Rickets is the softening and weakening of bones in children, usually because of an extreme and prolonged vitamin D deficiency. Rare inherited problems also can cause rickets. Vitamin D helps your child's body absorb calcium and phosphorus from food. Not enough vitamin D makes it difficult to maintain proper calcium and phosphorus levels in bones, which can cause rickets. Adding vitamin D or calcium to the diet generally corrects the bone problems associated with rickets. When rickets is due to another underlying medical problem, your child may need additional medications or other treatment. Some skeletal deformities caused by rickets may require corrective surgery. Rare inherited disorders related to low levels of phosphorus, the other mineral component in bone, may require other medications. Products & Services Book: Mayo Clinic Family Health Book, 5th Edition Symptoms Signs and symptoms of rickets can include: Delayed growth Delayed motor skills Pain in the spine, pelvis and legs Muscle weakness Because rickets softens the areas of growing tissue at the ends of a child's bones (growth plates), it can cause skeletal deformities such as: Bowed legs or knock knees Thickened wrists and ankles Breastbone projection

1. Imaging in Rickets & Scurvy
Presented by- Moderator-
Dr. Shivani Gupta Dr. Shalini
Agarwal
Junior Resident 1
Dept. of Radio-diagnosis
PGIMS Rohtak

2. PHYSIS/ GROWTH PLATE
 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.

3. 3 zones of
physis-
 Resting/ germinal zone
 Proliferating zone
 Hypertrophic
zone: zone of
maturation,
degeneration and
provisional
calcification

4. RICKET
S

5. INTRODUCTION
 It is a disease of childhood
characterized by failure of
mineralization of osteoid tissue in
developing skeleton, particularly at the
growth plate.
 Age: 6-12 months.
 At risk- Dark pigmented individuals,
infants breast-fed for prolonged
periods of time by a multiparous
mother, at higher altitudes

6. Pathology of rickets v/s
scurvy

7. PATHOLOGY
 Decrease in quantity of calcified
osteoid & increase in uncalcified
osteoid.
Osteopenia
 Cartilage cells at physis grow normally
but FAIL TO CALCIFY.
Growth plate is widened due to
overgrown & hypertrophied cartilage

8. CAUSES OF RICKETS
1.Vitamin-D deficiency
2.Abnormality in phosphate metabolism.
3.Calcium Deficiency

9. CLINICAL FEATURES
 First 6 months :Tetanic convulsions
 Irritability, weakness
 Delayed development
 Small stature
 Bony deformities and pain
 Rachitic rosary
 Swelling of wrist and costocartilage
 Thoracic kyphosis with pigeon chest
 Harrison’s sulcus
 Greenstick fractures are common

11. RADIOLOGICAL FEATURES
 MC and non specific finding : osteopenia
 Loss of provisional zone of calcification
 Changes are seen at open growth plate
 Especially visible at fast growing growth
plates like costochondral junction of the
middle ribs, knees, wrists & ankles.
 Earliest sign : distal ends of radius and
ulna. Ulnar growth plate grows more
rapidly so manifestations are seen
earlier in ulnar growth plate

12. WIDENING OF GROWTH PLATE
 Earliest and specific radiological
change
 Due to increase in cartilaginous cell
mass and loss of normal zone of
provisional calcification

13. METAPHYSEAL FRAYING
 Irregular
metaphyseal
margins
 Cause-
Disorganisation
of spongy bone
in metaphyseal
region

14. METAPHYSEAL CUPPINGAND
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
 Paint-brush
metaphysis

15. SHAFTABNORMALITIES
 Rarefaction of shaft due to loss of
mineral content
 Cortex becomes thin with a coarse
texture

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

17. RACHITIC ROSARY
 Bulbous
enlargement of
costochondral
junction
especially
middle ribs
 Cause-
Widening of rib
epiphyseal
cartilage.

18. 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

19. BOWING OF LONG BONES
 Cause-
Displacement of
growth centres
owing to
asymmetrical
musculotendino
us pull on the
weakened
growth plate

20. TRIRADIATE PELVIS
 Protrusion of
hip and spine
into the soft
pelvis with
protrussio
acetabuli

21.  PA radiograph of both hands shows
diffuse osteopenia, cupping, fraying &
splaying of metaphyses of b/l distal
radius and ulna.

23.  AP Radiograph of
both lower limbs
obtained 2 years
after active disease
phase shows
bowing of tibia and
fibula and
transverse sclerotic
bands at the
metaphysis parallel
to the growth plate
(Harris growth
arrest lines or park
lines)

24. 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
 Recalcification of subperiosteal osteoid
resulting in thick cortex surrounding the shaft
 Sharply defined ossification centres

25. FIRST E/O HEALING RICKETS:
REAPPEARANCE OF DENSE
ZONE OF PROVISIONAL
CALCIFICATION
 Seen as a
transverse line of
increased density
which appears
beyond the visible
end of shaft with
metaphysis
interposed
between two
radiolucent areas

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

27. SCURVY
 A.k.a. Barlow’s disease or
hypovitaminosis C

28. Introduction
 Scurvy is a nutritional bone disorder
which occurs due to long term
deficiency of Vitamin C.
 Infantile Scurvy: due to pasteurised or
boiled milk preparations
 Age: 8-14 months
 Latent period- 4 months before
symptoms and skeletal changes
become apparent.

29. PATHOLOGY
 Vitamin C is necessary for hydroxylation of
proline to hydroxyproline which is vital for
collagen synthesis.
 Vitamin C is also necessary for endothelial lining
Deficiency causes increased vascular fragility
 Osteoblasts require vit C to form mature osteoid
tissue.
 Decreased osteoblastic activity
Generalised osteopenia and osteoporosis
 Cartilage proliferation is decreased but
mineralisation is normal.

30. Clinical features
 Clinical hallmark : Spontaneous
haemorrhage i.e. cutaneous
petechiae,bleeding gums,melena &
hematuria.
 Progressive irritability with tender
edematous limbs and a tendency to lie
supine & motionless with the thighs
abducted (frog-leg position,
pseudoparalysis)
 Bulging at costochondral junction
(Scorbutic rosary-Sharp pain & tender)

31. WHITE LINE OF FRENKEL
 Dense zone of
provisional calcification.
 Radiodense line in the
zone of provisional
calcification at the
growing metaphysis
 Cause- Cartilage
proliferation decreased
with normal
mineralisation.
Conversion into bone is
delayed.

32. TRUMMERFELD ZONE
(Scorbutic zone)
 Transverse radiolucent
band directly beneath
the zone of provisonal
calcification.
 Cause- Suppressed
osteoblastic activity
with normal
mineralisation leading
to disordered osteoid
formation.
 Trabecular bone mass is
decreased.

33. PELKAN’S SPUR
 Bony protuberances at
the metaphyseal
margins at right angles
to the shaft.
 Cause- Zone of
provisional calcification
extends beyond the
margins of the
metaphysis resulting in
periosteal elevation
and marginal spur
formation

34. WIMBERGER'S
SIGN
(Ring epiphysis)
 Epiphysis is small &
sharply marginated by
sclerotic rim with central
portion more radiolucent.
 Cause- Decreased
cartilage proliferation
and unimpaired
mineralization
(sclerosis)
 Differentiates healing
rickets and scurvy

35. CORNER (ANGLE) SIGN
 Irregularity of the
metaphyseal
margins.
 Cause- Infarctions
of the epiphyseal-
metaphyseal
junction

36. SUBPERIOSTEAL
HEMORRAGES
 Seen in ends of long
bones(femur,tibia,
humerus)
 May cause
periosteal elevation
and new bone
formation
 Cause-Increased
capillary fragility

40.  Coronal T2-weighted fat-suppressed MR
image of both distal femoral
metadiaphyses shows heterogeneously
increased T2 signal intensity in the
marrow (*) and around the bone (arrows)

41. HEALING SCURVY
 On vitamin C therapy, all changes are
reversible though a single growth
arrest line may remain in metaphysis
as residual frenkel’s line.
 Following therapy, subperiosteal
hematomas rapidly calcify and
demarcate.

43. Thank you !