This document discusses rickets, including its causes, signs and symptoms, diagnosis, and treatment. Rickets is caused by a lack of vitamin D, calcium, or phosphate, which can result from inadequate sunlight exposure, poor nutrition, liver or kidney diseases, and some medications. Clinical features include bone deformities, muscle weakness, and growth delays. Diagnosis involves physical exam, lab tests showing low calcium and vitamin D levels and high alkaline phosphatase, and x-rays revealing bone changes. Treatment focuses on high dose vitamin D supplementation in the short term, followed by lower lifelong doses, along with ensuring adequate calcium and phosphate intake.

1. By
Dr Akkad Rafiq

2. Bone Structure
 Three main functions of bone
 support,
 protection
 leverage
 Composition
 Type I collagen fibers,
 mineral component
 Other non-collagenous proteins
 Osteopontin
 osteonectin
 Osteocalcin
 alkaline phosphatases
 Bone morphogenetic protein

3. Bone Minerals
 Almost half the bone volume is mineral
matter
 mainly calcium and phosphate in the
form of crystalline hydroxyapatite
 ‘demineralization’ of bone occurs only by
resorption of the entire matrix

4. Bone Cells
 Osteoblasts - concerned with bone
formation and osteoclast activation
 Osteocytes -These cells can be
regarded as spent osteoblasts
 Osteoclasts- These cells are the
principal mediators of bone resorption

5. Bone structure
 The mature tissue is lamellar
bone, in which the collagen
fibres are arranged parallel to
each other to form multiple
layers with the osteocytes
lying between the lamellae.

6. Minerals of bone
 Calcium
 Magnesium
 Vit D
 Phosphorus
 Calcitonin

7. Osteoporosis
 clinical disorder characterized by an
abnormally low bone mass and effects
in bone structure, which renders the
bone fragile and at greater risk of
fracture in a person of that age, sex and
race.

8. Pathology:
• results from an unhealthy imbalance
between two normal activities of
bone: bone resorption and bone
formation.
• The combined processes of bone
resorption and bone formation allow
the healthy skeleton to be
maintained continually by the
removal of old bone and its
replacement with new bone.

9. Pathology
 the destruction of bone begins to
exceed the formation of bone; this
imbalance leads to a net loss of
bone, and the beginnings of
osteoporosis.

10. PRIMERY RISK FACTORS
 Caucasoid (white) or Asiatic ethnicity
 Family history of osteoporosis
 History of anorexia nervosa and/or
amenorrhoea
 Low peak bone mass in the third decade
 Early onset of menopause
 Unusually slim or emaciated build
 Early hysterectomy
 Nutritional insufficiency
 Chronic lack of exercise

11. Causes of secondary
osteoporosis
 Nutritional
 Malabsorption
 Malnutrition
 Scurvy
 Inflammatory disorders
 Rheumatoid disease
 Ankylosing spondylitis
 Tuberculosis
 Drug induced
 Corticosteroids
 Excessive alcohol
consumption
 Anticonvulsants
 Heparin
 Immunosuppressives
 Endocrine disorders
 Gonadal insufficiency
 Hyperparathyroidism
 Thyrotoxicosis
 Cushing’s disease
 Malignant disease
 Carcinomatosis
 Multiple myeloma
 Leukaemia
 Other
 Smoking
 Chronic obstructive
 pulmonary disease
 Osteogenesis imperfecta
 Chronic renal disease

12. Investigations
 X-ray findings are
generally insufficient
• cannot reliably
measure bone density
• useful to identify
spinal factures,
explains back pain,
height loss or
kyphosis.
• X-rays may detect
osteopenia only when
bone loss is > 30%.

13. Patient who had a severe fracture and a
moderate fracture in her spine. Three years
later a second xray revealed a new fracture.
These fractures were in the lower spine.
Radiographic Fracture Assessment

15. DEXA
Dual energy x-ray absorptiometry (DEXA)
• This is the most popular and accurate test to
date
• non-invasive
• involves no special preparation.
• Radiation exposure is minimal,
• Can be used to measure bone mineral density in
the spine, hip, wrist, or total body.
•expensive
•not portable.

16. Screening- Ultrasound Densitometry
inexpensive,
portable
no radiation
can be used only in peripheral
sites (eg, the heel),

17. Fracture Reduction
 Goal: prevent fracture, not just treat
BMD
 Osteoporosis treatment options
 Calcium and vitamin D
 Calcitonin
 Bisphosphonates
 Selective Estrogen Receptor Modulators
 Parathyroid Hormone

18. Osteoporosis Treatment: Calcium and Vit
D
 Calcium and Vit D supplementation shown
to decrease risk of hip fracture in older
adults
 1000 mg/day standard;
 1500 mg/day in postmenopausal
women/osteoporosis
 Vitamin D (25 and 1,25): 400 IU/Day

19. Osteoporosis Treatment:
Bisphosphonates
 Decrease bone resorption
 decrease hip and vertebral fractures
 Alendronate, risodronate PO
 IV: pamidronate, zolendronate
 Ibandronate : once/month
Calcetonin
 not as effective as Bisphosphonates
 200 IU nasally/day

20. Osteoporosis Treatment:
Selective Estrogen Receptor Modulators
 Raloxifene
 Decrease bone resorption like estrogen
 No increased risk cancer (decrease risk
breast cancer)

21. Osteoporosis Treatment:
PTH
 Teriparatide
 INTERMITTENT PTH: overall improvement
in bone density

22. Current Guidelines
 US Preventive Task Force
 Test Bone Mineral Density in all women over
age 65, younger postmenopausal women
with at least one risk factor, and
postmenopausal women with a history of
fracture
 Treat patients with T score <-2 and no risk
factors, T score <1.5 if any risk factors, and
anyone with prior vertebral/hip fracture

23. Rickets:
Etiology, pathogenesis, clinical
features, diagnostics, treatment and
prevention

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

25. Etiology
1. Lack of sunshine due to:
 1) Lack of outdoor activities
 2) Lack of ultraviolet light in fall and winter
 3) Too much cloud, dust, vapour and smoke

26. Etiology
2. Improper feeding:
1) Inadequate intake of Vitamin D
 Breast milk 0-10IU/100ml
 Cow’s milk 0.3-4IU/100ml
 Egg yolk 25IU/average yolk
 Herring 1500IU/100g
2) Improper Ca and P ratio

27. Etiology
3. Fast growth, increased requirement
(relative deficiency)
4. Diseases and drug:
 Liver diseases, renal diseases
 Gastrointestinal diseases
 Antiepileptic
 Glucocorticosteroid

28. The history in patients with rickets may
include the following:
 The infant's gestational age, diet and degree of
sunlight exposure should be noted.
 A detailed dietary history should include
specifics of vitamin D and calcium intake.
 A family history of short stature, orthopedic
abnormalities, poor dentition, alopecia, parental
consanguinity may signify inherited rickets.
Evaluation

29. Clinical signs
Rickets
 is a systematic disease with
skeletons involved most, but the
nervous system, muscular system
and other system are also involved.

30. • Skeletal
deformities
1. Bow legs
2. pigeon chest
3. Bumps" in the rib
cage
4. odd-shaped
skull;

31.  Generalized muscular hypotonia is observed in the
most patients with clinical signs of rickets.
Clinical signs
• If rickets occurs at a later age,
thickening of the skull
develops. This produces
frontal bossing and delays
the closure of the anterior
fontanelle.

32. Protruding forehead
asymmetrical or odd-shaped skull

33. Chest deformity
Funnel chest – pectus
excavatum
Pigeon chest

34. Clinical signs
 In the chest, knobby
deformities results in the
rachitic rosary along the
costochondral junctions.
Rib beading
(rachitic rosary)

35.  Bowlegs and
knock-knees.
Clinical signs

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

37. A teenage male with rickets.
Note deformities of legs (bow legs)
and compromised height.

38.  The ends of the long bones demonstrate that same
knobby thickening. At the ankle, palpation of the tibial
Clinical signs
malleolus gives
the impression
of a double
epiphysis
(Marfan sign).

40.  Pain in the bones of Arms, Legs, Spine, Pelvis.
 Dental deformities
 Delayed formation of teeth
 Defects in the structure of teeth
 Holes in the enamel
 Increased incidence of cavities in the teeth (dental
caries)
Clinical signs

41.  Progressive weakness
 Decreased muscle tone (loss of muscle
strength)
 Muscle cramps
 Impaired growth
 Short stature (adults less than 5 feet tall)
 Fever or restlessness, especially at night
Clinical signs

42. The entire skeletal
system must be
palpated to search for
tenderness and bony
abnormalities.
Rickets should be
suspected in older
bowlegged children and
in cases associated with
asymmetry, pain, or
progression in severity.
Physical examination

43. Gait disturbances and
neurologic abnormalities
(such as hyperreflexia) in
all children should be
sought.
muscle cramps,
numbness, paresthesias,
tetany and seizures.

44. 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.

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

46. 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

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

48. Rickets in wrist - uncalcified lower ends of bones
are porous, ragged, and saucer-shaped
(A) Rickets in 3 month old infant
(B) Healing after 28 days of
treatment
(C) After 41 days of
treatment
A
B C

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

50. X-ray in rickets

52. Clinical manifestation
Stages
 Early stage
 Usually begin at 3 months old
 Symptoms: mental psychiatric symptoms
 Irritability, sleepless, hidrosis
 Signs: occipital bald
 Laboratory findings: Serum Ca, P normal or
decreased slightly, AKP normal or elevated
slightly, 25(OH)D3 decreased
 Roentgen-graphic changes: normal or
slightly changed

53. Clinical manifestation
Advanced stage
 On the base of early rickets, osseous
changes become marked and motor
development becomes delayed.
1. Osseous changes:
1) Head: craniotabes, frontal bossing, boxlike
appearance of skull, delayed closure of
anterior fontanelle
2) Teeth: delayed dentition with abnormal order,
defects
3) Chest: rachitic rosary, Harrison’s groove,
pigeon chest, funnel-shaped chest, flaring of
ribs

54. Clinical manifestation
4) Spinal column: scoliosis, kyphosis, lordosis
5) Extremities: bowlegs, knock knee,
greenstick fracture
6) Rachitic dwarfism
2. Muscular system: potbelly, late in standing
and walking
3. Motor development: delayed
4. Other nervous and mental symptoms

55. Clinical manifestation
Laboratory findings:
 Serum Ca and P decreased
 Ca and P product decreased
 AKP elevated
Roentgen-graphic changes:
Wrist is the best site for watching the changes
Widening of the epiphyseal cartilage
Blurring of the cup-shape metaphyses of long bone

56.  I Mild form: small changes of nervous
system, changes of one part of the skeleton;
 II Moderate form: changes of all organs and
systems, changes of two parts of the
skeleton;
 III Severe form: damaging function of all
organs and systems, changes of three parts
of the skeleton;
Classification

57. Types of Rickets
Nutritional
Nutritional rickets results from inadequate
sunlight exposure or inadequate intake of
dietary vitamin D, calcium, or phosphorus.

58. Vitamin D dependent
 Vitamin D-dependent rickets, type I is secondary
to a defect in the gene that codes for the
production of renal 25(OH)D3-1-alpha-
hydroxylase.
 Vitamin D-dependent rickets, type II is a rare
autosomal disorder caused by mutations in the
vitamin D receptor. Type II does not respond to
vitamin D treatment; elevated levels of circulating
calcitriol differentiate this type from type I.

59. Vitamin D resistant
 Rickets refractory to vitamin D treatment may be
caused by the most common heritable form,
known as vitamin D-resistant rickets or familial
hypophosphatemic rickets.

60. Other Conditions That Can Cause Rickets
 Medications
 Antacids
 Anticonvulsants
 Corticosteroids
 Loop diuretics
 Malignancy
 Prematurity
 Diseases of organs associated with vitamin D and
calcium metabolism
 Kidney disease
 Liver and biliary tract disease
 Malabsorption syndromes
 Celiac disease
 Cystic fibrosis (rare)

61. Diagnosis
 Assessed according to the followings:
 1. History
 2. Physical examination
 3. Laboratory findings
 4. Roentgen-graphic changes

62. Treatment for rickets
 The replacement of Vitamin D may correct rickets
using these methods of
ultraviolet light and medicine.
4000 IU of oral vitamin D per day for one month.
 Parents are instructed to take their infants outdoors
for approximately 20 minutes per day with their faces
exposed.
 Foods that are good sources of vitamin D include
cod liver oil,
 egg yolks,
butter
oily fish.
Some foods, including milk and breakfast cereals, are also
fortified with synthetic vitamin D.

63. Treatment
1. Special therapy: Vitamin D therapy
 A. General method: Vitamin D 2000-4000 IU/day
for 2-4 weeks, then change to
preventive dosage – 400 IU.

64. TREATMENT
1 STAGE
 VITAMINE D – - 2000 IU 1 TIMEDAY 30 DAYS
2 STAGE
 VITAMINE D – - 3500 IU 1 TIMEDAY 40 DAYS
3 STAGE
 VITAMINE D – - 5000 IU 1 TIMEDAY 45 DAYS
Then profilactic dose – 500 iu till the end of the second
– third year of life

65.  Vitamin D
 Fat-soluble vitamin used to treat vitamin D
deficiency or for prophylaxis of deficiency.

Cholecalciferol (Delta-D)
 Vitamin D-3 1 mg provides 40000 IU vitamin D
activity

66. Treatment
4. Calcium supplementation: Dosage: 1-3
g/day
 only used for special cases, such as baby
fed mainly with cereal or infants under 3
months of age and those who have already
developed tetany.
5. Plastic therapy:
In children with bone deformities after 4
years old plastic surgery may be useful.

67. Prevention
Vitamin D supplements
 Because of human milk contains only a small amount
of vitamin D, the American Academy of Pediatrics
(AAP) recommends that all breast-fed infants receive
400 IU of oral vitamin D daily beginning during the
first two months of life and continuing until the daily
consumption of vitamin D-fortified formula or milk
is two to three glasses, or 500 mL.
 AAP also recommends that all children and
adolescents should receive 400 IU a day of vitamin D.

68. Prevention
Vitamin D supplementation:
In prematures, twins and weak babies,
give Vitamin D 800IU per day,
For term babies and infants the demand
of Vitamin D is 400IU per day,
For those babies who can’t maintain a
daily supplementation, inject
muscularly
Vitamin D3 100000-200000 IU.

69. Prevention
Calcium supplementation:
0.5-1gm/day, for premature, weak babies and babies fed mainly with
cereal
 Recommended daily intake of calcium is as follows:
 1 to 3 years of age. 500 mg (two servings of dairy products a day)
 4 to 8 years of age. 800 mg (two to three servings of dairy products a
day)
 9 to 18 years of age. 1,300 mg (four servings of dairy products a day)
 19 to 50 years of age. 1,000 mg a day (three servings of dairy products
a day)

70. Sources of Vitamin D
 Sunlight is the most important source
 Fish liver oil
 Fish & sea food (herring & salmon)
 Eggs
 Plants do not contain vitamin D3