Rickets and osteomalacia

Rickets and osteomalacia by Dr. Bipul Borthakur

1. Rickets and Osteomalacia
By
Dr. Bipul Borthakur
Professor
Dept of Orthopaedics, SMCH

2. Syndromes of diverse etiology
Failure of normal
mineralization of bone and
epiphysealcartilage.
Rickets, the more obvious of
the two syndromes, occurs in
growing children and both
bone and epiphysealcartilage
are affected.

3. Osteomalaciaoccurs in
individuals in whom growth in
height has ceased
Regardless of specific
etiology, the rachitic
syndromes present a high
degree of stereotypy

4. ¬ Rickets and osteomalaciaare
an abnormality resulting in
lack of mineralization of the
bone due to deficiency of vit.
D.
¬ Diseases where the organic
matrix of the bone fails to
calcify

5. The manifestations of the two
diseases are different only with
respect to the stage in life at
which they occur
¬ Both are primarily due to
deficiency of VitD or a
disturbance in its metabolism

6. Rickets
Disease of growing skeleton
Failure of normal mineralisation
of bone seen prominently at the
Growth plates
Results in softening of bones and
development of deformities

7. Vit. D metabolism
Sunlight skin7 dehydrocholesterol to
cholecalciferol liverhydroxylation by
enzyme 25 hydroxylase 25 hydroxy
cholecalciferol kidneyhydroxylation
by enzyme 1 alpha hydroxylase
1,25 dihydroxycholecalciferol,
calcitriol ( active form)
24 hydroxylase 24,25
hydroxycholecalciferol (non active
form)

8. Minimum Daily Requirements for Calcium,
Phosphate and Vitamin D
Adults Children
Calcium 400-500 mg 400 to 700
mg
Phosphate 1000-1500 mg 1000-1500
mg
Vitamin D 1.5-10 mg 10 mg
(100-400 I.U.) (400 I.U.)

9. Etiologyand Nature of rickets
Nutritional : dietary
deficiency of vit. D,
calcium, phosphorus or
intestinal malabsorption
Lack of exposure to
sunlight

10. Genetic causes:
Type 1: deficiency of 1 alpha
hydroxylasein kidneys
Type 2 : receptor is abnormal
resulting in resistance

11. Chronic renal or liver
failure, renal
osteodystrophy,
cirrhosis
Others like oncogenic,
drug induced

12. Etiological Classification of Rickets
and Osteomalacia
I. Deficiency Rickets and
Osteomalacia
A. Vitamin D deficiency
B. Calcium deficiency
C. Phosphorus deficiency
D. Chelatorsin diet

13. II. Absorptive Rickets &
Osteomalacia
Gastric abnormalities
Biliarydisease
Enteric absorptive defects

14. III. Renal Tubular Rickets &
Osteomalacia
Proximal tubular lesions
Proximal and distal tubular lesions
Distal tubular lesions (renal tubular
acidosis)
–Primary.
–Secondary.
IV. Renal Osteodystrophy

15. V. Unusual Forms of Rickets &
Osteomalacia
A. Rickets with fibrous dysplasia
B. Rickets with neurofibromatosis
C. Rickets associated with soft-tissue
and bone neoplasm
D. Rickets due to anticonvulsant
medication
E. Hypophosphatasia.

16. Clinical features
General
¬ irritable child
¬ lethargy
¬ pot belly
¬ delayed milestone
¬ stunted growth

17. Craniotabes
Bossing of skull
Harrison’s sulcus
Pigeon chest
Rachitic rosary

19. Rachaticrosary

20. Harrison sulcus

21. Pectuscarinatum

22. Widening of physis
Kyphoscoliosis
Muscular hypotonia
Deformities
Pathological fractures

23. Investigations
Serum calcium is usually
normal or low
Serum phosphate is low
Serum alkaline
phosphataseis high

24. Radiological signs
¬ early radiological changes are
observed in lower ends of the
radius and ulna
¬ delayed appearance of epiphysis
¬ widening of the epiphyseal
plates

25. Cupping of the
metaphysis
Splaying of the
metaphysis
Rarefaction of
the diaphyseal
cortex
Bone deformities
¬ knock knees
¬ bow legs
¬ coxavara

28. Treatment
Medical
Nutritional rickets
*adequate exposure to sunlight
*dietary supplement of vit. D
*Vit D : ¬ 6 lacs units as a single oral dose
¬ if line of healing does not appear on X
rays by 3-4 wks then same dose may be
repeated
¬ if no response is seen after 2
nd
dose a
diagnosis of refractory rickets is made
¬if there is response then maintenance
dose of 400 I.U is given

29. Orthopaedic treatment
Conservative methods
¬ mild deformities correct
spontaneously when ricketheals
¬ splints can be used to correct
deformities
e.gMermaid splint, orthopaedic
shoes

30. Operative methods (Corrective
Osteotomy)
¬ moderate or severe deformities
often require surgery
¬ can be performed any time
after 6 months of starting the
medical treatment

31. Adult counterpart of rickets
Primarily due to deficiency of Vit. D
Results in failure to replace the
turnover of calcium and phosphorus
in the organic bone matrix
Bone content is demineralised and
the bony substance is replaced by
soft osteoidtissue
Osteomalacia

32. Etiology
Common in people with lack of
exposure to sunlight ( purdah
system in females)
Dietary deficiency of VitD
Undernutritionduring pregnancy
Malabsorptionsyndrome
After partial gastrectomy

33. Clinical features
In early stages signs and
symptoms are non-specific and
often missed
Bone pain
Muscular weakness
Spontaneous fractures usually in
spine leading to kyphosis

34. Investigations
Radiological features
¬ Diffuse rarefaction of
bones
¬ Looser’szone (
pseudo fractures )
¬ Triradiatepelvis in
females
¬ Protrusio-acetabuli

35. Triradiatepelvis

37. Serum
¬ serum calcium is low
¬ serum phosphate is
low
¬ alkaline phosphatase
is high

38. Bone biopsy
¬ diagnostic
¬ from iliac crest
¬ characteristic finding is
excessive uncalcified
osteoid

39. Treatment
Vitamin D supplementation in
case of defective intake
In patients with renal disease
Alfa-calcidiolmay be used
Calcium supplementation should
also be given
Treatment of the underlying
cause

40. THANK YOU