BONE TUMOURSBONE TUMOURS
Dr. SidharthYadav
Orthopaedic Dept.
N.K.P.SIMS
IntroductionIntroduction
Bone tumours are very diverse in morphology and
biological potential.
Most bone tumours are benign lesions
Most benign lesions are seen <30 years of age
Benign lesions typically present as incidental finding.
ApproachApproach
Age of the patient :- mature or immature skeleton.
Location of tumour :- Epi/Meta/Diaphyseal
Number of lesion :- solitary/multiple
Nature of lesion :- lytic/sclerotic/mixed
Matrix :- osteoid/chondroid/fatty
Zone of transition
Peiosteal reaction
LOCATION
1.In the transverse plane:
a) Central – Enchondroma
b) Eccentric -GCT, osteosarcoma,
chondromyxoid fibroma
c) Cortical - Non-ossifying fibroma,
osteoid osteoma
d) Parosteal - Parosteal osteosarcoma,
osteochondroma
2. In the longitudinal plane:
Diaphyseal: Ewings, Osteoid Osteoma, Mets, Adamantinoma,
Fibrous Dysplasia
Epiphyseal: Chondroblastoma,GCT.
Metaphyseal: Osteosarcoma ,Osteochondroma
• < 20 yrs - Osteogenic Sarcoma, Ewings. simple bone
cysts and chondroblastomas
• 20-40 yrs - GCT, Chondrosarcoma, MFH,
Lymphoma, Mets.
• >40 yrs - Mets, Myeloma, Chondrosarcoma, MFH
– Late Osteogenic, Fibrosarcoma.
Age of the patient
Clinical featuresClinical features
 Pain
- deep & consistant.
- may be present from a week to as long as 3-4 yrs.
- poorly localized.
- may be associated with antalgic limp with muscle waisting.
- night cries.
 Mass
 Pathological fractures due to excessive bone replacement by
tumour.
 Generalised weakness.
 Neurological symptoms such as paraesthesia.
 Deformity
InvestigationsInvestigations
Blood investigation
X-rays
Bone scan
Ct scan
MRI
Arteriography
Biopsy
Laboratory investigationsLaboratory investigations
Complete blood count.
ESR
C-reactive protein (CRP)
Urine for bence jones protein.
Serum electrophoresis.
Acid phosphatase.
Alkaline phosphatase.
RadiographsRadiographs
Exact location of the tumour
Borders of the tumour
Pattern of bone destruction
Matrix formation
Periosteal reaction
Pattern of bone destructionPattern of bone destruction
Bone destruction is due to osteoclastic resorptive
activity on both trabecular & cortical level.
2 stages :-
 Removal of mineral content
 Followed with enzymatic digestion.
3 types of bone destruction
 Geographic
 Moth eaten
 Permeative
Geographic bone destructionGeographic bone destruction
Seen as a well circumscribed hole in the
bone with a narrow zone of transition.
Divided into 3 types :-
A – with sclerotic margins
B – with out sclerotic margins
C – with ill defined margins
Type 1 a Geographic Lesion.
Eg. – unicameral bone
cyst, enchondroma.
Well-defined lucency with sclerotic rim.
Associated with benign / slow growing
Disorders.
Well-defined geographic lytic focus without
sclerotic rim , Endosteal scalloping seen.
Type 1 b Geographic Lesion
well-defined lucent lesion
without sclerotic rim.
myeloma
Large ill-defined lytic lesion , Codman’s triangle
Periosteal interruption, Tumor-induced new
bone .
.
Type 1 c Geographic Lesion
ill-defined lytic lesion.
Focally destructive & locally
Invasive.
Wider zone of transition.
osteosarcoma
IA: GEOGRAPHIC DESTRUCTION
WELL – DEFINED WITH SCLEROSIS
IN MARGIN
IB: GEOGRAPHIC DESTRUCTION
WELL – DEFINED BUT NO SCLEROSIS
IN MARGIN
IC : GEOGRAPHIC
DESTRUCTION
WITH ILL DEFINED
MARGIN
increasing aggressiveness
Margins: 1A, 1B, 1C
Type 2 Moth-eaten Appearance
Aggressive pattern.
Areas of destruction with
ragged borders
Implies more rapid growth
Presents as multiple scattered
hole vary in shape & size
These scattered hole coalesce
to form large defect.
osteosarcoma
Type 3. Permeative Pattern
Ewing sarcoma.
ill-defined lesion
with multiple “worm-holes”
Wide transition zone
Total penetration of cortex is
assumed.
Eg. Round cell tumours,
fibrosarcoma.
Leukemia
Patterns of Bone DestructionPatterns of Bone Destruction
Geographic Moth-eaten Permeative
Less malignant More Malignant
Periosteal reactionPeriosteal reaction
Periosteum of adult is minimally cellular & mainly fibrous in
inactive stage.
Reaction must mineralize to become visible on
radiographs.
Usually take 10 days – 3 wks.
Classified as :-
 Solid
 Interrupted
Ragsdale (1981) expanded this classification by adding
subclasses.
SolidSolid
Is further divided as :-
Smooth shell
Lobulated
Ridged
Solid Periosteal ResponseSolid Periosteal Response
Related to a slow form of
irritation osteoid osteoma
Slow-growing tumors provoke focal cortical thickening
A continuous layer of new bone that attaches to outer cortical surface
Single layer of reactive periosteum.
thick unilamellated periosteal reaction.
Smooth and continuous
Unilamellated periosteal reaction
Hypertrophic osteoarthropathy
Aggressive PeriostitisAggressive Periostitis
appearance of aggressive
periostitis in Ewing’s sarcoma
Layered, onion-skin, lamellated
• Alternating layers of opaque and
lucent densities
• Can be seen with aggressive
tumors and infections
growth spurt.
Spiculated periosteal reaction.
Perpendicular, brushed whiskers, hair-on-end, Fine linear
spiculations of new bone oriented perpendicular to the cortex or
radiating from a point source indicative of very aggressive bone
tumors
Osteosarcoma
Bone is formed in a disorganized fashion
Process may destroy spicules of bone as they are being
formed
This is a very aggressive process
Sunburst
Too fast growth for periosteum to respond
only the edges of raised periosteum will ossify
forming a small angle with the surface of bone.
Codman's triangle
seen in malignant bone tumors and in
rapidly growing lesions , aneurysmal bone
cyst, subperiosteal hematoma.
Solid onion-peel Sunburst Codman’s
triangle
Less malignant More malignant
Periosteal reaction
Matrix mineralizationMatrix mineralization
Matrix refers to acellular /intracellular substance
produced by mesenchymal cell.
Types :-
 Osteoid
 Chondroid :-
Solid
Patterns of mineralization of osseous matrix
Ivory-like
opacityCloud like
Osteoid tissue mineralise in a confluent manner that result in
radiographic density Ranging from hazy ground glass to ivory like
pattern.
Patterns of mineralization of cartilaginous tumour
matrix
Stippled Flocculent Ring and arc
CT ScanCT Scan
Very useful in early diagnosis
Determine intra/extramedullary extension.
More accqurate in demonstrating integrity of cortex in a area
contaning tumour.
Also demonstrate matrix mineralization.
Differentiate between solid & lytic lesion.
Early detection of pulmonary secondaries
Exact measurement for limb salvage procecures
(Prosthesis/allograft)
MRIMRI
Intra medullary extension
Soft tissue extension
Defines the relationship to the nearby major blood
vessels
T1 – differentiate tumour from fat.
T2 – differentiate tumour from surrounding muscle
Radio nuclide bone scanningRadio nuclide bone scanning
For pre biopsy staging
Dissemination of
tumour
Silent secondaries and
skip lesions
ArteriogramArteriogram
Planning limb sparing
surgery
Therapeutic
embolization
To assess vascularity of
tumour
BiopsyBiopsy
Closed biopsy
FNAC
Needle biopsy
Open biopsy
Incisional biopsy
Excisional biopsy
TreatmentTreatment
Chemotherapy
Radiotherapy
Surgical resection
RadiotherapyRadiotherapy
Radiation cause cell death by inducing formation
of free radicles that cause DNA damage.
Sensitivity of cell depends upon :-
 Cell’s position in cell cycle.
 Tissue oxygenation
 Cell’s ability to repair DNA damage or its inability to
undergo apoptosis.
Primary bone tumour’s are resistant to
radiotherapy except marrow cell tumour.
CarcinomaMetastatic to bone except renal cell
carcinoma are sensitive to radiation.
Radiation therapy is associated with
acute(erythema anorexia) & chronic
complications(oedema,fibrosis).
Rarely used for benign conditions.
Conventional external beam radiation can be
delivered by brachytherapy.
Hollow catheters are implanted in tumour bed at
the time of resection.
This techinique allow high dose of radiation to be
delivered to target cell.
ChemotherapyChemotherapy
With the use of new chemo protocol the 5 yrs survival
rate is approx 70% for osteosarcoma.
Similar rates has been noted for other maligant
conditions.
Chemotherapy is not useful for cartilagenous lesions &
other low grade malignancies.
Pre operative chemotherapy may decrease the spread of
tumour cells at the time of surgery.
2 types :-
 Adjuvant chemotherapy.
Administered post operatively to treat metastases.
 Neoadjuvant chemotherapy.
Administered before surgical resection of primary tumour.
Preoperatively chemo regress the primary tumour .
Drugs used in chemotherapy are more effective when they are
used against a small lesion.
They are more effective when used in combination rather then
single drug.
SurgerySurgery
In orthopaedic oncology surgical margins are
defined by :-
 Intralesional
 Marginal
 Wide
 Radical
Intralesional marginIntralesional margin
 Plane of surgical resection is with in the
tumour.
 This is a/k/a debulking because it leaves
behind gross residual mass.
 Procedure may be appropriate for
benign tumours when only option is to
sacrifice important anatomical
structures.
Marginal marginMarginal margin
 Tumours suppress the surrounding
tissue & appears to become
encapsulated .
 This surrounding is k/as pseudocapsule.
 A marginal margine is achieved when
the plane of dissection passes through
pseudocapsule.
 In high grade malignancy
pseudocapsule may contain satellite
lesion.
Wide & Radical marginWide & Radical margin
 Wide resection is acchieved when the
plane of resection is in normal tissue.
 If the plane of dissection touches the
pseudocapsule at any point then it
would be defined as marginal margin.
 Radical margine are achieved when all
the compartment that contain tumour
are removed en bloc.
CurettageCurettage
Many benign lesion can be treated adequately by curettage.
Local recurrence rate is high in curettage as compared to
resection.
Allows better functional results.
Curretage is first done by creating a large cortical window
over the lesion , atleast the size of lesion.
Bulk is removed with curets.
Cavity is enlarged by 1-2 cm in each
direction.
Cavity is filled with bone graft / cement.
THANK
YOU…

Bone tumours

  • 1.
    BONE TUMOURSBONE TUMOURS Dr.SidharthYadav Orthopaedic Dept. N.K.P.SIMS
  • 2.
    IntroductionIntroduction Bone tumours arevery diverse in morphology and biological potential. Most bone tumours are benign lesions Most benign lesions are seen <30 years of age Benign lesions typically present as incidental finding.
  • 3.
    ApproachApproach Age of thepatient :- mature or immature skeleton. Location of tumour :- Epi/Meta/Diaphyseal Number of lesion :- solitary/multiple Nature of lesion :- lytic/sclerotic/mixed Matrix :- osteoid/chondroid/fatty Zone of transition Peiosteal reaction
  • 4.
    LOCATION 1.In the transverseplane: a) Central – Enchondroma b) Eccentric -GCT, osteosarcoma, chondromyxoid fibroma c) Cortical - Non-ossifying fibroma, osteoid osteoma d) Parosteal - Parosteal osteosarcoma, osteochondroma 2. In the longitudinal plane: Diaphyseal: Ewings, Osteoid Osteoma, Mets, Adamantinoma, Fibrous Dysplasia Epiphyseal: Chondroblastoma,GCT. Metaphyseal: Osteosarcoma ,Osteochondroma
  • 5.
    • < 20yrs - Osteogenic Sarcoma, Ewings. simple bone cysts and chondroblastomas • 20-40 yrs - GCT, Chondrosarcoma, MFH, Lymphoma, Mets. • >40 yrs - Mets, Myeloma, Chondrosarcoma, MFH – Late Osteogenic, Fibrosarcoma. Age of the patient
  • 6.
    Clinical featuresClinical features Pain - deep & consistant. - may be present from a week to as long as 3-4 yrs. - poorly localized. - may be associated with antalgic limp with muscle waisting. - night cries.  Mass  Pathological fractures due to excessive bone replacement by tumour.  Generalised weakness.  Neurological symptoms such as paraesthesia.  Deformity
  • 7.
  • 8.
    Laboratory investigationsLaboratory investigations Completeblood count. ESR C-reactive protein (CRP) Urine for bence jones protein. Serum electrophoresis. Acid phosphatase. Alkaline phosphatase.
  • 9.
    RadiographsRadiographs Exact location ofthe tumour Borders of the tumour Pattern of bone destruction Matrix formation Periosteal reaction
  • 10.
    Pattern of bonedestructionPattern of bone destruction Bone destruction is due to osteoclastic resorptive activity on both trabecular & cortical level. 2 stages :-  Removal of mineral content  Followed with enzymatic digestion. 3 types of bone destruction  Geographic  Moth eaten  Permeative
  • 11.
    Geographic bone destructionGeographicbone destruction Seen as a well circumscribed hole in the bone with a narrow zone of transition. Divided into 3 types :- A – with sclerotic margins B – with out sclerotic margins C – with ill defined margins
  • 12.
    Type 1 aGeographic Lesion. Eg. – unicameral bone cyst, enchondroma. Well-defined lucency with sclerotic rim. Associated with benign / slow growing Disorders.
  • 13.
    Well-defined geographic lyticfocus without sclerotic rim , Endosteal scalloping seen. Type 1 b Geographic Lesion well-defined lucent lesion without sclerotic rim. myeloma
  • 14.
    Large ill-defined lyticlesion , Codman’s triangle Periosteal interruption, Tumor-induced new bone . . Type 1 c Geographic Lesion ill-defined lytic lesion. Focally destructive & locally Invasive. Wider zone of transition. osteosarcoma
  • 15.
    IA: GEOGRAPHIC DESTRUCTION WELL– DEFINED WITH SCLEROSIS IN MARGIN IB: GEOGRAPHIC DESTRUCTION WELL – DEFINED BUT NO SCLEROSIS IN MARGIN IC : GEOGRAPHIC DESTRUCTION WITH ILL DEFINED MARGIN increasing aggressiveness Margins: 1A, 1B, 1C
  • 16.
    Type 2 Moth-eatenAppearance Aggressive pattern. Areas of destruction with ragged borders Implies more rapid growth Presents as multiple scattered hole vary in shape & size These scattered hole coalesce to form large defect. osteosarcoma
  • 17.
    Type 3. PermeativePattern Ewing sarcoma. ill-defined lesion with multiple “worm-holes” Wide transition zone Total penetration of cortex is assumed. Eg. Round cell tumours, fibrosarcoma. Leukemia
  • 18.
    Patterns of BoneDestructionPatterns of Bone Destruction Geographic Moth-eaten Permeative Less malignant More Malignant
  • 19.
    Periosteal reactionPeriosteal reaction Periosteumof adult is minimally cellular & mainly fibrous in inactive stage. Reaction must mineralize to become visible on radiographs. Usually take 10 days – 3 wks. Classified as :-  Solid  Interrupted Ragsdale (1981) expanded this classification by adding subclasses.
  • 20.
    SolidSolid Is further dividedas :- Smooth shell Lobulated Ridged
  • 21.
    Solid Periosteal ResponseSolidPeriosteal Response Related to a slow form of irritation osteoid osteoma Slow-growing tumors provoke focal cortical thickening A continuous layer of new bone that attaches to outer cortical surface
  • 22.
    Single layer ofreactive periosteum. thick unilamellated periosteal reaction. Smooth and continuous Unilamellated periosteal reaction Hypertrophic osteoarthropathy
  • 23.
    Aggressive PeriostitisAggressive Periostitis appearanceof aggressive periostitis in Ewing’s sarcoma Layered, onion-skin, lamellated • Alternating layers of opaque and lucent densities • Can be seen with aggressive tumors and infections growth spurt.
  • 24.
    Spiculated periosteal reaction. Perpendicular,brushed whiskers, hair-on-end, Fine linear spiculations of new bone oriented perpendicular to the cortex or radiating from a point source indicative of very aggressive bone tumors Osteosarcoma
  • 25.
    Bone is formedin a disorganized fashion Process may destroy spicules of bone as they are being formed This is a very aggressive process Sunburst
  • 26.
    Too fast growthfor periosteum to respond only the edges of raised periosteum will ossify forming a small angle with the surface of bone. Codman's triangle seen in malignant bone tumors and in rapidly growing lesions , aneurysmal bone cyst, subperiosteal hematoma.
  • 27.
    Solid onion-peel SunburstCodman’s triangle Less malignant More malignant Periosteal reaction
  • 28.
    Matrix mineralizationMatrix mineralization Matrixrefers to acellular /intracellular substance produced by mesenchymal cell. Types :-  Osteoid  Chondroid :-
  • 29.
    Solid Patterns of mineralizationof osseous matrix Ivory-like opacityCloud like Osteoid tissue mineralise in a confluent manner that result in radiographic density Ranging from hazy ground glass to ivory like pattern.
  • 30.
    Patterns of mineralizationof cartilaginous tumour matrix Stippled Flocculent Ring and arc
  • 31.
    CT ScanCT Scan Veryuseful in early diagnosis Determine intra/extramedullary extension. More accqurate in demonstrating integrity of cortex in a area contaning tumour. Also demonstrate matrix mineralization. Differentiate between solid & lytic lesion. Early detection of pulmonary secondaries Exact measurement for limb salvage procecures (Prosthesis/allograft)
  • 32.
    MRIMRI Intra medullary extension Softtissue extension Defines the relationship to the nearby major blood vessels T1 – differentiate tumour from fat. T2 – differentiate tumour from surrounding muscle
  • 33.
    Radio nuclide bonescanningRadio nuclide bone scanning For pre biopsy staging Dissemination of tumour Silent secondaries and skip lesions
  • 34.
  • 35.
    BiopsyBiopsy Closed biopsy FNAC Needle biopsy Openbiopsy Incisional biopsy Excisional biopsy
  • 36.
  • 37.
    RadiotherapyRadiotherapy Radiation cause celldeath by inducing formation of free radicles that cause DNA damage. Sensitivity of cell depends upon :-  Cell’s position in cell cycle.  Tissue oxygenation  Cell’s ability to repair DNA damage or its inability to undergo apoptosis.
  • 38.
    Primary bone tumour’sare resistant to radiotherapy except marrow cell tumour. CarcinomaMetastatic to bone except renal cell carcinoma are sensitive to radiation. Radiation therapy is associated with acute(erythema anorexia) & chronic complications(oedema,fibrosis). Rarely used for benign conditions.
  • 39.
    Conventional external beamradiation can be delivered by brachytherapy. Hollow catheters are implanted in tumour bed at the time of resection. This techinique allow high dose of radiation to be delivered to target cell.
  • 40.
    ChemotherapyChemotherapy With the useof new chemo protocol the 5 yrs survival rate is approx 70% for osteosarcoma. Similar rates has been noted for other maligant conditions. Chemotherapy is not useful for cartilagenous lesions & other low grade malignancies. Pre operative chemotherapy may decrease the spread of tumour cells at the time of surgery.
  • 41.
    2 types :- Adjuvant chemotherapy. Administered post operatively to treat metastases.  Neoadjuvant chemotherapy. Administered before surgical resection of primary tumour. Preoperatively chemo regress the primary tumour . Drugs used in chemotherapy are more effective when they are used against a small lesion. They are more effective when used in combination rather then single drug.
  • 42.
    SurgerySurgery In orthopaedic oncologysurgical margins are defined by :-  Intralesional  Marginal  Wide  Radical
  • 43.
    Intralesional marginIntralesional margin Plane of surgical resection is with in the tumour.  This is a/k/a debulking because it leaves behind gross residual mass.  Procedure may be appropriate for benign tumours when only option is to sacrifice important anatomical structures.
  • 44.
    Marginal marginMarginal margin Tumours suppress the surrounding tissue & appears to become encapsulated .  This surrounding is k/as pseudocapsule.  A marginal margine is achieved when the plane of dissection passes through pseudocapsule.  In high grade malignancy pseudocapsule may contain satellite lesion.
  • 45.
    Wide & RadicalmarginWide & Radical margin  Wide resection is acchieved when the plane of resection is in normal tissue.  If the plane of dissection touches the pseudocapsule at any point then it would be defined as marginal margin.  Radical margine are achieved when all the compartment that contain tumour are removed en bloc.
  • 46.
    CurettageCurettage Many benign lesioncan be treated adequately by curettage. Local recurrence rate is high in curettage as compared to resection. Allows better functional results. Curretage is first done by creating a large cortical window over the lesion , atleast the size of lesion. Bulk is removed with curets.
  • 47.
    Cavity is enlargedby 1-2 cm in each direction. Cavity is filled with bone graft / cement.
  • 48.

Editor's Notes

  • #7 MFH – malignant fibrous histiocytoma.
  • #8 Question has to be asked about recent trauma which could have lead to the episode &amp; to differentiate it from stress fractures &amp; myositis ossificans. As the pain associated with stess fracture is aggravted on exercise &amp; relieved on taking rest where as pain associated with myositis ossificans relieved after some time. h/o of recent &amp; chronic infection should be taking as some times pain due to chronic osteomyelitis can mimic. Usually pat. With chronic infection give H/o of fever with chills . Mass :- questions about any other swelling should be asked &amp; any swelling near the joints should be asked so as to rule out OLLIER’S DISEASE &amp; MAFFUCCI’S SYNDROME. Pt. should be looked for café au laite spots &amp; subcutaneous neurofibromas :- sign’s of VON RECKLINGHAUSEN DISEASE. Extremity should be looked for raised temp ( infective pathology) , varicose veins ( due to obstruction of venous return coz of mass above ) &amp; mass should be checked for any trill or bruit. Chronic infection such as fungus or tb can mimic neoplasm.
  • #10 Cbc :- pt. might have anaemia coz of marrow involvement. ESR :- Raised coz of infection &amp; raised wbc count. Alkaline phosphatase :- its raised in new bone formation as it’s a active product of osteoblastic activity . Acid phosphatase :- if the metastasis is from prostrate. Serum electrophoresis :- m band protein ( albumin, alpha 1 globulin , alpha 2 ,beta globulis &amp; gamma globulin) gamma globulins are looked.
  • #21 Periosteal reaction is the formation of new bone in response to injury or other stimulai to the periosteum surrounding the bone.
  • #22 Smooth shells are caused by lesions that apply uniform pressure over the cortex. Lobulated - develop’s due to focal variation in growth rate. Rigded – a/k/a trabeculated septataed or soap bevel reaction. Develops when growth of a destrucyive lesion is uneven.
  • #31 Mineralization of the tumour bone is initally seen in the center of the lesion where cellular maturity is greatest. When a tumour bone is produced by the fibroblast which are converted to osteoblast through metaplasia , the pattern of bone formed is woven or fibrous in appearance. Woven bone of this type is usually less densely mineralized then the osteoid bone hence hazy glass appearance.
  • #40 Benign :- villonodular synovitis
  • #49 Autogenous bone graft provides most rapid &amp; reliable healing rate because its osteogenic ,osteoinductive &amp; osteoconductive. Cancellous allografts is reliable though its only osteoconductive.