Rickets is a childhood bone disease caused by vitamin D deficiency and lack of calcium and phosphate. It results in soft and weak bones in children. Symptoms include bone pain, bowed legs, and skull deformities. Risk factors include lack of sunlight exposure, dark skin pigmentation, malnutrition, and liver or kidney diseases. Diagnosis involves blood tests showing low calcium, phosphate, and vitamin D levels and x-rays showing bone changes. Treatment consists of vitamin D and calcium supplementation to strengthen and repair bones. Prevention involves adequate sunlight exposure, vitamin D supplementation, and calcium-rich nutrition during childhood bone growth.

1. ..
rickets
Osteomalacia

2. Rickets is a childhood disorder
involving softening and
weakening of the bones.
It is primarily caused by lack of
vitamin D, calcium, or
phosphate.

3. Sunlight as a source of vitamin D
Lack of vitamin D production by the skin may occur
if a person is confined indoors, or works indoors
during the daylight hours, or lives in climates with
little exposure to sunlight.
Sunlight is important to
skin production of
vitamin D and
environmental conditions
where sunlight exposure
is limited may reduce
this source of vitamin D.

4. Sunlight as a source of vitamin D
Adequate supplies of
vitamin D3 can be
synthesized with sufficient
exposure to solar
ultraviolet B radiation
Melanin, clothing or
sunscreens that absorb
UVB will reduce cutaneous
production of vitamin D3

5. Rickets
In rickets, another mechanism in the body works to increase
the blood calcium level. The parathyroid gland may increase
its functioning rate to compensate for decreased levels of
calcium in the bloodstream.
To increase the level of calcium in the blood the hormone
destroys the calcium present in the bones of the body and
this results in further loss of calcium and phosphorous from
the bones. In severe cases, cysts may develop in the bones.
Vitamin D deficiency could be caused due to numerous
reasons

6. • What are the causes for deficiency of
Vitamin D?

7. Etiology
• . * Vitamin D–deficient conditions :-
– Dietary lack of vitamin D
– Insufficient exposure to sunlight
– Vitamin D deficiency of

8. Etiology
. Diseases and drug:
• Liver diseases, renal diseases
• Gastrointestinal diseases
• Antiepileptic
• Glucocorticosteroid

9. Cholecalciferol (vitamin D-3) is formed in the skin from
7-dihydrotachysterol. This steroid undergoes hydroxylation in 2 steps.
- Metabolism of vitamin D
• The first hydroxylation occurs at position 25 in the liver,
producing calcidiol (25-hydroxycholecalciferol), which
circulates in the plasma as the most abundant of the vitamin D
metabolites and is thought to be a good indicator of overall
vitamin D status.

10. • Cholecalciferol (vitamin D-3) is formed in the skin from
7-dihydrotachysterol. This steroid undergoes hydroxylation in 2 steps.
Pathophysiology
• The second hydroxylation step occurs in the kidney at the 1 position,
where it undergoes hydroxylation to the active metabolite calcitriol
(1,25-dihydroxycholecalciferol - DHC). This cholecalciferol is not a
vitamin, but a hormone.

11. Vitamin D: The Sunshine Vitamin

12. Pathway of Vitamin D Production

13. Calcitriol acts on regulation of
calcium metabolism:
• Calcitriol promotes absorption of calcium and
phosphorus from the intestine,
• increases reabsorption of phosphate in the
kidney,
• acts on bone to release calcium and
phosphate;
• Calcitriol may also directly facilitate
calcification.
Calcitriol (1,25-DHC) – acts as a hormone rather than a
vitamin, endocrine and paracrine properties

14. CLASSIFICATION
• vitamin D deficiency rickets :-
– hypocalcemic rickets
– Poor vitamin D intake
– avoidance of sunlight
• pseudo-vitamin D–deficiency rickets :-
– familial hypophosphatemic rickets
– this syndrome present in the first year of life.
• growth retardation
• Rickets
• hypocalcemic seizures

15. Pathogenesis
• Vitamin D deficiency
• Absorption of Ca, P
• Serum Ca
• Function of Parathyroid

16. Pathogenesis
PTH
High secretion
P in urine Decalcification of old bone
P in blood Ca in blood normal or low slightly
Ca, P product

17. Pathogenesis
• Low secretion of PTH
• Failure of decalcification of bone
• Low serum Ca level
• Rachitic tetany
(Spasmophylia)

19. Causes and types
• 1/vit d defcincy –most common-duto
• 1-ditary diffcincy
• 2-lack exposure sun light
• 3-increase damened
• 2-defective vit d absorbation
• 3-defective activation
• 1- liver and renel dz

20. • 2-difcincy 1 alpha hydroxlyase enzyme
this called vit d depended rickets type 1
• 3-end organ rsistance to vit d this called
type 2
• 4-hypophsphatemia called vitamine d
resistant rickets
• 5-drugs

21. Clinical picture
Early rickets :
1- anorexia,irritabilit ,sweating of forhead
2- craniotabese
s (areas of thinning and softening of bones of
the skull).
3- knobby deformities called rachitic rosary
along the costochondral junctions :firstly
palpable not visible

22. • Advanced rackets
• A- Skeletal manifestation
• large head ::thickening of the skull develops. This
produces frontal bossing and delays the closure of
the anterior fontanelle
depression of nasal bridge
• Delay eruption of
primary teeth
Clinical signs
Frontal bossing

23. Protruding forehead
asymmetrical or odd-shaped skull

24. Clinical signs
• In the chest
knobby deformities results in the rachitic rosary along
the costochondral junctions.
• The weakened ribs pulled by muscles also produce
flaring over the diaphragm, which is known as Harrison
groove.
• Forward projection of the breastbone - pigeon chest or
pectus carinatum),

25. Pathway of Vitamin D Production
Rib beading (rachitic
rosary)

26. • Spine
deformities (spine
curves abnormally,
including scoliosis
or kyphosis).
• In more severe
instances in
children older than
2 years, vertebral
softening leads to
kyphoscoliosis
Clinical signs

27. Knock knee deformity
(genu valgum)
Bowleg deformity
(genu varum)

28. Bowlegs and knock-knees
Pelvic
deformities

29. Thikening and enlargment of the wrist and ankle
Distal Tibial bowing

30. Pelvic deformities
Bowlegs and
knock-knees

31. Clinical signs
• Increased tendency toward
bone fractures. Because the
softened long bones may
bend, they may fracture
one side of the cortex
(greenstick fracture).
• In the long bones, laying
down of uncalcified osteoid
at the metaphases leads to
spreading of those areas,
producing knobby
deformity (cupping and
flaring of the metaphyses).

32. •Extraskeletal manifsetation
Progressive weakness
•Decreased muscle tone (loss of muscle strength)
•Delayed of motor development (( in rickets
developing in infancy
•Protuberant abdomen ( due to hypotonia of
skeletal muscle of abdomen
•Fever or restlessness, especially at night
•Muscle cramps
•
Clinical signs

34. investigation
• Biochemical findings
Calciumdecrease or normal due to
compensatory mechanism
*Phosphatedecreas
*Alkaline phosphataseincrease
*Serum parathyroid hormone typically is ↑in
hypocalcemic rickets, in contrast it is N in
hypophosphatemic rickets

35. Decreases
in serum calcium,
serum phosphorus,
calcidiol, calcitriol,
urinary calcium.
The most common laboratory findings in
nutritional rickets are:
Parathyroid hormone,
alkaline phosphatase,
urinary phosphorus
levels are elevated.

36. • Classic radiographic findings include:
widening of the distal epyphysis, fraying
and widening of the metaphysis, and
angular deformities of the arm and leg
bones.

37. Classic radiographic findings include
Anteroposterior and lateral radiographs of the wrist of an 8-year-
old boy with rickets demonstrates cupping and fraying of the
metaphyseal region

38. • Classic radiographic findings include:
Radiographs of the knee of a 3-year-old girl with hypophosphatemia
depict severe fraying of the metaphysis.

39. Radiographic image of wrist and
forearm showing pathologic
fractures of radius and ulna with
rachitic changes of distal end of
radius and ulna.

40. X-ray in rickets

42. Prevention
**Sun exposure (5_10 min per day)
**Eat food high in vitamin D
fish, , milk and egg,.
**Take supplements of vitamin D and
calcium.
Sun exposureSun exposure

43. Treatment:-
**Vitamine D daily 50-150
mg(calciferol 2000-6000 I.U
per day ) after healing reduce
dose to400 iu per day
**Adequate dietary
Calcium & phosphorus
provided by milk, formula &
other dairy products.
Sun exposure .

44. 1. Exposure to sunlight.
2. Daily enough taken vitamin D &
Calcium.
3. Good exposure and vitamin D taken for
mothers

45. develop signs of rickets.