OSTEOMALACIA

1. z
OSTEOMALACIA
BY:
Mrs.Keerthi Samuel,
Asst.Professor,
VMCON

2. Osteomalacia in children is
known as rickets, and
because of this, use of the
term "osteomalacia" is
often restricted to the
milder, adult form of the
disease. Signs and
symptoms can include
diffuse body pains, muscle
weakness, and fragility of
the bones
INTRODUCTION

3. z
BONE MINERALIZATION
VITAMIN D(METABOLISM)

4. z VITAMIN-D FUNCTIONS
•Intestinal Calcium absorption
•Interaction with PTH in
regulation of blood Calcium
Re-absorption of Calcium from
Kidneys
Mineralization of Bone

5. z
Osteomalacia is the softening of
the bones caused by defective bone
mineralization secondary to
inadequate levels of available
phosphate and calcium, or because
of overactive resorption of calcium
from the bone which can be caused
by hyperparathyroidism (which
causes hypercalcemia).
 Metabolic disease characterized by
inadequate and delayed mineralization
of osteoid in mature compact and
spongy bone.
DEFINITION

6. z
INCIDENCE
 The prevalence of Vitamin D
deficiency ranged from 40% to 99%, with
most of the studies reporting
a prevalence of 80%–90%. It was prevalent
in all the age groups and high-risk groups
alike.

7. z
ETIOLOGY
 Inadequate mineralization of
the bone.
 There are two main causes
of osteomalacia:
 Insufficient calcium
absorption from the
intestine because of
lack of dietary calcium or
a deficiency of, or
resistance to, the action
of vitamin D; and
 phosphate deficiency
caused by increased

8. z
ETIOLOGY –Contd..
Vitamin D deficiency. Sunlight produces
vitamin D in your skin. Dietary vitamin D
is usually from foods to which the vitamin
has been added, such as cow's milk.
People who live in areas where sunlight
is limited, get little exposure to sunlight or
eat a diet low in vitamin D can develop
osteomalacia. Vitamin D deficiency is the
most common cause of osteomalacia
worldwide.

9. z
ETIOLOGY –
Contd..
 Celiac disease. In this
autoimmune disorder, foods
containing gluten, a protein
found in wheat, barley and rye,
can damage the lining of your
small intestine. A damaged
intestinal lining doesn't absorb
nutrients well, and can lead to
vitamin D and calcium
deficiency.

10. z
ETIOLOGY –
Contd..
 chronic liver disease:
 hepatocellular: 25-
hydroxylation vitamin D
 biliary: abnormal gut
absorption
 malabsorption syndromes such
as Crohn's
 partial gastrectomy (self-
restriction of fatty foods)

11. z
ETIOLOGY –Contd..
 Administration of phenobarbital (alternate liver pathway)
 Decreased deposition of calcium in bone (high PTH)
 Diphosphonates-(Bisphosphonates are a group of
medicines that slow down or prevent bone loss,
strengthening bones)
 Other causes
 Tumour induced osteomalacia
 Cadmium poisoning like Itai-itai
disease (Cadmium poisoning can also cause softening
of the bones and kidney failure).

12. z
ETIOLOGY-contd
 Drugs:
 Phenytoin
 Phenobarbital
 Carbamazepine
 Acetazolamide
 Aluminium Compound
 Flouride

13. z PATHOPHYSIOLOGY-I
HYDROXAPETITE(mineral saltin the osteoid
matrix, which is a crystalline complex of calcium
and phosphate) is responsible for hardness of
the bone
Defeciency of hydroxypetite leads to softening of
bone

14. z
PATHOPHYSIOLOGY-II
Deficiency of Vit-d
hypocalcemia
Osteomalcia/rickets
Increase in bone resorption
Increased plasma calcium and
decreased phosporous
Increased PTH

15. z
CLINICAL MANIFESTATIONS
 Diffuse joint and bone pain
(especially of spine, pelvis, and legs)
 Muscle weakness
 Difficulty walking, waddling gait
 Hypocalcemia (positive Chvostek
sign)
 Compressed vertebrae and
diminished stature
 Pelvic flattening, Bending of bones
 Weak, soft bones, Easy fracturing

16. COMPRESSED
VERTEBRAE

17. z
CLINICAL MANIFESTATIONS
 Osteomalacia in adults starts insidiously as aches
and pains in the lumbar (lower back) region and
thighs before spreading to the arms and ribs. The
pain is symmetrical, non-radiating and accompanied
by sensitivity in the involved bones. Proximal
muscles are weak, and there is difficulty in climbing
up stairs and getting up from a squatting position.
 Physical signs include deformities like triradiate
pelvis and lordosis. The patient has a typical
"waddling" gait.

18. z
SIGNS AND SYMPTOMS
 However, these physical signs may derive from a
previous osteomalacial state, since bones do not
regain their original shape after they become
deformed.
 Pathologic fractures due to weight bearing may
develop. Most of the time, the only alleged symptom
is chronic fatigue, while bone aches are not
spontaneous but only revealed by pressure or
shocks.
 It differs from renal osteodystrophy, where the
latter shows hyperphosphatemia.

19. z CARDINAL SIGNS
Pseudofracture
s, also called
Looser’s Zones.
Codfish
vertebrae.
Protrusion
Acetabuli, a hip
joint disorder-
Triradiant pelvis

20. z
NORMAL PELVIS TRIRADIANT PELVIS
Protrusion of hip and
spine into soft pelvis and
protrusion with
protrusion of acetabuli

21. z
NORMAL NECK OF
THE FEMUR
PSEUDO FRACTURE OF NECK
OF THE FEMUR(Milkman's
Syndrome)
Lucent bands that occur
due to a build-up of
osteoid, the unmineralized
organic component of
one.

22. z
z
Codfish vertebra' refers to the biconcave
deformity of the vertebral body and is more
common than anterior vertebral wedging and
flat vertebra signs.
NORMAL VERTEBRAE COD FISH VERTEBRAE

23. z
z
RICKETS

24. z
DIAGNOSTIC FINDINGS
 Biochemical features are similar to those of
rickets. The major factor is an abnormally low
vitamin D concentration in blood serum.
 Major typical biochemical findings include:
 Low serum and urinary calcium
 Low serum phosphate, except in cases of
renal osteodystrophy

25. zDIAGNOSTIC FINDINGS
 Elevated serum alkaline phosphatase (due to an
increase in compensatory osteoblast activity)
 Elevated parathyroid hormone (due to low
calcium)
 Furthermore, a technetium bone scan will show
increased activity (also due to increased
osteoblasts).

26. z RADIOLOGY
 Diffuse demineralization: osteoporotic-like pattern
 may show a characteristic smudgy "erased" or "fuzzy"
type of demineralization
 coarsened trabeculae
 insufficiency fractures
 Pseudofractures (looser’s zone)
 articular manifestations (uncommon)
 rheumatoid arthritis-like picture
 osteogenic synovitis
 ankylosing spondylitis-like picture

29. z TREATMENT
 Nutritional osteomalacia responds well to
administration of 10,000 IU weekly of vitamin D
for four to six weeks.
 Osteomalacia due to malabsorption may require
treatment by injection or daily oral dosing of
significant amounts of vitamin D.
 Calcitriol supplement for CKD.

30. z
TREATMENT
Exercise
 Exercise helps to strengthen the bones, especially weight-
bearing exercise (anything that involves walking or running).
However, you should avoid intensive exercise while any
fractures or cracks in the bones are healing.
Sunlight
 Where possible, going outside and exposing your arms and
face to sunlight is the best way to get vitamin D. From June
to August just 15 minutes a day is generally enough. Don’t
allow your skin to go red and take care not to burn,
particularly in strong sunshine and if you have fair or
sensitive skin.

31. Diet and nutrition
 A diet that includes vitamin D and calcium can help,
but this won’t prevent the condition by itself.
Nevertheless, a diet that provides vitamin D is
especially important if you don’t get enough
exposure to sunlight.