Changes due to pathology

Loss of bone density

This is usually a decrease in the amount of calcium present in the bone and therefore the bone becomes less dense in structure. The bone is more radiolucent and therefore appears ‘darker’ on a radiograph. This may be an overall loss of density or be specific to particular areas of bone.

Osteomalacia (‘adult rickets’) (Fig. 3.3)

An overall decrease in bone calcification.

Fig. 3.3 Osteomalacia, ulnar shaft.

(From Sutton 1987.)

(From Resnick Kransdorf, 2005.)

Cause –

congenital disorders (rare).

Osteitis fibrosa cystica

Loss of bone density due to the increase in blood calcium, the bones becoming decalcified. The skull appears mottled; bones develop cystic areas; bone is reabsorbed. Pathological fractures may occur.

Cause –

hyperparathyroidism: overactivity of the parathyroid glands and therefore excessive secretion of parathormone.

Increase in bone density

This is usually an increase in the amount of calcium present in the bone (osteosclerosis), resulting in the bone becoming denser in structure. The bone becomes more radiopaque and therefore appears ‘whiter’ on the radiograph.

Osteopetrosis (Fig. 3.5)

Increased density of bones which have been ossified from cartilage, but mainly in the ribs, pelvis, and vertebrae. Bones become hard but brittle and therefore fracture easily. A prominent line of calcification can often be seen along the epiphyseal plate.

Fig. 3.5 Osteopetrosis, vertebral bodies.

(From Sutton 1987.)

Cause –

disturbances when the bones are being formed during pregnancy.

Radiological signs –

appearance of ‘bone within a bone’.

Fluorosis

A generalised increase in bone density. Mottled discolouration of the teeth occurs.

Cause –

excessive ingestion of fluorine.

Lead poisoning (Fig. 3.6)

Radiographically dense transverse lines appear at the ends of the shafts of long bones.

Fig. 3.6 Lead poisoning, wrist. Note dense transverse lines on the radius and ulna.

(From Resnick Kransdorf, 2005.)

Cause –

excessive lead intake.

Myelosclerosis

A generalised increase in bone density. Secondary bone sclerosis and anaemia occur.

Paget’s disease (Figs 3.7, 3.8)

Sometimes described as a ‘cotton wool’ skull; some absorption of bone and excessive deposition of new bone occurs. There is increased vascularity and therefore increased bone destruction followed by bone repair with abnormal bone pattern and coarse, thickened trabeculae. It usually affects the skull, femora, tibiae, lumbar spine and pelvis and is common in old age.

Fig. 3.7 Paget’s disease, skull.

(Courtesy of Ernest Higginbottom.)

Fig. 3.8 Paget’s disease. Skeletal scintigraphy. Note increased uptake of radionuclide throughout the left hemi-pelvis.

Bone destruction

Necrosis of the femoral head following fracture

‘Bone death’ due to a poor blood supply. Radiographically the bone surfaces appear irregular.

Bone tuberculosis (Fig. 3.9)

Irregular bone destruction with little new bone formation. Most common sites are the vertebral bodies, long bones, fingers and joints.

Fig. 3.9 Bone tuberculosis, wrist and carpal bones.

(From Sutton 1987.)

Cause –

spread via the bloodstream from a tuberculous focus, usually in the lungs.

Radiological signs –

if the cartilage is destroyed the bones appear to be crowded.

Osteomyelitis (Figs 3.10, 3.11, Plate 1)

Bone infection, most common in children, usually from a Staphylococcus infection. It begins in the medullary cavity and may spread to the cortex and the periosteum. Bone destruction appears after 7 days when the periosteum becomes elevated. It can be treated with antibiotics and therefore gross bone destruction is now rare.

Fig. 3.10 Osteomyelitis, infant knee.

(Courtesy of Ernest Higginbottom.)

Fig. 3.11 Recurrent diabetic bone infection following amputation of the third toe at the level of the metatarsophalangeal joint, third and fourth metatarsal and head of second metatarsal. MR image.

(From Resnick Kransdorf, 2005.)

Caisson disease (bone necrosis) (Fig. 3.12)

Affects workers who experience high atmospheric pressure, e.g. divers and tunnel workers. Radiological signs appear late and include fatigue fractures, irregular areas of callus, necrosis with adjacent fibrous collapse and degenerative changes.

Fig. 3.12 Caisson disease, femur.

(From Sutton 1987.)

Hormone disturbances

Pituitary gland

The anterior lobe of the pituitary gland produces the growth hormone, which controls the rate of growth of the epiphyseal cartilage.

Gigantism

This occurs if hypersecretion takes place during childhood resulting in excessive growth.

Acromegaly (Fig. 3.13)

This occurs if hypersecretion takes place during adulthood. It results in enlarged and thickened bones, especially the hands and mandible, and dorsal kyphosis. Enlargement of the pituitary fossa occurs because the hypersecretion is caused by an adenoma (benign tumour).

Fig. 3.13 Acromegaly, distal phalanx, hand. Note prominence of the soft tissue, enlargement of the base of the phalanx, pseudoforamina, arrowed.

(From Resnick Kransdorf, 2005.)

Dwarfism (Fig. 3.14)

This occurs if hyposecretion takes place during childhood, resulting in a lack of bone growth and therefore a small individual.

Fig. 3.14 Hypopituitarism, wrist. Note the absence of closure of the epiphyses of the radius and ulna in a 23-year old-woman.

(From Resnick Kransdorf, 2005.)

Thyroid gland

Cretinism

Thyroxine from the thyroid gland is responsible for normal skeletal development and therefore hyposecretion results in retarded skeletal development.

Parathyroid glands

Hyperparathyroidism

Parathormone regulates the quantity of calcium and phosphorus in the blood and bones. Hypersecretion results in a calcium loss from bones causing a radiolucent appearance, subperiosteal bone reabsorption, deformity and fractures.

Adrenal glands

Osteoporosis

Prolonged hypersecretion of glucocorticosteroids affects calcium metabolism (as can large doses of steroids) resulting in osteoporosis of the axial skeleton.

Vitamin deficiencies

Vitamins C and D are responsible for the formation of healthy bone tissue.

Joint disorders

Septic arthritis

Inflammation of a joint due to a bacterial infection.

Osteoarthritis (Fig. 3.15)

Degeneration of the articular hyaline cartilage. The bone becomes thickened and spreads outwards forming ‘spurs’ round the joint margins. Synovial fluid may enter the bone giving it a cystic appearance. It is more common above the age of 60; the most common sites are the hips, knees and spine.

Fig. 3.15 Osteoarthritis, pelvis and hips.

(Courtesy of Ernest Higginbottom.)

Rheumatoid arthritis (Fig. 3.16)

Radiographically, this has the appearance of bone erosion, joint deformity and a narrowed joint space due to inflammatory tissue forming over and destroying the articular hyaline cartilage and eventually replacing it, causing the joint to swell and limiting its degree of movement. It affects several joints at once. The most common sites are the fingers, ankles, hips and knees.

Fig. 3.16 Rheumatoid arthritis, hands.

(Courtesy of Ernest Higginbottom.)

Osteochondritis dissecans (Fig. 3.17)

Caused by local bone necrosis (death of tissue) resulting in loose fragments of bone (loose bodies) in the joint space. The most common site is the knee.

Fig. 3.17 Osteochondritis dissecans, medial condyle of femur.

(From Sutton 1987.)

Juvenile osteochondritis (Fig. 3.18)

A non-inflammatory condition of epiphyses or centres of ossification. It may be due to poor blood supply causing necrosis.

Fig. 3.18 Osgood–Schlatter’s disease, knee. Note fragmentation of the tibial tubercle with overlying soft tissue thickening.

Radiological signs (late) – increased bone density and fragmentation of the epiphysis. Different names according to site, e.g. Perthes’ disease (see Fig. 7.17) – head of femur; Osgood–Schlatter’s disease (Fig. 3.18) – tibial tubercle.

Bone tumours

Bone cysts (not actual tumours) (Fig. 3.19)

These are cavities in the bone filled with fluid. They may be responsible for pathological fractures.

Fig. 3.19 Bone cysts, humerus, with pathological fracture.

(Courtesy of Ernest Higginbottom.)

Malignant tumours

Radiographically, these have ill-defined edges, destruction of the bone cortex, periosteal reaction and rapid growth. Blood-borne spread is usually to the lungs.

Osteosarcoma (osteogenic sarcoma) (Fig. 3.23)

A tumour of the osteoblasts, which can occur in any bone but is usually found at the end of a long bone. Most common in male adolescents. Spreads rapidly to patient’s lungs.

Fig. 3.23 Osteosarcoma, knee (pathology specimen).

(Courtesy of Ernest Higginbottom.)

Radiological signs –

area of radio-opacity with periosteal reaction.

Chondrosarcoma (Fig. 3.24)

A tumour of cartilage cells, metastasising to the lungs. Most common sites are the pelvis, long bones and round the knee joint.

Fig. 3.24 Chondrosarcoma, femur.

(From Sutton 1987.)

Fibrosarcoma

A rare tumour of fibrous tissue. Most common at the ends of long bones but may occur mid-shaft. Results in bone destruction.

Ewing’s tumour

A rare tumour, most common in adolescents. Thought to be a tumour of the reticulo-endothelial cells, metastasising through the bloodstream to the lungs and other bones.

Myelomatosis (multiple myeloma) (Fig. 3.25)

Probably a tumour of the bone marrow, most common in the 60-plus age group. Destroys bone tissue and produces multiple lesions. Pathological fractures are common. Common sites are the spine, skull, ribs, pelvis, upper femur, shoulder girdle and humerus.

Fig. 3.25 Myelomatosis, femur.

(From Sutton 1987.)

Secondary bone tumours (Figs 3.26, Figs 3.27, Plates 2, 3 and 4)

These may occur from a primary tumour of the prostate, breast, bronchus, kidney, stomach or thyroid. They produce simple or multiple, extremely pain-ful, lesions. Common sites are the vertebral bodies, upper ends of long bones, e.g. femur and humerus, pelvis, ribs and the skull. Nuclear medicine techniques will demonstrate metastases that are not demonstrated radiographically in the early stages.

Fig. 3.26 Bone metastases from prostatic cancer.

Fig. 3.27 Secondary bone tumours, spine. MR image.

(From Resnick Kransdorf, 2005.)

Fractures

A fracture is an abnormal break in bone continuity and may be complete or partial.

Causes

Direct trauma

Indirect trauma (usually rotational)

Repetitive strain (stress fracture, e.g. march fracture)

Underlying pathology (tumour, osteogenesis imperfecta, osteoporosis).

Types of fracture

Simple (closed) fracture

This is where the skin surface remains intact and therefore there is no risk of infection.

Orthopaedic management of fractures

Diagnosis

Signs and symptoms of a fracture may include:

pain

swelling

deformity, e.g. angulation or shortening of a limb

abnormal movement.

Diagnosis is usually confirmed radiographically

Reduction

The aim of reduction is to realign the bones to as near the normal position as possible and therefore promote faster healing.

Methods available include:

Closed manipulation –

usually performed under anaesthetic conditions when the bone ends are moulded together.

Mechanical traction –

usually used for fractures of the femur, where the contraction of muscles exerts a strong, displacing force. A weight is attached to the leg and this applies tension, which counteracts the muscular pull, slowly aligning the bones.

Open reduction –

a surgical operation where the bones are manipulated directly.

Immobilisation

This ensures that the manipulated fragments of bone maintain their alignment; it therefore encourages faster healing.

Methods available include:

Plaster of Paris bandages –

usually used after closed manipulation. Applied wet; when dry, provides a hard, protective cover.

Splints –

numerous types available; can be made of aluminium, plastic or polystyrene; tend to be used for fingers.

Screws and plates, pin and nails –

inserted during open reduction to internally fix the bone fragments. Used in comminuted fractures and when other methods are difficult to apply, e.g. for the neck of femur.

Rehabilitation

This takes place as soon after immobilisation as possible. The patient is encouraged to move parts of the body to increase the blood supply to the fracture site and therefore quicken healing, for example, in a fractured wrist the fingers are moved and muscle exercises are given.

Stages of healing of fractures

1. A blood clot is formed owing to damaged blood vessels in the medulla, cortex and periosteum.

2. Within 24 hours the haematoma is converted into vascular, fibroblastic granulation tissue.

3. After about 7 days cartilage and osteoid tissue are laid down by the osteoblasts, therefore forming irregular, new bone called provisional callus.

4. Provisional callus is converted into ‘normal’ bone containing haversian systems.

5. After a period of time the bone is moulded by the osteoclasts and osteoblasts to regain its original shape.

Healing of fractures

Radiological evidence of fracture healing

Appearance of callus.

Radiographic signs of bony union (Fig. 3.28)

Visible callus bridging the gap between the bone fragments.

Fig. 3.28 Radiographic signs of bony union, tibia and fibula.

(Courtesy of Ernest Higginbottom.)

Bone trabeculae continuing across the fracture site.

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Pathology

Osteoporosis (Figs 3.1, 3.2)

Osteomalacia (‘adult rickets’) (Fig. 3.3)

Osteogenesis imperfecta (Fig. 3.4)

Osteopetrosis (Fig. 3.5)

Lead poisoning (Fig. 3.6)

Paget’s disease (Figs 3.7, 3.8)

Bone tuberculosis (Fig. 3.9)

Osteomyelitis (Figs 3.10, 3.11, Plate 1)

Caisson disease (bone necrosis) (Fig. 3.12)

Acromegaly (Fig. 3.13)

Dwarfism (Fig. 3.14)

Osteoarthritis (Fig. 3.15)

Rheumatoid arthritis (Fig. 3.16)

Osteochondritis dissecans (Fig. 3.17)

Juvenile osteochondritis (Fig. 3.18)

Bone cysts (not actual tumours) (Fig. 3.19)

Chondroma (Fig. 3.20)

Osteochondroma (Fig. 3.21)

Osteoclastoma (giant cell tumour)(Fig. 3.22)

Osteosarcoma (osteogenic sarcoma) (Fig. 3.23)

Chondrosarcoma (Fig. 3.24)

Myelomatosis (multiple myeloma) (Fig. 3.25)

Secondary bone tumours (Figs 3.26, Figs 3.27, Plates 2, 3 and 4)

Radiographic signs of bony union (Fig. 3.28)

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