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Developmental Ortho Diseases - Coggle Diagram
Developmental Ortho Diseases
Hypertrophic Osteodystrophy - HOD
Metaphyseal osteopathy
Rapidly growing large and giant breed dogs
No known sex predilection
Trend to occur more in males
Higher incidence in: (odds ratios)
Great Dane = 190
Weimaraner = 21
Boxer = 18
Irish setters = 14
German shepherds = 10
Golden/Labrador retriever = 5/6
Possible etiologies
Vitamin C deficiency
inability to utilize vitamin C
inconsistent response to vitamin C therapy
Infections
canine distemper virus
CDV particles found in lesions
but no HOD in puppies infected with CDV (Koch’s postulate)
E. coli
Vitamin or mineral oversupplementation
Genetics
rapid growth
Weimaraners – multiple littermates affected
Proposed pathogenesis
Disturbance in metaphyseal blood supply
delay or failure in ossification of the hypertrophic zone
Zone elongates, extends into the metaphyseal trabeculae
See...
suppurative inflammation
hemorrhage
necrosis
fracture
extensive remodeling in the trabeculae
Trabecular fracture causes
lifting of the periosteum
new bone production
Signalment/signs
Onset
7 weeks - 8 months
Most 3 - 4 months
Orthopedic signs
Mild to severe lameness
Hot, painful, swollen, metaphyses of long bones
Episodic and bilaterally symmetrical
may involve..
ribs
mandible
scapula
metacarpals
Systemic signs
Fever
Anorexia
Depression
Weight loss
Hematology
Neutrophilia
Monocytosis
Mild anemia
Bacteremia - rare
Diagnosis
Changes can occur in days
Uneven radiolucent zones in the metaphysis
“double physeal line”
Metaphyseal lipping
Exostoses
Enostoses
Treatment
Supportive care
Activity restriction
Analgesia - NSAIDs vs corticosteroids (NEVER both)
Corticosteroids (0.75-1.5 mg/kg BID x 5 days)
effective when refractory to NSAID (recommended dosing)
More severe cases
Fluid therapy to maintain hydration
Enteral nutrition- proper diet (no supplements)
Vitamin C ??
Broad spectrum antibiotic if septic
Avoid pneumonia, cystitis, decubital ulcers
Death and skeletal deformities are rare
Prognosis
Good to excellent
Relapses may occur until skeletal maturity
Feeding recommendation
Avoid diet supplementation/top dressing
Monitor often - weekly from 3-6 months
Adjust food intake to maintain trim BCS
Change to adult food @ 1 year of age
Panosteitis
Spontaneous, self-limiting disease
Affects metaphyses and diaphyses
Large and giant breeds
Skeletally immature
AKA eosinophilic
panosteitis or enostosis
Signalment
5 -18 months old
males > females
Higher incidence in: (odds ratios)
Great Pyrenees = 5.3
Bassett hound, Mastiff, Shar pei = 3.5
Giant schnauzer = 3.4
German shepherds = 3.3
Bernese = 2.8
also Doberman, retrievers, St. Bernard
Etiology
Correlation of increased incidence and high calorie, protein-rich food
Excessive protein
osmotic effects
intraosseous edema
Clinical Signs
Acute shifting limb lameness
Intermittent fever, lethargy, anorexia
Affects ulna, radius, humerus, femur, tibia
Pain with direct pressure over diaphyseal bone
Recurrence is common up to 18 months
rarely in the same bone
pathogenesis
Endosteal osteoid/Ca deposits
Spreads proximally and distally
Vascular congestion stimulates
2°enostoses/exostoses and pain
Increased osteoblastic/fibroblastic activity
rad findings
Blurring of trabecular pattern
Medullary opacities are more delineated and begin to coalesce
Mild smooth periosteal reaction
Opacities, enostoses, exostoses
regress over time
Increased opacity in medullary canal around nutrient foramen
increased opacity of endosteum
treatment
Analgesia - NSAIDs
Rest/restricted activity
Supportive care
Prognosis
Excellent - self-limiting disease
Resolves at skeletal maturity (18-20 months)
Prolonged as it moves from bone to bone
Usually does not recur in same bone
Osteochondrosis (OC)
Disease of cartilage
Focal disturbance in endochondral ossification
Rapidly growing large and giant breeds
Only affected sites in dogs
Caudal aspect of the humeral head
Humeral trochlea
Lateral femoral condyle
Plantar aspect - medial trochlear ridge of the talus
Supported causes
Genetics
Polygenetic trait
breed dependent
Anatomy
Joint shape may lead to trauma to cartilage
Always in the same location
May cause dissecans from manifesta
Proposed pathogenesis
Clefts to articular surface leads to flap formation
Matrix and necrotic tissue exposed to synovial fluid
Inflammation results
Signalment
Large- and giant-breeds
Males > females
5-10 months of age
Bilateral disease (20 - 85%)
Breed prevalence differs by joint affected
clin signs
Usually gradual onset, but may be acute
Lameness worsens with exercise
Pain with palpation of affected joint
Joint effusion, stiffness, reduced ROM
Mild to moderate unilateral lameness
Diagnosis
Based on signalment, hx and PE findings
Confirmed with visualization of lesion
Radiography +/- contrast arthrogram
Ultrasound – user dependent
92% sens, 60% spec, 82.6% accuracy (shoulder)
MRI/CT
88.5% sens, 90% spec, 88.9% accuracy (shoulder)
96% sens, 88.9% spec, 94.4% accuracy (shoulder)
Arthroscopy – reference standard
Treatment
Conservative therapy
Rest
NSAIDs
+/- diet change
Surgical therapy if clinical signs persist
Remove flaps and/or joint mice
Trim edges
Expose bleeding subchondral bone
Blood clot/mesenchymal cells fill defect
matures to fibrocartilage over time
thoracic limbs
Shoulder
Remove flap - caudal medial
Check for joint mice
Caudal cul-de-sac
Biceps tendon
prognosis good to excellent
Younger dogs
Smaller lesions
Lameness resolves 7-60 days in > 90%
Mild OA long-term
Often bilateral
Elbow
Accuracy
Radiographs - 57%
CT - 87%
Remove flap - trochlea
Check for FCP too
Forage, microfracture, OATS
Prognosis - guarded
Dysplasia cannot be corrected
Moderate to severe OA despite treatment
pelvic limbs
Stifle
Male dogs ~ 75%
Lateral condyle – 96%
Lesions often very large
treatment
Forage or OATS
Prognosis - fair to guarded
OA long-term with large lesions
Bilateral 75%
Hock
Plantar aspect of medial – 79%
Lateral ridge
Lesions are larger
Rottweilers
Labradors
Younger dogs (8 vs 22 mo)
Skyline of talar ridges
Large lesions destabilize joint
Prognosis
correlates with size and location of lesion
Legg-Calvé-Perthes Disease
Prognosis
Dependent on
Age
Unilateral vs bilateral
Preoperative lesion size
Joint instability
Guarded to poor
Avascular necrosis of the femoral head
Toy and miniature breed dogs
Miniature pinscher (OR = 71.5)
Pug (OR = 65.6)
Yorkshire terrier (OR = 35.8)
West Highland white terrier (OR = 33.2)
Chihuahua (OR = 26.8)
Toy poodle (OR =22.6)
Age - 4-11 months
No sex predilection
Bilateral in 12-16% of cases
Etiology
Unknown
Possible form of osteochondrosis
Other possible causes
Infection
Trauma
Metabolic/hormonal imbalances
genetics - Inherited in Manchester terriers
disruption of blood supply to femoral head
Bone necrosis leads to cartilage collapse Clinical signs
CS
Hip pain
Crepitus in hip joints
Disuse muscle atrophy
Acute onset lameness (usually severe) in young small-breed dog
Diagnosis
Based on
Signalment
History
Physical exam findings
Radiographs
Early
Increased density epiphysis
Focal trabecular resorption
Late
Flattened femoral head
Collapse/thickening of neck
Neck fractures
DJD - very late
treatment
Lameness persists in 75%
Surgical
Femoral head and neck excision
good outcome (no pain/lameness) 84-100%
Does not depend on age or stage of disease
Total hip replacement ??
Conservative
Craniomandibular osteopathy (CMO)
Non-neoplastic bone proliferation
Affects flat bones of the skull (Lion’s jaw)
Uncommon
Breeds
Westies - autosomal recessive inheritance
Scotties and Cairn ± hereditary predisposition
Pathogenesis
Osteoclastic resorption of existing lamellar bone
Replaced by coarse, irregular woven bone
Primitive bone extends beyond normal periostealboundaries
Inflammatory cells invade the periphery of new bone
Mandible and petrous temporal area
Clinical Signs
Pain associated with opening the mouth
Lethargy
Anorexia
Fever
Temporal muscle atrophy
Weight loss
3-8 months old
Diagnosis
Bilaterally symmetrical periosteal lesions
Mandible and temporal bones
May affect TMJ
At skeletal maturity, lesions become static with smooth margins
treatment
Supportive care
Analgesia (NSAIDs)
Pharyngostomy tube, if necessary
Surgical debulking of bone mass
Resect condyloid process
Partial hemimandibulectomy
Self-limiting but prognosis usually good
Depends on degree of bony involvement
Complications and poorer prognosis if unable to open mouth
Hypertrophic Osteopathy - HO
Bilaterally symmetrical swelling of distal limbs
Secondary to pulmonary or urinary system lesions
Starts as soft tissue swelling
Progresses to diffuse periosteal reaction Clinical signs
Acute or gradual onset lameness all four limbs
Swelling starts in distal limbs, works proximally
Systemic signs associated with primary lesion
Radiographic findings
Bilaterally symmetrical, palisading periosteal reaction
Smooth/regular or rough/aggressive
Soft tissue swelling overlaying affected bone
Thoracic and abdominal radiographs/ultrasound to find primary lesion Treatment and Prognosis
Remove/treat primary lesion
Bone lesions regress within months
Prognosis dependant on primary lesion