This document discusses rickets, a disorder caused by abnormalities in calcium and bone metabolism leading to skeletal problems. It defines rickets and osteomalacia, outlines causes including vitamin D deficiency, and describes clinical features like bone deformities and biochemical abnormalities. The pathophysiology of rickets is explained as failure of bone mineralization due to lack of vitamin D. Diagnosis and treatment focus on vitamin D, calcium, and phosphate supplementation. Complications and prevention are also mentioned.

1. Dr. Omar Mahdi Abir
D-ortho Resident
Sir Salimullah Medical College
RICKETS

2. Heterogenous group of disorders
characterized by abnormalities in
calcium metabolism and/ or Bone cell
physiology.
They lead to an altered serum calcium
concentration and / or skeletal failure.

3. •Bone Mineralization related:
Osteomalacia/ Rickets
•Low Bone Content: Osteoporosis
•Bone Turnover related: Primary
Hyperparathyroidism, Secondary
Hyperparathyroidism , Paget’s Disease
•High Bone Content: Osteopetrosis

4. Distinct form of osteoporosis
This two are different expressions of the
same disease
Inadequate mineralization of bone in
children is called rickets
And In adults it’s called Osteomalacia
This leads to an increase in bone fragility
and fracture risk

5. Rickets is a clinical syndrome arising from an
excess of undermineralised bone matrix of
growing bone, occurs in children only before
fusion of the epiphyses.
 It results in
- short stature,
- bony deformity
- muscle weakness.

6.  :Rickets principally due to vitamin D deficiency
was rampant in northern Europe and the united
states during the early years of the 20th century. In
devoloping countries it remains as a significant
problem.
 In Africa finding the prevalence of rickets to
exceed 10% .UNICEF has estimated that 25%
children in China have some evidence of rickets.

7. 1 alpha Hydroxylase is
Upregulated by
• PTH
• Hypophosphatemia
And Downregulated by
• Hyperphosphatemia
• Calcitriol
• Increase serum Calcium

8. 3
Pathophysiology
 Combination of nutritional deficiency and lack
of sunlight ⬇️
Lack of 25-OHD
⬇️
Reduce Serum 1,25 –OHD
⬇️
Inability to calcify the intracellular matrix
in the growth plate causing
 Chrondrocyte to pile up irregularly ➡️
proliferative zone disorderly active
thickened plate .

9. 4
 Zone of calcification➡️poorly mineralized
 Zone of ossification ➡️sparse bone formation
⬇️
The new trabeculae are thin and weak and the
metaphysis becomes broad and cup shaped
⬇️
If the condition lasts for long time
⬇️
Stress deformity of the bone
⬇️
Indentation of pelvis (trefoil pelvis)
 Looser’s zone (pubic rami, femoral neck, scapula)
 Bending of femoral neck and shaft of long bones
 Biconcave vertebrae

10.  Nutritional Rickets
-Malnutrition
-malabsorbtion
-Biliary disease
 Vitamin-D dependent rickets
-Type-I VDDR (inability to hydroxylate)
-Type-II VDDR ( receptor insensitivity)
 Vitamin-D resistant rickets/Hypophosphatemic
Rickets(low serum phosphate and resistant to
treatment with vitamin –D)

11. -x linked dominant rickets(80%)
-Autosomal Dominant
hypophosphatemic rickets (20%
-fancony syndrome (inadequate
reabsorbtion of phosohate.
• Rickets due to other cause
-Tumor induced rickets(GCT, Non
ossifying fibroma)
-Drug induced
(phenytoin,phenobarbitone)
-Renal osteodystrophy

12.  Childhood and pregnancy when vit-D requirement are higher
 Strict veganism
 Dress codes which limits sun exposure.
 Nursing home resident Where poor diet is compounded by
reduced sunlight exposure
 Coeliac disease
 Defective vit-D activation(liver disease, anticonvulsant drug)
causing decrease hydroxylation.
 Phosphate deficiency(vit-D resistant rickets)

13. Restlessness, fretful, pale , flabby muscle
Delayed milestone of development
Delayed tooth eruption
In infant : may present with tetany or convulsion due
to hypocalcemia
Early sign
Failure to thrive
Listerness

14. • Muscular flaccidity
• Craniotobes (deformity of skull)
• Thickening of knee, ankles,wrists from
growth plate over growth
• Enlargement of costochondral junction (
rachitic rosary)
• Lateral indentation of chest (harrison’s
sulcus)
• Frontal and parietal bossing
• Delayed closure of anterior frontanalle
• Increased perspiration

15. In child
• Growth retardation
• Bony deformity(knock knee,
bow leg)
• Chest deformity(pectus
excavatum, pigeons chest)
• Pelvic deformity( trefoil pelvis)
• Epiphysis enlarged

16. Head
 Craniotabes
 Frontal bossing
 Delayed
frontanelle closure
 Delayed dentition,
caries
Skeletal
Deformities in
Rickets

17. In chest
• Rachitic rossary
• Harrison sulcus
• Pigeon’s
chest(pectus
carinatum
• Narrow chest
In abdomen
• Pot
belly/protubera
nt abdoment

18. Vertebral column
• Exaggerated
curvature (bi
concave shape)
• Kyphosis
• Lordosis
• Scoliosis
Pelvis
• Trefoil appearance
• Narrowing of pelvis.

19. Extremities
• Enlargement
/widening of wrist
and ankle
• Genu vulgum or
varus deformity
• Wind swept
deformity
• Coxa vara
• Femur – bowing
anterolaterally
• Bowing in tibia
Wind swept
deformity
Widening of
wrist and
ankle

21. 12

22. 12

23. Types
of
Rickets
Calcium Phosph
orus
ALP PTH 25(OH)
Vit-D
1,25(OH
)2
Vit-D
Nutrition
al
N N/⬇️ ⬆️ ⬆️ ⬇️⬇️ ⬇️
Vit-D
resistant
rickets
N ⬇️ ⬆️ N N N
Vit-D DR
Type-I
⬇️ ⬇️ ⬆️ ⬆️ ⬆️⬆️ ⬇️⬇️
Vit-DDR
type-II
⬇️ ⬇️ ⬆️ ⬆️ N/ ⬆️⬆️ ⬆️⬆️⬆️
Renal
osteody
strophy
N/⬇️ ⬆️ ⬆️ ⬆️⬆️ N ⬇️
Biochemical changes in Rickets

24.  Epiphysis: short/ small
 Metaphysis: widening and Cupping
 Diaphysis: Bowing
 Growth plate : thick and wide
 Decresed density of cortex
 Loss of transeverse Trabeculae and
decreased longitudinal trabeculae.
If calcium level is persistently
low,sign of secondary
hyperparathyroidism ,
 Subperiosteal Erosions at the
maximal remodelling

25. 15
Bone Biopsy
•Tetracycline lebeling shows that mineralization is
defective
•Osteoid seams are both wide and more extensive
Diagnosis
•Most cases of rickets are diagnosed based on the
presence of classic radiographic abnormalities.
•The diagnosis is supported by the physical
examination findings & a history and laboratory test
results.

26. 17
Treatment
General
 Counselling about the nature and future of the disease.
 The child likely to improve with calcium and vitamin D
supplementation.
 Vitamin D & calcium & phosphorus rich diet.
Specific:
Rickets due to vit-D deficiency:
 ‘Stoss’ therapy- 300000-600000 IU vit D are
administered as 2-4 divided doses over one day.
 High dose vit-D 2000-5000 iu/day over 4-6 wk. Either
strategy should be followed by daily vit-D intake 400IU
/day
 Calcium supplementation

27. Vitamin D resistant rickets
Inj vitamin D3 0.1-1 lac IU/ day to produce
healing
Inorganic phosphate -3gm/day
Renal Rickets
 contact nephrologist for CRF
Advise to decreased phosphate use
aluminium containing antacid
For chelating phosphate –use alumonium
containing antacid + use desferoxamin
Calcium supplementation

28. Other treatment of
Rickets
• Supportive
Management
-Brace (eg: mermaid
splint in knock knee)
-Corrective plaster
• Surgical Treatment:
Excessive deformity in
1st visit :corrective
osteotomy

29. 20
:
Follow up
 Blood and urine Ca, Ca:Cr should be done
while the child getting vit-D every 2-3 month.
 X-ray of wrist and hand /ankle
 Radiographic improvement is expected
within 6 weeks of therapy.

30.  Most children have an excellent response to treatment
with radiologic healing within few months.
 Children with severe disease may have permanent
deformities.
 Short stature dose not resolve in some children,
 Rarely patients may benefit from orthopedic
intervention for leg deformities.

31. 21
Complication:
Repeated infections
bronchopneumonia
 Bony deformities
 Pigeon chest
 Knock knee
 Bow leg
 Spinal curvature.
 Contracted pelvis

32. :
 Exposure to sunlight.
 Oral administration of vit-D 400 IU/day.
 Prematurely born infant should receive
supplement vit-D daily from 2nd week after
birth.
Vit -D should be administered to pregnant
& lactating mother.

33. References
•Apley’s and Solomon’s System of Orthopaedics
and Trauma.
•Cambell’s Operative orthopaedics
•Turek’s Orthopaedics Principles and Their
application
•Internet