This document discusses osteomalacia and osteodystrophy in animals. Osteomalacia is a disease affecting bone in adults where bone formation is incomplete, leading to weak and fractured bones. It is caused by calcium, phosphorus or vitamin D deficiencies. Osteodystrophy is abnormal soft tissue bone formation causing weak, distorted and enlarged bones. It is caused by nutritional imbalances or deficiencies, especially too high a calcium to phosphorus ratio, and can lead to lameness and fractures. Diagnosis involves history, symptoms, and lab/radiographic testing, while treatment focuses on correcting nutritional deficiencies.

1. Osteomalacia
Karima Al salihi

2. Definition
•It is a disease of adult animals affecting bone
in which endochondral ossification completed.
It is characterized by osteoperosis and
formation of excessive uncalcified matrix
which lead to lameness and easily fracture.
•Causes
(1) Calcium, phosphorus and/or vitamin D
deficiency.
(2) Lactation and pregnancy are predisposing
causes.

3. Pathogenesis
(1) Osteomalacia occurs in adults under
the same conditions of rickets and is
mainly confined to the diaphyses of bone.
(2) It is formed during the normal process of rebuilding the
bone. Osteoid tissue under the periosteum (especially at the
site of ligament and tendon attachment and in the Haversian
systems) gradually replaces the calcified tissues causing
weakness of the bones which break or become deformed and
uncalcified callus is unable to support weight.
(3) It mainly occurs in cattle area deficient in ph or in feedlot
animals take more ph with low Ca and vitamin D.

4. (4) Pathogenesis occurs by:
1) Increase resorption of bone mineral to
supply the needs of pregnancy, lactation
and endogenous metabolism leads to
osteoporosis, weakness and deformity of
bone.
2) Large amount of uncalcified osteoid
tissue are deposited in the diaphysis.

6. Symptoms
!In the early stages (The main
cause is ph deficiency):
(1) Lower productivity and
infertility.
(2) Loss of condition.
(3) Licking and chewing of foreign
object & pica.

7. !In the late stage:
(1) Stiff gait, moderate lameness and shifting
from leg to leg due to painful condition of the
bone and joints.
(2) Arched back.
(3) Crackling sound during walking.
(4) Bone deformity leads to fracture of bone
and separation of tendon. Dystocia may occur
in deformity of pelvis.
(5) Finally weakness lead to disinclination to
move, permanent recumbence and death from
starvation.

8. •Diagnosis
(1) Case history and
symptoms.
(2) Laboratory examination:
Increase serum alkaline
phosphatase and decrease
phosphorus level.
(3) Radiographic examination.

9. Treatment
(1) Calcium therapy: Ca gluconate 500 ml IV
& SC in cattle.
(2) Phosphorus therapy: Tonophosphan
25-30cc IV or IM in cattle or sodium dibasic
phosphate 100-200 ml of 20% solution SC.
(3) Vitamin D3 therapy.
(4) Mineral mixture: 50g /daily/ cattle.
(5) Bone meal (100 g) and bran daily in the
ration.
NB: In severe deformity treatment is of no
value.

10. Osteodystrophy
(Osteodystrophy
Fibroses)
Definition
•It is an abnormal soft cellular
fibrous tissue formation of
bones. It includes weakness,
distortion & enlargement of
bones, susceptibility of bone
to fracture & interference with
gait & posture.

11. Occurrence
•It occurs mainly in horses at
any age specially after
weaning 2-7 years. The
disease may occur within 5
months.

12. Etiology
(1) Nutritional causes
A. Imbalance of Ca: ph ratio in diet 1: 2.9 or greater.
B. Calcium deficiency due to very low calcium intake.
C. Prolonged feeding of diet high in calcium.
D. Excess ph feeding lead to secondary Ca deficiency (such as cereal
hays combined with heavy grain or bran feeding).
E. Continuous ingestion of oxalate in specific grasses with normal
dietary intake of calcium & phosphorous.
F. Disease of parathyroid gland (adenoma).
G. Deficiency in dietary protein, copper, vitamin A & or multivitamin,
multi- mineral deficiency
H. Hypervitaminosis A

13. (2) Chemical agents: Chronic
lead or fluorine poisoning.
(3) Congenital causes;
Chondrodystrophy in dwarf
calves; exostosis in horse;
angular deformities of joints of
long bones.
(4) Physical causes: as trauma.

14. Pathogenesis
(1) Weakness of bones and a fibrous dysplasia occurs
around the affected bone in response to:
A. Defective in mineralization of bones follows the
imbalance of Ca and ph in the diet and a fibrous dysplasia
occurs.
B. Hyperparathyroidism stimulated by the excessive
intake of ph.
(2) Weakness of bone lead to fractures and separation of
muscle and tendinous attachment.
(3) Articular erosions occur commonly and displacement of
bone marrow may cause the development of anemia.

15. Symptoms
(1) Shifting lameness (no physical deformity can be
found) occurs in early stage.
(2) Arching of the black
(3) Crackling of the joints due to relaxation and or
sprain of tendons and ligament.
(4) Lameness may occur due to articular erosions.
(5) Weakness of the bones
(6) In more advanced cases severe injuries
including fracture and distortion.
(7) Fracture & distortion in growing animals.
(8) Unexpected fractures in mature animals.

16. (9) Local swelling of the lower mandible and
facial bones which may lead to difficulty in
respiration and snoring.
(10) Flattening of the ribs, fractures and
detachment of ligaments.
(11) Obvious swelling of joints and curvature of
long bones.
(12) Pressure of spinal cord or nerves may
lead to paralysis.
(13) Severe emaciation and anemia.
(14) Chronic wasting & lameness in cow with
calcinosis

17. Diagnosis
(1) History and clinical signs
(2) Laboratory examination: Increase
serum level of alkaline phosphatase
and ph and decrease serum Ca level.
(3) Radiographic examination.

18. Treatment
(1) Correct Ca: ph imbalance in
ration.
(2) Cereal hay may supplement with
alfalfa or clover hay or finely ground
lime stone.