42 David Sutton

DAVID SUTTON PICTURES

DR. Muhammad Bin Zulfiqar PGR-FCPS III SIMS/SHL

• Fig. 42.1 Rickets. There is obvious 'fraying' of the visible metaphyseal margins.

• Fig. 42.2 Rickets. There is splaying of all of the visible metaphyses, with widening of the epiphyseal plates. In addition, there is so chaaracteristic bowing of the femora and bones of the lower leg.

• Fig. 42.3 Rickety rosary. Widening of the anterior ribs is clearly demonstrated (arrows). The classic metaphyseal changes of rickets are also seen in the proximal humeri.

• Fig. 42.4 Renal tubular acidosis. The combination of nephrocalcinosis and osteomalacia (Looser's zone-arrow) in the right 11th rib is characteristic, although symptomatic bone disease affects only a minority of patients. (Courtesy Dr. Dl Stoker and Institute of Orthopaedics.)

• Fig. 42.5 Looser's zone. The characteristic lucency of the mid ulna is seen.

• Fig. 42.6 Looser's zone. There is lucency with surrounding sclerosis in the lateral border of the scapula-a common site.

• Fig. 42.7 Sites of incidence of Looser's zones in osteomalacia. In a group of middle-aged and elderly patients with dietetic osteomalacia. (Courtesy of Dr D. J. Stoker and Institute of Orthopaedics.)

• Fig. 42.8 Looser's zones. Symmetrical lucencies are seen involving the medial cortex of the proximal femur bilaterally-another characteristic site.

• Fig. 42.9 Osteomalacia. Marked biconcavity of the vertebral bodies (codfish vertebrae). (Courtesy of Dr D. J. Stoker and Institute of Orthopaedics.)

• Fig. 42.10 Hypophosphatasia. In this child metaphyseal ossification is delayed in the ulnae while the distal radii contain islands of non-ossified tissue. (Courtesy of Dr D. J. Stoker and Institute of Orthopaedics.)

• Fig. 42.11 Familial hyperphosphataemia. (A) The femur is abnormal with some bowing, increased width, and prominent but irregular cortex, somewhat resembling Paget's disease. (Courtesy of Dr C. S. Resnik.)

• Fig. 42.11 Familial hyperphosphataemia. (B) The radiological appearances in this child are diagnostic. The bones are widened with loss of differentiation of cortex and medulla. A coarse trabecular pattern and bowing are also evident. Again, these features resemble those of Paget's disease. (Courtesy of Dr D. J. Stoker and Institute of Orthopaedics.)

• Fig. 42.12 Scurvy. The margins of the epiphyses are sclerotic (Wimberger's sign). There is a narrow epiphyseal plate, with increased density of the zone of provisional calcification (Frankel's line). The lucent zone beneath this is due to lack of mineralized osteoid (Trumerfeld zone).

• Fig. 42.13 Scurvy. Subperiosteal haemorrhage has elevated the periosteum. The healing stage shows marked periosteal new bone formation. The metaphyseal lucency (Trumerfeld zone) is again visible, as is Pelkan's spur, at the medial border of proximal tibial metaphysis.

• Fig. 42.14 Postmenopausal osteoporosis. Serial films in this patient show the progressive development of kyphosis as a result of anterior wedging of the thoracic vertebral bodies during the course of 6 months. (Courtesy of Dr D. J. Stoker and Institute of Orthopaedics.)

• Fig. 42.15 Osteoporosis. In this patient, resorption of the secondary trabeculae has left the primary trabeculae to delineate the lines of stress within the femoral neck.

• Fig. 42.16 Cushing's disease. Excessive callus formation is seen at multiple fracture sites in the ribs. The patient had functional adrenal carcinoma.

• Fig. 42.17 Cushing's disease. Generalised reduction in bone density simulates postmenopausal osteoporosis in this patient. The compression fracture of the superior border of the body of L4 has characteristically produced dense callus. This feature is almost, but not entirely, pathognomonic of glucocorticosteroid excess. (Courtesy of Dr D. J. Stoker and Institute of Orthopedics).

• Fig. 42.18 Thyroid acropachy. A dense periosteal reaction is seen along the first metatarsal. Although this can occur in any of the digits, the first is a characteristic site.

• Fig. 42.19 Hypertrophic (pulmonary) osteoarthropathy. There is marked periosteal reaction along most of the visualised bones, with, in addition, some periarticular osteoporosis, most likely secondary to disuse, resulting from the severe pain experienced in this condition.

• Fig. 42.20 Hypertrophic osteoarthropathy: periosteal reaction is identified along the medial aspect of the distal femur.

• Fig. 42.21 Cretinism. Marked skeletal retardation was present in this 12- month-old child. Note that the carpal and proximal femoral centres have not yet appeared. (Courtesy of Dr D. 1. Stoker and Institute of Orthopaedics.)

• Fig. 42.22 Adult cretinism. This 39-year-old man received no therapy until 4 years before this film was obtained. Coxa vara is present, while the femoral heads are deformed and irregularly ossified in the absence of thyroid hormone during development. (Courtesy of Dr D.J. Stoker and Institute of Orthopaedics.)

• Fig. 42.23 Acromegaly. The frontal sinuses are markedly enlarged, and there is frontal bossing. A double floor is seen in the pituitary fossa with' ballooning’.

• Fig. 42.24 Acromegaly. The vertebral bodies show bony overgrowth. Mild posterior scalloping is also seen at several levels. (Courtesy of Dr. C. S. Resnik.)

• Fig. 42.25 Acromegaly. There is obvious enlargement of the soft tissues and phalanges with prominent joint spaces due to increased cartilage thickness. The distal phalanges show the characteristic 'arrowhead' configuration.

• Fig. 42.26 Acromegaly. There is marked prominence of the soft tissues of the heel pad which measures approximately 35 mm.

• Fig. 42.27 Acromegaly. There is overgrowth of the bone in the iliac crests and irregular bony prominence of the sites of muscle attachments throughout the pelvis.

• Fig. 42.28 Pseudohypoparathyroidism. A markedly short fourth metacarpal bone is seen. Although not specific for pseudohypoparathyroidism, this is a characteristic finding. (Courtesy of Dr C. S. Resnik.)

• Fig. 42.29 Hyperparathyroidism. There is marked subperiosteal resorption of the radial aspect of several of the phalanges and erosion of the tufts.

• Fig. 42.30 Hyperparathyroidism. There is subperiosteal erosion of the medial side of the proximal tibia.

• Fig. 42.31 Hyperparathyroidism. There is subperiosteal erosion of the distal end of the clavicle, as well as on the inferior surface at the site of the attachment of the coracoclavicular ligament.

• Fig. 42.32 Hyperparathyroidism. Intracortical bone resorption is seen, with multiple small oval lucencies within the cortical bone. A brown tumour is seen in the proximal femur.

• Fig. 42.33 Severe disuse osteoporosis. There is marked intracortical bone resorption, particularly evident in the tibia.

• Fig. 42.34 Hyperparathyroidism. 'Pepper-pot' skull. There are multiple characteristic lucencies throughout the skull.

• Fig. 42.35 Brown tumour of hyperparathyroidism. There is a well defined, lytic, mildly expansive lesion of the proximal humerus.

• Fig. 42.36 Brown tumour of the mid tibia. The patient was found to have a parathyroid adenoma.

• Fig. 42.37 Renal osteodystrophy. Rugger-jersey spine of renal osteodystrophy. Typical end-plate sclerosis is seen with alternating bands of lucency (Courtesy of Dr D. J. Stoker and Institute of Orthopaedics.)

• Fig. 42.38 Uraemic osteodystrophy in childhood. In this child with chronic renal failure, the combination of rickets and secondary hyperparathyroidism affects the skeleton. The femoral metaphysis is irregular and the capital epiphysis shows considerable displacement. This has been likened to a rotting fence post.

Fig. 42.39 Chronic renal failure: haemodialysis patient. (A) There is an appearance resembling a Charcot spine, or even infection. (B) A destructive arthropathy of the shoulder is also seen, without evidence of infection or neuropathy.

• Fig. 42.40 Oxalosis. There is a generalised but slightly patchy increase in density of much of the visualised skeleton, due to calcium oxalate deposition.

• Fig. 42.41 Ochronosis. Gross narrowing of the joint spaces of both hips is associated with other evidence of severe degenerative disease. The intervertebral disc spaces are calcified and narrowed. (Courtesy of Dr D. J. Stoker

• Fig. 42.42 Ochronosis. The intervertebral disc spaces are narrowed and calcified. Such widespread change is uncommon in uncomplicated degenerative spondylosis. (Courtesy of Dr D. J. Stoker and Institute of Orthopaedics.)

• Fig. 42.44 Lead lines: metaphyseal bands of increased density.

• Fig. 42.45 Bismuth poisoning: dense metaphyseal lines are present, similar to those seen in lead poisoning.

• Fig. 42.46 Vinyl chloride poisoning. Inhalation or ingestion of vinyl chloride may produce this characteristic resorption of the central portions of the terminal phalanges. (Courtesy of Dr D. J. Stoker and Institute of Orthopaedics.)

• Fig. 42.47 Fluorosis. There is markedly increased density of all the visualised bones.