Clinical

1. Metabolic &Endocrine
Disorders
Affecting Bone
Dr. Santosh Atreya
MD Resident (Phase B)
Radiology and Imaging
BSMMU

2. • Introduction
Metabolic & endocrine
bone diseases-with
radiological features
• Rickets
• Osteomalacia
• Scurvy
• Osteoporosis
• Hyperpituitarism
• Hyperthyroidism
• Hypothyroidism
• Hyperparathyroidism
• Hypoparathyroidism
• Toxic effects on the
skeleton
TOPICS TO BE
DISCUSSED TODAY

3. • Metabolic & Endocrine bone
disease is an umbrella term referring
to abnormalities of bones caused by a
broad spectrum of disorders.
Introduction

4. Metabolic bone diseases affects the skeleton in two
ways; either by too much or too little calcified bone .
Radiographic evaluation of changes in bone density is
difficult, as upto 40% of bone mass may be lost, before it
becomes apparent radiographically.

5. Composition of bone
Bone cells
Osteocytes
Osteoblasts
Osteoclast
Bone matrix
Organic components.
Inorganic components.

6. Organic components
A.Type -1 collagen fibers ( 95% of
organic matter)
B. Ground substances
Sulfatedglycosaminoglycans
Chondrotin sulfate
Keratin sulfate
Glycoprotiens
Osteocalcin
Osteopontin
Sialoprotien
Inorganic material
( about 5% of dry weight of bone
matrix)
Calcium
Phosphorus
Bicarbonate
Citrate
Magnesium
Sodium
Potassium

7. Physis
• It is the anatomical difference
between growing and mature
bone.
• It appears radiologically as a
lucency between the epiphysis
and the metaphysis.
• It represents the site where
longitudinal bone growth occurs.
• It is the primary site for the
effect of metabolic and
endocrine bone disorder.

8. DISEASES

9. History of Rickets
• 2nd century-Romans described
individuals who may have had
rickets
• 1640’s-Rickets was extremely
common in england
• 1920’s-Cause of Rickets
identified
• 1930’s-Public health initiative
to fortify milk with vit.D

10. • It is a disease of childhood characterized by failure
of mineralization of osteoid tissue in developing
skeleton, particularly at the growth plate.
• Age: 4-18 months.
• Causes:
1.Abnormality in vitamin-D metabolism.
2.Abnormality in phosphate metabolism.
3.Calcium Deficiency.
RICKETS

12. Serum calcium- low
Serum phosphorus- low
Serum alkaline phosphatase-
elevated
Serum 25(OH)D- low
Biochemical examination

13. Clinical features
Tetany
Convulsion
Protruding abdomen
Pigeon chest
Failure to thrive
Restlessness
Muscular flaccidity
craniotabes
Swelling of wrist and ankle
Stunted growth
Rickety rosary
Spinal curvature ( eg: kyphosis,
scoliosis )
Bowing and or # of long bones.
Mnemonic
R-Rachitic rosary
I-Pigeons Chest
C- Craniotabes
K-Knock Knees
E-Ends of long bones becomes
widened
T-Teeth: Delayed eruption of teeth
S-Skull: Bossing of skull in children
<6 months

14. Pot Belly in rickets
Widening of Wrist
Rickets : Valgus deformity
( knock Knee)

15. What to look for on X-rays??

16. •Earliest radiological sign is
loss of normal zone of
provisional calcification
adjacent to metaphysis.
•Later, metaphyseal margin
becomes indistinct
& frayed.
•Growth plate become
widened.
Radiological Features

17. Rickets pre-treatment: irregular
widened epiphyseal plates, with
cupping and fraying of the
metaphyses, and bowing of long
bones.
Rickets post-treatment: the
epiphyses and metaphyses assume
a more normal appearance

18. • Splaying & cupping of
metaphyseal margin occurs.
• Indistinct cortex as
subperiosteal osteoid fails to
calcify.
• Reduction in generalized bone
density.
• In epiphysis, haziness of
cortical margin may be found.

19. In long standing cases:
• Bowing of long bone(particularly lower limb).
• Fracture of wt bearing bone.
• Looser’s zones but less than osteomalacia.
• Stunted growth
Changes in Thorax:
• Thoracic kyphosis may be present with deep narrow
chest- ‘pigeon chest’.
• Harrison’s sulcus –indrawing of the lower chest
caused by the pull of the diaphragmatic attachment to
the soft ribs.
• Enlargement of growth plates at costochondral
junction---Rachitic rosary.

20. Changes in the pelvis:
• Triangular/ Tri-radiate pelvis
• Protrusioacetabuli may be seen
• Slipped capital femoral epiphysis.
Changes in the skull:
• Frontal bossing of skull
• Basilar invagination.
Changes in the appendicular bone:
• Characteristic lateral bowing of legs may be
present from age of 2-3 yrs with associated
varus deformity of hip and knee.

21. ‘Rachitic rosary’: costochondral
junction enlargement (arrowheads)

22. Vitamin D resistant rickets
X-linked hypophosphatasia
Rare X-linked dominant disorder of renal tubular
reabsorption characterized by impaired reabsorption of
P04 in prox. renal tubule (due to defect in renal brush
border membrane).
 Hypophosphataemia, hyperphosphaturia, elevated
serum alkaline phosphatase, normal plasma &urine
calcium, normal serum vit-D.
 Rickets clinically become evident at about 6-12
months of age.

23. • Avariety of renal dysfunction syndromes produce
rickets and osteomalacia. These include:
-Hypercalcaemia
- Renal po4 loss
-Secondary hypophosphataemia
- Aminoaciduria & renal tubular acidosis.
• In renal tubular acidosis, affected patients demonstrate
growth retardation ,short stature, changes of rickets/
osteomalacia, nephrolithiasis, nephrocalcinosis.
Vitamin D resistant rickets associated
with renal tubular disorders

24. Renal tubular acidosis. The combination
of nephrocalcinosis and osteomalacia
(Looser's zone) in the right 11th rib is
characteristic.

25. Osteomalacia
Osteomalacia refers to lack of mineralization of
osteoid in the mature skeleton resulting from
Vitamin D deficiency .
C/F:
• Bone pain
• Malaise
• Muscular weakness
Biochemical findings:
Serum calcium
Serum phosphorus
SerumALK phosphatase

26. Radiological features
Common sites
-Pubic rami
-Proximal femur
-Scapula
-Lower ribs & ulna
Generalised
bone density
Looser’s
Zones
Coarsened indistinct
trabecular pattern
Bone
softening
Biconcave vertebra
Bowing of long bones
Protrusio acetabuli
Tri-radiate pelvis
Basilar invagination
Common sites

27. Osteomalacia. ‘Looser”s zone’ of the proximal
femoral metaphysis

28. Osteomalacia. Marked biconcavity of the
vertebral bodies(codfish vertebrae Pattern).

29. Bilateral Looser’s zones

30. Scurvy
•Scurvy is a nutritional disorder occurs due to long term
deficiency of vitamin C.
•Vitamin C is necessary for hydroxylation of proline to
hydroxyproline which is vital for collagen synthesis.
About 90% of the matrix of mature bone is collagen &
hence a lack of collagen will have a severe effect on
bone formation . In children, this gives rise to scurvy.
•Age : Scurvy is rare before 6months of age.
•Predisposed by feeding with pasteurized /boiled milk

31. Radiological features:
1. Wimberger’s sign-Epiphyses is small,sharply
marginated by sclerotic rim
2. white line of Frankel-Zone of provisional calcification
is dense
3. Trumerfeld zone-a lucent zone
4. Pelkan’s spur

32. Scurvy. The margins of the epiphyses are sclerotic . There is a
narrow epiphyseal plate, with increased density of the zone of
provisional calcification. Lucent zone beneath this is
trumerfeld zone.

33. Scurvy:
Subperiosteal hge
has elevated the
periosteum.
Wimberger’s sign
Frankel’s line
Marked periosteal
new bone formation

34. OSTEOPOROSIS
• Most frequent metabolic bone disease.
• Decrease in bone mass.
• Radiographically best described as osteopenia.
Age:
• Usually begins around 5th decade in
women and around 6th decade in men.
•Loss of bone mass approx 3-10%/decade.

35. Normal bone
Osteoporosis-destuction of trabeculae
reuslting in loss of continuity &
interconnectivity.

36. Post menopausal osteoporosis
• Occur in women of 50-65 years.
• There is a disproportionate loss of trabecular bone.
• Fractures involving vertebral bodies (crush
fractures)and distal radius (colles’fracture).
Senile osteoporosis
• Both men and women over 75 yrs of age.
• Proportionate loss of both cortical and trabecular bone.
• Fracture occur in the femoral neck, vertebral
body(wedge fracture), proximal humerus, tibia and
pelvis.
• M:F=1:2

37. R/F of osteoporosis:
General:
• Decreased radio-density of bone
• Low trauma fracture- common in vertebrae, distal forearm,
proximal femur.
Spine:
•Vertical striated appearance to several vertebral body on lateral
radiograph.
•Vertebral fracture
Hand:
•Thinning of cortex of the tubular bones.
•Accentuation of primary trabeculae with loss of secondary
trabeculae.

38. Osteoporosis—vertebral osteoporosis and fracture. (A) Lateral radiograph of
normal vertebrae. (B) There is loss of the transverse trabeculae, resulting in
prominence of the vertical trabeculae, giving a striated appearance. (C)
Lateral thoracic radiograph with multiple wedge and end-plate osteoporotic
vertebral fractures of varying grades.

39. 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.

40. Osteoporosis. The hand
of an elderly women
shows reduced bone
density, thinned cortex
and reduced number of
trabeculae, those which
remain appearing more
prominent.

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

42. Rare self-limiting disease, affects both sexes.
Typically occurs before puberty
Osteoporosis, mostly in thoracic & lumbar vertebrae.
Metaphyseal fractures
Compression of the vertebrae with kyphosis may result
Biochemical findings normal
Idiopathic Juvenile osteoporosis

43. Fig.4 : Idiopathic juvenile osteoporosis

44. Steroid induced osteoporosis (Cushing’s disease)
Excess of adrenocortical steroid hormones
Endogenous cushing’s disease:
Adrenal hyperplasia
-Secondary to pituitary overstimulation
-Tumors of the adrenal gland
Exogenous cushing’s disease:
More common than endogenous
Results from excessive treatment with steroid medication
Age : 30—40 years
Sex : M : F = 1:3

45. Radiological features:
• Osteoporosis.
 Exuberant callus formation
seen at fractures of long bone,
ribs and vertebral bodies.
 Characteristic increased density
of end plates of vertebral
bodies (marginal
condensation).
•Avascular necrosis of femoral
head.
• Rib fracture- multiple, painless.
• In children, growth retardation.
Cushing’s disease : Excessive
callus formation is seen at multiple
fracture sites in the ribs.

46. Exogenous Cushing’s Disease- Lateral view of the lumbar spine shows
osteoporosis and biconcave vertebral bodies. The increase density in
the vertebral body adjacent to the end plate is the result of exuberant
callus formation. This is referred to as marginal condensation.

47. Hyperpituitarism
• Increase GH secretion from pituitary tumor
usually from pituitary macroadenoma.
• GH excess therefore produces
– Gigantism in children (before epiphyseal closure) &
– Acromegaly in adult ( after epiphyseal closure)
47

48. Acromegaly
• This is due to pituitary tumor in almost all
cases.
• C/F-
• Headache
• Enlargement of lips,tongue and nose
• Prognathism- overgrowth of lower jaw
• Cardiomyopathy
• Hypertension

49. • Thickened skull vault, specially inner table with
encroachment of diploic space.
• Paranasal sinuses and mastoid air cells are enlarged,
Frontal bossing.
• Pituitary fossa : Ballooning of the sella with
undercutting of ant. clinoid process,
backward growth of dorsum , downward
enlargement of floor of sella into the
sphenoid bone
• Prognathism

50. Acromegaly: frontal sinuses markedly enlarged & there is frontal
bossing.

51. Appendicular Skeleton:
• Hands show characteristics enlargement of bones &
soft tissue with spade like appearance of terminal tufts
or arrow head distal phalanges.
• Widening of the joint spaces (overgrowth of
articular cartilage).
Feet show increased thickness of heel pad
• Long bones of the feet are elongated.
• Prominence of muscle attachments
• Chondrocalcinosis (rare).

52. Acromegaly the vertebral bodies show mild
posterior scalloping

53. Acromegaly: Enlargement of soft tissue& phalanges with prominent
joint spaces. Distal phalanges show arrowhead configuration.

54. Acromegaly: Overall
enlargement of the hand
with spade-like terminal
phalanges; wide joint
spaces and hook-like
appearance to the distal
metacarpals.

55. Acromegaly: increase heel pad thickness
measures approx 35mm.

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

57. HYPERTHYROIDISM
R/F:
• Generalized osteoporosis.
• Increase cortical tunneling or striation.
• Vertebral body deformity-wedge/biconcave.
• Accelerated skeletal maturation in childhood( rarely).
 Hyper-function of thyroid gland.
 There is an increased metabolic ratio with an increase
in bone formation and resorption.
C/F:
Tachycardia, wt loss, muscle weakness, anxiety,
temperature tolerance.

59. Thyroid acropachy
•It is a triad of pre-tibial myxoedema, exophthalmos &
clubbing of the fingers.
•Radiologically there is characteristic periosteal
thickening in the extremities; commonest &
characteristic site of involvement is the first metacarpal
or metatarsal.

60. Thyroid acropachy: dense periosteal
reaction along the first metatarsal.

61. Hypertrophic osteoarthropathy
There is a marked periosteal reaction along most of the visualized
bones,with,in addition some periarticular osteoporosis,most likely
secondary to disuse,resulting from the severe pain experienced in this
condition.

62. HYPOTHYROIDISM
Deficiency of thyroid hormone produces a spectrum of
musculoskeletal abnormalities termed cretinism in
infants, Juvenile myxoedema in children and
myxoedema or hypothyroidism in adults.
Incidence: 1: 4000 live birth have congenital hypothyroidism.

63. Radiological features:
• Retarded skeletal maturation.
• Epiphyses are late in appearing & fragmented
( bilateral & symmetrical).
• Wide sutures with delayed closure.
• Wormian bones.

64. • The sella is small bowl-shaped in young children;
or large rounded in older children.
• Bullet shaped vertebral bodies with kyphosis (at
thoracolumbar junction).
• All long bones are short.
• PNS are underdeveloped.
• Slipped capital femoral epiphysis.
• Pelvis often narrow with coxa vara deformity.

65. Cretinism: skeletal retardation in 12 month old child
Carpal and proximal femoral centers have not yet appeared.

66. AP view of the pelvis in a child with hypothyroidism (cretinism). There
is irregular fragmentation of the proximal femoral epiphyses & evidence
of constipation.

67. HYPERPARATHYROIDISM
This condition is divided into primary,
secondary and tertiary forms.

68. PRIMARY HYPERPARATHYROIDISM
• Increase parathyroid hormone production occur as
a result of-
ParathyroidAdenoma (75%)
Parathyroid Hyperplasia- 15-20%
Parathyroid Carcinoma- 0.5%
•Age:middleagedandelderlypeople.
•M : F - 1:2

69. Radiological Features:
 Subperiosteal bone resorption
Subchondral bone resorption
Subligamentous bone resorption
Intracortical bone resorption
Generalized osteopenia
Erosive arthopathy
Renal calculi

70. Hyperparathyroidism: marked subperiosteal resorption
of the radial aspect of phalanges and erosion of the tufts.

71. Brown Tumour:
Brown tumours are locally destructive areas
of intense osteoclastic activity. They present
as well defined multi loculated lytic lesion
which may be expansive & destroy over
lying cortex. Pathological fracture may
occur.
Chondrocalcinosis-
Deposition of calcium pyrophosphate dihydrate in
articular & fibrocartilage -identified on hand
(triangular ligament), knees(articular cartilage &
menisci) ,symphysis pubis.
Brown tumour in
tibia
Chondrocalcinosis
as illustrated in the
knee & symphysis
pubis.

72. cortical ‘tunnelling’ in the
proximal phalanges.

73. Primary hyperparathyroidism: granular
appearance of the vault—the so-called salt-and-
pepper skull.

74. SECONDARY HYPERPARATHYROIDISM
Occurs
in response to persistent hypocalcaemia
Observed
Rickets, osteomalacia
and chronic renal failure
•The skeletal changes are similar to those of primary
HPT, although brown tumours are less seen.
•Calcification of arteries and soft tissues occure.

75. Renal diseases secondary to srtuctural
abnormality in urinary tract
RENAL OSTEODYSTROPHY
The term used to describe bony changes in patients
suffering from long standing renal disease.
Causes:
Chronic glomerulonephritis .
Bone changes results from a combination of different
processes including:
Secondary hyperparathyroidism
Rickets/ Osteomalacia
Osteosclrosis
Aluminium toxicity

76. 1. Subperiosteal bone resorption, subchondral resorption, intra-
cortical tunnelling, brown tumour.
2. Calcification of arteries, articular cartilage and periarticular
tissue.
3. Looser’s zones
4. Osteosclerosis-may be the only manifestation.Common sites
are vertebral end plate(rugger-jersy spine), pelvis, ribs and
clavicle.
5. Osteopenia- In 85% patients.
6. In children metaphyseal change resembling rickets together
with cortical erosion , particularly at femoral neck. Slipped
capital femoral epiphysis also seen.
7. Fractures particularly in 2nd 3rd and 4th ribs due to aluminium
toxicity.
R/F of Renal Osteodystrophy:

77. Rugger-jersy spine of renal
osteodystrophy.Typical end plate
sclerosis is seen with alternating
bands of lucency.

79. • This term implies to cases in which
secondary hyperparathyroidism give rise to
autonomous hyperthyroidism.Treatment of
the underlying causes fails to control
hyperparathyroidism.
• Surgical removal of the autonomous
parathyroid is necessary.
Tertiary
hyperparathyroidism

80. HYPOPARATHYROIDISM
•Hypoparathyroidism results from reduced or
absent parathyroid hormone production which
causes hypocalcaemia, hyperphosphataemia and
neuromuscular symptoms like tetany and fits.
•The most common cause for hypoparathyroidismis
parathyroid glandremoval at thyroid surgeryor 131
Iodine-labelled thyroidtherapy.

81. Radiological Features:
• Basalgangliacalcification.
• Osteosclerosis of pelvis,inner tableof the skull vault,
proximalfemur andvertebralbodies.
• Softtissuecalcification
• Enthesopathy

82. Hypoparathyroidism. Soft tissue
calcification may be present, seen here
in the basal ganglia.

83. TOXIC EFFECTS ON THE
SKELETON

84. Lead poisoning:
Findings:
Lead deposition in
growing metaphysis
causes metaphyseal
bands of increased
density.
Fig: Child with lead poisoning. The diagnosis
is indicated by the presence of a sclerotic
metaphyseal band.

85. Fig:Bismuth poisoning. Dense
metaphyseal lines seen similar to lead
poisoining.
Bismuth poisoning:
Findings Similar
to that of lead
poisoning.

86. Fluorosis:
1. Generalised increased density of
bone.
2. Ossification of ligamentous &
musculotendinous attachment.
3. Vertebral osteophytosis.
Fluorosis. There is marked increased
density of all bones.