BONE TUMOURSBONE TUMOURSDr. Sidharth YadavOrthopaedic 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.

ApproachApproachAge 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 fibromac) Cortical - Non-ossifying fibroma,

osteoid osteomad) Parosteal - Parosteal osteosarcoma,

osteochondroma2. In the longitudinal plane:

Diaphyseal: Ewings, Osteoid Osteoma, Mets, Adamantinoma, Fibrous DysplasiaEpiphyseal: 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

Investigations Investigations Blood investigationX-rays Bone scanCt scanMRIArteriography Biopsy

Laboratory investigationsLaboratory investigationsComplete blood count.ESR C-reactive protein (CRP)Urine for bence jones protein.Serum electrophoresis.Acid phosphatase.Alkaline phosphatase.

RadiographsRadiographsExact location of the tumour

Borders of the tumour

Pattern of bone destruction

Matrix formation

Periosteal reaction

Pattern of bone Pattern of bone destructiondestruction

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 Geographic bone destructiondestructionSeen as a well circumscribed

hole in the bone with a narrow zone of transition.

Divided into 3 types :-

A – with sclerotic marginsB – 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 growingDisorders.

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 & locallyInvasive.Wider zone of transition.

osteosarcoma

IA: GEOGRAPHIC DESTRUCTIONWELL – DEFINED WITH SCLEROSISIN MARGIN

IB: GEOGRAPHIC DESTRUCTIONWELL – DEFINED BUT NO SCLEROSISIN MARGIN

IC : GEOGRAPHIC DESTRUCTIONWITH 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 reactionPeriosteum 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.

Solid Solid 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 thickeningA 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 mineralization Matrix mineralization

Matrix refers to acellular /intracellular substance produced by mesenchymal cell.

Types :-

Osteoid

Chondroid :-

Solid

Patterns of mineralization of osseous matrix

Ivory-like opacity Cloud 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 ScanVery 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)

MRIMRIIntra 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

BiopsyBiopsyClosed biopsy FNAC Needle biopsy

Open biopsy Incisional biopsy Excisional biopsy

Treatment Treatment Chemotherapy Radiotherapy

Surgical resection

Radiotherapy Radiotherapy 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 oxygenationCell’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.

ChemotherapyChemotherapyWith 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.

Surgery Surgery In orthopaedic oncology surgical

margins are defined by :-

Intralesional

Marginal

Wide

Radical

Intralesional marginIntralesional marginPlane 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.

Curettage Curettage 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.

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