Osteomalacia, also known as adult rickets, is a metabolic bone disease characterized by inadequate mineralization caused by vitamin D deficiency, leading to softening of bones, pain, and fractures. Key factors contributing to the disease include poor diet, lack of sunlight, and various medical conditions affecting calcium and phosphate metabolism. Management involves dietary modifications, vitamin D supplementation, and potentially surgical interventions for orthopedic deformities.

1. 0STEOMALACIA
Ms.Shanmugapriya.S
Bsc.,Nursing

3. X ray
.

4. Introduction
 Osteomalacia also known as adult rickets,is
a disease in the bone becomes abnormally soft
because of a disturbed calcium and phosphorus
balance secondary to vit-D deficiency,resulting
in marked deformities of the weightbearing
bones and pathologic fractures.

5. Definition
 Osteomalacia is a metabolic bone disease
characterised by inadequate mineralisation of
bone.As a result the skeleton softens and
weakens,causing pain,tenderness to
touch,bowing of bones and pathologic fractures.

6. Etiological factors
 VITAMIN D DEFICIENCY:
 classical-lack of sunlight exposure
 poor diet
 gastrointestinal diseases
 FAILURE OF 125 VITAMIN D SYNTHESIS
 chronic renal failure
 vitamin d resistant rickets type 1

7. # VITAMIN D RECEPTOR DEFECTS:
* Vitamin D resistant rickets type 1
# DEFECTS IN PHOSPATE AND PYROPHOSPHATE
METABOLISM:
* Hypophosphatemoic rickets
* Autosomal recessive phospatemic rickets
* Autosomal dominant phosphatemic rickets
* Tumor induced hypophosphatemic
osteomalacia
# IATROGENIC AND OTHER CAUSES:
* Biphosphonate therapy
* Aluminium
* Floride

8. Due to etiological factors
such as,
Renal failure GI disorders Deficiency in
vitamin D
Acidosis
Poor
absorption of
fat and fat
soluble
vitamins
To maintain
homeostasi
s, body
uses serum
calcium and
activates ph

9. Ph stimulates the
release of skeletal
calcium
Poor absoption
of calcium in
intestine
Increased
excretion of
calcium in
faeces
Increased
excretion of
phosphate in
urine
Decreased
calcium level

10. Demineralisation of
bone
Bony fibrosis and
bone cyst
formation

11. Clinical manifestation
 Bone pain
 Tenderness
 Muscle weakness from calcium deficiency
 Waddling or limping gait
 Pathological fractures
 Softened vertebrae become
compressed,shortening patient’s trunk and
deforming thorax

12.  Weakness and unsteadyness,presenting risk of
falls and fractures
 Craniotabes
 Bossing of frontal and parietal bones
 Delayed anterior frontal closure
 Enlargement of epiphysis

13. Assesment and diagnostic findings
 X ray studies
 Study of vertebrae may show a compression
fracture with indistinct vertebral end plates
 Laboratory studies show low calcium level and
phosphorus level and a moderately elevated
ALP
 Urine excretion of calcium and creatinine is low

14.  Bone biopsy demonstrates an increased
amount of osteiod,a demineralised,cartilagious
bone matrix that is sometimes refered to as
prebone
 Routine biochemical screen with measurement
of serum 25(OH)D levels are low or
undetectable and PTH is elevated.
 Radiographic osteopnea is common and the
presence of vertebral crush fractures may
cause confusion with osteoporosis.

15. Medical management
 Dietary modifications(eg.vitamin D and calcium
supplementsetc.,)
 Exposure to sunlight may be recommended
 Diet with adequate calcium and protein is
necessary
 Long term monitering is undertaken to ensure
stabilization or reversal

16. Surgical management
 Orthopedic deformities may be treated with
braces or surgery-osteotomy

17. Nursing management
 Vitamin D administered daily until signs of
healing takes place
 Adequate intake of calciom and phosporusas
well as protein should be ensured
 Supplemental calcium in the form of lactate or
gluconate is administered
 Administration of 2000-10000IU of vit-d
cholecalciferol by orally.