Bhaskar & Bernier in
1958
.
• Is a non-neoplastic, reactive lesion of bone
generally
consisting of several cavities filled
with blood and deprived of an endothelial
• Not a true cyst, sinusoidal blood filled
lining.
space.
• Word “Aneurysm” was used to describe the blown out

appearance of the contour of the affected

area.
• Exist in two clinico-pathologic forms:

1. Primary

2. Secondary – arising in other osseous conditions like

Fibrous Dysplasia, Ossifying Fibroma, CGCG,

Osteoblastoma, Osteosarcoma, Ameloblastoma

Etiology:
Cause is controversial, the theories put forth regarding
the

pathogenesis of the lesion are:

- Trauma

- Local changes in haemodynamics

- Reparative response to the hematoma

C/F:
• Occurs below 20 yrs of age.

• Predilection towards female.

• Mandible > maxilla, molar region is the most common

site.

• Slow growing, may expand the

cortical plate, does not destroy
them.
• Aggressive lesions may perforate cortical plate with soft

tissue extension.
• Teeth may be tender, missing or
displaced.
• Pain is occasional
complaint.
• On palpation: egg-shell crackling, non-
pulsatile.
• On surgical exploration: ‘welling up’ of
blood.
• Gross examination: blood-soaked
sponge.
R/F:
• Well defined
radiolucency
• Extreme expansion of

cortical plates -
honey - comb or soap -
bubble appearance

• Can displace teeth

• Cortex may be destroyed

H/F:
• Consist of a
fibrous
connectiv tissu stro
e
containin e of ma
g
sinusoidal many filled
blood
spaces.
• Fibroblast are
numerous as well
multinucleated giant
cells.
• Vascular spaces lack any
endothelial lining, and
giant cells form part of
their walls.
Treatment:
• Surgical curettage & partial resection are primary means
of

treatment.

• Cryotherapy.

• Recurrence rate is high, ranging from 19% to about 50%.

• Follow up is necessary.
• Differencial
diagnosis
• CGCG
• Hyperparathyroidism
• Cherubism
 TRAUMATIC BONE
CYST
Etiology:
• Trauma → Failure of organization of blood clot

→ Degeneration of clot → Empty cavity

within bone.

C/F:
• Young persons (<20 yrs).

• Male predilection.

• Mandible frequently affected.

• Asymptomatic, pain or tenderness rarely
present.
• Rarely expansion of
jaw.
• Teeth - vital, No tipping /
migration.
• Aspiration –
negative.
• On surgical exploration – usually empty cavity,
sometimes
filled with little straw colored
fluid.
R/F:
• Well defined,
scalloped
margin.

• Oval / round shape.

• No root resorption.

• Lamina dura intact.

• Usually located

above mandibular
canal.
H/F:

• Thin connective

tissue membrane.
• No epithelial lining.

•Presence of giant cells.

Treatment:
• Curettage

• Re-establish bleeding
into the lesion.
 OSTEOBLASTOMA
• It is a benign neoplasm of bone that arises from
• osteoblasts.
Osteid osteoma is thought to represent a smaller version
of
the same
tumor.
C/F:
• Occurs mostly in young persons
• (<30yrs).
Slight male
• predilection.
Affects both the jaws, more in post
• region.
Characterized by Pain and swelling at tumor
• site.
Size: 2-4cm ,but may be larger than
10cms,
measuring <1.5cm is osteoid
osteoma.
R/F:
• Well circumscribed.
• Radiolucent -
radiopaque
mixed -
pattern.
• A thin radiolucency may
be surrounding
calcified
central tumor mass.
• Occasional sun-
appearance-
ray
resembling
osteosarcoma.
H/F:
• Irregular osteoid
trabeculae
&
immature
within the stroma. of
• Prominent vascular bon
network. e
• Actively
proliferating osteoblasts
& moderate no. of
multinucleatedgiant cells.
Treatment :
• surgical excision.

• Recurrence is rare.

• Malignant transformation into osteosarcoma has also

been reported.
•Differential diagnosis
Cementoblastoma
Ossifying fibroma
Fibrous dysplasia
 CHERUBISM
• Rare developmental jaw condition.

• The condition is named due to the facial

appearance
-plump cheeked little angels with
upward directed look depicted in renaissance
painting.

Etiology:
• Inherited as an autosomal dominant trait.

• Gene for cherubism present on chromosome 4p16.3.

• Disturbance in development of
permanent II & III molars.
• Dysregulation of mesenchymal bone
formation and development of giant cell
granulomas.
C/F:
• Occurs between the age of 2-5yrs.

• Progressive, painless, symmetric

swelling of the jaws- mandible

or maxilla.
• Cherub like facies arise from
bilateral involvement of posterior
mandible that tends to include the
angles & rami region - angelic
chubby cheeks.
• Eyes ‘up turned to heaven’
appearance – due to b/l maxillary
involvement.
• Lesion grows slowly but no perforation of cortex.

• Marked cervical lymphadenopathy.

• Premature shedding of deciduous teeth.

• Permanent dentition – teeth missing, failure of

teeth eruption, teeth displacement.

• Speech difficulty.

• Bony lesions regresses after puberty.

R/F:
• B/L expansion & thinning of cortical plates.
• Multilocular cystic appearance – teeth floating in
spaces.
• Numerous unerupted & displaced teeth.
H/F:
• Consists variable number
of multinucleated giant
cells.
• Foci of extravasated blood
are commonly present.
• Cuff like deposits
surrounding small blood
vessels throughout the
lesion.
Treatment:
• The lesions tend to show varying degree of remission

after puberty.
• By 4htdecade facial feature approach normalcy.

• Early surgical intervention for cosmesis has given good

results.
• Some studies showed the use of calcitonin, but still not

proved.
BROWN TUMOR OF
HYPERPARATHYROIDISM
• Parathormone (PTH) is normally produced by
parathyroid
glands, which regulates the Ca+
metabolism.
• Excessive production of PTH results in a condition
known
as
Hyperparathyroidism.
• It is an exaggerated form of ‘Osteitis fibrosa
cystica’

discovered by von Recklinghausen in 1891.

Three
types:
• Primary
hyperparathyroidism
• Secondary
hyperparathyroidism
• Tertiary
hyperparathyroidism
C/F:
• Incidence: 1 in 500

• Predilection for females.

• Describes the features ‘Stones , Bones, Abdominal

-

Groans & Psychic Moans’

• Metastatic calcifications - Nephrocalcinosis, blood
vessels.
• Jaw - not as frequent as in long bones and
• skull.
Vague aches, severe bone pain, tenderness
fractur
following
• es.
Swelling develops, firm in consistency,
• tender . of
Mobility
teeth.
R/F:
• Sub-periosteal erosion
of middle phalanges is
the hallmark.
• Very rarely jaw
affected first.
• Generalized loss of
lamina dura.
• Ground glass appearance.
• Cortical plate may
be
thinned or
lost.
• There is a cystic
type
of
radiolucency.

• On gross examination-Vascularity, hemorrhage & deposits

of haemosidrin imparts a dark reddish brown color to the

lesion –”Brown Tumor”

H/F :
• Giant cells of
osteoclastic
origin scattered
fibrovascular over the
stroma foci of
which in
hemosiderin are present.

Lab.
investigations: leve
• alkaline
Serum phosphatasel,
& PTH level will be
calcium
raised
Treatment:
 Primary:
 Surgical excision of parathyroid adenoma.
 Bone lesions resolve spontaneously.

Secondary:
 Management of kidney disorders.

Tertiary:
 Oral Ca supplement
 Vit. D analogue