Pathology

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3 Pathology

Chapter contents

Changes due to pathology

Loss of bone density
Increase in bone density
Bone destruction

Hormone disturbances

Pituitary gland
Thyroid gland
Parathyroid glands
Adrenal glands

Vitamin deficiencies

Joint disorders

Bone tumours

Benign tumours
Malignant tumours
Secondary bone tumours

Fractures

Types of fracture
Orthopaedic management of fractures

Pathology is the study of disease. This chapter covers some of the more common diseases which can be detected radiographically. Pathology concerning specific areas of the body will be discussed in later chapters following the relevant bone or joint. Radiographs have been included to demonstrate some of the pathology; these are often advanced examples and it should be remembered that early signs will not be as obvious.

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.

Osteoporosis (Figs 3.1, 3.2)

A deficiency in the bone matrix due to a reduction in bone formation – therefore the bones fracture easily.

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Fig. 3.1 Osteoporosis, resulting in a compression fracture of the first lumbar vertebra.

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Fig. 3.2 Osteoporosis, femoral head. MR image. Note the joint effusion.

(From Resnick Kransdorf, 2005.)

Causes –

lack of vitamin C (scurvy). Old age. Disuse, for example due to immobilisation following fracture; if activity returns the bone returns to normal. Cushing’s syndrome. Overuse of steroid hormones. Post-menopausal, related to reduced oestrogen levels.

Radiological signs –

bone affected appears radiolucent. The primary trabeculae may appear more prominent.

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

An overall decrease in bone calcification.

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Fig. 3.3 Osteomalacia, ulnar shaft.

(From Sutton 1987.)

Causes –

diet low in vitamin D, calcium or phosphorus. Malabsorption syndromes, e.g. coeliac disease, Crohn’s disease, renal disease.

Radiological signs –

narrow bands of decalcification 2–3 mm wide called Looser’s zones (‘pseudo fractures’).

Osteogenesis imperfecta (Fig. 3.4)

Bone formation is defective. The bones become small, thin and prone to fracture. Growth becomes stunted and limb deformity results.

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Fig. 3.4 Osteogenesis imperfecta, lower extremities. Note a decrease in bone density associated with thin long bones, multiple fractures and bowing of the long bones.

(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.

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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.

image

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.

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Fig. 3.7 Paget’s disease, skull.

(Courtesy of Ernest Higginbottom.)

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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.

image

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.

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Fig. 3.10 Osteomyelitis, infant knee.

(Courtesy of Ernest Higginbottom.)

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