Radiological imaging features of bones in metabolic & endocrinal diseases.

1. Metabolic & Endocrinal
diseases affecting bone
DR SAHIDUL ISLAM
PGT RADIOLOGY, FAAMCH
dr.sahidul@gmail.com

2. Topics to be discussed here
Introduction
Features of
Rickets Osteomalacia
Scurvy Osteoporosis
Thyroid Disease
Parathyroid
disease
Toxic effects

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

4. Normal Bone Remodelling

5. Normal Bone Remodelling

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

7. Normal Bone Metabolism
Calcium & Phosphate Vitamin D3 & Vitamin C
PTH Calcitonin
Metabolic factors influencing
normal Bone REMODELLING

8. Calcium
 Bones are the reservoir for 99% of body calcium
 Absorbed mainly from duodenum
 Healthy adult needs 750mg of elemental ca /day ; post
menopausal women or fracture healing need
1.5gm/day
 Calcium equilibrium requires Vit D3 & PTH in the body

9. Phosphate
 More than 85% stored in the bone
 Absorption occurs in kidney- proximal
tubule.
 Optimum phosphate level is essential for
mineralization & provides strength to bone.
 Phosphate homoeostasis depend upon PTH
& Vit D3

10. Vitamin D3
 Its active metabolite is 1,25-Dihydroxycholecalciferol
 In Bone it maintains homeostasis by 2 actions
 Mobilisation of calcium & Phosphorus (requires PTH)
 Promotion of mineralization & maturation.
 It Promotes absorption of calcium & phosphorus in the intestine.

11. Vitamin D3

12. PTH

13. Calcitonin

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

16. Metabolic diseases

17. Abnormality of Vit D
Lack of action of Vitamin D
inadequate or delayed mineralization of newly synthesized organic matrix (osteoid) in growing bone
(Rickets) OR mature bone (Osteomalacia)
RICKETS
In Children
OSTEOMALACIA
In Adult

18. Rickets
Vit D Dependant
Type I
Defect of 25 (OH)Vit D 1a hydroxylase (Renal)
Inactive Vit D to active Vit D conversion is
impaired
Type II
The defect is in intracerllular 1,25 (OH)2 Vit D
Vit D Resistant
Familial Hypophosphatemic Ricket
Impared Renal tubular reabsorption of
Phosphate

19. Rickets
 Lack of mineralization of osteoid
tissue/lack of calcification.
 Most obvious changes are at the
metaphysis (rapid growth)
 Initially Loss of the normal zone
of provisional calcification seen.

21. Rickets
 Earliest radiological sign is loss of
normal zone of provisional
calcification adjacent to
metaphysis.
 Later, metaphyseal margin
becomes indistinct& frayed.
 Growth plate become widened.

22. Rickets

23. Rickets
 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

24. Rickets
 Enlargement of
growth plate at
costochondral
junction

25. Rickets
Frontal Bossing Pigeon Chest Widened Wrist

27. Osteomalacia
 Changes resulting from vit d deficiency in mature skeleton
 Failure of mineralization
 Changes in the physis- increased width & disorientation
 Changes in the bone – cortical thining & bowing
 Bone pain, mascular weakness & malaise is the hallmark c/f

28. Osteomalacia

29. Osteomalacia

30. LOOZER’S ZONE

31. Osteomalacia
 Triaradiate Pelvis Potrusio Acetabuli

32. Osteomalacia

34. Vitamin C deficiency - Scurvy
 Vitamin C is essential for formation of Hydroxyproline which is vital for collagen.
 90% of the bone matrix is collagen.
 Children affected by Vit C deficiency leads to Scurvy. Adult counterpart is
Osteoporosis.
 Rare before 6month of age.
 Presents with limb pain & irritability.

35. Radiological Features - SCURVY
• Epiphysis is small & sharply marginated by a sclerotic rim
Wimbergers sign
• Zone of provisional calcification at the growing
is dense giving a white lineFrankels Line
• Beneath this is a lucent zone due to lack of mineralization
of osteoid.Trumerfeld Zone
• Finally as this area is weakened it is prone to fracture
manifest at the cortical margins.Pelkans Spur

36. SCURVY
• Epiphysis is small & sharply
marginated by a sclerotic rim
Wimbergers
sign
• Zone of provisional calcification at
the growing metaphysis is dense
giving a white line
Frankels Line
• Beneath this is a lucent zone due to
lack of mineralization of osteoid.
Trumerfeld
Zone
• Finally as this area is weakened it is
prone to fracture which manifest at
the cortical margins.
Pelkans Spur

37. Scurvy
 Due to capillary fragility subperiosteal
haemorrhages occurs giving rise to
periosteal elevation & new bone
formation.

38. Osteoporosis
 Most frequent metabolic bone disease
 Decrease in bone mass
 Microstructure of the bone is normal but the
quantity of the bone is diminished.
 Radiographically best described as osteopenia
 Age- usually begins around 5th decade in
women & 6th decade in men
 Loss of bone mass aprox 3-10% /decade

39. Causes of Generalised Osteoporosis
 Age related – senile &
postmenopausal
 Deficiency states
 Malnutrition
 Calcium deficiency
 Scurvy
 Drugs
 Steroids
 Metabolic
 Hyperthyroidism
 Hyperparathyroidism
 Cushings disease
 Acromegaly
 Pregnancy
 Diabestes mellitus
 Hypogonadism
 Alcoholism
 Chronic liver dis
 Anaemia
 Idiopathic

40. Osteoporosis

41. Postmenopausal osteoporosis
 Occurs in women of 50-65 years
 Osteoporotic changes are linked to reduced
estrogen level.
 There is disproportionate loss of trabecular bone
 Fracture involve vertebral bodies (Crush fracture)&
distal radius (Colles fracture)
 Marked Kyphotic deformity due to loss of height &
anterior wedging

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

43. Post menopausal osteoporosis
 (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.

44. Post menopausal osteoporosis
 A common fracture
encountered in
post menopausal
osteoporosis is
fracture of distal
radius.

45. Post menopausal 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

46. Senile Osteoporosis
 Both men and women over 75 yrs of
age.
 Reduced intestinal absorption,
diminished adrenal function & secondary
hyperparathyroidism plays role.
 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

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

48. Senile osteoporosis
 There is a severe osteoporotic
fracture of the T12 vertebral body
 with a mild osteoporotic fracture of
the L1 vertebral body .
 There is a lumbar scoliosis with
obliquity of the lower three lumbar
vertebrae

49. Idiopathic Juvenile Osteoporosis
 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

50. Idiopathic Juvenile Osteoporosis

51. Steroid induced osteoporosis
 Age group mostn affected 30-40years
 M:F=1:3
Cushings disease
Excess of adrenocortical steroid hormones
Endogenous
Adrenal Hyperplasia
Secondary to pituitary overstimulation
Tumor of the adrenal gland
Exogenous
Excessive treatment with steroids
commonest

52. Cushings Disease
 Exuberant callus formation seen at fractures of long bone,ribs and
vertebral bodies.
 Characteristic increased densityof end plates of vertebral bodies (marginal
condensation).
 Avascular necrosis of femoral head.
 Rib fracture- multiple, painless
 In children, growth retardation

53. Cushings disease

54. Cushings disease
 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.

56. Hyperpituitarism
 Increase GH secretion from
pituitary tumor usually from
pituitary macroadenoma.

57. Growth Hormone
Excess
Gigantism
In children
Before epiphyseal closure
Acromegaly
In Adult
After epiphyseal closure

58. Acromegaly
 Due to pituitary tumor in almost all cases
 C/F includes
 Headach
 Enlargement of lips,tongue and nose
 Prognathism- overgrowth of lower jaw
 Cardiomyopathy
 Hypertension

59. Acromegaly
 Skull Changes
 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

60. Acromegaly
 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)

61. Acromegaly
 The vertebral bodies show
mild posterior scalloping

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

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

64. Acromegaly
 Increase heel
pad thickness
measures approx
35mm.

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

66. Hyperthyroidism
 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.

67. Hyperthyroidism : Radiology Feature
 Generalized osteoporosis.
 Increase cortical tunneling or
striation.
 Vertebral body deformity-
wedge/biconcave.
 Accelerated skeletal maturation in
childhood( rarely)

68. 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.

69. Thyroid Acropachy
 Thick, wavy periosteal reaction is
seen along the shafts of the 1st
through 4th metatarsals bilaterally

70. 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.

71. Hypothyroidism
 Deficiency of thyroid hormone produces a
spectrum of musculoskeletal abnormalities
–
 cretinism in infants,
 Juvenile myxoedema in children
 myxoedema or hypothyroidism in adults
 1: 4000 live birth have congenital
hypothyroidism

72. Hypothyroidism : Radiological feature
 Retarded skeletal maturation. (CRETINISM)
 Epiphyses are late in appearing & fragmented ( bilateral & symmetrical).
 Wide sutures with delayed closure.
 Wormian bones
 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

73. Hypothyroidism

74. Hypothyroidism
 Bullet shaped vertebral
bodies with Kyphosis

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

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

77. Hyperparathyroidism
 This condition is divided into primary, secondary and tertiary forms.

78. Primary Hyperparathyroidism
 Increase parathyroid hormone production occur as a result
of-
 Parathyroid Adenoma (75%)
 Parathyroid Hyperplasia- 15-20%
 Parathyroid Carcinoma- 0.5%
 Age: middle aged and elderly people.
 M : F - 1:2

79. Primary Hyperparathyroidism Radiology
 Subperiosteal bone resorption
 Subchondral bone resorption
 Subligamentous bone resorption
 Intracortical bone resorption
 Generalized osteopenia
 Erosive arthopathy
 Renal calculi

80. Hyperparathyroidism
 marked subperiosteal
resorption of the
radial aspect of
phalanges and
erosion of the tufts.

81. 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.

82. Chondrocalcinosis
 Deposition of calcium
pyrophosphate
dihydrate in articular
& fibrocartilage -
identified on hand
(triangular ligament),
knees(articular
cartilage & menisci)
,symphysis pubis.

83. Hyperparathyroidism
 cortical ‘tunnelling’ in the
proximal phalanges.

84. Hyperparathyroidism
 Granular
appearance of the
vault—the so-called
salt-and pepper
skull.

85. Secondary Hyperparathyroidism
 Occurs in response to persistent hypocalcaemia ;
 Observed in 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.
 Associated with Renal Osteodystrophy.

86. Renal Osteodystrophy
 The term used to describe bony changes in patients suffering from long
standing renal disease.
 Caused by Renal diseases secondary to structural abnormality in urinary
tract & Chronic Glomerulonephritis.
 Bone changes results from a combination of different processes including
 Secondary hyperparathyroidism
 Rickets/ Osteomalacia
 Osteosclrosis
 Aluminium toxicity

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

88. Renal Osteodystrophy
 Rugger-jersy spine of renal osteodystrophy.Typical end plate sclerosis is seen with
alternating bands of lucency.

89. Renal Osteodystrophy
 Slipped capital femoral epiphysis

90. Tertiary Hyperparathyroidism
 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.
 Radiological features are same as primary hyperparathyroidism.

91. Hypoparathyroidism
 reduced or absent parathyroid hormone production causes
hypocalcaemia, hyperphosphataemia and neuromuscular
symptoms like tetany and fits.
 The most common cause for hypoparathyroidism is
parathyroid gland removal at thyroid surgery or 131 Iodine-
labelled thyroid therapy

92. Hypoparathyroidism : Radiology
 Basal ganglia calcification.
 Osteosclerosis of pelvis, inner table of the skull vault, proximal femur and
vertebral bodies
 Soft tissue calcification
 Enthesopathy

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

94. Toxic effects on the skeleton

95. Lead Poisoning
 Lead deposition in
growing metaphysis
causes metaphyseal bands
of increased density.
Child with lead poisoning.
The diagnosis
is indicated by the
presence of a sclerotic
metaphyseal band.

96. Bismuth Poisoning
 Findings Similar
to that of lead
poisoning
Dense
metaphyseal lines seen
similar to lead
poisoining.

97. Fluorosis
 Generalised increased
density of bone
 Ossification of ligamentous
& musculotendinous
attachment.
 Vertebral osteophytosis
There is marked
increased
density of all
bones

98. Thank You
Source :
 Textbook of Radiology & Imaging , 7th Edition (David Sutton)
 Radiopedia website (www.radiopedia.com)