Author, Donkey, Bureaucrats, Administrators
53,803
edits
Changes
Created page with "right|thumb|100px|<small><center>Rickets in dog (Image sourced from Bristol Biomed Image Archive with permission)</center></small> *Essentially the s..."
[[Image:Rickets in dog.jpg|right|thumb|100px|<small><center>Rickets in dog (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
*Essentially the same disease as osteomalacia
*Caused by Vitamin D and phosphorus deficiency
*In young animals
*Failure of:
**Mineralisation of osteoid at sites of membranous growth
**Cartilage vascularisation and mineralisation at sites of endochondral ossification
*Osteoid and catilage build up at those sites
*Histologically:
**Lines of hypertrophic cartilage cells are lenghtened and disorganised
**Ossification at metaphysis is poor
**Persisting osteoid and cartilage -> shaft modelling failure
**Thuckened physes due to normal chondrocyte proliferation but defective removal
*Ends of bones enlarge -> club-like thickening of metaphysis + compression of epiphysis
**Most affected:
***Proximal humerus
***Distal radius
***Ulna
***Ribs
****Enlargement of costochondral junction - called 'rachitic rosary'
*Weight bearing leads to:
**Thickening of the physis and
**Flaring of the excess matrix at the metaphysis
*Histological lesions heal whn diet corected
*Minor deformities correct but major deformities remain
*Occurs after weaning because:
**''In utero'' and in milk - adeqaute nutrients obtained at expense of dam
*In Foals
**Rare - long nursing period and relatively slow rate of growth
*In Calves and lambs
**When diet deficeint of phosphorus and poor exposure to sunlight
*In Puppies, Kittens and Piglets
**Rapid growth, weaned early -> fulminating rickets if poor exposure to sunlight and lack of vitamin D in diet
[[Category:Bones - Metabolic Pathology]]
*Essentially the same disease as osteomalacia
*Caused by Vitamin D and phosphorus deficiency
*In young animals
*Failure of:
**Mineralisation of osteoid at sites of membranous growth
**Cartilage vascularisation and mineralisation at sites of endochondral ossification
*Osteoid and catilage build up at those sites
*Histologically:
**Lines of hypertrophic cartilage cells are lenghtened and disorganised
**Ossification at metaphysis is poor
**Persisting osteoid and cartilage -> shaft modelling failure
**Thuckened physes due to normal chondrocyte proliferation but defective removal
*Ends of bones enlarge -> club-like thickening of metaphysis + compression of epiphysis
**Most affected:
***Proximal humerus
***Distal radius
***Ulna
***Ribs
****Enlargement of costochondral junction - called 'rachitic rosary'
*Weight bearing leads to:
**Thickening of the physis and
**Flaring of the excess matrix at the metaphysis
*Histological lesions heal whn diet corected
*Minor deformities correct but major deformities remain
*Occurs after weaning because:
**''In utero'' and in milk - adeqaute nutrients obtained at expense of dam
*In Foals
**Rare - long nursing period and relatively slow rate of growth
*In Calves and lambs
**When diet deficeint of phosphorus and poor exposure to sunlight
*In Puppies, Kittens and Piglets
**Rapid growth, weaned early -> fulminating rickets if poor exposure to sunlight and lack of vitamin D in diet
[[Category:Bones - Metabolic Pathology]]