Canine Juvenile Bone Disease Flashcards
Congenital issues
Apparent at or soon after birth
Uncommon
Ex - radial agenesis
Developmental issues
Apparent during growth
Common
Elbow or hip dysplasia, OCD
Idiopathic issues
During growth
Fast growing large breeds
Uncommon-common
Panosteitis, HOD
Infectious issues
Any age
Uncommon
Septic arthritis, osteomyelitis
Traumatic issues
Any age
Common
Fractures
Nutritional/metabolic issues
Any age, susceptible during growth
Uncommon w commercial diets
2nd hyperPT, hypovitaminosis D
Neoplastic issues
Any age
Cancer can peak under 1 year and then in old age
Osteosarcoma
OCD
Osteochondritis dissecans, Failure of endochondral ossification
Osteochondrosis: thickening of cartilage
Non-clinical in SA
Osteochondritis dissecans: clinical form of disease, flap formation
Normal progress of epiphysis
Outlayer becomes articular cartilage
Inner later becomes the epiphyseal ossification center
- undergoes endochondral ossification
- responsible for epiphyseal enlargement
- proliferation of chondrocytes near periphery = growth
- conversion of cartilage to bone in center = calcification
Progress of OCD
Failure of ossification =
Cartilage thickens (drosis), loss of deep chondrocytes forms a cleft, causes a flap, flap can fall off = Dritis dissecans
Can lead to exposure of subchondral bone = jt inflame, DJD
Common locations for OCD
Shoulder - caudal humeral head
Elbow - medial portion of condyle
Stifle - lateral > medial condyle
Tarsus - medial > lateral trochlear ridge
Risk factors for OCD
Fast growing dogs
4-8 months
Male>female
10-45% heritable, large/giant breeds
Nutrient excess, micro trauma
Presentation of OCD
4-8m old or later
Gradual onset, v rest, ^ exercise
Unilateral or bilateral
Joint effusion & pain on manipulation
Diagnosing OCD
Radiographs
- distraction of subchondral bone
- flattening or convacity of normal contour
- sclerosis in margins
Contract arthrogram, ultrasound, CT, MRI
Conservative management of OCD
NSAIDS, exercise v, diet changes, weight control
Surgery treatment for OCD
Best options
Flap removal: open or arthroscopic
Debride all poorly attached cartilage, edges 90*, debride to bleeding subchondral bone
Osteochondral grafts & synthetic cartilage for OCD
Grafts : OATS system, transfer cartilage from a non articular area
Synthetic : synACART, synthetic cartilage plug, no donor site morbidity
Prognosis for joints w OCD
Shoulder - good/excellent
Elbow - guarded/fair
Stifle - guarded/fair
Tarsus - guarded
Will ultimately develop arthritis
HOD
Hypertrophic osteodystrophy
Metaphyseal pain, swelling, hyperthermia
signalment for HOD
Males>females
2-6 months
Rapidly growing, large/giant breeds (retrievers, GS, Weimaraner, Irish setters, boxers)
Causes for HOD
Unknown
Could be heritable
Infection, nutritional, k9 distemper
Effected bones & histo findings for HOD
Radius, ulna, tibia > all other bones
Disrupted metaphyseal trabeculae
- hemorrhage, hemosinderin deposits, necrosis, inflame, fibrosis adjacent & parallel to physis)
Irregular physis, subperiosteal hemorrhange/reactive bone
Presentation of HOD
Swelling of metaphyseal regions of long bone
Variable degrees of pain, lameness, inflammation
Also systemic illness
- hyperthermia, hyporexia, anorexia, depression, diarrhea
Diagnosing HOD
Radiographs
- lucent line at metaphyseal “double physis” appearance
Periosteal /endosteal prolif, widening of physis
Blood culture - immunocompromised
HOP vs HOD
HOD - swelling near metaphyseal, lesion near physis
HOP - diffuse periosteal prolif condition secondary to distant neoplastic or infectious masses
Treatments for HOD
Pain meds, diet
Systemic support - IV meds/fluids, nutrition, antibiotics
Prognosis for HOD
Selflimiting, 7-10 days
Mild = good prognosis
Severe + systemic = guarded
Recurrent, could lead to angular limb deformity - bridging physis, slowing physis growth on one side but bone grows on the other /hypertrophy
Panoestitis
Self limiting inflammation disease of bone marrow in long bones
Signalment of panosteitis
Large/giant breeds
5-18 months
Males>females, 4:1 ratio
Presentation of panosteitis
Acute onset, no trauma, shifting leg lameness, variable degrees of lameness, systemic illness is uncommon, painful on bone palpation
Commonly affected bones - panosteitis
Ulna, radius, humerus, femur, tibia
Forelimbs > hind limbs
Histology for panosteitis
Early stages - empty space near adipose BM, vascular prolif, local bone formulation around nutrient foramen
- vascular congestion & ^ interosseous pressure
- ^ local bone, 2* periosteal reaction, enlarged haversian system
- remodeling over time
Diagnosing panosteitis
Early stages - difficult to observe
Hall mark = intramedullary increase in radio density
- loss of Normal trabecular pattern
- changes in endosteum
Treating panosteitis
Can spontaneously resolve
Exercise restriction, analgesics, diet
Prognosis of panosteitis
Mild = good
Can reoccur
PCLS
Puppy carpal laxity syndrome
PCLS features
Young puppies, 6-16 weeks
Hyperextension > 190
Hypoextension < 180
Genetics, environment, stress
Conservative treatment for PCLS
Excellent prog!
Exercise restriction, splinting (2 wks), adult diet (helps soft tissue form properly)
Surgical treatment for PCLS
Rare, common in older dogs who were untreated as puppies & require tenotomy or Arthrodesis
