Imaging of bone disease 1- plain x-ray

2-radio isotope

3- CT scan

4- MRI

PLAIN X-RAY

1-BONE DENSITY

2-PERIOSTEAL REACTION

3-CORTICAL THICKENING

4- ALTERATION IN TRABECULAR PATTERAN

5-ALTERATION IN THE SHAPE OF BONE

Decrease bone density Generalized :

a-osteoporosis

b-osteomalacia and rickes

c-hyperparathyroidism,renal

osteodystrophy

d- mutiple myeloma

e-osteogensis imperfecta

Localized :

Fracture of one bone

Sudeck atrophy -sever osteoporosis

Increase bone density

a-osteopetrosis

b-myelosclerosis

c-sclerotic metastasis

d-paget s disease

e-prostatic metastasis

Periosteal reaction

Excess bone prodused by the

periosteum which occurs in response to

such condition

a-neoplasm

b-inflammation

c-trauma

Cortical thickening

Laying down of new bone ,there is no

separated lines or spicules of calcification as

seen in periosteal reaction

Causes:

1-chronic osteomylitis

2-healed trauma

3- response to chronic teroids

4- benign neoplasm

Alteration in the trabecular pttern

Reduction in number of trabeculae and alteration

in the remaining ones

a-osteoporosis :thick cortex ,long trabeculae

b-paget s disease:thick trabeculation in cortex and

medulla

c-haemolytic anemia :biconcave bone marrow

Alteration in the shape of the bone a-achondoplasia

b-multiple stenosis

c-acromegaly

e-expnding bone tumor

osteoporosis

Due to defenciency of the protein matrix

Matrix reduced in quantity

Caueses:

1-idiopathic

2-cushing syndrome

3-postmenopausal

osteomalacia

Lack of calciumin the body tissue

With poor mineralization of osteoid

If this occurs before epiphyseal closure

It is called rickets while in adults it is called osteomalacia

Periosteal Reactions

Benign

None

Solid

More aggressive or malignant

Lamellated or onion-skinning

Sunburst

Codman’s triangle

Chronic osteomyelitis

Benign

None

Solid

Aggressive/malignant

Onion-skinning

Sunburst

Codman’s triangle

Periosteal Reactions

Benign

None

Solid

Aggressive/malignant

Onion-skinning

Sunburst

Codman’s triangle

Periosteal Reactions

Ewing’s sarcoma

Ewing’s-Codman’s

triangle

Benign

None

Solid

Aggressive/malignant

Onion-skinning

Sunburst

Codman’s triangle

Periosteal Reactions

Osteosarcoma

Benign

None

Solid

Aggressive/malignant

Onion-skinning

Sunburst

Codman’s triangle

Periosteal Reactions

Periosteal Reactions

Solid Lamellated Codman’s Sunburst

Less malignant More malignant

Alteration in trabecular

patteran

1-haemolytic anemia

2-paget s disease

3-marrow hyerplasia

CT SCAN

1-disc herniation

2-imaging of complex shapd bone

3- extend of bone tumors both within

bone and adjacent soft tissue

Radioisotope scanning 1-detecion of metastasis

2-detection of osteomylitis

3- to decide if an abnormality on

rdiograph no seen

4- other abnormalities

Infection of bone

An invading organism may attack bone by direct invasion

from an infected wound, or from an infected joint, or it may

gain access by

haematogenous spread from distant foci, usually in the skin

Haematogenous osteomyelitis usually occurs during the period

of growth, but all ages may be affected and cases are even

found in old

age.

In infants, Streptococcus usually causes osteomyelitis. In

adults, Staphylococcus is more common

osteomyelitis

In the infant, vessels penetrate the epiphyseal plate in

both directions. Metaphyscal infections can thus pass

to the epiphysis and then the joint. Acute pyogenic

arthritis is therefore a relatively

common sequel of osteomyelitis in infants. The

periosteum in nfants is very loosely attached to

underlying bone.

osteomyelitis

In childhood, between 2 and 1 6 years, few vessels

cross the epiphyseal

plate though the periosteum is still relatively

loosely

attached. The epiphysis and joint are thus less

frequently infected.

The metaphyseal vessels terminate instead in

slow-flowing sinusoids

which promote blood-borne infective change

osteomyelitis

In the adult, after the epiphyseal plate has fused,

metaphyseal

and epiphyseal vessels are again connected so

that septic arthritis

can recur. Periostcum, however, is well hound

down and articular

i nfections via a metaphyseal route are less

likely.

Osteomyelitis The formation of pus in the bone deprives local cortex and

medulla of its blood supply.

Dead bone is resorbed by granulation tissue. Pieces of dead bone,

especially if cortical or surrounded by , pus, are not resorbed and

remain as sequestra .

As sequestra are devitaliscd they remain denser than surrounding

vital bone, which becomes demineralised due to hyperaemia and

immobilisation.

Absorption of sequestra is also facilitated by the presence of

an im'olucrum.

The involucrum forms beneath vital periostcum • which bas been elevated by pus.

As periostcum is poorly attached in nfants, involucrum formation is

greater and so is the resorption of dead bone, and healing.

osteopmyelitis

Acute osteomyelitis:

1-oedema

2-soft tissue swelling

3- bone destruction

osteomyelitis

Chronic osteomyelitis :The preliminary radiograph :

1- There is cortical thickening

2- evidence of intramedullary cavitation and angulation.

3-Linear calcified densities in the

soft tissues may represent extruded sequestra.

4- sequestrum in bone

Chronic osteomyelitis

MR image shows

1- muscle wasting;

2-the deformity of the bone is again

demonstrated.

3-There is extensive increase in signal within the medulla, indicating

a fluid collection.

4- A band of high signal can be seen extending from

the medulla superiorly, through the cortex laterally and into the

adjacent

soft tissues.

5-There is an effusion in the knee joint and oedema of the

subcutaneous

soft tissues.

osteomyelitis

Osteomyeltis

I n areas of dead periostcum, defects in the

involucrum occur..

These cloacae allow pus and sequestra to

escape, sometimes to the

skin via a sinus. The track and its deep

connection to bone can then

be demonstrated by sinograpby using water-

soluble contrast medium

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