Rickets etiology, gross lesions, signs and symptoms, diagnosis vitamin D deficiency oestomalacia vs rickets

1. Rickets/ Oestomalacia
Urusha Ghimire
Roll no: 39
Sem 6th, HICAST

2. Rickets Vs Oestomalacia
• Rickets is a disease of growing children that affects how the
growth plates of bones develop. Rickets can cause bowing of
the legs and bone pain. It can also increase a child’s risk of
fracture (broken bone).
• Osteomalacia affects both children and adults and is a
disease in which the bones don’t contain enough bone
mineral (mostly calcium and phosphate). Like rickets,
osteomalacia can cause bone pain and increase the risk of
fracture.
• These two conditions are closely linked – usually a child
with rickets will also have osteomalacia.

3. Definition
• Rickets is a disorder affecting the
skeleton of growing animals.
• Osteomalacia refers to a marked
softening of bones. The softened bones
of children and young adults with
osteomalacia can lead to bowing during
growth, especially in weight-bearing
bones of the legs. Osteomalacia in older
adults can lead to fractures

4. Etiology
•Primary causes are insufficient dietary phosphorus or calcium, an inappropriate
ratio between these minerals in the diet, or insufficient amount of activated vitamin
D.
•Kidney and renal dysfunction
•Some medical conditions, such as celiac disease, can affect how a child’s gut
absorbs vitamin D from food.

5. Gross Pathology
• The main gross lesions were
marked retardation of body
growth, enlargement of the
ends of the long bones,
hypertrophy of the bones,
widening of the epiphyseal
plate, thickening of the cortical
bone, softening of the bone,
and enlargement of the
parathyroid gland.

6. Histopathology
Typical microscopic lesions associated
with rickets are impaired endochondral
ossification, which are most prominent in
fast-growing bones. Growth plates are
widened and irregular, and joints appear
enlarged. Trabecula of the spongiosa are
thinner, predisposing to infarctions and
hemorrhage. Growth plates appear
widened and irregular.
Microscopic view of trabecular bone from swine with ricket
Haversian systems are filled with pale pink, unmineralized osteoid
[HE; 100x].
Parietal pleural surface, increased volume of costochondral joints
(arrow)

7. Clinical Findings and Lesions
The characteristic lesions of rickets are failure of both
vascular invasion and mineralization in the area of
calcification of the physes. This pathology is most obvious in
the metaphysis of the long bones. The predominant clinical signs
are posterior lameness, and ataxia.
There may be a wide variety of clinical signs, including:
•bone pain
•stiff gait
•swelling in the area of the metaphysis
•difficulty in rising
•bowed limbs
•pathologic fractures

8. Swine kept in confined housing are
susceptible to rickets because of their rapid
growth rate combined with lack of exposure
to sunlight.
In ruminants, deficiency of vitamin D is due
to a lack of exposure to sunlight and to a
lesser extent dietary phosphorus deficiency.
In Corriedale sheep, a gene defect
associated with enhanced degradation of
activated vitamin D has been reported.
Inherit Rickets in Sheep

9. Diagnosis
• Checking for the abnormalities
• Blood and Urine test for mineral and vitamin D levels,
• radiographs of long bones and bone biopsies
• X-rays