1. By
Dr. Tarek Mansour
Faculty of medicine
Al-Azhar university

2. The amount of bone at any part of
skeleton at ant time depend up on
the balance between bone
resorption and formation.

3. The three hormonal regulators include
1. Parathormone (PTH), produced by the
four parathyroid glands on the back
side of the thyroid gland.
2. The active form of vitamin D produced
in the proximal renal tubule 1,25(OH)2.
3. And calcitonin produced by the
parafollicular cells in the thyroid gland.

4. PTH
The major function of PTH is to prevent the
dangerous reduction in the serum calcium
level by:
1. Increasing the production of 1,25,(OH)2
vitamin D in the kidney which then
increases the absorption of calcium from
the gut and renal tubule.
2. PTH also activates osteoclastic
mobilization of calcium from bone mineral.
3. PTH is to promote urinary excretion of
phosphorous.


5. 
The major function of 1,25,(OH)2
vitamin D is to activate the absorption of
calcium from the gut and bone.

The least important calcium regulator is
calcitonin which is designed to prevent
an increase of serum calcium by
inhibiting the osteoclastic mobilization of
calcium at the bone level.

7. Hormonal regulation of calcium
and phosphate



The crude inactive form of vitamin D comes
from the gut and the skin that is exposed to
sun light which is then transported to the liver
for its first phase of activation by a
hydroxylation process at the 25 position of the
sterol ring.
This still inactive form then goes to the kidney
for its finial activation by a hydroxylation
process on the 25 position of the sterol ring.
This now activated vitamin D acts as a
hormone similar to PTH to help absorb
calcium from the gut and bone.

8. Calcium and phosphate
metabolism

9. Mobilization of Ca from
Bone



When the serum calcium level drops below
normal the parathyroid gland puts out PTH
which then activates resting bone cells to
differentiate into an active lytic osteoclast.
On the bone surface the active brush border of
the cell secrets collagenase enzyme which
dissolves bone mineral thus liberating calcium
and phosphorous ions which are then
transported across the cell to its outer
membrane
Where a 1,25,(OH)2 pumping mechanism
transports the calcium and phosphorous into
the blood stream.

10. Metabolic, endocrinal and nutritional
bone diseases affect the skeleton
through too much or too little calcified
bone.
 Too little calcified bone is either due to
- Decrease bone formation.
- increase bone resorption.


12. Radiographic criteria of
endocrinal, metabolic and
nutritional diseases

They are commonly diffuse or at least
multifocal, although isolated bone lesion
may be found as in brown tumor.

They tend to involve specific
location, and tend to be symmetrical in
the body.

14. Endocrinal disorders









Acromegaly.
Gigantism.
Cushing syndrome.
Hyperparathyroidism.
Hypoparathyroidism.
Pseudohypoparathyroidism.
Pseudo-pseudohypoparathyroidism.
Hyperthyroidism.
Hypothyroidism.

15. Acromegaly
(hyperpituitrism).
Result from excess production of growth
hormone by anterior pituitary gland.
 In adult
Acromegaly.
 In children
Gigantism


16. Radiological findings
Skull





Thickened
calvarium.
Frontal bossing.
Prognathism.
Enlarged mastoid air
cells and sinuses.
Enlargement of
pituitary fossa.

17. Spine.
 Enlarged vertebral
bodies with posterior
scalloping.
 Increase disc height.

18. Hands.
 Enlarged bone and
soft tissue shadow.
 Spade like terminal
tufts or arrowhead
distal phalanges.

19. Measurments
Sesamoid index of the thumb.
< 40 mm. in male.
< 32 mm. in female.
 Tuftal width of the third finger.
< 10 mm. in female.
< 12 mm. in male.
 Joint space of the second
MCP joint.
= 2.5 mm. in both men and
female.
 Thickness of phalangeal soft
tissue
< 26 mm. In male.
< 23 mm. in female.


20. 




Joint spaces
Wide joint spaces due to enlarged articular
cartilage
Feet
Increase thickness of fat pad
Long bone
Elongated with prominent muscle attachment.
Calcifications
Ear pinna
Chondrocalcificinosis
Cardiomegaly + visceromegaly

22. Gigantism
Imaging findings.
Proportional yet exaggerated bone
growth.
 Bone increase in length and diameter.
 Enlarged sella turcica.


24. Cushing disease
It is hyperadrenocorticism due to
 Anterior lobe tu.
 Adrenal cortex tu.
 Complication of therapy.
Imaging findings.
 Osteoporosis (more at trabecular bone).
 Increase insufficiency fractures in
vertebra, scapula, ribs and pubic bones.

27. Hyperparathyroidism
It is defined by increase level of
parathormone and parathormone
peptides in the serum.
 It can be divided in to three types.
 Primary.
 Secondary.
 Tertiary.


28. Primary
hyperparathyroidism
May be the result of.
 Adenomas (single or multiple) 90%
 Diffuse hyperplasia.
 Carcinomas.
In all cases : serum Ca level is increased.


This disorder is due to a primary defect in the
parathyroid glands >>> increased secretion of PTH
>>> increase serum calcium and decrease serum
phosphorus.
The increase in serum calcium concentration is due
in part to activation of the osteoclastic system.

29. Secondary hyperparathyroidism

Is induced by any condition or circumstance
that cause serum calcium to fall.
It may be the result of:
 Vit. D deficiency.
 Chronic renal failure.
 Intestinal malabsorption of Ca (rare).

In diseased kidney>>> decrease active Vit. D
>>> decrease int. ca absorption>>>
hypocalcaemia>>> stimulate parathyroid
gland>>> increase PTH

30. Tertiary
hyperparathyroidism

It is result of long standing secondary
hyperparathyroidism due to chronic
renal failure.

In tertiary hyperparathyroidism, the
parathyroid glands function
autonomously.

31. Clinical presentation
In primary hyperparathyroidism may be:
 Asymptomatic hypercalcemia.
 In younger patients, the most common
presentations are:
1. Renal stone and Nephrocalcinosis (25-35%).
2. High blood pressure (40-60%).
3. Acute arthropathy (pseudogout).

Other symptoms as osteoporosis, peptic ulcer,
acute muscle weakness & mild non specific
symptoms.

32. To understand radiological changes
in PTH you have to know:
An elevated level of parathormone :
In early phase>>>> increase bone mass
In later stages>>>> trabecular bone
resorption may occur.


Because HPT today is usually detected
early through increased level of serum
calcium, we observe more patients with
more bone formation and fewer patients
with less bone.

33. Radiological findings in primary
hyperparathyroidism.
Subperiosteal bone resorption.
Subchondral bone resorption.
Subligamentous bone resorption.
Intracortical bone resorption.
Osteopenia.
Brown tumor.
Erosive arthropathy.
Chondrocalcinosis.
Renal calculi, rarely Nephrocalcinosis.
10. Rarely osteosclerosis.
1.
2.
3.
4.
5.
6.
7.
8.
9.

34. Radiologic findings of
HYPERPARATHYROIDIS
M The M/C radiologic abnormality is generalized

osteopenia.

Bone resorption, bone sclerosis, brown
tumors, chondrocalcinosis, soft tissue
calcification, and vascular calcification.

Brown tumors appear as well-defined lytic lesions.

After resection of parathyroid adenomas, the lesions may
become sclerotic and may mimic blastic metastasis.
Bone resorption, the most characteristic finding, is
usually classified as


subchondral, trabecular, endosteal, intracortical, subperios
teal, subligamentous, and subtendinous.

35. Subperiosteal resorption - M/C




Usually occurs in the hands and feet.
M/C affected site: radial aspects of the middle
phalanges.
Acro-osteolysis or phalangeal tufts resoption may also
be present.
Trabecular resorption


Often seen in the diploic space of the skull, where it has
a characteristic salt and pepper appearance.
Subchondral resorption


May be seen in the sacroiliac joints, sternoclavicular
joints, acromioclavicular joints, symphysis pubis, and
discovertebral junction .

36. AP radiograph of the hand in a 66-yearold woman with primary
hyperparathyroidism owing to
parathyroid adenoma shows
subperiosteal bone resorption (
arrows) along the radial aspect of
2nd, 3rd, and 4th middle
phalanges.

37. AP radiograph of the knee in a child with hyperparathyroidism
shows subperiosteal bone resorption ( arrow) along the
proximal medial tibia.

38. Subchondral bone
resorption
Sites :
 Outer and sometimes inner end of the
clavicle.
 Symphysis pubis.
 Sacroiliac joints.
 Vertebral end plates.

39. Subligamentous resorption:
Sites:
 Greater & lesser trochanter.
 Ischial tuberosity
 Inferior calcaneum
 Inferior surface of clavicle.

41. Intracortical bone resorption
Linear translucencies within the cortex
(cortical tunnelling), esp. tubular bones of
the hands, 2-5 mm. oval or cigar shaped.
 Loss of corticomedullary junction.
 In the skull, granular or mottled
appearance (pepper-pot) or salt and
pepper.

Not specific for hyperparathyroidism.

44. Osteopenia
More common in postmenopausal
women and the elderly.
 Loss of corticomedullary junction may
occur.


45. Chondrocalcinosis


1.
2.
3.
4.

Due to deposition of calcium
pyrophosphate dihdrate (CPPD) in the
cartilage.
It can be seen in:
Hand (triangular ligament).
Knees (artigular cartilage & menisci).
Symphesis pubis.
Less common, the shoulder and hip.
Chondrocalcinosis of the symphysis pubis
and nephrocalcinosis on the abdominal x
ray is diagnostic of hyperparathyroidism.

49. Brown tumor (ostitis fibrosa
cystica).
These are cystic lesions within bone due
to excessive osteoclastic resorption
(osteopenia).
 Radiographically, brown tumors appear
as low density multiloculated cysts that
can occur in any skeletal site and may
cause expansion of bones.


50. Brown tumor

51. PHPT
 Erosion of the terminal
tufts.
 Resorption of the
radial side of the
middle phalanx of the
index and middle
finger.
 Coarsened
trabeculae.
 Thinned cortices.
 Brown tumor.

52. Osteosclerosis.

Occurs uncommonly
in PHPT but is a
common feature of
SHPY secondary to
chronic renal failure.

53. A, AP radiograph of the spine in a patient with secondary
hyperparathyroidism shows generalized bone sclerosis, small kidneys,
and left renal calculi. B, Lateral radiograph of the lumbar spine in another
patient with secondary hyperparathyroidism shows horizontal, bandlike
("rugger jersey") sclerosis of the vertebral bodies ( arrows).

54. Erosive arthropathy.

Involving hands, wrists, and shoulders.
Differentiate from RHD arthritis
1. Subperiosteal resorption.
2. Affection of distal interphalangeal joints.


55. Radiological findings of
secondary
hyperparathyroidism.
Similar to 1ry hyperparathyroidism.
 Less frequent brown tumor.
 Calcification of arteries and soft tissue.
 Osteosclerosis more common.

56. 
Primary
•
Chondrocalcinosis
•
usually seen in
the menisci of the
knee, the
triangular
fibrocartilage of
the wrist, and the
pubic symphysis
Secondary



Bony sclerosis;
focal or
generalized.
Rugger-jersey
appearance of
spine.
Soft tissue and
vascular
calcification.

58. AP radiograph of the hand in a 50-year-old man with
renal osteodystrophy shows acro-osteolysis ( short
arrows), subperiosteal bone resorption ( long
arrows), and vascular calcifications.
Secondary HPT Radiograph of the hand
showing resorption of the first to third
tufts with soft tissue calcification 1
There is articular calcification
2 , and subperiosteal and
subligamentous resorption 3

59. The differential diagnosis of
HYPERPARATHYROIDIS
M Focal subperiosteal resorption involving a single bone


Neoplasms or osteomyelitis.
Bone sclerosis in patients with secondary
hyperparathyroidism.


Metastatic disease, radiation-induced bone
disease, hypoparathyroidism, myelofibrosis, mastocytosis,
sickle-cell disease, and Paget's disease.
Chondrocalcinosis


Pyrophosphate arthropathy (CPPD) or hemochromatosis.
Brown tumors


includes other focal lytic lesions, such as giant cell tumor
and fibrous dysplasia.

60. Hypoparathyroidism
It result from:
 The M/C cause is
excision of or
trauma to the
parathyroid glands.
 may not be
recognized for years
after surgery.

I 131 therapy.
Clinical presentation:
Neuromuscular
dysfunction.
 Short stature.
 Delay or failure of
tooth eruption.
 Gastrointestinal
complaints.


61. Radiologic findings of
HYPOPARATHYROIDISM
Radiologic findings are varied.

Bony sclerosis. = M/C finding
 Focal or generalized







Subcutaneous calcification.
Calvarial thickening
Basal ganglia calcification
Hypoplastic dentition
Premature physeal fusion
Spinal ossification.
Occasionally :
Osteoporosis, Enthesopathy, Dense
metaphyseal bands.

63. differential diagnosis of
HYPOPARATHYROIDISM

Widespread bony sclerosis.
 Blastic metastasis, myelofibrosis, renal
osteodystrophy, sickle-cell disease, and
fluorosis.

Dense metaphyseal.
 Leukemia therapy, heavy-metal poisoning, or
hypothyroidism.

Calcifications of the basal ganglia
 Toxoplasmosis or cytomegalovirus infections,
after radiation therapy, and after carbon
monoxide exposure.

Subcutaneous calcifications.
 Collagen-vascular diseases, hypervitaminosis
D, and renal osteodystrophy.

64. Pseudohypoparathyroidism
It is an x linked genetic disorder.
 Normal or enlarged parathyroid gland.
 End organ resistance (kidney & bone).


65. Imaging findings in pseudohypoparathyroidism.






Thickening of the skull.
Basal ganglia calcification.
Abnormal dentition with hypoplasia &
cranial defects.
Connective tissue calcification in
skin, ligaments, tendons & facial planes.
Coxa vara, coxa vulga and bowing of long
bones.
Exostosis prependicular to long bone axis.

66. Hands




Short metacarpals
esp. 1st , fourth and
fifth.
Metacarpals &
phalanges esp. 1st
digit may be wide with
cone shaped
epiphysis.
Metatarsals may be
affected.
+ve metacarpal sign.

69. Hyperthyroidism
Imaging findings:
 Generalized
osteoporosis.
 Increased cortical
striations in long
bones.
 Thyroid acropachy:
Periosteal thickening
in extremities esp.
hands.
 Exophthalmus &
pretibial myxodema.

70. AP radiographs of the hand in a 46-year-old man with thyroid
acropachy who presented with hand swelling and hypothyroidism
2 years after a thyroidectomy. Note the dense, solid periosteal
reaction with feathery contour ( arrows) along the shafts of
2nd, 3rd, and 4th proximal and middle phalanges.

71. Thyroid acropachy. (A,B) Radiographs of the hands showing diaphyseal periostitis
arrows) and generalized swelling. (C) Radiograph in a different patient
showing marked soft tissue prominence.

72. Differential for
HYPERTHYROIDISM

Thyroid acropachy
Periosteal reaction involving multiple bones
 Hypertrophic osteoarthropathy:
○
long bones.
○ Feathery contour is absent.

Pachydermoperiostosis:
○
Long bones.
○ Periosteal reaction extends to the
metaphyses and epiphysis.

73. Hypothyroidism
Deficiency of thyroid hormones (T4 and
T3) produce a spectrum of musculoskeletal
abnormalities termed (cretinism) in
infant, (juvenile myxoedema), in
children, and (myxoedema or
hypothyroidism) in adults.
It results from:
 Primary disorder of the thyroid gland
 Decrease stimulating hormones secondary
to disorders of the pituitary or
hypothalamus (tertiary).
 Rarely end organ resistance.


74. Imaging findings in
hypothyroidism.
Delayed skeletal maturation in children.
Skull:
 Wormian bones.
 Small bowel shaped cherry sella (older
children).
 Paranasal sinuses underdeveloped.
Spine:
 Bullet shape vertebrae esp. thoracolumbar.
 Kyphosis may occur.

75. 






Long bones;
Short.
Epiphyses appear
late and frahmented.
Pelvis;
Narrow
Coxa vara deformity
Slipped femoral
capital epiphysis.

77. Osteoporosis & delayed
closure of growth plate
After treatment

79. METABOLIC DISORDERS
Osteoporosis.
 Hypophosphatasia.
 Hyperphosphatamia.


80. Osteoporosis
Definition : reduced bone mass of normal composition.
•Most common metabolic bone disease.
•One of the most prevalent conditions associated with
aging.

81. 
Clinical definition: requires the presence
of a nontraumatic fracture.

Histologic definition: requires normally
mineralized bone to be present in
reduced quantity.

82. Ostoporosis Classification

Primary osteoporosis. (idiopathic) : more common
 Type 1 (postmenopausal)
 Type 2 (age-related or senile)

Secondary osteoporosis.
 Metabolic (acromegaly, hypercorticism, hyperthyroidism,
hyperparathyroidism, hypogonadism, pregnancy, diabetes
mellitus)
 Congenital (osteogenesis imperfecta, Ehlers-Danlos
syndrome, homocystinuria, mastocytosis, ochronosis,
Gaucher's disease)
 Nutritional (alcoholism, malnutrition, calcium deficiency,
scurvy)
 Drug-related (steroids, heparin).

83. osteoporosis



1.
2.
3.
Most common metabolic bone disease.
Is defined as qualitatively normal bone
present in deficient quantities.
It has three major categories.
Generalized: affecting majority of the
skeleton.
Regional: affecting one limb or section of
body.
Localized: focal osteopenia in one or more
discrete portions of bone.

85. Imaging findings in
osteoporosis
Requires 30-50% bone loss to be detected by plain x ray.
Bones:
 osteopenia with thin cortex.
 Resorption of horizontal trabeculae.
 Accentuated residual trabeculae more at weight bearing
areas.
 Fracture neck femur is common.


The bone surfaces are well defined, with sharp margins.
Spine:
 Biconcave (cod-fish vertebrae) and anterior wedging.
 Decreased density with more dense end plates (penciling
in).
 Fracture (wedge shaped or vertebra plana).

89. DXA

91. Differential considerations
for diffuse osteopenia
Osteomalacia.
1.


indistinct trabeculae and poorly defined
interfaces between cortical and trabecular
bone.
Presence of Looser's zones.
Hyperparathyroidism.
2.

bone resorption at characteristic sites.
Multiple myeloma.
3.

MR imaging may show areas of marrow
replacement.

92. Regional or localized
osteoporosis
Immobilization and disuse
Reflex sympathetic dystrophy syndrome
(RSDS)
Transient regional osteoporosis
1.
2.
3.


4.
5.
6.
Transient osteoporosis of the hip.
Regional migratory osteoporosis.
Inflammatory arthritis.
Tumors
Infection.

93. This patient had a long-standing immobilization due to a fracture of the right humerus
The appearances in the right hand are classical for reflex sympathetic dystrophy, or
Sudeck’s atrophy, and include
1 Pronounced demineralization of the bones, particularly in the periarticular region
2 No joint involvement.
3. Associated soft tissue atrophy
This condition has been recently renamed the “complex regional pain syndrome”

94. Hypophosphatasia






It is an autosomal
recessive disease.
Imaging findings:
In sever cases
exaggerated fraying
of metaphysis is
seen.
Craniostenosis.
Nephrocalcinosis.
Deformities of distal
phalanges and tibia.

96. Hyperphosphatamia
Autosomal recessive disorder, presents
in early infancy
Imaging findings:
 Similar to Paget`s disease but occur in
infancy & more symmetrical.
 Skull vault is thickened.
 Long bones are tubular, enlarged and
bowed with cortical irregularity.


97. Bowed extremities with
osteopenic bones and
heart shaped pelvis similar
to rickets
Deformed bell shaped rib
cage with osteopenia like
ricket
s

100. NUTRITIONAL
DISORDERS
Hypervitaminosis A.
 Hypervitaminosis D.
 Osteomalacia.
 Rickets.
 Scurvy (Hypovitaminosis C).


101. Hypervitaminosis A:
X ray findings
 Subperiosteal cortical thickening.
 Osteoporosis.
Hypervitaminosis D:
X ray findings
 Generalized osteopenia.
 In young patients, alternating areas of
sclerosis and lucencies in the metaphysis.

102. Hypervitaminosis A

103. Hypervitaminosis D
Dense sclerotic bands seen in
metaphyses similar to cretinism
and phosphorous poisoning
Dense calvarium as osteopetrosis

105. Rickets and osteomalacia



Rickets and osteomalacia are similar
histologically.
Abnormality in vitamin D metabolism.
Incomplete mineralization of normal
osteoid tissue.
Rickets
Osteomalacia
Occurs in children
Occurs in adult
Affects immature bone
Affects mature bone

106. Clinical findings of
Rickets and Osteomalacia
Depend in part on the etiology and severity of the disorder, as well as the
age of the patient at presentation
Rickets: stunted skeletal growth.
 Apathetic, Irritable, Hypokinetic.
 Frontal bossing, softening of the skull,
dental caries, rachitic rosary, kyphosis,
joint enlargement, or bowing of long
bones.
 Fractures and slipped capital femoral
epiphyses.

108. Clinical findings of
Rickets and Osteomalacia
Depend in part on the etiology and severity of the disorder, as well as the
age of the patient at presentation
Osteomalacia: more subtle.
 Fatigue, malaise, or bone pain.
 Proximal muscle weakness and
abnormal gait may be present.

109. Osteomalacia

Presence of poor quality bone (delayed
or defective mineralization of osteoid
matrix) due to vit. D deficiency.

110. Imaging finding in osteomalacia

Generalized osteopenia with coarse, hazy
appearing trabeculae.

Poorly defined interfaces between
cortical and trabecular bone.
Pseudo fracture (Looser`s zone): narrow
zone of lucency, usually perpendicular to
bone cortex, usually bilateral &
symmetrical.
Common sites are:
 Femoral neck, scapula, pubic bone, ribs,
occiput and long bones.


111. Looser's zone.
 Linear areas of undermineralized
osteoid that occur in a bilateral and
symmetric distribution.
 Characteristic sites; inner margins of
femoral neck, proximal ulna, axillary
margin of the scapula, pubic rami, and
ribs.
 DDx; Paget's disease or fibrous
dysplasia.

112. Looser zone

113. Coarse trabeculae

114. Imaging finding continue


1.
2.
3.
4.
5.
Vertebrae: Penciling in of the vertebral
bodies, loss of vertebral height (cod fish).
Bone softening producing:
Bowing of long bones
Shepherd`s crook deformity
Protrusio acetabulae.
Basilar invagination.
Compression wedge fracture (less
common than osteoporosis).

115. Shepherd`s crook deformity

116. Protrusio acetabulae.

117. Basilar invagination

118. Rickets

The skeletal effects are due to a lack of
calcification, So, the most obvious
changes are at metaphysis, where the
most rapid growth is occurring.

119. Imaging findings in rickets



Generalized osteopenia.
Skull bossing.
Epiphysis are enlarged, flaring, cupping &
irregularity of metaphysis.






Earliest; Slight axial widening of the physis
Next; Increased lucency of the zone of provisional
calcification.
More advance; The physis widens and its contour
becomes irregular.
Thoracic kyphosis with pigeon chest.
Enlarged costochondral junction (rosary
beads).
Bowing of the legs.

120. 
The regions of highest yield on
radiologic evaluation of rickets are
those that are undergoing rapid growth.





Costochondral junctions of middle ribs
(rachitic rosary)
Distal femur
Both ends of the tibia
Distal radius and ulna
Proximal humerus.
Differential diagnosis of rickets includes
Hypophosphatasia and the Schmid-type of
metaphyseal chondrodysplasia.

121. The complication of rickets.
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Skeletal deformities.
In neonates; posterior flattening and squaring
of the skull, or craniotabes, may be seen.
In early childhood; bowing deformities of arms
and legs are common.
Older children: scoliosis, vertebral end plate
deformities, basilar invagination of the skull
may be seen.
Advance disease: Slipped capital femoral
epiphysis.

122. A, AP radiograph of the knee in a 2-year-old girl with rickets
shows generalized osteopenia and widening of the metaphyses
of the proximal tibia and fibula. B, AP radiograph of the wrist in
another child with rickets shows generalized osteopenia, as well
as widening and irregularity of the metaphyses of the distal radius
and ulna.

123. Rickets in a young child with growth plate widening and irregularity in the wrist
A) and knees (B). Note the small epiphyses in the knees.

124. Vitamin D-resistant rickets in a -year-old child. (A) AP radiograph of the knees
showing irregularity and widening of the growth plates. The epiphyses are
small and irregular as well. (B) Three years after high-dose vitamin D
therapy, the knees appear normal. There is residual femoral bowing.

125. Rachitic rosery nodularity at costochondral junctures

128. 4 year old rachitic child with knockknee deformity
Healing rickets in 2 yr male with
epiphyseal rings second to
treated rickets

129. Scurvy
Dietary deficiency of vit. C (rare before 6
month).
Imaging findings:
 Small epiphysis, sharply demarcated by
sclerotic rim (Weinberger's sign).
 Dense zone of provisional calcification at
metaphysis. (Franket`s line).
 Lucent zone due to defective mineralization
(Trumerfeld zone).
 Cortical fractures (Pelkan`s spurs).
 Subperiosteal haemorrhage.
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130. Hemorrhagic Periostitis in
Scurvy

131. 1 year old child with multiple slipped
epiphyses second to scurvy