This document discusses skeletal disorders of metabolic and endocrine origin. It begins by describing normal bone structure and the parts of long bones, including growth plates. It then discusses various causes of rickets and osteomalacia, including nutritional rickets, hereditary forms, oncogenic osteomalacia, drug-induced rickets, and others. The clinical, pathological, and radiological features of each condition are described. The document also covers hyperparathyroidism and the actions of parathyroid hormone on calcium metabolism and bone resorption seen on imaging.

1. SKELETAL DISORDERS
OF METABOLIC AND
ENDOCRINE ORIGIN
DR. NAVNI GARG
DNB RESIDENT
, MEDANTA–THE MEDICITY

2. MATURE BONE
 Lies within the
medullary canal
 Meshwork of primary
longitudinal and
secondary transverse
trebaculae
 Normally in ends of
long bones and axial
skeleton
 Consists of
haversian system :
haversian canal
surrounded by bony
lamellae with
volkman’s canal
connecting them
TREBACULAR/
CANCELLOUS/ SPONGY CORTICAL

4. PARTS OF LONG BONE

5. GROWTH PLATE / PHYSIS
 Located at end of long bones between epiphysis
and metaphysis
 Site at which proliferation and orderly maturation
of cartilage cells occur
Functionally part of shaft of long bone
Four zones
 Resting/ germinal zone
 Proliferating zone
 Hypertrophic zone : zone of maturation,
degeneration and provisional calcification
 Zone of primary and secondary spongiosa

6. GROWTH PLATE
 Proliferating :
cartilage cells multiply
 Hypertrophic : marks
the end of lucent
growth plate and
beginning of calcified
metaphysis
 Spongiosa : calcified
cartilage column,
produce bone via
enchondral
calcification

7. BONE FORMATION

8. CLASSIFICATION
 Defect in osteoid formation : scurvy
 Defect in mineralization : rickets/ osteomalacia
 Disorder with increased bone resorption :
hyperparathyroidism
 Disorder with decreased bone mass :
osteoporosis
 Miscellaneous : fluorosis, heavy metal
poisoning, hypervitaminosis

9. CAUSES OF RICKETS AND
OSTEOMALACIA

10. NUTRITIONAL RICKETS

11. PATHOLOGY
 Characteristic changes of rickets are identified
in the growth plate prior to closure
 Disorganisation of growth plate and adjacent
metaphysis
 Zone of maturation affected with disorganised
increase in number of cartilageneous cells :
increase in length and width of growth plate
 Zone of provisional calcification shows
deficient mineralisation : Increased uncalcified
osteoid and decrease in calcified osteoid

12. CLINICAL FEATURES
 First 6 months : tetanic convulsions
 Irritability, weakness
 Delayed development
 Small stature
 Bony deformities and pain
 Rachtic rosary
 Swelling of wrist and costocartilage

14. RADIOLOGICAL FEATURES
 MC and non specific finding : osteopenia
 Changes seen at open growth plate
 Especially visible at fast growing growth plates
like costochondral junction of the middle ribs,
distal femur, proximal humerus, both ends of
tibia, distal ulna and radius
 Earliest sign : distal ends of radius and ulna.
Ulnar growth plate grows more rapidly so
manifestations are seen earlier in ulnar growth
plate

15. WIDENING OF GROWTH
PLATE
 Earliest and specific radiological change
 Due to increase in cartilageneous cell mass

16. METAPHYSEAL FRAYING
 Irregular
metaphyseal
margins occuring
due to fraying and
disorganisation of
spongy bone in the
metaphyseal region

17. METAPHYSEAL CUPPING AND
WIDENING
 Protrusion of bulky
mass of
cartilageneous cells in
the zone of
hypertrophy into the
poorly mineralized
metaphysis
 Cupping is common
in both ends of fibula
and distal end of ulna
and tibia
 Not seen in bones of
elbow

18. EPIPHYSEAL
ABNORMALITIES
 Osteopenia
 Irregural and indistinct borders
 Delayed appearance of ossification centres

19. SHAFT ABNORMALITIES
 Rarefaction of shaft due to loss of mineral
content
 Cortex becomes thin with a coarse texture

20. SKELETAL DEFORMITIES
 Skull : Craniotabes
 Long bones : bowing deformities
 Ribs : rachitic rosary
 Spine : scoliosis and vertebral end plate
deformities (when weight bearing becomes
prominent)
 Pelvis : triradiate configuration

21. CRANIOTABES
 Excess osteoid
deposition in frontal
and parietal regions
with posterior
flattening of skull due
to supine posture of
infant
 Squared configuration
of skull
 Demineralisation of
skull

22. BOWING OF LONG BONES
 Result of
displacement of
growth centres
owing to
asymmetrical
musculotendinous
pull on the
weakened growth
plate

23. RACHITIC ROSARY
 Bulbous
enlargement of
costochondral
junction especially
middle ribs
 May indent pleural
surface or thymic
shadow

24. TRIRADIATE PELVIS
 Protrusion of hip
and spine into the
soft pelvis with
protrussio acetabuli

25. SIGNS OF HEALING RICKETS
 Seen within 2-3 weeks of adequate therapy
 Total calcification is usually complete in 2
months
Signs :
 Reappearance of dense zone of provisional
calcification : first evidence
 Increase in cupping of healing metaphysis
 Recalcifiaction of subperiosteal osteoid
resulting in thick cortex surrounding the shaft
 Sharply defined ossification centres

26. REAPPEARANCE OF DENSE
ZONE OF PROVISIONAL
CALCIFICATION
 Seen as a
transverse line of
increased density
which appears
beyond the visible
end of shaft with a
metaphysis
interposed between
two radiolucent
areas

27. Complete healing and restoration of
normal structure is the rule in rickets
even if severe changes are present
during the active stage !!!!

28. HEREDITARY VITAMIN D
DEPENDANT RICKETS

29.  1 alpha hydroxylase
deficiency
 Dec levels of 1,25
dihydroxy D 3
 Presents within 3
months
 Convulsions and
muscle weakness,
severe rachitic bone
changes, pathologic
fractures
 Rx : 1,25- dihydroxy D3
 End organ resistance
to 1,25-dihydroxy D3
 Elevated levels of
1,25 dihydroxy D3
 Severe rickets,growth
retardation, dental
changes, alopecia
 Rx : Calcium
supplements
TYPE 1 (Psuedo vitamin D
deficiency )
TYPE 2 (Calcitriol resistant
rickets )

30. X LINKED
HYPOPHOSPHATEMIA

31.  Familial Vitamin D resistant/ refractory rickets
 MC form of renal tubular rickets and osteomalacia
 X linked dominant
 Rickets develops between 12-18 months of age
 Lifelong hypophosphatemia due to impaired
reabsorption of phosphate from proximal tubules
 Also impaired conversion of 25 hydroxy D3 into
1,25 dihydroxy D3
 Low serum phosphate, normal serum calcium,
normal PTH

32. RADIOLOGIC FEATURES
 Bowing of legs
 Coarsening of trebacular
pattern with increasing age
 Generalized
increase/normal bone
density especially axial
skeleton
 Calcification and
ossification in
paravertebral ligaments,
ligamentum flavum,
iliolumbar and sacroiliac
ligaments
 Osteoarthritis in ankle,
knee, wrist, sacroiliac
joints

33. ONCOGENIC
OSTEOMALACIA
 Seen in adults with some vascular neoplasms
like hemangiopericytoma
 Tumors produce phosphatonin which inhibits
absorption of phosphate in proximal tubule
resulting in hypophosphatemia
 Advanced rachitic changes may be present
 Refractory to vitamin D therapy
 Respond to tumor removal

34. DRUG INDUCED RICKETS
 Due to high doses of ifosfamide
 Nephrotoxic Metabolites cause tubular
damage
 Results in fanconi syndrome and
hypophosphatemic rickets

35. METAPHYSEAL
CHONDRODYSPLASIA

36.  Generalised symmetric disturbance of enchondral
bone formation primarily at metaphysis
 Seen in childhood : short stature, bowing of long
bones
 Normal serum calcium, phosphorus,ALP levels
 Widening of growth plate with multiple bony
projections growing from metaphysis into growth
plate
 Metaphysis is well mineralised and shows
increased density with absence of loosers zone
 Spontaneous improvement, no response to
vitamin D therapy

38. HYPOPHOSPHATASIA

39.  Defective skeletal mineralisation with normal
serum calcium and phosphorus, low levels of
alkaline phosphatase
 Increased amount of phosphoethanolamine
amino acid in blood and urine
 Usually presents in infancy and childhood
 Neonatal death may occur in severe disease

40. RADIOLOGICAL FEATURES
 Growth plate changes
similar to rickets with
multiple radiolucent
extensions into the
metaphysis
(uncalcified bone
matrix)
 Coarse trebacular
pattern
 Bowing deformity,
fractures
 Wormian bones,
craniosynostosis

41. ATYPICAL AXIAL
OSTEOMALACIA

42.  Axial skeletal involvement with sparing of
appendicular skeleton
 Dense coarse trebacular pattern : most
marked in cervical region , may be seen in
Lumbar spine, pelvis or ribs
 Normal serum calcium, phorphorus,ALP
 No response to vitamin D therapy

43. OSTEOMALACIA

44. PATHOLOGY
 Abnormalities are seen in mature areas of
trebacular and cortical bone
 Defective mineralisation of cortical and spongy
bone with Increase in unmineralised osteoid
 C/F : fatigue, malaise , bone pain , proximal
muscle weakness

45. RADIOLOGICAL FEATURES
 Osteopenia : Uniform involving all the bones
 Coarse indistinct trebacular pattern
 Thin cortex of long bones
 Pseudofractures
 Bone deformities : medial acetabular migration
(protrussio acetabuli ), triradiate pelvis, bowing
of legs
 Spine : kyphoscoliosis , increased endplate
concavity

46. Pseudofractures /
umbauzonen/loosers
zone/milkman’s fracture
 More specific but less common manifestation
 Loosers zone : linear areas of
undermineralised osteoid that occur in
bilateral, symmetric distribution
 Oriented at right angles to the cortex
 Occur due to vascular pulsation acting on the
softened bones
 May show mild-moderate sclerosis with
absence of callus formation

47. Site of increased stress resulting in fracture
Accelerated bone turnover
Inadequately mineralised osteoid
Radiolucent area

48. LOOSER’S ZONE
Sites :
 Axillary margins of
scapula
 Superior and inferior
pubic rami
 Inner margin of
proximal femur
 Posterior margin of
proximal ulna
 Ribs

49. SPINE
 Defective
mineralisation
 Overall decrease in
number of bony
trebaculae within all
the bones enhancing
the contrast of
remaining trebaculae
giving coarse mottled
appearance
 Decreased bone
mass without any
defect in
mineralisation
 Trebaculae are thin
and sharp
OSTEOMALACIA OSTEOPOROSIS

50. HYPERPARATHYROIDISM

51.  Occurs due to excessive production of PTH
 Primary : due to excess production by
abnormal gland like adenoma, hyperplasia ,
carcinoma
 Secondary : abnormality in gland induced by
sustained hypocalcemic stimulus like CRF,
malabsorption states
 Tertiary : due to long standing secondary HPT
who develop autonomous parathyroid function

52. ACTIONS OF PTH

53. CALCIUM METABOLISM

54. RADIOLOGICAL FEATURES
 Bone resorption
 Brown tumors
 Joint disorders
 Osteosclerosis
 Renal osteodystrophy

55. BONE RESORPTION
 Hallmark of hyperPTH
 Due to increased osteoclastic activity
 Can be subperiosteal, intracortical, endosteal ,
subchondral and trabecular
 Cortical bone is affected more than cancellous
bone
 Seen as poor definition of cortical surfaces ,
increased cortical striations (tunneling ),
cortical thinning , distortion and blurring of
trabecular bone

56. SUBPERIOSTEAL
RESORPTION
 Pathognomic of HPT
 Earliest site : radial
aspect of middle
phalanges of middle
and index fingers and
terminal tufts of
fingers
 Others : medial
aspect of proximal
end of tibia, humerus
and femur, superior
and inferior margins
of ribs, lamina dura

57. LOSS OF LAMINA DURA
 Seen in dental sepsis, pagets disease, fibrous
dysplasia, osteomalacia also

58. INTRACORTICAL BONE
RESORPTION
 Osteoclasts tunnel through volkman’s and
haversian canals causing tiny linear striations
within the cortex parallel to long axis of bones
 Tubular bones of hands and feet esp cortex of
second metacarpal
 Almost always associated with subperiosteal
resorption

59. ENDOSTEAL BONE
RESORPTION
 Leads to cortical thinning, scalloping and
irregularity of the endosteal surface esp bones
of hand
 Mostly occurs in conjuction with subperiosteal
and intracortical resorption

60. SUBCHONDRAL BONE
RESORPTION
 Common manifestation of hyperPTH
 Seen in joints of axial skeleton, sacroiliac,
sternoclavicular , acromioclavicular , pubic
symphysis, discovertebral junctions
 Surface irregularity with increased joint space
 Most severe in distal ends of clavicle

61. SUBPHYSEAL BONE
RESORPTION
 Seen in children with primary or secondary
hyperHPT
 Irregular radiolucent areas in metaphysis
adjacent to growth plate

62. SUBLIGAMENTOUS AND
SUBTENDINOUS BONE
RESORPTION
 Occurs at sites of tendon and ligament
attachment to bone
 Involves femoral trochanter, ischial and
humeral tuberosities, elbow , inferior surface of
calcaneum, inferior aspect of distal end of
clavicle

63. TREBACULAR BONE
RESORPTION
 Occurs throughout skeleton in advanced stage
of disease
 Osteoclasts dissect through the centre of
trabecula giving a stippled, mottled, granular
appearance of skull ( SALTAND PEPPER
SKULL)
 Definition of inner and outer table is lost

64. SALT AND PEPPER SKULL

65. BROWN TUMORS
 Osteitis fibrosa cystica
 Cystic lesions within the bone due to extensive
bone resorption
 May cause swelling, pathological fracture or
pain
 Represent hemorrage and deposition of
breakdown products of hemoglobin
 Risk of pathological fracture is more when
brown tumor involves more than two thirds of
the cortex of long bone especially in weight
bearing areas

66.  Multiple Iytic,
expansile ,cystic
lesion
 Eccentric or cortical
location
 Sites : mandible,
clavicle, ribs, pelvis
and tubular bones

67. JOINT DISORDERS
 Erosive arthropathy of hands, wrists and
shoulders
 Almost always associated with typical
subperiosteal resorption of phalanges and
occur on ulnar aspect of metacarpal heads
 Chondrocalcinosis or calcification of
hyaline/fibrocartilage of knee, pubic symphysis
or wrist due to calcium pyrophosphate
dihydrate deposition

68. OSTEOSCLEROSIS
 Increased bone density due to stimulation of
osteoblastic activity by PTH in addition of
osteoclastic activity
 Sec HPT : diffuse increase in bone density
 Pri HPT : localized / patchy sclerosis
 Focal bone sclerosis seen in metaphyseal
regions of long bones, skull , vertebral end
plates

69.  Skeletal features
 Less florid skeletal
features
 Sclerosis rare
 Brown tumors and
chondrocalcinosis
more common
 Soft tissue and vasc
calcification less
common
 Skeletal features with
changes of renal
osteodystrophy
 More florid
 Sclerosis common
 Brown tumors and
chondrocalcinosis less
common
 Soft tissue and vasc
calcification more
common
PRIMARY HYPERPTH SECONDARY HYPERPTH

70. DIALYSIS ASSOCIATED
ARTHROPATHY

71.  Axial and appendicular skeleton destructive
arthropathy due to long term dialysis
 Chronic, progressive ,symmetric
polyarthropathy involving large and small
peripheral joints
 Periarticular cysts , erosions , loss of joint
space , loss of articular surface, osteopenia

72. SPINE DRSA
 usually after 3-5 years of dialysis, cervical
spine involved MC .
 Narrowing of disc height, subchondral cysts,
endplate erosions, collapse, erosion of
contiguous vertebral bodies, facet erosion ,
spondylolisthesis, peridiscal calcification.
 Calcification in subcutaneous regions,
vascular, muscular , visceral organ .

73. RENAL OSTEODYSTROPHY

74.  Bony changes seen in patients with chronic
renal insufficiency
 Children : structural abnormalities of urinary
tract
 Adults : chronic glomerulonephritis

75. RADIOLOGIC FEATURES
Sec hyperparathyroidism
 Bone resorption (subperiosteal, intracortical ,
endosteal , subligamentous)
 Brown tumors
 Soft tissue and vascular calcification
 Osteosclerosis ( focal / diffuse ): rugger jersey
spine, pelvis , ribs , clavicles
 Osteopenia : end result of osteomalacia, bone
resorption, osteoporosis

76. RENAL OSTEODYSTROPHY
 Deposition of bone
in subchondral
areas of vertebral
bodies
 Radiodense bands
across superior and
inferior vertebral
margins
Rugger jersey spine

77. CALVARIAL THICKENING

78. HYPOPARATHYROIDISM

79. CAUSES OF HYPOPTH
 MCC : excision/ trauma to parathyroid gland
during thyroid surgery
 Idiopathic hypoparathyroidism due to
circulating antibodies to PTH , adrenal and
thyroid glands
 Radiation induced damage to the gland
 Low serum calcium and PTH , high phosphate

80. RADIOLOGICAL FEATURES
 Focal or generalised bone sclerosis
 Pelvis, proximal femur , vertebral bodies
 Calvarial thickening
 Hypoplastic Dentition
 Band like areas of increased radiodensity in
metaphysis of long bones
 Calcifiction and ossification of anterior
longitudinal ligament and spinal osteophytes
 Calcification in basal ganglia, cerebrum,
cerebellum

81.  Mineralization of
iliolumbar ligament (pink
arrow), broad ossification
at the lateral margin of
acetabulum (white arrow),
osseous proliferation and
irregular bony
excrescences above the
acetabulum (arrowhead),
and lesser and greater
trochanters and ischial
tuberosities (open arrows)
 Capsular calcification of
the hip joint (black arrow)
and internal fixator for the
right femoral shaft fracture.

82.  Bilateral basal
ganglia calcification

83. PSEUDOHYPOPARATHYROI
DISM

84.  Autosomal dominant
 Due to end organ resistance to parathyroid
hormone
 Due to defect in adenyl cyclase cyclic AMP
system in renal tubules and bones
 Second decade, F>M
 Short , obese , mentally retarded,
brachydactyly
 Low calcium, high PTH and phosphate

85. RADIOLOGICAL FEATURES
 Shortening of fourth
metacarpal
 Soft tissue calcification and
ossification, basal ganglia
and calcification
 Calvarial thickening
 Short metatarsals and
phalanges
 Premature closure of
epiphysis
 Exostoses projecting at
right angles to the bone
 Features of hypoPTH

86.  Not seen  Short first and fourth
metacarpal
 Exostosis
perpendicular
surface of bone
HYPOPARATHYROIDISM
PSEUDOHYPOPARATHYROIDI
SM

87. PSUEDOPSEUDOHYPOPARATHYR
OIDISM

88.  Result of incomplete genetic manifestation of
PHP
 Caused by end organ resistance to PTH
 Pts with PPHP have normal calcium
 Radiological features like PHP except higher
rate of short metacarpals in PPHP and short
distal phalanges in PHP

89. HYPERCORTISOLISM

90. CAUSE
 Tumor of adrenal gland
 EctopicACTH production
 Iatrogenic
 Basophil pituitary adenoma

91.  Inhibiton of bone formation
 Stimulation of bone resorption
 Decrease in intestinal absorption of calcium
 Decrease in synthesis of collagen
Osteonecrosis, osteoporosis, muscle wasting

92. RADIOLOGICAL FINDINGS
 Generalized loss of bone density : spine, pelvis,
ribs, cranial vault (trebacular bone > cortical bone)
 Accentuation of primary trebaculae, with central
endplate depressions in the vertebral bodies
(biconcave fish like appearance )
 Increased radiodensity of superior and inferior
margins of compressed / collapsed vertebrae (d/t
exuberant callus formation )
 Exuberant callus at fracture sites in long bones
and ribs
 Local regions of osteonecrosis esp after
exogeneous steroids ( AVN at femoral and
humeral heads)

93. Skeletally immature child
 Suppresses growth : short child
 Osteoporosis , truncal obesity , delayed bone
age
 Osteonecrosis at growing epiphysis may lead
to abnormal development at ends of long
bones
 Early development of osteoarthropathy

94. HYPOPITUITARISM

95.  Delay in skeletal maturation : delay in
appearance and closure of epiphysis
 Retarded skeletal growth
 Overall loss of bone density

96. HYPOTHYROIDISM

97.  Thyroid neoplasm
 Thyroiditis
 Thyroid ablation
 Disturbance in
iodine metabolism
 Def of TSH
PRIMARY SECONDARY

98.  Infant : cretinism
 Child : juvenile myxedema
 Adult : myxedema

99. CONGENITAL
HYPOTHYROIDISM
XRAY WRISTAND XRAY KNEE
 Delay in skeletal maturation with bone age lagging
behind chronological age : short stature and late
appearance of epiphyseal ossification centres
 Normally , distal femoral epiphysis is ossified at
36 wks and proximal tibial epiphysis at 38 wks :
dec size/ absence indicates hypothyroidism
 Deformed , irregularly shaped epiphysis
(EPIPHYSEAL DYSGENESIS ): bilateral and
symmetrical
 Delayed closure of epiphyseal plates

100.  Skull : sutures may remain open and show
wormian bones, small sella in young or large,
rounded in old children
 PNS are underdeveloped
 Pelvis : narrow with coxa vara deformity , inc
incidence of SCFE
 Spine : bullet shaped VB , kyphosis

101. ADULT HYPOTHYROIDISM
 Mild skeletal manifestations
 Generalized osteoporosis

102. HYPERTHYROIDISM

103.  Accelerated skeletal
maturation therefore
bone age ahead of
chronological age
 Osteoporosis with
VB fracture and
kyphosis
CHILD ADULT

104. RADIOLOGICAL FINDINGS
 Osteoporosis : spine, pelvis, skull, hands and feet
 Progression of thyrotoxic osteoporosis is faster
than post menopausal osteoporosis but same
radiologically
 DL vertebra more affected : Biconcave VB ,
wedge deformities , kyphosis, fractures
 Tubular bones of hands, feet : cortical tunneling
and striations due to inc osteoblastic and
osteoclastic activity
 Thyroid acropachy in treated pts : exophthalmos,
soft tissue swelling of fingers and toes, pretibial
myxedema or clubbing

105.  Dense , solid, periosteal new bone formation
with feathery margins
 Asymmetric periosteitis : most prominent
along the radial margin of metacarpals and
phalanges in the diaphyseal region

106.  Hands and feet
 Feathery contour
 Long bones
 Absent
THYROID ACROPACHY
HYPERTROPHIC
OSTEOARTHROPATHY

107. TURNERS SYNDROME

108.  Skeletal maturation is usually normal till 15 years
of age following which delayed epiphyseal closure
occurs esp apophysis of iliac crest
 Depression or slanting of the medial tibial plateau
with concomitant overgrowth of medial condyle of
femur
 Short fourth and fifth metacarpal
 Narrow ribs
 Small sella
 Android pelvis
 Hypertelorism

109. ACROMEGALY

110.  Reactivation of enchondral bone formation
 Stimulates periosteal bone formation
 Connective tissue proliferation

111. CLINICAL FEATURES
 3-4 decade
 Coarse facial features
 Thick skin
 Dental occlusion
 Deepening of voice
 Prominent tongue
 Broad hands and feet
 Organomegaly

112. DEFINITIVE DIAGNOSIS
 24 hours serum GH levels
 GH secretion not suppressed by oral glucose
 Serum level of insulin like growth factors

113. RADIOLOGICAL FINDINGS
SKULL
 Cranial vault thickening
 Prominence of supraorbital ridges and zygomatic
arches
 Prominence of ext occipital protruberance
 Enlargement of sella
 Prominence and enlargement of maxillary and
frontal sinuses
 Excessive pneumatisation of mastoid
 Enlargement and elongation of mandible with
widening of mandibular angle

114. HANDS AND WRIST AND
FEET
 Soft tissue thickening of fingers
 Thickening and squaring of phalanges and
metacarpals
 Overconstriction of shafts of phalanges
 Abn wide articular surfaces : MCP, MTP, IP
 Bony excrescences at site of tendon and ligament
attachment to bone
 Prominence of ungal tufts ( spade like )
 Keel shaped deformity : resorption of cortex along
plantar aspect

115. INDICES
 Increased phalangeal soft tissue thickness at
prox mid phalanges > 27 mm (men) and > 26
mm (women)
 Widening of second MCP joint > 2.5 mm in
men and women
 Bone excrescences and marginal spurs
 Inc width of phalages : spade like
 Large sesamoid index > 40 mm(M) and >
32mm (F)
 Inc interstyloid distance

116. HEAL PAD THICKNESS
 Shortest distance between calcaneum and
plantar surface of skin
 > 21.5 mm (f) and >23 mm (m) : suggestive
 >23 mm (f) and > 25 mm (m) : diagnostic

117. MALE FEMALE
HEEL PAD THICKNESS > 23 > 21.5
SESAMOID INDEX >40 >32
TUFTAL WIDTH >12 >10
PHALANGEAL SOFT TISSUE >27 >26
JOINT SPACE >2.5 >2.5

118. VERTEBRAL COLUMN
 Elongation and widening of vertebral bodies
 Increase in vertebral height
 Ant and lat osteophytes
 Inc height of IVD
 Scalloping of post margins of VB
 Inc thorasic kyphosis
 Exagerrated lumbar lordosis

119.  Enlarged thorax due to elongation of ribs and
prominence of costochondral junction
 Pelvis : enlargement and beaking of symphysis
pubis
 Feet : soft tissue enlargement , prominence of
tufts and base of terminal phalanges, bone
proliferation at sites of tendon and ligament
attachment like undersurface of calcaneum
 Articular abnormalities : knee, hips, glenohumeral
joints. Widening of articular space seen at MCP,
MTP and IP joints

120. ACROMEGALIC
ARTHROPATHY
Hypertrophy causing
 Fissuring
 Ulceration
 Denudation
(Degenerative
arthropathy , changes
of OA )
 Hypertrophy
 Brisk regeneration :
chronic > thickened
cartilage > inc joint
space > enlarged
bones > hypertrophy
of periarticular soft
ts.
HYALINE CARTILAGE FIBROCARTILAGE

121. FIBROCARTILAGE
HYPERTROPHY
 Calcification and ossification > calcinosis +
osteophytes > at atypical sites like
glenohumeral and elbow joint
 Presence of beaklike osteophytes at inferior
part of head of humerus , lateral aspect of
acetabulum , medial part femoral head , sup
margin pubic symphysis , radial head , tibia

122. GIGANTISM

123.  Extreme height with normal body proportions

124. SCURVY

125.  Due to long term vitamin c deficiency
 Infantile : due to pasteurised or boiled milk
formula
 6 months – 2 years
 C/F : progressive irritability with tender
edematous limbs, subcutaneous / mucous
membrane hemorrages, anaemia, bleeding
gums, malena, bulging at costochondral
junction

126. PATHOLOGY
 Vitamin C necessary for Endothelial lining :
deficiency causes increased vascular fragility
 Decreased osteoblastic activity and cartilage
proliferation resulting in decreased formation
of bony matrix
 Normal mineralisation
 Osteoporosis

127. WHITE LINE OF FRENKEL
 White line in the
zone of provisional
calcification at the
growing metaphysis
 Cartilage
proliferation
decreased with
normal
mineralisation
resulting in widened
and dense zone of
provisional
calcification

128. TRUMMERFELD ZONE
(SCORBUTIC ZONE)
 Transverse
radiolucent band
adjacent to zone of
provisonal
calcification due to
suppressed
osteoblastic activity
with normal
mineralisation
 Trabecular bone
mass is decreased in
zone of primary and
secondary spongiosa.

129. WIMBERGER SIGN
 Epiphysis is small
sharply marginated
by sclerotic rim with
central portion more
radiolucent.
 Due to decrease
cartilage
proliferation and
unimpaired
mineralization
(sclerosis)

130. CORNER (ANGLE) SIGN
 Irregularity of the
metaphyseal
margins secondary
to infractions of the
epiphyseal-
metaphyseal
junction

131. PELKAN’S SPUR
 Zone of provisional
calcification extends
beyond the margins
of the metaphysis
resulting in
periosteal elevation
and marginal spur
formation

132. SUBPERIOSTEAL
HEMORRAGES
 Due to increased
capillary
permeability
 Seen in ends of long
bones(femur,tibia,
humerus)
 May cause
periosteal elevation
and new bone
formation

134.  On vitamin C therapy, all changes are
reversible though single growth arrest line may
remain in metaphysis as residual frenkel’s line.

135. FLUOROSIS

136. ETIOLOGY
 Chronic ingestion of flouride in excess of 8
ppm in drinking water
 Industrial expose to fluorine compounds
for many years
 In laboratory personnel due to inhalation
of fluorine vapors
 Agricultural fluoride contamination
 Habitual drinking of wine containg fluorine
i.e. wine fluorosis

137. PATHOLOGY
 Generalized increase in bone density due to
osteoclastic response to fluorine
Excess fluorine
Osteoclastic activity increases,
Disturbed normal collagen synthesis
 Fluoride have strong affinity for bone salts replacing
hydroxyl ion; Hydroxipatite converted into
fluoropatite which is more resistant to dissolution

138. CLINCAL FEATURES
 Initially asymptomatic
 Rare in children because it takes 12 or
more years after exposure to develop
changes
 Polydipsia
 Anemia
 Mottling of enamel of teeth
 Crippling stiffness and pain
 Pathological fractures

139. RADIOLOGIC FEATURES
 Thickening of the
cortex of affected
bones
 Ribs : Inferior
margin may show
irregularity/fringed
appearance (rose
thorn appearance )
Osteosclerosis
 most marked in
spine, pelvis, ribs
 Skull and tubular
bones are spared
 Calvarium :
sclerosis of base of
skull and posterior
clenoid

140.  Ossification and
calcification of
ligaments of
sacrospinous,
sacrotuberous
 Ossification of
interosseus
membrane
 Vertebral
Osteophytes
 Paraspinal and
intraspinal ligament

141. OSSIFICATION OF
INTERROSEUS MEMBRANE

142. THANK YOU ALL