GCT

1. GIANT CELL TUMOR
Presenter: Dr. Sudheer kumar
Moderator : Dr. Y. Siva prasad
professor of orthopaedics

2. INTRODUCTION
• It is one of the most common bone tumors encountered.
• Though benign tumor, it is locally aggressive and has
malignant potential
• They have significant bone destruction ,local recurrence
and occasional metastasis

3. DEFINITION
• Distinct neoplasm arising from non-bone forming
supportive connective tissue of marrow with network
of stromal cells regularly interspersed with giant cells
• Tumor is called GCT because Giant cells are found
• These Giant cells resemble osteoclasts…..hence called as
OSTEOCLASTOMA

4. EPIDEMOLOGY
Only 5% of PRIMARY bone tumors & 20% of benign bone
tumors
Almost affects skeletally mature patients in the age group of
15 to 40 with peak incidence in later half of 3rd decade
Female to male ratio -----1.5 : 1
But malignant GCT more common in MALES
.

5. SITE OF INVOVLMENT
Usually SOLITARY lesions
1-2% may be multi-centric !!
Seen at
distal end of femur
proximal end of tibia
distal end of radius
upper end of humerus
lower end of tibia
i.e., cancellous disposed bone ends which
are sites of high bone turn over
and osteoclastic activity
Others like
hand , spine and pelvis

6. CLINICAL FEATURES
SWELLING :
An epiphyseo-metaphyseal , eccentric swelling is seen at the
ends of long bones
Overlying Skin is stretched & shiny but no engorged veins
On palpation, swelling is warm ,tenderness present with bony
consistency
EGG SHELL CRACKLING may be elicitable when there is too
much thinning of cortex/pathological fracture

8. CLINICAL FEATURES
PAIN :
Vague persistent pain at the end of long bones in relation
to activity of the joint
Pain may increase after a pathological fracture
Limitation of joint movements due to mechanical block
Pathological fracture :
usually uni-cortical than a complete fracture
Neurological deficit may be seen in cases involving the spine and sacrum.
Metastasis is present in 1-5% cases. most common site being lung..k/a
LUNG IMPLANTS

9. INVESTIGATIONS
• Blood
serum calcium
phosphorus
ALK.PHOSPHATASE
• To rule out hyperparathyroidism

10. PLAIN RADIOGRAPHS
Epiphyseo-metaphyseal in location
Expansible lesion
Eccentrically situated
Confined to bone…cortical break-through
indicates more aggressiveness of tumor
Lysis with or without trabeculations giving
rise to soap bubble appearance
Geographic distribution rarely extending
to articular cartilage
Absence of margin of bone sclerosis or
punctuate calcification
Absence of intra- lesional bone formation
or ominous periosteal reaction

11. COMPUTED TOMOGRAPHY
• Confirms the integrity of cortex and outline tumor extent
• Sub-cortical destruction can be well appreciated
• Soft tissue extension & relationship to adjacent structures
cannot be studied!!

12. MRI
• Morphologic analysis & extent of tumor can be
assessed.
• Intra-medullary tumors are best seen in T1 weighted
images
• Extra osseous portion is best appreciated on T2 weighted
images

13. ANGIOGRAPHY
• Not routinely done
• To assess the relationship of major vessels to large
tumors
• To know major feeding vessels to tumor

14. BONE SCAN
• Gct takes up increased uptake of technetium 99
• Does not correlate to grading or nature of tumor
• Useful when multi-centric lesions suspected

15. BIOPSY
Final diagnostic tool for GCT
Types
FNAC (22 GAUGE NEEDLE)
CORE NEEDLE BIOPSY (14 GAUGE NEEDLE)
OPEN INCISIONAL BIOPSY

16. OPEN INCISIONAL BIOPSY
• Reliable
• Allows pathologists to evaluate cellular morphologic
features & tissue architecture from different sites of
lesion
• Use the smallest longitudinal incision
• Use a cautery knife & avoid crushing specimen texture
• Use meticulous heamostasis

17. PATHOLOGY
GROSS APPEARANCE
EARLY LESION:
Homogenous ,friable ,reddish
brown mass
LATE LESION:
Variegated appearance ,blood
filled areas

18. HISTIOGENESIS & MICROSCOPY
Composed of many multi-nucleated Giant cells
(40-60 nuclei/cell) in a sea of mono-nuclear stromal cells
Stromal cells are the main neoplastic component of the
tumor which regulate giant cell mediated
bone destruction.
Nuclei of stromal cells are identical to that of nuclei of
giant cells, a feature that distinguishes from other tumors
containing giant cells

19. HISTIOGENESIS & MICROSCOPY
Stromal & giant cells in the GCT contain
ACID PHOSPHATASE (TUMOR MARKER) Where as other
giant cell variants contains ALKALINE PHOSPHATSE
Areas of storiform spindle cell formation, reactive bone
formation or foamy macrophages may be seen
Secondarily ANEURYSMAL BONE CYSTS may be present
Indicators of aggressiveness:
Increased no. of stromal cells, hyperchromatism,
greater mitotic activity

20. GRADING OF GIANT CELL TUMOR
• CAMPANNCI’S RADIOGRAPHIC GRADING
• JAFFE et al PATHOLOGICAL GRADING
• ENNEKING STAGING OF GCT

21. CAMPANACCI RADIOGRAPHIC GRADING
GRADE I: CYSTIC LESION
GRADE II: Expansile lytic lesion with
THIN CORTEX but no break in cortex
GRADE III: Destructive radiolucent lesion with
cortical break and soft tissue extension

22. JAFFE et al PATHOLOGICAL GRADES
BASED ON MITOSIS & ATYPIA OF STROMAL CELLS
GRADE 1: numerous giant cells
mononuclear cells are rare
mitotic activity is absent
GRADE 2: mononuclear cells are numerous
moderate atypia & mitotic activity
GRADE 3: giant cells are few& small
atypia & pleomorphism are common
high mitotic activity

23. ENNEKING : STAGING OF GCT
STAGE 1 STAGE 2 STAGE 3
LATENT (10-15%) ACTIVE( 70-75%) AGGRESSIVE(10-15%)
ASYMPTOMATIC SYMPTOMATIC SYMPTOMATIC
DISCOVERED INCIDENTALLY ---------- RAPIDLY GROWING
MASS
MAY CAUSE PATHOLOGICAL # OFTEN ASSOC.
PATHOLOGICAL #
INTRACAPSULAR INTRACAPSULAR EXTRA CAPSULAR
WELL DEFINED MARGINS HAS EXPANDED/
THINNED OUT CORTEX
CORTICAL
BREAKOUTWITH
SOFTT-ISSUE EXT.
SCLEROTIC RIM ON XRAY/CT ACTIVE ON BONE
SCANS
ACTIVTY ON BONE
SCAN EXTENDS
BEYOND LESION ON
XRAY

24. DIFFERENTIAL DIAGNOSIS
• Brown tumor of hyperparathyroidism
other skeletal manifestations like
Osteopenia,
sub-periosteal resorption,
resorptive changes at distal phalanges
loss of lamina Dura of teeth
Elevated AKP & serum calcium levels & decreased
phoshophorus levels

25. • Chondroblastoma
adolescent with open physis
polygonal stromal cells
multiple punctuate calcifications
CHICKEN WIRE APPEARANCE on radiograph
• Aneursymal bone cyst
75% located in metaphysis
double density fluid-fluid level on CT/MRI
• Unicameral bone cyst
below 20 years of age
metaphyseal lesion
fallen fragment sign on radiographs

26. • Giant cell rich osteosarcoma
metaphyseal lesion
aggressive bone destruction
ill-defined margin
• Chondromyxiod fibroma
metaphyseal lesion
10 to 30 age group
pseudo-trabeculations are denser & thicker
• Non-ossifying fibroma
less than 15 years age
open physis
metaphyseal or diaphyseal lesion
well defined scalloped margins
rim of reactive host bone sclerosis

27. TREATMENT

28. The Tumour Is Invasive And Aggressive
It commonly recurs, may become malignant after
unsuccessful removal.
Recurrence is treated with en bloc excision.
En bloc excision is also indicated if the tumour has eroded
the cortex and extended into the soft tissues.
Eradicate the growth completely at the initial surgery
28
PRINICIPLES OF TREATMENT

29. PRE-OP PLANNING
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

30. TREATMENT OPTIONS
SIMPLE CURETTAGE: Intra- lesional curettage ALONE
EXTENDED CURETTAGE :
curettage along with use of adjuvants to augment curettage
EN BLOCK EXCISION
IRRADIATION THERAPY
EMBOLISATION
BISPHOSPHONATES
AMPUTATION

31. INTRA LESIONAL CURRETAGE
• Adequate exposure with
large cortical window
• High power burr
• Pulsatile jet lavage
• Curettage alone has high
recurrence rate

32. ADJUVANTS TO CURRETAGE
Advantage of using adjuvants
It eliminate the microscopic disease and reduces recurrence
Curettage and cementation causes a 2mm osteolytic lesion
zone surrounding the cement due to thermal injury
PHENOL-12-50% conc
Easily absorbed
Nephrotoxic
Soft tissue complication
HYDROGEN PEROXIDE

33. ADJUVANTS TO CURRETAGE
PMMA BONE CEMENT
Bone cement +ADRIAMYCIN+METHOTREXATE to reduce
recurrences
PRINICIPLE: heat of polymerization or direct toxicity of
monomer
CRYOSURGERY WITH LIQUID NITROGEN
it create 1-2cm zone of tissue necrosis.
Local complications…thermal shock,dehydration,wound
healing problems
Not easily available & costly
Storage difficulties

34. RECONSTRUCTION OF RESIDUAL DEFECT
• Bone grafting
autogenous bone graft
allograft
artificial bone graft substitutes
demineralised bone matrix
• Bone cement

35. ADVANTAGE DRAWBACK
Remodelling along stress
lines
Auto graft quantity is less
Reconstruction is permanent Donor site morbidity
Restores bone stock Allograft is
expensive..requires bone
bank
Restores normal
biomechanics at joint
surface(theortical)
Recurrence is difficult to
distinguish from graft
resorption
BONE GRAFT

36. PMMA BONE CEMENT
ADVANTAGE DISADVANTAGE
Immediate structural support
and early ambulation
MMA monomer is cytotoxic
Thermal effect
Radiographic detection of
recurrence is easier
Not a biological material.
Though strong in
compression but weak when
subjected to shear and
torsional forces
Fear of long term
degeneration of articular
cartilage in sub-chondral
lesion in wt bearing stress

37. SANDWICH TECHNIQUE
when tumor is <1cm from articular surface,
the incidence of degenerative changes in cartilage after the
use of cement alone is 2.5 times greater than when tumor is
>1cm away
In such conditions,
multilayer reconstruction technique is recommended
Interposing bone graft between the cartilage & cement reduces
heat damage and the resultant degenerative changes

38. Sandwich technique
• A layer of gel foam is layered over cement to reduce heat
damage to graft.

39. EN BLOC RESECTION AND SUBSEQUENT
RECONSTRUCTION/ARTHODESIS
Initial procedure of choice in more aggressive tumors .
2 cm of normal tissue is also excised.
Defects are filled with cancellous bone grafts, freeze dried
allografts or prosthesis.
This technique has low recurrence rate

40. Resection :Indications
 stage 3 lesions
cortex destroyed and soft tissue extension
present
 Recurrences
Large defects are expected
Joint surface destroyed or cannot be salvaged
Certain bones which can be sacrificed such as
• Lower end of ulna
• Upper end of fibula

41. RECONSTRUCTION OPTIONS
BIOLOGIC
AUTOGRAFT ARTHRODESIS
LIVE MICROVASCULAR FIBULAR GRAFT
OSTEO-ARTICULAR ALLOGRAFTS
ILIZAROV METHOD
ENDOPROSTHETIC JOINT REPLACEMENT
eg: custom mega prosthesis

43. EMBOLISATION
• Trans-catheter Embolisation of blood supply of
Certain un-resectable tumors like sacrum & pelvic
PREOP EMBOLIZATION also
Brings down size of tumor & provides pain relief
Re-embolisation needed at monthly intervals

44. AMPUTATION
• Malignant tumour
• Fungation
• Recurrence after surgery and irradiation
• Deep seated associated infection
• Extensive destruction of bone
• Severe disability

45. RADIOTHERAPY
• When complete excision or curettage is not possible
• Aggressive, multiple/ recurrent tumor
• Lesions of spine & sacrum
• The recommended dosage is 1,500 to 5,000 rads for 5 to 6
weeks using mega voltage therapy cobalt 62
• It may induces malignant change if it is given to the
benign lesion.

46. BISPHOSPHONATES
• Pamidronate / Zoledronate can be given
• They target osteoclast-like giant cells.
• Limit tumor progression