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Benign bone tumor ppt
1. GUIDED BY: PRESENTED BY:
DR. MAHESH BHATI SIR DR. PRADEEP CHOUDHARY
SENIOR PROFESSOR & PG 2ND YEAR
UNIT HEAD DEPT. OF ORTHOPEDICS
BENIGN BONE TUMORS
5. COMMON FEATURES:-
Well defined margins
Sclerotic rim
No periosteal reaction
Expanding lesion
No extra-osseous soft tissue involvment
Narrow zone of transition
6. TREATMENT
1.INTRA LESIONAL:
-plane of surgical dissection is
within the tumour.
-Symptomatic benign lesion.
-palliative in metastatic disease.
2.MARGINAL:
-plane of dissection passes
thro’the pseudocapsule formed by
the tumour.
-most benign lesion & low
grade malignancies.
7. 3.WIDE:
-plane of dissection is thro’ normal tissue.
-no specific distance is defined.
-quality of the margin is more important than the quantity.
- hiogh grade malignancy.
4.RADICAL:
All compartments containing tumour are removed en bloc
-deep soft tissue tumours
In case of bone tumour: removing entire bone and the
compartments of any involved muscle.
8.
9. EXTENED CURETTAGE:
- use of adjuvants, ( liq N2 , phenol ,
methacrylate, thermal cautery)
recurrence rate can be reduced
FILLING THE CAVITY:
-autogenous bone graft
-allograft
-demineralised bone matrix
-artificial bone graft substitute
-bone cement ( immediete stability
11. OSTEOMA
Benign bony outgrowth of membranous bones.
Multiple osteomas are associated with Gardner's
syndrome[multiple cut./subcut.lesion]
Highest incidence in the sixth decade
Male: female is 2:1
Asymptomatic,[sinonasal osteoma- sinusitis,
nasal discharge,headache]
Xray- 3-4cm homogenous round radiodense
mass
Excision if symptomatic
12. OSTEOID OSTEOMA
Commonest benign osseous tumour
Common in 1st& 2nd decade of life
10% of all benign bone tumours
M:F – 2:1
SITE: diaphysis, metaphysis of long bones [prox
femur mc>proximal tibia], posterior elements of
spine
On basis of CT/MRI-
subperiosteal,intracortical,endosteal
13. CLINICAL FEATURES
Dull pain, worse at night (night cries) & responds to
salicylates ( aspirin)
Swelling uncommon
Tenderness
RADIOLOGICAL FEATURES
A sharp round or oval lesion.
Less than 2 cm in diameter.
Radiolucent nidus surrounded by reactive sclerosis
Nidus- osteolytic/partially/entirely calcified
14. Nidus –central well defined
hypervascular area of
rarefaction[reduction of density of
bone]
15. INVESTIGATIONS
CT SCAN: IOC
Nidus is best localized with CT (1 mm cuts)
Bull‟s eye lesion
BONE SCAN: Tc99
Due to intense radioisotope uptake by nidus
and decreased uptake by surrounding sclerotic
bone, a double density image is created that is
typical of osteoid osteoma.
Headlight in fog appearance
17. MANAGEMENT
Course: Self limiting
On maturation, ossify and merge with surrounding
bone
No reports of malignant transformation till date
Treatment:
Conservative - not recommended because of
severity of pain
Surgical: En Bloc resection, Burr down
Percutaneous radiofrequency ablation (PRA) –drill
hole made & rf probe inserted with temp 90c for 5-6
min
18. OSTEOBLASTOMA
Benign vascular osseous tumour similar to
osteoid osteoma
Progressive growth, absence of reactive
perifocal bone formation &>2cm nidus
2nd, 3rd decade.
M > F
Sites: vertebrae- posterior elements
dull aching Pain, long duration ,not relieved by
nsaids, spine –stiffness, painful scoliosis
19. xray/CT scan- radiolucent well
circumscribed lesion with central calcification
& thin peripheral shell of reactive
bone„[cotton wool‟ if calcified ]
Spine-spinous process,pedicle markedly
enlarged
t/t – intralesional curettage or en-
bloc resection
Neurologic involvement-
decompressive laminectomy
21. ENCHONDROMA
Benign hyaline cartilage tumor occur in medulla of
bone and cause destruction of cancellous bone
Replaces normal bone with mineralized/un. Hyaline
cartilage
AGE: Most common between 2nd & 4th decades
SITES: Short tubular bones of hand (phalanges and
metacarpals), followed by metaphysis femur,
humerus and ribs
c/o- painless swelling,pain due to patho#
RADIOGRAPHS: well circumscribed distinct area of
rarefaction, expands the cortex ,
Calcification in older lesions -
spotty/punctate/stippled-rings & arcs
24. MANAGEMENT
Asymptomatic lesions - follow-up with serial
radiographs
Symptomatic – PET Scan or biopsy to r/o
any malignancy
Curettage and bone grafting
Wide excision to avoid recurrence
Pathologic fractures are allowed to heal
with closed treatment, curettage and bone
grafting is then required after fracture
healing.
25. OLLIERS DISEASE
Multiple enchondromatosis unilaterally
Non-hereditary disorder common in children
Affects metaphysis of long bones
Presentation – bony swellings leads to thickening
and shortening and deformities
25% risk of malignancy
MAFFUCCI SYNDROME -50%risk of malignancy
• hereditary familial disease
• multiple enchondroma and cavernous
haemangioma
26. OSTEOCHONDROMA
Also known as: Osteocartilaginous Exostosis
Cartilage capped bony projection on external
surface of bone containing a marrow cavity that
is continuous with underlying bone
Commonest benign tumour of bone.
Lesion has its own growth plate, usually stops
growing at skeletal maturity.
AGE GROUPS: first two decades
SEX PREDILECTION: M:F-1.5:1
27.
28. SITES OF PREDILECTION: Around the
knee(40%) and proximal humerus.
LOCATION: Metaphysis of long bones.
Asymptomatic- hard,immobile, nontendor
swelling of long duration
Pain: Mechanical irritation, Ischemic
necrosis, Perilesional ,bursitis, Fracture of
stalk, Malignancy <1%
29.
30. Growth disturbance of the extremity
Block to joint motion
No growth after skeletal maturity
X RAY
Pedunculated / sessile – exophytic
metaphysis / diaphysis
Marrow and cortices of lesion continuous with
bone
Directed away from growing end
Cartilage cap not seen on x ray
31. PATHOGENESIS:
Herniation of a fragment of growth plate through
periosteal bone cuff
Misdirected growth of that portion of physis
HISTOLOGY:
Lesion has three layers- periosteum,cartilage,bone
Cartilage cap resembles layers of the normal growth
plate
The cartilage is more disorganized than normal
Binucleate chondrocytes in lacunae
Covered with a thin layer of periosteum.
32. Cartilage cap 1-3 mm thick, thicker in children
SIGNS OF MALIGNANCY:
>2 cm after skeletal maturity indicates
possible malignant transformation
Growth spurt of lesion beyond skeletal
maturity
Development of soft tissue with calcifications
Dispersed calcifications within the
cartilaginous cap
33. MANAGEMENT
Surgical excision
Indication- cosmetic
-limitation of joint function,
-fracture,
- secondary impingment of nerve,
tendon, or vessals,repeated
-bursitis,
-suspicion of malignancy
34. HEREDITARY MULTIPLE EXOSTOSES (H.M.E)
Also known as: Multiple Exostoses, Diaphyseal
aclasis
Autosomal dominant hereditary disorder, 10% no
family history. EXT1,2,3 genes [EXT1 –severe dis]
Knees, ankles and shoulders are most frequently
affected.
Knobby appearance, Short stature
Forearm deformity, Tibio-fibular synostosis, Genu
valgum, Coxa valga
Rx - Excision of symptomatic exostosis
Correction of deformity and limb length discrepancy
35. CHONDROBLASTOMA
ALSO KNOWN AS: Codman’s Tumour
Arises from immature cells of epiphyseal
cartilage
AGE GROUPS: 10 to 20 yrs.
SEX PREDILECTION: Males more affected
than females.
SITES OF PREDILECTION: Proximal part of
the tibia, proximal part of the humerus and
femur.
LOCATION: Epiphysis/ apophysis
SYMPTOMS: Pain and local swelling of joint
without h/o trauma
36. RADIOGRAPHS:
Well defined oval lytic lesion
Sclerotic margin
Epiphysis
Eccentric
Cottonwool calcification
HPE: Chicken-wire calcification
37.
38.
39. Highly cellular and relatively undifferentiated
tissue,made up of polygonal chondroblast
like cells and multinucleated giant cells of
osteoclast type.
Presence of cartilagenous intercellular matrix
with areas of focal calcification is typical.
d/d- gct, tb,abc
t/t- intralesional curettage with reconstruction
40. GIANT CELL TUMOUR (OSTEOCLASTOMA)
INCIDENCE : 5% of biopsied primary bone
tumors.
F>m,1.5:1
Epiphysiometaphysel region
5Es- Elderly
Epiphysis
Eccentric
Expansive
Egg shell
crackling
41. c/f- pain,swelling, joint restriction, ms
wasting,pathological fracture
Patho- end of bone is expanded, thin
periosteum,fleshy dark brown soft friable
mass, cystic spaces seen with vascularised
network of round oval stromal cells &
multinucleated giant cells
42. Campanacci Grading:
Grade I: Tumour associated with well defined
margins and thin rim of mature bone [cystic
lesion]
Grade II: Tumour is well defined but has no
radiopaque rim[thin cortex but no break in
cortex]
Grade III: Tumour has fuzzy borders [cortex
break & soft tissue extension]
44. Radiological Signs
Lytic lesion
Epiphysis
Narrow zone of transition
Thinning of cortex
Honey comb appearance
Soap bubble appearance
45. DD: GCT has to be differentiated from giant
cell variants.
Unicameral bone cyst -<20 yrs
age,metaphyseal region, fallen fragment sign
Aneurysmal bone cyst-metaphyseal,double
density sign on ct
Non-ossifying fibroma - <15yr age,
metaphysis/diaphysis,well defined scalloped
margins,rim of reactive host bone sclerosis
46. Chondroblastoma –adolescent with open
physis,polygonal stromal cells with punctate
calcification,chiken wire appr.
GCT of hyperparathyroidism (Brown tumor )-
osteopenia,subperiosteal resorption,high ca
&ALP,PTH
48. Treatment :
Curettage and bone grating
Curettage and placement of bone cement
Curettage and cryosurgery
Enbloc resection: 2cm normal tissue
include,Endoprosthesis, Arthrodesis
Angioembolization
Zolindronic acid –traget osteoclast like giant
cells.Follow-up : Follow-up examination is
essential for at least 5 years
49. SANDWICH TECHNIQUE
When tumor is<1cm from articular surface
Incidence of degenerative changes in
cartilage after the use of cement alone is 2.5
times greater than when tumor is>1cm away
Than multilayered reconstruction is
recommened- interposing bone graft b/t
cartilage &cement reduces heat damage &
degenerative changes.
55. ANEURYSMAL BONE CYST
expansile, blood filled cystic cavity separated
by connective tissue{not lined by
endothelium}
<20 yr age
Etiology:
Primary ABC (65-99%): Unknown
Secondary ABC (1-35%): preexisting bone
56. C/F :
5-20 yrs, 60% in females.
Presents with pain at the site.
80% of lesions – long bone like femur and tibia-
fibula
Spinal lesions affect the neural arch, spinous
process, transverse process, and lamina. The
thoracic and lumbar spine are the common regions.
Histology: ABC consists of multiple blood filled
sinusoid spaces. The solid, numerous multinucleated
giant cells.
58. CT scan features: “blood filled sponge‟‟, fluid
levels due to sedimentation of blood.
MRI : Multiple cysts: Fluid – fluid levels [double
density fluid level & intralesional septa]sbc vs
abc
Nuclear study: “ donut sign ” i.e. peripheral
increased uptake.
Angiography: hypervascularity in the periphery
of the lesion.
Rx: Surgical curettage with bone grafting.
Recurrence rate is high
62. NONOSSIFYING FIBROMA (FIBROUS CORTICAL
DEFECT)
1st & 2nd decade
Site- femur ,tibia,humerus
•Solitary & well defined
•Eccentric
•radiolucent, ovoid, bubbly
• metaphysis
Rim of sclerosis
Doesn’t expand cortex & no periosteal rxn
63. FIBROUS DYSPLASIA
Developmental anomaly of bone formation.
Replacement of normal bone by fibrous
tissue &small woven bone
GNAS 1 MUTATION
C/F : 3-15 yrs,pain and sk deformity
M:F 1:1, site –rib ,femur ,humerus
Bowing deformities and pathologic fractures,
Café-au-lait spots are present in 30% of
patients.
65. Fibrous dysplasia with Shepherd‟s crook
deformity and pathological fracture
Well defined Geographic
lytic lesion
Groundglass matrix
Rx –curettage & grafting
Int fixation with osteotomy
66. BROWN TUMOR(OSTEITIS FIBROSA CYSTICA)
Replacement of bone by vascularized fibrous
tissue secondary to PTH stimulated osteoclastic
activity.
Not true neoplasm,mimic like tumor
Eccentric, expansile lytic lesion with well defined
non sclerotic margin.
Haemorrhage & giant cell rxn within the fibrous
stroma may give rise to brownish,tumor like
mass,whose liquefaction leads to fluid –filled
cysts
67. Subperisteal cortical resorption of middle
phalanges
High PTH & ALP, HIGH Calcium & low P
Rx – calcium &vit d
parathyroidectomy