giant cell tumor or osteoclastoma

1. GIANT CELL TUMOR
Dr. PATEL YAHYA ISMAIL

2. INTRODUCTION
 One of the most common bone tumors
 Benign tumor, but locally aggressive and has malignant potential
 First described by Sir Astley Cooper in 1818

3. DEFINITION
 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
 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
 GCT of small bones occur in younger age group with high
incidence of multicentricity

5. SITE OF INVOVLMENT
 Solitary or multicentric (1%)
1. distal end of femur
2. proximal end of tibia
3. distal end of radius
4. upper end of humerus
5. lower end of tibia
 cancellous disposed bone ends
which are sites of high bone turn over
& osteoclastic activity
 Others like hand , spine and pelvis

6. CLINICAL FEATURES
1. 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

7. 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
 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

8. INVESTIGATIONS
 serum calcium,
 phosphorus,
 ALK.PHOSPHATASE
 To rule out hyperparathyroidism

9. PLAIN RADIOGRAPHS
 Epiphyseo-metaphyseal
 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

10. 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!!

11. 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

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

13. 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

14. BIOPSY
 Final diagnostic tool for GCT
1. Types FNAC (22 GAUGE NEEDLE)
2. CORE NEEDLE BIOPSY (14 GAUGE
NEEDLE)
3. OPEN INCISIONAL BIOPSY

15. 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

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

17. 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

18. 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

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

20. 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

21. 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

22. ENNEKING : STAGING OF GCT

23. GIANT CELL TUMOUR VARIANTS
1.Brown tumor of hyperparathyroidism
 Osteopenia,
 sub-periosteal resorption,
 resorptive changes at distal phalanges
 loss of lamina Dura of teeth
 Elevated AKP & serum calcium levels &
 Decreased phoshophorus levels

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

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

26. TREATMENT
 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

27. 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

28. 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

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

30. 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

31. 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
1. thermal shock,
2. dehydration,
3. wound healing problems
 Not easily available &
 costly Storage difficulties

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

33. BONE GRAFT
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
Recurrence is difficult to
distinguish from graft
resorption

34. 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

35. 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

36. 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

37. 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

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

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

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

41. 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

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

43. THANK YOU