Generalised Increased Bone Density (Adult)
Solitary sclerotic bone lesion
Multiple sclerotic bone lesions
Bone sclerosis with periosteal reaction
Coarse trabecular pattern
Coarse trabecular pattern
Skeletal metastases by their common radiological appearance
MIXED/SCLEROTIC:
- breast
- prostate
- carcinoid
- cervical
- testis
- gastric
LYTIC, EXPANSILE:
- Renal cell carcinoma
- Thyroid
- Pheochromocytoma
- Melanoma
LYTIC:
- SCC
- lung
- rectal, colon (occ sclerotic)
- uterus, ovary
- Wilm’s tumor
- bladder (occ sclerotic)
- neuroblastoma (occ sclerotic)
Sites of origin of primary bone neoplasm
Non-aggressive lucent lesion in the medulla (well-defined, marginal sclerosis, no expansion)
Indeterminate lucent lesion in the medulla (well-defined, NO marginal sclerosis, no expansion).
Aggressive lucent lesion in the medulla (ill-defined)
LUCENT BONE LESION IN THE MEDULLA
– WELL-DEFINED, ECCENTRIC
EXPANSION
LUCENT BONE LESION – GROSSLY
EXPANSILE
Malignant bone neoplasms:
1. Metastases – renal cell carcinoma and thyroid; less commonly melanoma, bronchus, breast and phaeochromocytoma.
2. Plasmacytoma
3. Central chondrosarcoma/lymphoma of bone/fibrosarcoma:
– when slow growing may have this appearance.
4. Telangiectatic osteosarcoma
Benign bone neoplasms:
1. Aneurysmal bone cyst
2. Giant cell tumour
3. Enchondroma
Non-neoplastic:
1. Fibrous dysplasia
2. Haemophilic pseudotumour (see Haemophilia) – especially in the iliac wing and lower limb bones. Soft-tissue swelling.
± Haemophilic arthropathy.
3. Brown tumour of hyperparathyroidism*.
4. Hydatid.
‘MOTH-EATEN BONE’ IN AN ADULT
Neoplastic:
1. Metastases.
2. Multiple myeloma.
3. Leukaemia – consider when there is involvement of an entire bone
4. Long-bone sarcomas:
(a) Ewing’s sarcoma.
(b) Lymphoma of bone.
(c) Osteosarcoma.
(d) Chondrosarcoma.
(e) Fibrosarcoma and malignant fibrous histiocytoma.
5. Langerhans’ cell histiocytosis.
Infective:
Acute osteomyelitis.
Osteomalacia and rickets
Vitamin D deficiency
1. Dietary.
2. Malabsorption.
Renal Disease
1. Glomerular disease (renal osteodystrophy*).
2. Tubular disease
(a) Renal tubular acidosis.
(i) Primary – sporadic or hereditary.
(ii) Secondary.
– Inborn errors of metabolism, e.g. cystinosis,
galactosaemia, Wilson’s disease, tyrosinosis, hereditary
fructose intolerance.
– Poisoning, e.g. lead, cadmium, beryllium.
– Drugs, e.g. amphotericin B, lithium salts, outdated
tetracycline, ifosfamide.
– Renal transplantation.
(b) Fanconi syndrome – osteomalacia or rickets, growth
retardation, RTA, glycosuria, phosphaturia, aminoaciduria and proteinuria.
(c) Vitamin D-resistant rickets (familial hypophosphataemia,
X-linked hypophosphataemia)
Hepatic disease:
1. Parenchymal failure.
2. Obstructive jaundice – especially biliary atresia.
If the patient is less than 6 months of age then consider:
1. Biliary atresia.
2. Metabolic bone disease of prematurity – combined dietary deficiency and hepatic hydroxylation of vitamin D.
3. Hypophosphatasia.
4. Vitamin D-dependent rickets.
PERIOSTEAL REACTIONS – BILATERALLY
SYMMETRICAL IN ADULTS
HYPERTROPHIC OSTEOARTHROPATHY
Pulmonary:
1. Carcinoma of bronchus.
2. Lymphoma.
3. Abscess.
4. Bronchiectasis – frequently due to cystic fibrosis.
5. Metastases.
Pleural:
1. Pleural fibroma – has the highest incidence of accompanying HOA, although it is itself a rare cause.
2. Mesothelioma.
Gastrointestinal
1. Ulcerative colitis.
2. Crohn’s disease.
3. Dysentery – amoebic or bacillary.
4. Lymphoma*.
5. Whipple’s disease.
6. Coeliac disease.
7. Cirrhosis – especially primary biliary cirrhosis.
8. Nasopharyngeal carcinomas (Schmincke’s tumour).
Avascular necrosis (Toxic, traumatic, metabolic/endocrine, inflammatory/infective, Hb disorders)
Toxic:
1. Steroids – probably does not occur with less than 2 years of treatment.
2. Alcohol – possibly because of fat emboli in chronic alcoholic pancreatitis.
3. Immunosuppressives, Anti-inflammatory drugs
Traumatic:
1. Idiopathic – e.g. Perthes’ disease
2. Fractures – especially femoral neck, talus and scaphoid.
3. Radiotherapy.
4. Fat embolism.
Inflammatory:
1. RA (probably vasculitis)
2. SLE (probably vasculitis)
3. Scleroderma
4. Infection: pyogenic arthritis
Metabolic and endocrine:
1. Pregnancy.
2. Diabetes.
3. Cushing’s syndrome.
4. Hyperlipidaemias.
5. Gout.
Haemopoietic disorders:
1. Haemoglobinopathies – especially sickle-cell anaemia.
2. Polycythaemia rubra vera.
3. Gaucher’s disease.
4. Haemophilia
Erosion/absent outer end of clavicle
Focal rib lesion (SOLITARY OR
MULTIPLE)
NEOPLASTIC:
Secondary more common than primary. Primary malignant more common than benign.
NON-NEOPLASTIC:
1. Healed rib fracture.
2. Fibrous dysplasia.
3. Paget’s disease.
4. Brown tumour of hyperparathyroidism.
5. Osteomyelitis – bacterial, tuberculous or fungal.
Inferior rib notching
ARTERIAL:
- coarctation of the aorta: Bilateral 4th to 8th ribs conventionally. Unilateral and right-sided if coarc is prox. to left subclavian artery. Unilateral and left-sided if coarc associated with anomalous right subclavian artery distal to coarc.
- Subclavian obstruction (unilateral rib notching of 1-4th ribs on operated side of Blalock operation for TOF repair)
VENOUS:
- SVCO
NEUROGENIC:
- neurofibromatosis (ribbon ribs may be a feature)
Superior rib notching
Connective tissue diseases:
1. Rheumatoid arthritis.
2. Systemic lupus erythematosus.
3. Scleroderma*.
4. Sjögren’s syndrome.
Metabolic:
Hyperparathyroidism*.
Miscellaneous
1. Neurofibromatosis.
2. Restrictive lung disease.
3. Poliomyelitis.
4. Marfan’s syndrome.
5. Osteogenesis imperfecta*.
Wide/thick ribs
Madelung deformity. It comprises: (a) short distal radius, which shows a dorsal and ulnar curve;
(b) triangular shape of the distal radial epiphysis;
(c) premature fusion of the ulnar side of the distal
radial epiphysis;
(d) dorsal subluxation of the distal ulna;
(e) enlarged and distorted ulnar head; and
(f) wedging of the triangular-shaped carpus between the distal radius and ulna.