GIANT CELL

TUMOUR

OSTEOCLASTOMA
GIANT CELL TUMOUR

 IT is an aggressive lesion characterised

by well vascularised tissue made up of
plump spindly or ovoid cells in addition to
numerous multinucleated giant cells
uniformly dispersed through out the
tumour tissue .
 This lesion represents about 5% of all
primary bone tumours
GIANT CELL TUMOUR

 It is distinct neoplasm of undifferentiated

cell
 Locally aggressive
 Usually Benign neoplasm
 Involves the end of the bone
 At the epiphysio metaphysial area
 Usually after epiphyseal closure
GIANT CELL TUMOUR

 Exact cell of origin not known

 Can be from marrow monocyte
 Consists of proliferating mononuclear
cells and multinucleated giant cells
HISTORY
 HISTORY
 JOHN HUNTER &JOHN ABERNETHY-1804 –
first classified about tumour

 In 1818 SIR ASTLEY COOPERS and TRAVERS

first described about this lesion
They called this fungus medullary exostosis
This tumor was thought to be malignant and often
treated with amputation
HISTORY

 1853-PAGET called it BROWN or

MYLEOID tumour
 1912-BLOODGOOD first coined the
phrase GIANT CELL TUMOUR OF THE
BONE then only the nonmalignant
behavior of this lesion was first
established
GIANT CELL TUMOUR
 INCIDENCE-
Peak incidence 20-40
Can occur before
physial closure then
it will be in
metaphysis
female :male =1.5 :1
In SEA countries
incidence is 20% of
primary tumour
GIANT CELL TUMOUR
LOCATION
 Distal femur 27
 Proximal tibia
20
 Distal radius
 Sacrum
11
 Distal tibia 5
 Proximal humerus 4
 Proximal femur 4
CLINICAL FEATURES
 PAIN –near articular
cartilage

 SWELLING
-eccentric
Clinical features
 JOINT SYMPTOMS
Weakness
limitation of motion
Pain when there is pathological fracture
Tenderness with EGG SHELL CRACKING
Due to jt invovement disuse atrophy ,jt
effusion,
RADIOLOGY

 ECCENTERIC expansible
osteolytic lesion
 Well demarcated or merges
with metaphysis
 Trabeculae- SOAP BUBBLE
APPEARANCE
 No periosteal new bone
formation
 Pathological fracture
 Subchondral bone
involvement
 Closed physis will be seen
CAMPANACCI GRADING
According to Radiology
 Stage I-Normal bony contour
 Stage II- Expansile lytic lesion but no break in cortex
 Stage III-Destructive radiolucent lesion, cortical break
and soft tissue involvement
 BETTER PROGNOSIS-
Outer border-intact
Inner margin-sharp
 AGGRESSIVE –
Cortical break
Soft tissue involvement
MRI AN CT

 It helps in early diagnosis

and soft tissue
involvement.
 FALSE POSITIVE or
NEGATIVE
 In the spine ,tumors such
osteoblastoma, ABC and
metastasis may be found
in the same location as
GCT
 They may have
overlapping MRI
characterstics
PATHOGENESIS
 Hypothesis by GESHICKTER and
COPELAND-
Spindle shaped neoplastic mononuclear
cells stimulate immigration of blood
monocyte into the tumour tissue and
promote formation of OSTEOCLAST
LIKE GIANT CELLS
The giant cells are innocent lookers but the
culprit are SPINDLE CELLS
 MONONUCLEAR SPINDLE SHAPED
CELLS
Chromosome abnormality
Neoplastic oncogene-p53
,C-myc ,C-fox, N-myc
CYTOKINE DIFFERENTIATE
FACTOR
Macrophage recruitment activation
TNF ,IFN‫ ע‬,M- CSF

Fusion of mononuclear cells

MULTINUCLEATED GIANT
CELLS
TYPICAL HISTOLOGY
 Multinucleated
giant cells
 Round
mononulear
cells
 Spindle shaped
cells

SPINDLE
SHAPED
CELLS
ATYPICAL HISTOLOGY
 Giant cells with
predominance of
spindle cells and this
can be mistaken for
FIBROSARCOMA
 Tumour in blood
vessels
MONONUCLEAR CELLS
 Phenotypically
resembles
connective tissue
stromal cells
 Receptors for
parathyroid hormone
 Produce collagen
 Don’t express
macrophage surface
antigen
MULTINUCLEATED GIANT
CELLS
 Multinucleated giant cells
(50-150nuclei,10-15
microns) are formed from
mononuclear cells
 PREDOMINANT TYPE-
Large multinucleated cells
where individual nuclei are
identical to stromal cells
 MINORTY-Small size, dark
pyknotic nuclei ,bright
eosinophilic cytoplasm
MULTINUCLEATED GIANT
CELLS
STROMAL CELLS DERIVED
FROM
 TYPE I-Fibroblast or undifferentiated
bone marrow mesenchymal cells
 TYPE II-monocyte –macrophage
osteoclast lineage
 Rarely contain foci of reactive bone so
not to confuse with OSTEOSARCOMA
PATHOLOGY
 Giant cells are not diagnostic
 They are also seen in
ABC,UBC
Nonossifying fibroma
Chondroblastoma
Brown tumour
Fibrous dysplasia
Osteogenicsarcoma
These are variant of GCT
STAGE
EVING
STROMA
and JAFFE
GIANT CELLS
GRADING
I CONSPISIOUS PLENTY

II PROMINENT REDUCED NUMBER

III SARCOMATOUS SPARSE

SECONDARY CHANGES IN GCT
TREATMENT AIM

 Eradicate the growth completely at the

initial surgery
 Local ablation without sacrificing joint
function
 Lowers the risk of reccurence
 The appropriate treatment has been
controvorsial
CHONDROBLASTOMA(histology)

 In nuclei there will be folding or cleft

 Stromal background
 Mononuclear cells will be rounded
whereas it will be spindle shaped in
GCT.
Preop management and
planning
 Aggressive nature of this lesion so firm
diagnosis should be established ie
malignancy should be ruled out by prior
biopsy and other investigation.
OPERATIVE PLAN MUST INCLUDE THIS
THREE FACTORS
1.type of resection.
2.The use of adjuvant therapy
3.Type of material to be used to fill the defect

TREATMENT
Intralesional curettage.
 EN BLOCK exicision
 Curettage (if the joint surface can be saved)
 Curettage and bone grafting
 Curettage with adjuvant chemotherapy and
biphosphonate
 Curettage and acrylic bone cementation
 Curettage and cryosurgery
 Excision and reconstruction
 Irradiation
 Embolisation
EN BLOCK EXCISION

Lesions of sacrificial part

 Lower end of ulna
 Upper end of fibula
 Phalanges
 Metatarsals rays
INTRALESIONAL CURRETAGE

 Adequate exposure with

large cortical window
 High power burr
 Pulsatile jet lavage

If Curratage only used than

recurrence rate is 40%
(mayo clinic study)
ADJUVANT TO AUGMENT
CURRATEGE
 PHENOL-12-50% conc
Disadvantage-
Easily absorbed
Nephrotoxic
High nonunion rate
Soft tissue complication
HYDROGEN PEROXIDE
 ADJUVANT S
 BONE CEMENT
 Bone cement
+ADRIAMYCIN+METHOTREXAT
E to reduce recurrences
 Cementation with calcium
phosphate
CRYOSURGERY WITH
LIQUID NITROGEN
-196’ ;it create 1-2cm zone of
tissue necrosis.
Cost
Local complication
Not easily available
Storage difficulties
# rate increased
DO THESE ADJUVANT HELP
 YES
 It eliminate the microscopic disease
 Curettage and cementation causes a 2mm osteolytic lesion
zone surrounding the cement due to thermal injury

REMOVAL of tumour seems to be more important factor

Trieb et al- recurrence rate is same

 CEMENTING
ADVANTAGE DISADVANTAGE
The monomer is cytotoxic Not biological material so
Thermal effect strong in compression but
weak in shear and
Radiographic detection of
torsional forces
recurrence is easier
Fear of long term
Immediate structural
degeneration of articular
support and early
ambulation cartilage in subchondral
lesion in wt bearing stress
TREATMENT

 Chen-chen 2005
-when residual
subchondral bone
after an extended
curretage is
<5mm then
multilayer
reconstruction
technique is
recommended
REINFORCEMENT PINS

 STEINMANN pins has been used to to

reinforce bone cement used to fill large
subchondral defects
 SOME FORM OF INTERNAL FIXATION
SHOULD BE THERE
ARGON CAUTERIZATION
 BONE GRAFT(if no cryotherapy is
used )
ADVANTAGE DRAWBACK

Remodelling along stress Autograft quantity is less

lines
Reconstruction is permanent Donor site morbidity

Allograft is expensive

Recurrence is difficult to spot

EXCISION AND
RECONSTRUCTION
 TURN O PLASTY
 Arthrodesis
 Arthroplasty
WIDE RESECTION AND
RECONSTRUCTION
 Larger the area of subchondral bone
affected worse prognosis
Thus even in benign tumour resection may
be the preferred option
When the skeletal integrity is unlikely to be
restored after healing leading to
compromise in ultimate function
OPTION

 MEGA JOINT REPLACEMENT

 Biological reconstruction like autograft
arthrodesis microvascular fibular
reconstruction
 ILIZAROV method
 Osteoarticular allograft
CHEMOTHERAPY

 NO effective chemotherapy agent

available
RADIOTHERAPY
 When complete excision or curratage is
not possible
 Aggressive, multiple recurrent tumor
 The use of modern megavoltage
radiation may reduce the rate of
malignant transformation
EMBOLIZATION

 Transcatheter embolization of blood

supply
Reembolisation monthly
Certain unresectable tumor like
sacral,pelvic
PREOP EMBOLIZATION
Resectable tumor-perop bleed and size
BIPHOSPHONATE

 Pamidronate, zoledronate
 It induces apoptosis in osteoclast like
giant cells
 Help in limiting tumour progression
AMPUTATION

 Malignant tumour
 Fungation
 Recurrence after surgery and irradiation
 Deep seated associated infection
 Extensive destruction of bone
 Severe disability
RECCURENCE

 Mainly due to incomplete initial removal

of tumor
 majority occurs with in 2 years
MANAGEMENT-
 Steyern et al-same as that of primary
DIAGNOSIS OF RECCURENCE

 Curretage and cementation causes a

2mm osteolytic zone surrounding the
cement due to thermal injury
 A thin sclerotic rim forms by 6 months
 Failed development of sclerotic margin
ay suggest reccurence
 Akhane et al-total ser acid phosphatase
can be used as tumour marker
METASTASIS
 Mean interval is 2-5 years
 LUNG-commonest
Good prognosis unlike other tumour
 Regional LN, mediastinum
 Scalp, pelvis
 It looks like primary
 Treatment is wide resection like lobectomy
 MALIGNANT GCT
 Tender mass in the region of
previously treated GCT
 Skin changes from prior radiation
therapy
 c/o pain
 H/O previously GCT average
10yrs back
Commonly post irradiation 75%
Rarely at the treated surgical site of
GCT
POOR PROGNOSIS
TREATMENT-
Preop chemotherapy+wide surgical
resection or amputation
 MULTICENTRIC
 Multicentric GCT occurs in <1% of all patients
with GCT.
 ONLY 43 patients are reported till now
 MALIGNANT GCT
 X RAY DD
Benign GCT,reccurence GCT
Osteomyleitis
PATHOLOGY-tumour breaks
cortex, necrosis,soft tissue
extension ,hemmoragic
foci,
Histology-nuclear
pleomorphism
 DIFFERENTIAL DIAGNOSIS
RADIOLOGICAL

Chondroblastoma Malignant fibrous

Osteosarcoma histiosarcoma
fibrosarcoma

PATHOLOGICAL
Benign malignant

ABC,chondroblastoma, Malignant fibrous

GCreparative granuloma histiosarcoma,Malginant
GCT,Osteosarcoma
containing GCT
IF not treated then it Leads to
destruction of cortical bone to soft
tissue invasion and finally
ulceration of skin
CONCLUSION
 GIANT CELL TUMOUR is challenging surgical
problem due to its divergent unprediticable and
biological behaviour
 Modality of treatment is essentially surgical
 For conservation of limb en block resection with
reconstruction is best
But commonly used is intralesional curettage
 Irradiation is for nonaccessible lesion
 Amputation is resort of desperation
FUTURE GENETIC
 No recurrent chromosomal structural or numeric
aberation of importance has been detected yet…
 When confronted with rearrangemnt ,especially
concerning 16q22 or 17p3,an associated ABC
should be excluded
 Cytogenetic morphological
The most frequent anamoly is telomeric
association,the most most frequent association
11p,13p,14p,15pand 19,20,21q
FUTURE

 Clinical studies on treatment on GCT

with CALCITONIN have shown positive
results probably due to control of
OSTEOCLASTOGENESIS
 OSTEOPROTEGRIN influences
osteoclastogenesis and may be used for
the treatment of GCT