different between rickets and osteomalacia

1. Rickets
&
Osteomalacia
Hamad Emad Dhuhayr

2. CONTENTS
1. SOEPEL
2. DEFINITION
3. EPIDEMIOLOGY
4. BASIC BACKGROUND
5. AETIOLOGY
6. RISK FACTORS
7. CLINICAL MANIFESTATIONS
8. INVESTIGATION
9. MANAGEMENT
10.REFERENCES

3. SUBJECT:
• S , a four year old girl is brought to the primary health centre for not being to
walk properly. On examination, there are skeletal deformities of both upper and
lower limbs with marked bowing General examination shows pallor, otherwise
there are no other signs.The abdomen is distended, otherwise systemic
examination is normal.
SOEPEL

4. OBJECTIVE:
taking history, physical examination ( musculoskeletal and neurological )
EVALUATION (DD):
Ricket
Hypophosphatamia
Metaphyseal dysostoses
Blount's syndrome
PLAN: History, physical examination, plain X-ray
ELABORATION: vit D
SOEPEL

5. LEARNING GOALS:
Rickets and Osteomalacia
SOEPEL

6. Normal Development
• calcium/ PO4
• Vit D
• PTH
• calcitonin
Bones….What do they need to be strong?

8. VIT D LEVEL IN SERUM -
• 25 (OH) D3 level ng/ml
DEFICIENT < 10
INSUFFICIENT 10 - 20
OPTIMAL 20 - 60
HIGH 60 - 90
TOXIC >90

9. PARATHYROID HORMONE
• Stimulus for its secretion : fall in serum Ca.
• PTH promotes bone resorption process and is adversely affected by calcitonin.
• PTH also stimulates the excretion of phosphates by the kidneys; this inhibition of phosphate resorption
in turn enables calcium resorption.
• In GIT - indirectly increases calcium absorption by increasing the synthesis of active vit D 3 by
stimulating alpha hydroxylase

10. CALCITONIN
• It is produced by para follicular c cells of thyroid.
• It is a calcium lowering hormone in serum by inhibiting bone resorption by decreasing the no &
activity of osteoclasts .
• So calcitonin acts counter to PTH. Calcitonin inhibits bone resorption thus causing serum calcium
levels to fall.

11. Metabolic bone diSeases

12. Metabolic bone diseases include:
•Rickets
•Osteomalacia
•osteoporosis

13. Rickets
• Disease of growing bones of children(in it epiphyseal plate
not closed )in which defective mineralization occurs in both
bone and cartilage of epiphyseal growth plate.
Osteomalacia
• Disorder of mature bones in adult (after epiphyseal plate
closure )in which mineralization of new osteoid bone is
inadequate or delayed

14. Types of Rickets
• (1)Vitamin D deficient rickets: there is decrease in vitamin D inside body.
• (2)Vitamin D dependent rickets: there is defect in the process of vitamen D
activation.
• (3)Vit D resistant rickets: either
-Hypophosphatemic rickets
• - End organ resistance to 1,25 Dihydroxy Vit D3

15. causes of rickets :
• 1- Nutritional deficiency: commonest cause in the developing countries also Excess of phytate in diet
which form insoluble compounds with calcium so prevent its absorption (chapati flour)
• 2-Malabsorption as in Celiac disease,Pancreatic insufficiency
• 3-Hepato-biliary disease
• Biliary Artesia
• Cirrhosis
• neonatal hepatitis
• 4-Drugs
• Anti-convulsants
• Phenobartbitone
• Phenytoin
5-Renal causes :
-Renal osteodystrophy
- Renal tubular acidosis.

16. pathogenesis ofVitamin D deficient rickets
• The predominant cause of rickets is a deficiency in vitamin D, which is
required for normal calcium absorption from the gut. Malabsorption leads
to low levels of calcium in the blood.This not only prevents proper bone
growth, but can also lead to calcium being released form the bones to
increase its blood level.

17. Hypophosphatemic rickets
• Nutritional phosphate deficiency
• Prematurity
• Decreased intestinal absorption of phosphate
• Ingestion of phosphate binders (aluminum hydroxide)
• Renal phosphate wasting

18. Rickets
Clinical feature
General
Failure to thrive
Apathetic , listless, irritable
Shorter, lower body weight and anemic
Excessive sweating particularly at hand & face

19. Rickets
Clinical feature
Head
• craniotabes(soft skull)
• frontal bossing
• Widening of suture,
persistent fontanelae
• Delayed dentition, caries

20. Rickets
Clinical feature
Chest
• Rachitic rosary
• Harrison groove
• Pigeon chest
• Respiratory infection and
atelectasis

21. Rickets
Characteristic feature
• Widening of wrist, knee and ankle due to physeal over
growth

22. Rickets
Characteristic feature
Abdomen
- prominent
muscle weakness (floppy baby, delayed walking)
Pelvis - narrow inlet

23. Rickets
Characteristic feature
Deformity
• Toddlers: Bowed legs
(genu verum)

24. Rickets
Characteristic feature
Deformity
• Older children: Knock-knees
(genu velgum)

25. Rickets
Characteristic feature
Deformity
• windswept knees
• CoxaVera
• String of pearls deformity

26. Rickets
Characteristic feature
• Thoracic kyphosis (rachitic cat – back)
• increased tendency for fracture, especially green stick #
• Growth disturbance
• Bone pain or tenderness
• Less common tetany, laryngeal, stridor and convulsion
• Sign of PEM

27. Rickets
Radiographic feature

28. Rickets
Radiographic feature

29. Rickets
Radiographic feature

30. Rickets
Radiographic feature

31. Rickets
Diagnosis
• History & physical examination finding
• Radiographic abnormality
• Special etiology confirmed with lab. test

32. Diagnosis of rickets
• A-Clinical features of rickets:
(1)Skeletal manifestations
(2) extraskeletal manifestations
• B-investigations

33. (1) Skeletal manifestations
• The earliest sign of rickets in infant is craniotabes (abnormal softness of skull)
• Delayed closure of anterior fontanel
• Frontal and parietal bossing :Rounded prominence of the frontal and parietal
bones in an infant’s cranial vault
• Delayed eruption of primary teeth
• Enamel defects and caries teeth.
• Rachitic rosary
• Swelling of the costo-chondral junction
• Harrison’s groove
• Lateral indentation of the chest wall at the site of attachment of diaphragm
because the patients lack the mineralized calcium in their bones necessary to
harden them; thus the diaphragm, which is always in tension, pulls the
softened bone inward.
• Enlargement of long bones around wrists and ankles
• Bow legs,
• knock knees
• green stick fractures
• Deformities of spine, pelvis and leg – rachitic dwarfism

34. (2)Extra – skeletal manifestations
• SEIZURES
• TETANY i.e periodic painful muscular spasms and tremors,
caused by faulty calcium metabolism and associated with
diminished function of the parathyroid glands.
• HYPOTONIA AND DELAYED MOTOR DEVELOPMENT
Muscle weakness
• PROTUBERANT ABDOMEN, BONE PAIN, WADDLING
GAIT AND FATIGUE.
In older children presenting with rickets

35. B - Investigations
• BASIC INVESTIGATIONSTO CONFIRM RICKETS
• SerumCa, P and X rays of ends of long bones at knees or wrists
• Hypocalcemia
If Serum Calcium less than 8.0 mg/dl
• Widening, fraying, cupping of the distal ends of shaft.
• Tetracycline-labelled bone biopsy. Gold stansar.

36. Difference Between Osteoporosis &
Osteomalacia
• Osteoporosis refers to the degeneration of already constructed bone,
making them brittle,
• while osteomalacia is an abnormality in the building process of bone,
making them soft.

37. Osteomalacia
Clinical feature
Insidious course
Pt may present with bone pain, back ache and bone tenderness
proximal muscle weakness
Fracture may be first sing of Osteomalacia
Vertebral collapse, kyphosis or knock knee perhaps due to
adolescent rickets- may increase in later life.

38. Osteomalacia
Clinical feature
Long standing case sign of secondary hyperparathyroidism
• Depression
• Polyuria
• Increased thirst
• Constipation
• Nephrolithiasis
• ?Peptic Ulcer Disease

39. Osteomalacia
X- ray
• Looser zone

40. Osteomalacia
• X- ray -Looser zone

41. Osteomalacia
X- ray
• lateral indentation of the
acetabulam (trefoil pelvis)
• Biconcave vertebrae

42. Osteomalacia
• Long standing case sign of secondary
hyperparathyroidism

43. Osteomalacia
• Long standing of Osteomalacia
Cortical erosion
Pathological #
Brown tumor

44. Osteomalacia
Deferential diagnosis
1. Osteomalacia osteoporosis
• Unwell well
• Generalized chronic ache pain after #
• Muscles weakness muscle normal
• Looser’s zone absent
• Ph3 decrease normal
• Alk. Ph3ase increase normal

45. Osteomalacia
Deferential diagnosis
2. Primary Hyperparathyroidism
Hypercalcaemia
hypophosphaetemia
Raised PTH & alkaline phosphatase
3. Myeloma
 Anemia
Increase ESR
Blood and urine electrophoresis raised of single Ig
Bence jones protein

46. Rickets & Osteomalacia
Treatment
• Depending on etiology, severity and metabolic abnormality
• In general the combination ofVit-D, Ca and phosphate
• Orthopedic measure require in very less no. of cases
1 mg of vit-D = 40,000 IU
1 IU = 0.025 microgram

47. Rickets & Osteomalacia
Target of therapy
low -N = Ca
N- = phosphate
high - N = alkaline
phosphatase
Over dosing side effect
ofVit – D prevented

48. Rickets & Osteomalacia
Treatment
1.Vit-D deficiency state
Vit –D 1,000 – 10,000 I.U./day4- 6 wk
Adherence is poor (stoss therapy)
Vit –D 300,000-600,000 IU
Im /Orally in a day (2-4dose)
Calcium --- 1g/ day
General nutrition , sunlight ?
Followed by
400 IU / day

49. Rickets & Osteomalacia
Treatment
2. Absorption defect
Vit- D 1,500 – 25,000 IU / day
Calcium 1 g/ day
Treatment of underling pathology; where appropriat, low fat
or gluten free diet

50. Rickets & Osteomalacia
Treatment
3.Vit – D resistant
Vit – D 20,000- 60,000 IU/day
Or dihydrotachysterol (dose 1/3 of vit D)
Neutral phosphate-1.5- 6 g/ day (4-5 dose)
Calcium – 1 g / day

51. Rickets & Osteomalacia
Treatment
4.Vit – Dependent type – I
1, 25Vit – D 250 IU – 800 IU /day
Calcium 1 g/day

52. Rickets & Osteomalacia
Treatment
5.Vit – Dependent type – II
Respond with high dose of
 1, 25 Vit – D
1,000- 20,000 IU /day for 3-6 mth
Calcium - - 1-3 g / day
i/v Ca with oral
supplement

53. Rickets & Osteomalacia
Treatment
6. Renal tubular
Vit- D 1,000 – 4,000 IU/ day
Alkalizing solution; K supplement