Neoplasm(Dorland) : New & Abnormal growthUncontrolled &

Progressive.
Malignant Neopl : Anaplasia & Metastasis.
Synonim : Tumor.
Precursor lesion
High Risk : - Olliers disease / Mafucci syndrome
- Familial Retinoblastoma syndrome
Moderate Risk :
- Diaphysial aclasis/multiple
osteochondromatosis
Low Risk : - F.D., Osteomielitis chronic, metalic implant

TUMOR : enlargement of a body part

Inflammation swelling
Accumulation of fluid haematoma, effusion, pus
collection
Neoplasms
Others
NEOPLASM: neoplasia of a tissue
Abnormal growth
Progressive
Abnormal cells

Majority bone neoplasma arise de

novo/idiopathic
Genetic/chromosomal aberration
Radiation injury

Etiologi

Types of Musculoskeletal
Neoplasm
Based on the primary site:
Primary neoplasm
Secondary neoplasm
Based on malignity:
Benign tumor
Malignant tumor
Conditions that mimic neoplasm

Origin of Primary Musculoskeletal Neoplasm

Osteogenic
Chondrogenic
Fibrogenic
Hematopoietic
Angiogenic
Lipogenic
Neurogenic
Uncertain origin

Classification (Aegerter,1975)
I.Reactive Bone
Lesion

A.Osteogenic
1. Osteoid osteoma
2. Osteoblastoma

II.Hamartomas
Affecting Bone
A. Oteogenic
1.
Osteoma
2.
Osteochondroma
B. Chondrgenic
1.
Enchondroma

B.Collagenic
1. Subperiosteal
cortical defect
2. Non-osteogenic
fibroma

C. Collagenic
1.
Angioma
2.
Aneurysmal bone
cyst

III.True Neoplasms
of Bone
A. Osteogenic
1.
Osteosarcoma
2.
Parosteal sarc
B. Chondrgenic
1.
Benignchondrobla
stoma
2.
Chondromyxoid
fobroma
3.
Chondrosarcoma
C. Collagenic
1.
Fibrosarcoma
2.
Angiosarcoma
D. Myelogenic
1.
Ewings tumor
2.
Reticulum cell
sarc
3.
Hodgkins disease
E. Osteoclastoma

Diagnosis
Clinical history
Physical signs
Biochemical findings (lab)
Radiographic features
Scintigraphy (bone scan)
Computed tomograpphy
Arteriography (angiography)
MRI
Biopsy
Microscopic appearance

Clinical features
Non Spec. long time may-elapse until tumor is diagnosed
Cardinal symptoms :
- Pain, swelling and general discomfort
- Limited mobility, pathologic Fx.
Pain
First and most common symptom in malignant B.T
Initially as rheumatic pain intermittent, at rest more
intense disturb sleep spread into
adjacent joint
arthritis post traumatic
phenomenon

 History: - Duration, progression, pain

- Trauma ?
- Family history of neoplasma
- Previous tx: radiotherapy ?
Bone tumors Pain
Typically deep seated and dull, may resemble a
toothache
Initially intermittent, usually progresses in intensity
and becomes constant
Night pain
May be a long standing mild to moderate pain (lowgrade tumors), or a shorter course (high-grade)
Soft tissue tumors Lump

Basic orthopaedic clinical examination

Clinical examination for neoplasm
Color
Temperature
Venous dilatation
Smoothness of the mass smooth/rough
Overlying skin changes , peau de orange, skin retraction
Size
Consistency cysteous, hard, bony-hard, pulsative
Margins/borders well/ill-defined border
Mobility of the mass mobile/fixed to surrounding tissue
Tenderness
Auscultation bruit
Adenopathy

Laboratory Studies
Nonspecific
Phosphatase alkali
Serum globulin-albumin ratio
Bence-Jones protein

Blood routine
ESR: - infection & neoplasm
> 80

- Benign neoplasm (n)

- Active benign malignant neoplasm esp. Ewing , but not
mm/h, if > infection

CRP: indicates systemic inflammation/process

 Enzyme profile
- Serum alkaline phosphatase (SAP)
- Indicates increase bone turn over
- Present in most tissues in the body
- Predominant source: hepatobiliary system and bone
- Pediatric conventional OsteoSa: SAP
- NOT all OsteoSa has SAP , BUT normal SAP does NOT
exclude
OsteoSa
- Minimal SAP positive in many process even in healing
fracture
- Adult with SAP due to bone disease: Paget or diffuse
metastatic Ca
- Liver disease: SAP also GOT/GPT which not in primary BT
- Ca & PO4 serum & urine metabolic/metastatic bone disease
- Serum Latic Dehydrogenase (LDH)
- in some patient OsteoSa, Ewing Sa prognostic factor
- Initial SAP/LDH (n) can be used as monitoring for relapse/
reccurencies

Radiography
Plain film orthogonal view
Bone scan Technetium bone scan
CT-scan
MRI
Others angiography, etc
Pay attention to:
Race predilection
Age predilection
Sex predilection
Location of the mass within the bone

Grade 1
1a. Sclerotic margin without complete
cortical
penetration
1b. Sharp margin, non-sclerotic
margin
without total cortical
penetration
1c. Poorly defined margin, totally
penetrated the cortex
Grade 2
geographic lesion + moth-eaten
and/or permeative destruction
Grade 3
motheaten and/or permeative
destruction only

Radiographic Features

Osteosarcoma

Osteolysis: bone resorption

Osteosclerosis: bone
deposition
Expansion
Codmans triangle
Onion skin
Sunburst appearance
Pathological fracture

Biopsy
Role of biopsy in orthopaedic neoplasm:
Confirm diagnosis
Decision-making in treatment
Prognosis

Biopsy Method:
Needle biopsy

Fine needle aspiration

Core biopsy
Open biopsy
Incisional biopsy take tissue sample at least 1 cm 3
Excisional biopsy

STAGING FOR ORTHOPAEDIC NEOPLASIA

Musculoskeletal Tumor Society / Enneking system most

popular,easy and useful

AJCCs TNM system not widely accepted in Orthopaedy
Enneking System Based on:

Mass site/spread (T)

T1: Intracompartmental
T : Extracompartmental
2
Histologic grading (G)
G0: Benign lesion
G1: Low-grade malignancy
G : High-grade
2
Distant metastasis (M)
M0: No metastasis
M1: Metastasis present

TREATMENT
Based on staging
Method:

Radiotherapy alone, or in combination with

chemotherapy and surgery
Chemotherapy multi-agents, adjuvant, neo-adjuvant
Operative
Operative Treatment
Based on staging stage determines the resection margin
Method:
Limb-salvage complex operation

Amputation

Planning after staging

Benign tumors
Stage 1 tumors: Intracapsular excision (or curettage)
is
adequate.
Stage 2 tumors: Extracapsular excision passing
through the
reactive zone is needed.
Stage 3 tumors: Wide margins of resection are
required
in stage 3 or aggressive benign lesions.
In areas not amenable to wide excision,
marginal excision together with adjuvant
treatment (eg, radiation therapy) may be
acceptable.

Planning after staging

Malignant tumors
Stage 1A: Tumors are treated with wide excision and usually are

amenable to
limb salvage procedures.
Stage 1B: Tumors may be treated with wide excision but the choice
between
amputation and limb salvage depends on the
estimated amount of
residual tumor left behind after a limb
salvage procedure.
Stage 2: Tumors are high grade and usually are
extracompartmental and
have a significant risk for skip
metastases. They usually are not
amenable to limb
salvage operations and require radical
amputation or
disarticulation in most patients. However, bone
tumors responsive to chemotherapy may be treated successfully
using wide excision and adjuvant therapy.
Stage 3: Tumors are responsive to chemotherapy and may be
treated with
aggressive resection. Tumors not responsive to
adjuvant
therapy
should be treated with palliative
resection.

Suggestive for malignancy:

Pain in previously painless lump
Rapid increase in size
Poor demarcation
Attached to adjacent tissues
Sonogram discrete echo pattern

REHABILITATION
Rehabilitation of function reconstructive

surgery may be needed

Rehabilitation of psychological state
Rehabilitation of social factors

CLASSIFICATIONS OF PRIMARY TUMOURS

INVOLVING BONES
Metastatic cancers are the most frequent malignant tumors found in bone
Histological Types

Benign

Hematopoietic (40%)

Malignant
Myeloma
Malignant lymphoma

Chondrogenic (22%)

Osteochondroma
Chondroma
Chondroblastoma
Chondromyxoid fibroma

Chondrosarcoma
Dedifferentiated
chondrosarcoma

Osteogenic (19%)

Osteoid osteoma
Osteoblastoma

Osteosarcoma

Unknown origin (10%)

Giant cell tumour

Ewing tumour
Giant cell tumour
Adamantinoma

Histiocytic origin
Fibrogenic
Notochordal
Vascular, Cystic, lipogenic
neurogenic

Fibrous histiocytoma
Fibroma

MFH
Fibrosarcoma
Chordoma

AGE(probably the most important clinical clue).

Age group

Most common benign lesions

Most common malignant tumors

0 - 10

simple bone cyst

eosinophilic granuloma

Ewing's sarcoma
leukemic involvement
metastatic neuroblastoma

non-ossifying fibroma
fibrous dysplasia
simple bone cyst
aneurysmal bone cyst
osteochondroma (exostosis)
osteoid osteoma
osteoblastoma
chondroblastoma
chondromyxoid fibroma

osteosarcoma,
Ewing's sarcoma,
adamantinoma

enchondroma
giant cell tumor

chondrosarcoma

osteoma

metastatic tumors
myeloma
leukemic involvement
chondrosarcoma
osteosarcoma (Paget's associated)
MFH
chordoma

10 - 20

20 - 40

40 & above

SITE OF LONG BONE INVOLVEMENT

(most primary bone tumors have favored sites within long bones; this may provide a clue to
diagnosis).

Diaphyseal lesions centered in

the cortex:
Adamantinoma, osteoid
osteoma

Metaphyseal intramedullary lesions:

Osteosarcoma is usually centered in the
metaphysis. Chondrosarcoma and
fibrosarcoma often present as
metaphyseal lesions. Osteoblastoma,
enchondroma, fibrous dysplasia, simple
bone cyst, and aneurysmal bone cyst are
common in this location.

Metaphyseal exostosis:
Osteochondroma

Diaphyseal intramedullary lesions:

Favored location for Ewing's
sarcoma, lymphoma, myeloma.
Common for fibrous dysplasia and
enchondroma

Metaphyseal lesions centered in the

cortex:
Classic location for a non-ossifying
fibroma (NOF). Also, a common site
for osteoid osteoma.

Epiphyseal lesions:
Chondroblastoma (Ch) and Giant
Cell Tumor (GCT) are almost
invariably centered in the
epiphysis. Chondroblastoma is a
rare tumor seen in children and
adolescents with open growth
plates. GCT is the most common
tumor of epiphyses in skeletally
mature individuals with closed
growth plates. GCT often shows
metaphyseal extension.

OSTEOID OSTEOMA
characterized by:

a small size,
limited growth potential,
tendency to cause extensive reactive changes in
surrounding tissues.

The lesion tissue, called a "nidus: a small

radiolucent focus, less than 1 cm in size, either

within the cortex or adjacent to it.
The lesion is thought to produce prostoglandin/
prostocyclin-mediated effects on the surrounding
tissues

inducing
exuberant,
reactive,
periosteal sclerosis, soft tissue edema and pain

OSTEOID OSTEOMA
Incidence
Predominant: males between the ages of 10 - 25 years
femur and tibia (50% of cases)
Other: humerus, the small bones of the hands and feet, and

the spine.
If the lesion occurs in a close proximity to the articular
surface of the joint it causes severe reactive synovitis

Sign and Symptoms

Pain.
Pain is often slowly progressive, relieved by rest, most intense at
night
Swelling and redness.
Joint effusion~ the lesion may impairment of join function
because of reactive synovitis and effusion.
Scoliosis
Abnormalities in bone growth.
Some osteoid osteoma of long bones present in infancy and
located close to a growth epiphyses result in lengthening of the
segment.

OSTEOID OSTEOMA

Pathological Findings
If the nidus is removed
intact, it appears as a
circumscribed portion of
red,
trabecular
bone,
usually less than 1cm in
size

Low-power view shows

thelesion tissue ("nidus"),
well demarcated from the
surrounding sclerotic bone.

OSTEOID
Radiological Findings
OSTEOMA

Plain film shows a small, intracortical,

radiolucent focus (nidus), surrounded

by dense reactive periosteal bone.
The Lesion is located in the mid
portion of the humeral shaft.

Differential Diagnosis
Osteoblastoma

is a benign boneforming neoplasm, histological findings

may be identical. But osteoblastoma is
characterized by a larger size (more than
1.5 cm) and absence of diagnostic
clinico-radiological findings of osteoid
osteoma.
Intracortical osteosarcoma. Look for
the presence of significant nuclear
atypia and invasive growth pattern
indicative of malignancy.

OSTEOID OSTEOMA
Treatment
The only effective treatment is complete removal of

the nidus
Less destructive method:
such as laser coagulation or coring out the lesion
under CT control,
Non-invasive procedure:
called heat vascularity ablation, involves placing an
electrode into the tumor, which is heated causing a
'microwave' treatment to the tumor.

Prognosis
Complete removal of the focus of tumor tissue results in
cure. Incomplete removal of this focus may lead to
recurrence of symptoms and the necessity for reoperation

NON-OSSIFIYING FIBROMA
Definition
NOF is a common, non-neoplastic, self-healing lesion

occuring in skeletally immature individuals.

Incidence
NOF usually occurs between the ages of 5 and 20

years. The larger lesions occupying more than a half of

the bone diameter may present with a pathologic
fracture.

Sign and Symptoms

This lesion is commonly silent clinically. Local pain,

usually of short duration, is sometimes produced.

pathologic fracture

NON-OSSIFIYING
FIBROMA
Pathological Findings

Low power view showed a

moderately
cellular
lesion
composed of uniform spindle cells
in a storiform pattern and
scattered giant cells; Spindle cells
had bland appearance.

Radiological findings

Plain radiograph shows a sharply

demarcated, lucent, loculated,
metadiaphyseal lesion surrounded
by a rim of sclerotic bone.
The lesion predominantly involves
the lateral portion of the bone and
produces mild cortical expansion.

NON-OSSIFIYING
FIBROMA
Treatment
Treatment is usually unnecessary.
If the defect is very large or has led to repeated

fractures, it can be treated by curettage and

bone grafting.

Prognosis
Many resions have been shown to undergo

spontaneous regression. There is no risk of

malignancy change.

Simple bone cyst

Occurs before 15 years of age.
50% develop in the proximal end of the humerus.
Other common sites include: the proximal femur , the proximal

and distal tibia , iliac wing and calcaneus.

Common presentation : incidental discovery when radiographs
are taken for other reasons or by pathological fracture after
minor trauma.
Solitary or unicameral bone cyst:
Expansion of bone & thinning of the bone cortex through
endosteal erosion.
Pathological fracture.
Extensive bone destruction resemble a neoplasm

Simple bone cyst

The cavity is filled by a serous fluid.The fluid will be

stained by hemorrhage if pathological fracture occurred.

Radiographically appear as symmetric well demarcated
radiolucent expansile lesions at bone metaphyses, often
extending up to the physeal plate and the cortex may
be thinned. as the bone grows away from the cyst , the
lesion may come to lie in the diaphysis.
When pathological fracture occurs a fragment of thin
cortex may separate and fall in the cavity {fallen leaf
sign} .
No periosteal reaction except after stress fracture

Simple bone cyst

Simple bone cyst

Simple bone cyst

Simple bone cyst

With skeletal growth and maturation, simple bone

cysts tends to spontaneous healing.

Most fractures of simple bone cysts heal rapidly
with closed treatment as callus formation induces
cystic healing as well as fracture consolidation.
Methods of treatment:
1- observation and restriction of activity until the cyst

heals in asymptomatic lesions .

2- curettage and bone grafting in active lesions.

Aneurysmal bone cyst

ABCs arise primarily as a skeletal osteolytic lesion or may arise

as a reaction to hemorrhage within a pre-existing tumoral lesion.

The primary lesion is found mostly in the second decade of life.
Common sites are metadiaphysis of long bones preferably in the
lower limb bones.
The lesion usually is eccentric subperiosteal in origin, so
pathological fracture is unusual presentation, but it may arise
centrally within the bone.
The diagnostic features are :
Marked expansion of the involved bone, cystic bone destruction and

periosteal new bone formation.

The lesion rapidly destroys the original bone cortex and is contained
only by a thin rim of periosteal new bone.
During curettage there may be a considerable bleeding from the
fleshy lining membrane [welling or pouring of blood ]

Aneurysmal bone cyst

Radiographic features:
a well defined radiolucent subperiosteal osteolytic
lesion elevating and inflating the periosteum and
progressively eroding the cortex, with scarce periosteal
reaction observed as a thin shell of reactive bone at
the metaphysis of long bones [egg shell].
The cyst initially appears as an eccentric osteolytic
area .

Aneurysmal bone cyst

Aneurysmal bone cyst

Aneurysmal bone cyst

Methods of treatment :
The treatment of choice is curettage and
autogenous grafting. [during curettage
copious bleeding may be encountered ].

osteochondroma
Osteocartilaginous exostoses: [cartilage capped

exostosis] the most common tumors of bone.

Are hamartomas and occur during skeletal
growth as a small overgrowth of cartilage at the
edge of the physeal plate and develops by
enchondral ossification into a bony protuberance
still covered by the cap of cartilage.
They continue to grow and mature , undergoing
enchondral ossification.
Once skeletal maturity occurs, growth of
exostosis ceases.

osteochondroma
Radiographic features are usually classic and

other studies are rarely required to make

the diagnosis.
The pathogonomonic feature of an exostosis is

that the medullary bone is contiguous in the

stalk of the exostosis and the underlying bone.
Lesions are usually pedunculated but can be
sessile, the lesion initially is adjacent to the
physeal
mechanism
and
becomes
more
diaphyseal as the child ages.
Pedunculated lesions extend away from the
epiphysis of origin toward the diaphysis of the
involved bone.
It looks smaller than it feels because the
cartilage cap is usually invisible

osteochondroma

osteochondroma

osteochondroma
The exostosis is covered with a cartilaginous

cap and undergoes enchondral ossification to

from the underlying cancellous bone.
The thickness of the cap is variable depending
on the age of the person and diminishes
following skeletal maturity. The cells of the
cartilaginous cap are arranged in columns
similar to an epiphyseal mechanism.

osteochondroma
Common problems of osteochondromas:
1.
2.
3.
4.

5.

Fracture of the stalk in pedunculated type.

Entrapment of the adjacent neurovascular
structures.
Adventitious
bursa
formation
over
the
cartilaginous cap which is liable for bursitis.
Malignant transformation to chondro sarcoma
{ more in lesions arising in the pelvis, scapula,
ribs and spine }.
Pressure atrophy on adjacent bone when arise
from the leg or forearm bones.

osteochondroma

osteochondroma
Malignant transformation :
Malignant transformation of a single osteochondroma
is a rare event {<1%} and is less common than in
patients with MHE {6%}.
Lesions arising in the pelvis, scapula, ribs and spine
are at higher risk for malignant transformation than
those in the appendicular skeleton.
Transformation does not occur before skeletal maturity
Methods of treatment :
Surgical excision should be reserved for lesions that

cause discomfort or deformity or are cosmetically

unappealing.
To avoid the local recurrence, the entire cartilaginous
cap must be excised.

osteochondroma
Multiple Heritable Exostoses :
MHE is a syndrome of being multiple, heritable and

associated with skeletal deformity and short stature,

and by having a significant frequency of transformation
into secondary peripheral chondrosarcoma.
The ratio of solitary exostoses to MHE is at least 10:1.
Exostoses usually are identified earlier in persons with
MHE [usually by 10 years of age] than with solitary
lesions.
MHE are transmitted as an autosomal dominant trait.
The lesions tend to be diffuse and relatively symmetric.
The long bones are affected most severely, with the
greatest involvement around the knee, shoulder, hip,
wrist and ankle.
The pathogenesis and histopathologic features are the
same as for solitary exostoses.

osteochondroma
Multiple Heritable Exostoses:
Radiographically:
the lesions are larger than the solitary one and
the underlying bones are shorter than normal, with a widened

metaphysis [ due to failure of bone remodeling as the

periosteum is tethered in all direction at the metaphysis ] .

Malignant transformation:
occurs in around 1-6% and
central lesions [ pelvis, scapula, ribs, and spine] are at great

risk
of
malignant
osteochondromas.

transformation

as

with

solitary

Excision of one or more exostoses often is necessary in

persons with MHE because of discomfort or for mechanical
reasons as fracture of a stalk in pedunculated lesion or
due to bursitis and pressure on nearby vital structures.

osteochondrom
a

Enchondroma
Clinical Features:
Enchondromas

are hamartomatous collections of mature

hyaline cartilage within bone.
They usually present as solitary lesions.
Multiple lesions known as enchondromatosis or Ollier`s
disease.
It arise from the lack of normal enchondral ossification below
the growth plate.
They are asymptomatic unless a pathological fracture occurs.
They commonly involve the small tubular bones in the hand
and foot, the proximal humerus, the femur and the ribs.

Radiological features:
A

well defined radiolucent central lesion within the

metaphysis or diaphysis of the involved bone, sometimes the
bone is slightly expanded.
Calcification may be present and usually is stippled or flecks,
smoke ring or popcorn ossification.

Enchondroma

Enchondroma

Pathological findings

Low-power
microscopic
examination
of
the
biopsy
specimen
shows
three
characteristic :
a)
b)
c)

vague lobularity;
abundant cartilaginous matrix,
which can be focally calcified;
low cellularity.

High-power view shows clustered

and scattered chondrocytes with
small, uniform, darkly stained
nuclei. Occasional bi-nucleated
chondrocytes
are
present.
Importantly,
there
were
no
mitotic figures.

CHONDROMA (ENCHONDROMA)
Differential Diagnosis
a low-grade (Grade 1) chondrosarcoma. The

presence of pain, large size of the lesion > 5cm,

certain skeletal locations and "aggressive"
radiological features of the lesion favor the
diagnosis of chondrosarcoma.
Histologically, Grade 1 chondrosarcoma shows
moderate cellularity, mild nuclear atypia, "open"
chromatin, small nucleoli, frequent. binucleated
cells and rare mitotic figures. Infiltrative growth
pattern is indicative of malignancy

CHONDROMA (ENCHONDROMA)
Treatment
Treatment is not always necessary. An
asymptomatic chondroma does not need
excision or other treatment
follow-up xrays are indicated to rule out
disease progression..
If the tumor appears to be enlarging, or if
it presents as a pathological fracture,
should be removed as thoroughly as
possible by curettage; the defect is filled
with bone graft.

Fibrous Dysplasia
present in a variety of ways: monostotic, polyostotic,

and with or without associated syndromes

Most cases are diagnosed within the first three
decades and have a distinct female predilection
monostotic presentation is more common than
polyostotic This condition is a dysplastic anomaly of boneforming mesenchymal tissue with an inability to produce
mature lamellar bone. Accordingly, the bone is arrested in the
woven state with a resultant proliferation of spindle cell
fibroblasts

In the polyostotic form, it tends to involve one side of

the body rather than bilaterally. Nevertheless, it can involve any
bone of the body

Fibrous Dysplasia
The most common location is the proximal femur,

where it results in the so-called shepherd's crook

deformity. Other areas frequently involved include the
tibia, pelvis, humerus, radius, and ribs.
In addition to bony involvement, patients can
demonstrate caf au lait skin pigmentation seen in
neurofibromatosis. Patients with fibrous dysplasia may
have associated endocrine problems.
5% of patients with the polyostotic form of fibrous dysplasia also

exhibit precocious puberty (McCune-Albright syndrome).

endocrine

abnormalities include hyperthyroidism, acromegaly,

Cushing disease, and hypophosphatemic osteomalacia. Polyostotic
fibrous dysplasia with soft-tissue myxomas is known as Mazabrand
syndrome.

Fibrous dysplasia can also involve the skull and jaw

bones, mimicking ossifying fibroma of jaw bone.

Fibrous Dysplasia
Macroscopy
The bone is often expanded and the lesional tissue has a tan

grey colour with a firm-to-gritty consistency.

There may be cysts, which may contain some yellow-tinged
fluid, When cartilage is present, it often stands out as sharply
circumscribed of blue-tinged translucent material

Histopathology
The lesion is generally well circumscribed and composed of

fibrous and osseous components.

The fibrous component is composed of cytologically bland
spindle cells with a low mitotic rate. The osseous component
is comprised of irregular curvilinear trabeculae of woven (or
rarely lamellar) bone. Occasionally, the osseous component
may take the form of rounded psammomatous or cementumlike bone. Secondary changes such as foam cells.

Fibrous Dysplasia

Fibrous dysplasia. A Characteristic C shaped bony spicules with liypocelljlan^pindle cell stroma. B
High power appearance showing the typical appearance of bone which seems to be dissected by
spindle cell proliferation. Note that there is no osteoblastic rimming.

Fibrous Dysplasia

Fibrous Dysplasia

Fibrous dysplasia tends to be active during the growing years and

then burns out in adult life. > 1% of lesions convert to

osteosarcoma, fibrosarcoma, or even chondrosarcoma. If
conversion does occur, it almost always happens during
adulthood.
In pediatric patients with active disease, curettage and grafting
should be avoided because of high recurrence rates. The goals
in treating pediatric patients should be the prevention and
treatment of deformity, especially in the lower extremity.
Most cases should become quiescent with skeletal maturity. If not,
the best surgical treatment in adults consists of rigid fixation with
an intramedullary implant with strut grafting as needed.
The best surgical treatment in adults consists of the use of long
autogenous fibular struts combined with autogenous cancellous
bone graft. Medical management with bisphosphonates is of
benefit in some cases.
Irradiation is contraindicated because it may lead to irradiationinduced sarcoma at a later date.

Giant cell tumor

Although benign, GCTs show a tendency for significant

bone destruction, local recurrence, and occasionally

metastasis .
Frequency:

GCTs represent approximately 5% of all primary bone tumors

and 18-21% of all benign bone tumors.

The most common bone tumor in the young adults aged 25 to
40 years, GCTs occur most commonly in the third decade of
life.

giant cell tumors only occur after the epiphyseal

plates have closed and a diagnosis of GCT in a patient

with open growth plates should be questioned.
Approximately 50% of GCTs are located about the
knee at the distal femur and proximal tibia, with the
proximal humerus and distal radius representing the
third and fourth most common sites.

Giant cell tumor

Pathological Findings

Microscopic
examination showed a
cellular
lesion
composed of numerous
multinucleated
giant
cells in a background of
small,
ovoid,
mononuclear
stromal
cells.

Giant cell tumor

Radiologic features:
The

lesions are expansile, osteolytic, radiolucent without

sclerotic margins and usually without a periosteal reaction and
eccentrically located within the bone.
There is a well-defined defect in the metaphysis and epiphysis,
with destruction of the medullary cavity and adjacent cortex.
The destruction may stop just short of the joint.

Giant cell tumor

Giant cell tumor

Giant cell tumor

GIANT CELL TUMOR

Treatment
Well-confined, slow growing lesions with benign

histology can savely be reated by thorough

curettage ang stripping of the cavity with burrs
and gouges, followed by swabbing with hydrogen
peroxide or by the application of liquid nitrogen;
the cavity is then packed with bone chips.
More aggressive tumors, and recurrent lesions
should be treated by excision followed, if
necessary, by bone grafting or prosthetic
replacement.
Amputation is indicated as primary treatment
only for huge, neglected giant cell tumors.

Osteosarcoma
Osteosarcoma

is the most common primary

malignant tumor of bone, characterized by the
direct formation of bone or osteoid by tumor cells.
The incidence of osteosarcoma peaks in those aged
10-20 years; (maximum period of skeletal growth).
osteosarcoma occurs most commonly in the
metaphyses of long tubular bones, particularly
around the knee joint (distal femur, proximal tibia).
The proximal humeral metaphysis is another
common site. The disease commonly extends from
the metaphysis into the adjacent diaphysis or
epiphysis.

Osteosarcoma
Radiographic appearances:
shows a mixture of lytic and sclerotic areas. Soft

tissue extension of osteosarcoma is common and

seen on radiographs as a soft-tissue mass.
Cloud like areas of sclerosis due to malignant osteoid
production and calcification may be seen within the
mass.
Periosteal reactions are commonly seen once the
tumor extends through the cortex ( Codman triangles
and multilaminated, spiculated, and sunburst
reactions).

Osteosarcoma

Osteosarcoma

Osteosarcoma

Chondrosarcoma
Chondrosarcoma is a malignant tumor that

produces cartilage matrix.

Primary chondrosarcoma is very uncommon,
arises centrally in the bone, and is found in
young adult. Secondary chondrosarcoma
arises from benign cartilage defects such as
osteochondroma or enchondroma.
Chondrosarcoma can also be classified as
intramedullary, which generally arise from
enchondromas, and surface which arise from
osteochondromas

Chondrosarcoma
It is most common in the femur, humerus, ribs

and on the surface of the pelvis.

Radiographic features:
chondrosarcoma is a fusiform,
lucent defect with scalloping of the inner cortex

and periosteal reaction.

Extension into the soft tissue may be present as
well as punctate or stippled calcification of the
cartilage matrix.
May shows a lobulated appearance like a
cauliflower mass.

Chondrosarcoma

Chondrosarcom
a

Chondrosarcoma

Ewing's sarcoma
Ewing's sarcoma is a highly malignant tumor that is

found in the lower extremity more than the upper

extremity, but any long tubular bone may be affected.
The most common sites are the metaphysis and
diaphysis of the femur followed by the tibia and
humerus.
Ewing's sarcoma is most common in the first and
second decade.
The clinical presentation of Ewing's sarcoma includes

pain and swelling of weeks or months duration.

Erythema and warmth of the local area are sometimes seen.
Osteomyelitis is often the initial diagnosis based on
intermittent fevers, leukocytosis, anemia and an increased ESR.

Ewing's sarcoma
Radiologically,
Ewing's sarcoma is
often
associated
with a lamellated
or "onion skin"
periosteal
reaction.

Radiograph of periosteal response in Ewing

sarcoma of the femur in a 15-year-old boy

Ewing's sarcoma

Ewing's sarcoma
Ewing sarcoma is an aggressive malignancy with a high

local recurrence and metastatic rate.

Patients with locally resectable disease treated with multidrug

chemotherapy have a 5-year survival rate of approximately
70%.
Unfortunately, 1525% of patients present with nonlocalized
disease.
For the patient who presents with advanced, metastatic
disease, the 5-year survival rate is 30%. Resection of lung
metastasis, if possible, does improve survival.

Ewing sarcoma is a radiosensitive tumor.

Because of the not insignificant risk of secondary sarcomas,

surgery was investigated as the primary modality for local
control.
If the margins are contaminated, local irradiation must still be
used postoperatively.

Multiple Myeloma
Clinical Features:
(Plasmacytoma)

Multiple myeloma is a malignant tumor of plasma cells that

causes widespread osteolytic bone damage.

Multiple myeloma is the most common primary tumor of bone
and is found in the spine, skull, ribs, sternum and pelvis but
may affect any bone with hematopoietic red marrow.
The average patient age is over fifty years old.
Monoclonal immunoglobulin is found on serum protein
electrophoresis.
BenceJones proteins are present in urine.

The radiological appearances:

multiple myeloma is characterized by irregular lytic defects of

different sizes. These lytic areas are often described as

"punched out" and have no periosteal reaction.
Erosion begins intramedullarly and progresses through the
cortex.
It may causes generalized osteoporosis

Multiple Myeloma

Multiple Myeloma

BONE SECONDARIES
COMMONEST MALIGNANT BONE TUMOURS
SITE OF PRIMARY:
breast, prostate, thyroid, kidney, lung
2/3 come from cancer breast or prostate
16 % from thyroid, kidney, lung
17 % unknown primary
SITE OF SECONDARIES:
bones rich in cancellous bone
trunk bones e.g spine, pelvis, skull, ribs
root bones e.g upper humerus, upper femur
ROUTES :
1. Local invasione.g rectum invades pelvis
2. Blood born from tumour drain via vena cava to
heart, to lung to systemic circulation to bone
3. LYMPPHATICS

BONE SECONDARIES
TYPES :
Osteolytic 90 %... Bone destruction ( breast )
osteosclerotic
Bone sclerosis
( prostate )
PRESENTATION:
1- Pain
2- Pathologic fracture ( fr. Spine )
3- Swelling
4- Anaemia, cachexia
TREATMENT :
Hormonal
Radio & Chemo..
Surgical:
.

Internal fixation
Amputation
Resection