Lecture 27: Developmental Bone Disease (Exam 3) Flashcards

1
Q

What are some primarily inflammatory dev bone diseases & who are they seen in

A
  • Panosteitis
  • Hypertrophic osteodystrophy (HOD)
  • Appear during growth period of large & giant breeds
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2
Q

Define canine panosteitis

A

Disease of young dogs causing lameness, bone pain, endosteal bone production & occasional periosteal bone production (There is an infiltration of eosinophils)

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3
Q

Describe the pathophysiology of canine panosteitis

A
  • Etiology is unknown
  • Osseous compartment syndrome (more dominant etiology theory)
  • Disease of adipose bone marrow
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4
Q

What is osseous compartment syndrome

A
  • Animals one protein rich - high calorie diet (potential cause)
  • Excessive protein causes intraosseous edema -> increased medullary pressure & ischemia
  • Endosteal bone formed as marrow invaded by bone trabeculae
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5
Q

What is the common signalment of panosteitis

A
  • Male large breed dogs
  • young dogs < 2 Y
  • Older dogs occasionally dx
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6
Q

What is the common hx of px w/ panosteitis

A
  • Shifting leg lameness
  • Pain on deep bone palpation
  • May present as acute lameness on single limb or of chronic intermittent shifting leg lameness
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7
Q

What is seen on a PE if the px has panosteitis

A
  • Gait analysis (single or multi leg involvement)
  • Severity of lameness varies (wt-bearing lameness)
  • Pain on direct palpation of affected bone(s)
  • Seen in dogs after growth has ceased
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8
Q

Describe the use of radiographs for assessing panosteitis

A
  • Make dx w/ radiographs
  • Clinical signs may precede radiographic changes by up to 10 D
  • Repeat radiographs in 7 to 10 D
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9
Q

What are the radiographic findings for a px w/ panosteitis

A
  • Widening of Nutrient foramen
  • intramedullary radiocapicity (radiopaque patchy or mottled bone; blurring & accentuation of trabecular patterns)
  • Endosteal thickening
  • Periosteal new bone
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10
Q

What is this Xray showing

A

Intramedullary radiocapacity (cloudy)

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11
Q

How is panosteitis treated

A
  • Medical - only if it is self-limiting disease, NSAIDs, Exercise restriction when lame, warn owner that recurrences are common
  • Surgical treatment not indicated
  • Long-term prognosis is excellent for complete recovery
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12
Q

Define hypertrophic osteodystrophy (HOD)

A
  • Disease causing disruption of metaphyseal trabeculae
  • Usually in the long bones of young rapidly growing dogs
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13
Q

What is the etiology of HOD

A
  • Unknown
  • Thought to be due to vitamin C def
  • Viral causes suspected (usually w/ a hx of recent GI/resp prob, possible relationship to distemper virus, vax protocol assoc w/ dev of HOD, weimaraner pups & irish setters)
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14
Q

What is the pathophysiology of HOD

A
  • Disturbance of metaphyseal BS (Changes in physis and adjacent metaphyseal bone, delayed ossification of physeal hypertrophic zone, increased width of the hypertrophied chondrocyte zone of the physis)
  • No bone bormed on calcified cartilage, instead there is inflammatory infiltration of neutrophils & mononuclear cells
  • Osteoclastic resorption of recently formed metaphyseal trabecular bone
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15
Q

What is the common signalment of px w/ HOD

A
  • Young rapidly growing large breed
  • Male > females
  • Usually sx @ 3 to 4 M old
  • Seen early as 2 M old
  • Weimaraners @ increased risk
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16
Q

What is the common hx of px w/ HOD

A
  • Acute onset of lameness
  • May be severely affected (not able to walk)
  • Inappetence & lethargy
  • Hx of recent diarrhea may precede lameness
17
Q

What will be seen in the PE of a possible HOD

A
  • Mild to severe lameness of all 4 limbs
  • Long bone metastases swollen, warm, & painful on palpation
  • Swelling is often present in all 4 limbs
  • Swelling in forelimbs may be more obvious (in the distal radial metaphyses)
18
Q

What are the radiograph findings w/ HOD

A
  • Irregular radiolucent line on the metaphyseal side of physis (“double physis”)
  • Widening of the physis - as the disease progresses periosteal new bone formation may span active physis
  • Usually on multiple limbs
  • “second growth plate”
19
Q

Label A & B

A
  • A: active physis
  • B: osteolysis
20
Q

What is this showing

A

The progression of HOD

21
Q

What is the treatment of HOD

A
  • Self limiting so focus on supportive tx
  • Analgesics to control pain - NSAIDs +/- opioids
  • Severely affected animals - IV fluid support, corticosteroids, antibiotics, & vitamin C (should be considered & bacteremia needs to be ruled out before corticosteroids)
22
Q

What is the prognosis of a px w/ HOD

A
  • Most recover fully in 7 to 10 D (can have relapses)
  • Severe debilitation or multi severe relapses = consider euthanasia
23
Q

Describe Retained Ulnar cartilaginous core (AKA Retained endochondral cartilage core)

A
  • Cones of growth plate cartilage
  • Projects from distal ulnar growth plate into distal metaphysis
  • Consist of viable hypertrophic chondrocytes (retained hypertrophic chondrocytes = failure of growth plate cartilage to convert to metaphyseal bone)
24
Q

What is the clinical presentation of retained ulnar cartilaginous core

A
  • Large to giant immature canines
  • Growth plate manifestation of osteochondrosis (OC)
  • If assoc w/ reduced ulnar length growth there will be cranial bowing of radius, rotation & valgus deviation of forepaw, & subluxation of carpal & elbow joint (CARPAL VALGUS)
  • Forelimb deformities may be identical to premature closure of distal ulnar & radial growth plates
25
Q

How to dx retained ulnar cartilaginous core

A
  • Through radiographs
  • Determine cause of deformity
  • No correlation noted btw/ size of lesion, histopathology, & severity of forelimb deformity
26
Q

What will be seen on radiographs of a px w/ retained ulnar cartilaginous core

A
  • Radiolucent core (triangle) of cartilage in distal ulnar metaphysis +/- sclerotic zone
  • Core can extend 3 to 4 cm into metaphysis
27
Q

What is the tx of retained ulnar cartilaginous core

A
  • W/ no forelimb deformity = not tx
  • Moderate to marked forelimb deformities = surgical correction of deformity may be req, all px should be prescribed well balanced diet, & cores may disappear spont.
28
Q

What is Legg-Calve-Perthes Dx

A
  • Noninflammatory aseptic necrosis of femoral head
  • Found in young px before capital femoral physis closure
  • Synonyms - Avascular necrosis of femoral head
29
Q

What is the causes of Legg-Calve-Perthes Dx

A
  • Collapse of femoral epiphysis caused by interruption of blood flow
  • Etiology unknown
  • Autosomal recessive gene is the proposed genetic cause
30
Q

What is the pathophysiology of Legg-Calve-Perthes Dx

A
  • Vascular supply to the femoral head in young animals & comes from the epiphyseal vessels the metaphyseal vessels do not cross the physis to contribute to femoral head vascularity
  • Epiphyseal vessels course along the femoral neck surface, cross the growth plate, & penetrate the bone this supplies nourishment to femoral epiphysis
  • Synovitis or sustained abnorm limb position - may increase intra articular pressure & collapses fragile veins & inhibits blood flow
  • Cell death occurs & reparative process begins
  • Bone substance weakened during revascularization process
  • Norm physio wt.bearing forces = collapse & fragmentation of femoral epiphysis, incongruence of femoral epiphysis & acetabulum (results in DJD), fragmentation & DJD cause pain and lameness
31
Q

What is the common signalment of a px w/ Legg-Calve-Perthes Dx

A
  • Young small breed dogs (under 10 kg)
  • Peak incidence during 6 to 7 MO
  • Ranges from 3 to 13 MO
  • Males & females affected equally
  • Occurs bilaterally in 10 to 17% of affected px
32
Q

What is the common hx of a px w/ Legg-calve-perthes dx

A
  • Slow onset of wt bearing lameness worsens over 6 to 8 W
  • lameness may progress to non weight bearing (NWB)
  • May present as acute onset of lameness - sudden collapse of epiphysis may cause acute exacerbation of lameness
  • Other sx - irritability, reduced appetite, & chewing @ skin over the hip
33
Q

What will be found on the PE of a px w/ Legg-calve-perthes dx

A
  • Hip joint pain
  • Limited range of motion, muscle atrophy, & crepitus if it is advanced disease
34
Q

What DDx should also be considered when looking at the PE of a px w/ Legg-calve-perthes dx

A
  • Physeal trauma & medial patella luxation (MPL)
  • Small dogs may have concurrent bilateral MPLs
35
Q

What will be seen on radiographs of a px w/ Legg-Calve-Perthes Dx

A
  • shows femoral head deformity
  • Femoral neck shortening &/or lysis
  • Foci of decreased bone capacity w/in femoral epiphysis
36
Q

What is the medical management of Legg-Calve-Perthes Dx

A
  • Do in early stages of dx if not painful
  • If made before collapse of femoral head - limited wt bearing on limb during revascularization to prevent collapse of femoral head
  • Conservative tx - NSAIDs, leash limited or NWB exercise, can provide pain relief in small % of px
  • Dx often made after collapse of epiphysis
  • Results in joint incongruity & DJD
37
Q

What is the surgical management of Legg-Calve-Perthes Dx

A
  • Most dogs req sx to relieve lameness
  • Excision of the femoral head & neck (FHO ) is the tx of choice
38
Q

What is the postop care for a px w/ Legg-Calve-Perthes Dx

A
  • Limb usage imm after sx (include immediate rehab exercise)
  • NSAIDs to reduce pain & encourage early fxn
  • Passive flexion-extension of hip done 2x daily
  • PT initiated (canine rehab) - small movements & ROM gradually increased over 5 to 10 min
39
Q

What is the prognosis of px w/ Legg-Calve-Perthes Dx

A
  • Good after FHO - small size of affected dogs
  • Slight intermittently lameness may occur - Heavy exercise or period of inactivity
  • Poor occasionally w/ - NWB before sx, severe preop muscle atrophy, & incorrect sx technique