Seminar 1 Ortho

8/6/2019 Seminar 1 Ortho

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Seminar 1

Musculoskeletal Tumours

Prepared by: Ong Siew Hoon, Lim Seng Fatt,

Wong Chui King, Ooi Yin Chuin,

Goh Jin Yi, and Chong Siew Mei.


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Bone ossification


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Ossification = osteogenesis

2types

- intramembranous ossification

- endochondral ossification

Heterogenous ossification = atypical bone

tissue formation at extra skeleton location.


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Intramembranous ossification

Transformation of mesenchyme (primitive

connective tissue) bone.

Mesenchyme is an embryonic cell consist ofmesodermdevelop into CT eg bone

Occurred mostly in fetal development phase.

Forms skull & clavicle Occur in healing # treated by OR+metal

plate/screw


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STEPS OF INTRAMEMBRANOUS

OSSIFICATION

1.Selected mesenchymal cells cluster osteoblasts

2.Ossification centre is formed

3.Osteoblats begin to secrete osteoid, later mineralized

4. Trapped osteoblasts differentiate into osteocytes5. Accumulating osteoid is laid down between

embryonal bv trabeculae

6. Trabeculae just deep to the periosteum thicken

bone collar

mature compact bone7. Spongy bone, consisting of distinct trabeculae, arepresent internally. Bv differentiate into red bonemarrow.


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Endochondral ossification

Cartilage is replaced by bone.

essential process during the rudimentary

formation oflong bones, the growth of thelength of long bones.

Forms all the bones except for skull & clavicle

Occur in healing fractures of long bonestreated with POP


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STEPS OF ENDOCHONDRAL OSSIFICATION

Primary site of ossification -> middle of diaphysis1. Formation of periosteumThe perichondrium becomes the periosteum (containslayers of osteoprogenitor cells which becomeosteoblasts)2. Bone collar

Osteoblasts secrete osteoid against the hyalinecartilage diaphysisbony collar

3.Calcification of matrixChondrocytes in the ossification center hypertrophy,stop secreting collagen, begin ALP calcificationApoptosis of the hypertrophic chondrocytes cavities


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4. Invasion of periosteal bud

Hypertrophic chondrocytes (before apoptosis) secreteVEGF-> sprouting of bv from the perichondrium-

>periosteal bud->invade cavity Bv carry hemapoietic cells, osteoprogenitor cells

5. Formation of trabeculae

Osteoblasts from progenitor cells entered the cavity, usethe calcified matrix as scaffold-> begin to secreteosteoidtrabecula

Osteoclasts from macrophages, bdown spongy bone toform BM


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At about time of birth, a secondary ossification

center appears in each end (epiphysis)of long bone.

The cartilage between the primary and secondary

center is called the epiphyseal plate,it continues to

form new cartilage, which is replaced by bone incr.

bone length


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Bone tumourPrimary Secondary

Due to hyperactivity of pluripotent

neoplastic cells

Due to implantation of neoplastic cells

Usually solitary lesion One/ several sites

Less common More common

Primary site

-Prostate

-Urinary bladder&cervix

-breast

-lung-intestine,stomach,colon,rectum

-kidney

-thyroid


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Classification of bone tumoursCell types Benign Malignant Tumour-like lesions

Osteoblasts Osteoma

Osteoblastoma

Osteoid osteoma

Osteosarcoma ABC ( Aneurysmal

bone cyst)

UBC (Unicameral)

Chondroblast Chondroma

Chondroblastoma

Osteochondroma*

Chondrosarcoma Non-ossifying

fibroma

Fibrous dysplasia

Eosinophilic

granuloma

Browns tumour

Osteoclasts Osteoclastoma Malignant giant cell

tumour


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Classification of bone tumoursCell types Benign Malignant Tumour-like lesions

Medullary Ewing SA

Reticulum cell SAMultiple myeloma*

Hodgkins disease

Vascular Hemangioma Angiosarcoma

Fibrous tissue Fibroma Fibrosarcoma


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Commonest malignant primary tumour

1.Multiple myeloma 2. Osteosarcoma

Commonest benign bony tumour

osteochondroma

Metastatic lesions > common then primarylesion

2/3 of secondary : CA breast & prostate

Benign lesions are painless except Osteoid

osteoma


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Diagnosis/ investigations

Imaging

Plain Xray

CT scan

MRI

Radionuclide scanning reveal small tumours


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Aneurysmal bone cyst


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Multiple Echondroma with fractures


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Chondrosarcoma with snow flake

calcification


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MRI shows Multiple myeloma


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Biopsy

Open Biopsy

Needle biopsy


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Lab investigations

Hb

ESR

Serum Ca & P

Serum alkaline phosphatase ( hign in

osteogenic SA)

Urine analysis bence jones protein in MM


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Differential Dx

Chronic OM

Pain+swelling

Xray:

1.bone destruction

in the metaphysis

2. periosteal new

bone formation


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Stress fracture

Young adults

Localized pain near large

jt

Xray

1. Cortical destruction

2. periosteal new bone

Typical stress fracture of the distal shaft of the

second metatarsal not seen on initial

radiograph (left). Callus formation is seen at 4

weeks follow up


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Stress #

A stress fracture is an overuse injury.

Bone is constantly attempting to remodel andrepair itself, especially when extraordinary

stress is applied.

When enough stress is placed on the bone, itcauses an imbalance between osteoclastic and

osteblastic activity and a stress fracture mayappear.


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O

steoidO

steoma


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Osteoid Osteoma

Benign OSTEOBLASTIC tumour

More common in male 2-3:1

90% occur in people ages


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osteoid-rich nidus in a highly loose, vascular

connective tissue

Nidus is WELL DEMARCATED, has some

calcifications, and surrounded by sclerotic

bone.

Most commonly occur in the cortex of shafts

ofLONG BONES.

50-60% occurs in femur and tibia (Barei et al)


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Pathology

a discrete central nidus(well circumscribedcavity) usually < 1 cm with diffuse peripheral

sclerosis.

irregular lacelike osteoid and calcified matrix

lined by plump osteoblasts and osteoclasts

with a well-vascularized but bland stroma.

Appearance vary with the degree of lesional

maturity.


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Clinical features

Localised, continuous, deep, aching, and

intense pain with varying quality and severity.

Pain affect gait May produce radicular/ referred pain to lower

limbs/ shoulder

50-75% of patients responds to oral

salicylates.

Swelling (for those occuring in diaphysis)


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Physical Examination

Tenderness*( prostaglandins )

Epiphyseal lesion mimic intra articular

deragement. Decrease ROM

Joint effusion (mimic inflammatory arthritis)

Neurological abnormalities like monoparesisand paraparesis (uncommon)


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Ix

X-ray

a radiolucent area of about 1 cm in diameter

(nidus) surrounded by sclerotic bone.

May not appear months after onset

CT Scan (delineate nidus better)

Diagnosis can be confirmed only with pathologic

examination percutaneous needle biopsy


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OO - AP and lateral


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Management

Initial treatment aspirin and NSAIDs

Surgical intervention for patients whose pain is

unresponsive to medical therapy, cannot tolerate

prolonged use ofNSAIDs, unable to adapt to

activity restrictions, severe scoliosis

Complete surgical excision of the nidus

Contraindicated if lesions in femoral head/neckdue to complications

Recurrence in 9-28% after surgery within 1 year


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EosinophilicGranuloma


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Eosinophilic granuloma

Eosinophilic granuloma (EG) is the benignform of the 3 clinical variants of Langerhans

cell histiocytosis, which include Letterer-Siwe

disease, Hand-Schller-Christian disease, andEG.

Also known previously as histocytosis X.

single or multiple skeletal lesions.

more common sites include the skull,

mandible, spine, ribs, and long bones.

Affects children, adolescent and young adults.


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clonal proliferation of Langerhans cells,

abnormal cells deriving from bone marrow &

capable of migrating from skin to lymphnodes.

Lung involvement occurs in 20% of patients

with eosinophilic granuloma (caused bysmoking)

Presence of diffuse pulmonary inflitrates

May present as aggressive peridontitis- Lyticjaw lesion


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Clinical Features Solitary, minimally symptomatic lesion in a young

child/ adult.

Local pain, swelling and tenderness are common

and the ESR may be elevated

Low grade fever & mild peripheral eosinophilia are

occasionally associated findings

Mandibular involvement , loosening or loss of teeth

can be encountered

Vertebral body involvement may result in

compression fracture and possible neurological

impairment


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Ix

X-ray is diagnostic

destructive bone lesion arising from the

marrow cavity

Skull lesions* are lytic, with a beveled edge or

sharp and serrated margins and the absence

of sclerosis in calvarial lesions.


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Skull: lesion may have sharp, punched out borders that is uneven

across the inner and outer table causing a "beveled edge


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Anteroposterior radiograph of the mandible (left image) in a 10-

year-old boy who presented with swelling of the left mandible. Alytic expanding lesion is seen within the ramus of the leftmandible. An oblique view of the mandible (right image) showsfloating teethwithin the lytic bone lesion


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Plain radiograph of the pelvis in a 10-year-old girl shows a lytic lesion of eosinophilicgranuloma within the left ileum. Biopsy results confirmed the diagnosis of eosinophilic

granuloma.


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CT scan better for difficult areas like mastoids,

atlantoaxial joints, and posterior elements of

the vertebral bodies.

Histology


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Proliferating Langerhans cells are ovoid or round histiocyte-like cells that arearranged in aggregates, sheets, or individually within a loose fibrous stroma. Thecells have eosinophilic cytoplasm and contain central ovoid 'coffee bean' shapednuclei with typical nuclear grooves. Langerhans cells are frequently admixed withinflammatory cells including large numbers of eosinophils, as well as lymphocytes,neutrophils and plasma cells


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Management

Treatment of EG depends on the form of the

disease

Localized disease often a biopsy alone is

enough to incite healing

Other treatment modalities: curettage, excision,

steroid injection, radiation and observation

Chemotherapy is recommended for systemic

disease. [interleukin-2 (IL-2) and antitumor

necrosis factor-alpha (antiTNF-alpha)]


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Osteochrondoma


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Osteochrondoma

MOST common benign bone tumour. (35%

) Cartilaginous neoplasm in bone that

undergoes endochondral ossification (long

bones)

knee and the proximal humerus

Incidental finding

mechanical symptoms Present in age


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Pedunculated Sessile


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Pathophysiology

located adjacent to growth plates and develop

away from the growth plate with time.

isolated growth plates affected by growth

factors.


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Clinical Features

Asymptomatic

Occasionally, painless mass.

Pain, if present, is due to mechanical effect onsoft tissue.

# of stalk.


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Ix

X-ray

MRI

Rx

Excision-symptomatic

Do not leave behind remnants-recurrence (2-5%)


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Enchondroma


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Enchondroma

benign cartilaginous neoplasms

Solitary lesions

Intramedullary bones

Small incidence of malignant transformation

Pathological #


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Pathology

lesions replace normal bone with mineralized

or unmineralized hyaline cartilage

lytic area containing rings and arcs of

chondroid calcifications

Multiple enchondroma-enchondromatosis


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Frontal radiograph of the right hand demonstrates

a lytic expansile lesion in the fifth metacarpal bone,

with thinning of the cortex that has a somewhat

scalloped appearance. A pathologic fracture is

noted, but no appreciable calcifications are seen in

the lesion.


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62-year-old woman with enchondroma involving the proximal end

of the proximal phalanx of her middle finger. The lesion has a lobular

morphology and punctate calcifications. Because of pain, the lesion

was curetted and packed with morselized allograft bone.


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Multiple enchondromas may occur in 3 distinct disorders:

Ollier disease is a nonhereditary disorder characterized by

multiple enchondromas with a predilection for unilateral

distribution. The enchondromas can grow large and can be

disfiguring.

Maffucci syndrome is nonhereditary and is less common

than Ollier disease. This syndrome results in

multiple hemangiomas in addition to enchondromas.

Metachondromatosis consists of multiple enchondromas

andosteochondromas. Of the 3 disorders,metachondromatosis is the only one that is hereditary,

which is by autosomal dominant transmission.


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Ix

X-ray (rings/ arcs on the HANDS)

CT Scan

MRI

Biopsy (to differentiate from Chrondosarcoma)


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Treatment

Surgical(Bone grafting)

Non-Surgical(Observation)

+ Malignant risk


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FIBROUS DYSPLASIA


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Introduction

Developmental disorder in which areas oftrabecular bone are replaced by fibrous tissue,osteoid and woven bone

If lesions are large, bone is weakened andpathological fractures or progressive deformitymay occur

Can affect one bone (monostotic), one limb(monomelic) or many bones (polyostotic)

Malignant transformation occurs in 5-10% ofpatients with polyostotic lesions, rare inmonostotic


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Pathology

Coarse, gritty feel due to specks of immature

bone

Histological picture- loose cellular fibrous

tissue with patches of woven bone and

scattered giant cells


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Clinical Features

Small, single lesions are asymptomatic

Large, monostotic lesions may cause pain andbone deformity

Can be discovered after a pathological fracture Patient with polyostotic disease present in

childhood or adolescence with pain, limp, bonyenlargement, deformity or pathological fracture

May be associated with caf-au-lait patches onthe skin and (in girls) precocious sexualdevelopment (Albrights syndrome)


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Investigations

X-Ray:

-Cyst-like areas in metaphysis or shaft have ahazy (ground glass) appearance (fibrous tissue

with diffuse spots of immature bone)-Weight-bearing bones may be bent

-Shepherds crook deformity of the proximal

femur Radioscintigraphy- marked activity in the

lesion


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Resemble bone forming tumour and

hyperparathyroidism both clinicaly and

histologically- detailed X-ray and lab test to

exclude


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Treatment

Small lesions need no treatment

Large and painful or threatening to fracture lesioncan be curetted and grafted (tendency to recur)

Mixture of cortical and cancellous bone graftsmay provide added strength even lesion is noteradicated

For very large lesion, grafts can be supplementedby methylmethacrylate cement

Deformities require correction by suitablydesigned osteotomies


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NON-OSSIFYING FIBROMA (

FIBROUS CORTICAL DEFECT)


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Introduction

Commonest benign lesion of bone

Developmental defect in which a nest of

fibrous tissue appears within the bone and

persists for some years before oosifying

Incidental finding on X-ray

Commonest site- metaphysis of long bones,

occasionally multiple


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Pathology

Solid lesion consisting of unremarkable fibrous

tissue with a few scattered giant cells

As bone grows, defect heal spontaneously

Occasionally, enlarges to several centimetres

in diameter and cause pathological fracture

No risk of malignant change


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X-Ray

Oval radiolucent area surrounded by a thin

margin of dense bone


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Treatment

Usually unnecessary

If defect is large and led to repeated fracture ,

then curettage and bone grafting should be

done


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ANEURYSMAL BONE CYST


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Introduction

May be encountered at any age and in almostany bone, more often in young adults and inlong bone metaphyses

Occasional sites- vertebrae and flat bones Arises spontaneously or after degeneration or

haemorrhage in some other lesion

Clinical features: with expanding lesions,patient may complain of pain, large cyst maycause a visible or palpable swelling of bone.


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Pathology

Cyst contain clotted blood and during

curettage, considerable bleeding from the

fleshy lining membrane

Histological- lining consists of fibrous tissue

with vascular spaces, deposits of hemosiderin

and MNG


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X-Rays

Well-defined radiolucent cyst, often

trabeculated and eccentrically placed

Often situated in the metaphysis in tubular

bone and may resemble a simple cyst or one

of the other cyst like lesion

In an adult, an aneurysmal bone cyst may be

mistaken for a giant-cell tumour but it usuallydoes not extend up to the articular margin


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Treatment

Cyst should be carefully opened, thoroughly

curetted and then packed with bone grafts

Sometimes graft is resorbed and cyst recurs

further operations and packing with

methymethacrylate cement

If cyst is in a safe area where there is no risk

of fracture, lesion may occasionally healsspontaneously


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SOLITARY EXOSTOSIS ( CARTILAGE-

CAPED EXOSTOSIS)


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Introduction

One of the commonest tumours of bone

starts as a small overgrowth of cartilage at the edge ofphyseal plate and develops by endochondralossification into a bony protuberance still covered by

the cap of cartilage

Any bone that develops in cartilage. Commonest- fastgrowing ends of long bones and crest of ilium

Stop growing at the end of the normal growth period.

Any furtherenlargementaftertheend ofthegrowth

periodissuggestive ofmalignanttransformation!


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Clinical features

Patient usually a teenager or young adult whenthe lump is 1st discovered

Pain due to an overlying bursa or impingement

on soft tissues Paresthesia due to stretching of an adjacent

nerve. Rare.

Multiple lesions may develop as part of a

heritable disorder- hereditary multiple exostosis(abnormal bone growth resulting in characteristicdeformities)


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X-RAY

Well-defined exostosis emerging from

metaphysis, its base co-extensive with the

parent bone

It looks smaller in x-ray than it feels

Large lesion- bony exostosis surrounded by

clouds of calcified material. ( cartilage

degeneration and calcification)


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Pathology

Cartilage cap is seen surmounting a narrow

base of pedicle of bone

Large lesion- cauliflower appearance with

degeneration and calcification in the centre of

the cartilage cap

Malignant transformation 1% for solitary

lesion and 6% for multiple lesions


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Treatment

If it causes symptoms, excision required

In adult, recently become bigger or painful

urgent operation (MALIGNANCY)

If suspicious features present, further imaging

and staging should be carried out before biopsy

If histology suggestive of benign cartilage but the

tumour is known for certain to be enlarging afterthe end of growth period, it should be treated as

chondrosarcoma.


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Simple BoneC

yst


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Introduction

A.k.a. solitary cyst/unicameral cyst

Straw-colored fluid filled cavity in bone

Benign condition

Appears during childhood (


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Introduction

Some heals spontaneously, while othersenlarge

More invasive cysts can grow to fill most of

the bone's metaphysis pathological#/destroys growth plate -- leading toshortening of the bone

Causes unknown (disorder of growth plate?developmental anomaly in the veins of theaffected bone? repeated trauma?)


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Symptoms

No symptoms

Usually discovered after pathological #/

incidental finding on x-ray

May be abnormal angulation of limb

secondary to fracture or shortening of the

limb if adjacent growth plate is involved


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Diagnosis

Plain x-ray

Radiolucent area in metaphysis,

often extending up to physeal plate

Clear margin Bone expanded

Intact cortex but thinned

Atypical appearance/unusual location-- MRI, CT scan


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In doubtful case, fine needle aspiration under

x-ray control straw-colored fluid

Biopsy / histological examination if

necessary


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Management

Asymptomatic left alone, can be watchedwith repeated X-rays and doctor examinations,caution to avoid injury which might cause #

Symptomatic aspiration of fluid & injectionof 80-160mg methylprednisolone

If continue enlarged, curettage and packedwith bone chips

Risk of recurrence more than 1 operationmay be needed


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Prognosis

Generally good

Most heals with proper Tx

If left alone, most heals spontaneously by the

time the skeleton ceases to grow

Recur

Continuous follow-up care is essential for the

successful treatment


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G

iantC

ell Tumor


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Introduction

Rare, benign but locally aggressive bone

tumor of unknown etiology

Accounts for 4-5% of primary bone tumors

and ~20% of benign bone tumors

Slightly more common in females

Predominant in Chinese

Occurs chiefly in men between 20-50 yrs (after

epiphyseal closure)


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Cause

Occur spontaneously

Not known to be a/w trauma, diet,environmental factors

Not inherited

In rare case, a/w hyperparathyroidism

- may produce brown tumors that areradiographically & histologically similar to giant

cell tumor of bone

- unlike brown tumors, serum Ca is normal in GCT


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Symptoms

Pain at the area of tumor

Slight swelling

History of trauma is common

Pathological # occurs in 10-15% of cases

Palpable mass with warmth of overlying

tissues on examination

i i


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Diagnosis

Plain x-ray

- well-defined lytic lesion (radiolucent) thatinvolves the metaphysis and epiphysis

- Extend to articular surface, bounded bysubchondral bone plate

- Centre soap-bubble appearance d/t ridging ofsurrounding bone

- Cortex is thin and sometimes expanded

- Aggressive lesions ill-defined, extend into softtissue

X-ray of a typical giant cell tumor in


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X ray of a typical giant cell tumor in

the end of the radius bone

l il l d & l i


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multiloculated & pure lytic

Di i


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Diagnosis

CT scan- helps determine extact amount of cortical destruction and optimal

location of the cortical window

MRI

- help determine extent of tumor destruction

- may be indicated when the tumor has eroded thru the cortex andallows determination of whether concomitant neurovascularstructures are involved

- may help evaluate subchondral penetration

Bone scan

- shows a "hot spot" in the bone where the tumor is (show

decreased radioisotope uptake in the center of lesion)

An x-ray or CT scan of the chest will often be done to look for possiblespread to the lungs

Di i


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Diagnosis

Biopsy for histological examination

Gross: reddish, fleshy appearance, friable, cystic cavities oftenfilled with blood

Histologically: abundance of multinucleated giant cells(osteoclastic type) scattered on a background of stromalcells with little / no visible intercellular tissue

- Aggressive lesions show more cellular atypia and mitotic

features- Histological grading unreliable as predictor of tumor

behavior

St i


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Staging

stage I:

- benign latent giant cell tumors

- no local aggressive activity

stage II:

- benign active GCT

- imaging studies demonstrate alteration of the cortical bonestructure

stage III:

- locally aggressive tumor

- imaging studies demonstrate a lytic lesion surrounding medullary

and cortical bone- there may be indication of tumor penetration through the cortex

into the soft tissues;

M t


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Management

Well-defined, slow growing lesions with benignhistology thorough curettage and stripping ofcavity, followed by swabbing with hydrogenperoxide/ application of liquid nitrogen, then

packed with bone chips Aggressive/recurrence lesions excision,

followed, if necessary, by bone grafting/prosthetic replacement

Tumors in awkward sites (spine) diff eradicate Radiotherapy is sometimes recommended, risk of

malignant transformation


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L

ipoma

I t d ti


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Introduction

Most common benign soft tissue tumor

Arises in subcutaneous layer

May occur anywhere

Commonly torso, neck, upper thighs, upper

arms, and armpits

Multiple lesions

Occurs at all age, not common in children

Eti l


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Etiology

Cluster of fat cells, become over-active & so

distended with fat that they have become

palpable lumps

Not completely understood

Inherited

Triggered by injury

Being overweight does not cause lipoma

P t ti


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Presentation

Painless swelling

Slow growing, rarely regress

Spherical, lobulated surface, come in all sizes

Soft, irregular edge, compressible, +ve slip

sign

Not fluctuate, solid in room temperature

Pseudo-fluctuation and pseudo-

transillumination, radiolucent

Management


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Management

Dx by its appearance alone

Biopsy is usually unnecessary, only essential if there areany atypical features

Surgically removed if symptoms develop or d/tcosmetic reason

Complete surgical excision with the capsule to preventlocal recurrence

Liposuction small incision and may be remote from

the actual tumor

Recurrence is uncommon, unless excision is incomplete


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Primary malignant bone tumours

Osteosarcoma

Chondrosarcoma

Introduction


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Introduction

Pathology: neoplastic osteoid is produced by aproliferating spindle cell stroma

Common age group: aldolescent and 30/40s

Male>Female

Classification: Classic form

Telangietactic

Periosteal

Parosteal

significant number of osteosarcomas in adultsassociated with Pagets disease

Clinical features


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Clinical features

Pain

Swelling

Common sites: (long bone metaphyses)

Knee

Proximal end of femur

Investigation


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Investigation

X ray

osteolytic lesion

new bone formation (sun burst appearance)

periosteal reaction ( Codmans triangle)

visible soft-tissue mass

Bone tissue biopsy

CT/MRI: extent of the tumour

Lung metastases

Osteosarcoma


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Osteosarcoma

Treatment


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Treatment

Local

Surgery

Adjuvant chemotherapy

Metastases

Surgical resection of lung metastases

It requires good local disease control and no extra-pulmonary metastasis

Treatment


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Treatment

Surgery

Limb salvage surgery

Amputation

Relative indications:- associated pathologic fracture

- tumors encasing the neurovascular bundle

- tumors that enlarged during preoperative

therapy that contact neurovascular bundle;

Prognosis


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Prognosis at time of dx, most osteosarcomas are stage IIb lesions that have

infiltrated the soft tissue.- 70% of patients without detectable metastases: remain disease

free with appropriate surgical resection and chemotherapy;- 50% of adolescent pts, tumor penetrates growth plate into

epiphysis.

metastasis:- single most important prognostic factor- early hematogenous metastasis is common- 10% of patients will have pulmonary or lymph node

metastases at time of presentation

survival:- greater than 50% with adjunctive chemotherapy- metastatic disease evident at presentation also indicates

presence of more aggressive disease & poor prognosis

Chondrosarcoma


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Chondrosarcoma

Common age group: 40/50 age group

Low grade/ high grade

Primary

Secondary

usually arises in the cartilage cap of

osteochondroma that present since childhood

Any osteochondroma increase in size after the endof normal bone growth= malignant!

Clinical features


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Clinical features

Dull, persistent pain

Common sites:

Hip

pelvis

Investigation


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Investigation

X ray

Radiolucent lesion

With patchy/central calcification

X ray of chondrosarcoma


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X ray of chondrosarcoma

Treatment


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Treatment

tumor does not respond to either radiotherapy irchemotherapy

Current available treatment: surgical treatment (wideexcision and prosthetic replacement)

low grade tumors: more common- rarely metastasize- rarely recurs after wide limb salvaging excision- the involved bone is resected along w/ a small cuff of

surrounding muscle

high grade tumors

- have higher rate ofrecurrence after limb salvage(requires amputation)

- are prone to pulmonary metastases.

Ewings Sarcoma


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Ewing s Sarcoma

Malignant round cell tumour of long bones

(typically diaphysis) and limb girdles

Believed to arise from endothelial cells in the

bone marrow

Most commonly between the ages of10 and

20 years

Usually in a tubular bone (eg tibia, fibula orclavicle)

Ewings Sarcoma


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Ewing s Sarcoma

Macroscopically tumour is lobulated & fairly

large

Microscopically sheets of small dark

polyhedral cells with no regular arrangementand no ground substance are seen

Clinical Features


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Clinical Features

Pain (throbbing in nature)

Swelling

Generalized illness

Pyrexia

Warm tender swelling

Raised ESR (suggest / mistaken as

osteomyelitis)

Investigation


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Investigation

X-ray

Bone destruction (in mid-diaphysis)

New bone formation (along the shaft / appears as fusiformlayers of bone around lesiononion peel effect

CT & MRI

Reveal large extraosseous component

Radioisotope scans Disclose multiple lesions elsewhere in the skeleton

Treatment


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Treatment

Prognosis always poor

Surgery alone does little to improve

Radiotherapy has dramatic effect on tumour

but overall survival is not much enhanced Chemotherapy much more effective5 year

survival rate of 50%

Best results are achevied by combination of all3 methods

Secondary bone tumours


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Secondary bone tumours

Common source of carcinoma

Breast

Prostate

Kidney

Lungs

Thyroid

Bladder GI Tract

Commonest sites for bone metastases


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Commonest sites for bone metastases

Vertebrae

Pelvis

Proximal half of femur

Humerus

Clinical features


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Clinical features

Aged 50-70 years

Pain

After pathological fracture

Hypercalcemia (in patients with skeletal

metastases)

Investigations


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Investigations

X rays- skeletal deposits appears as rarefied areas in the medulla / patchesbones destruction in cortex

- osteoblastic deposits in late prostate carcinoma

MRI

99m Tc bone scintigraphy

- most sensitive method detecting silent metastasis

US, mammography, TFT, PSA , biopsy(1 tumour)

FBC, LFT,RP

Management


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Management

Mostly palliative

Radiotherapy and/or chemotherapy

Assessment for pathological fracture

Stabilize lesion with high risk of fracture

Surgical intervention: are to preserve stability

and function of the musculoskeletal system as

well as alleviate pain


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The End

Seminar 1 Ortho

Documents

Transcript of Seminar 1 Ortho