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Bones / Joints Flashcards

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1
Q

Developmental skeletal dysplasias

A

K9 chondrodysplastic dwarfism
Osteogenesis imperfecta
Osteochondrosis/osteochondritis dissecans

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2
Q

Types of Cartilage

A

Hyaline cartilage - shock absorber, template for endochondral ossification

Fibrocartilage - connections between connective tissue, tendon/ligament insertions

Elastic cartilage - flexible structures

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3
Q

Generalized chondrodysplasias

A

Congenital defects involving cartilage template and generalized (polyostotic) defect in ECO

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4
Q

Origin of chondrodyplasias

A

Defect in cartilage template required for EO

Spontaneous or heritable mutation

Defect in any part of skeleton from cartilage template

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5
Q

Disproportionate (chondrodysplastic) dwarfism

A

Breed standard in Bassett hound/corgis (autosomal dominant FGF4 mutation)

Lethal mutation in bulldog calves (Dexter, Holstein) (Col2A1 and aggrecan mutations) —> shortened malformed limbs

Secondary defects in cells or ECM (lysosomal storage) —> limb, spine, skull malformations (+other organs)

+/- early DJD (from malformation in shape of epiphysis —> joint instability / incongruency

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6
Q

K9 Chondrodysplasia

A

Chondrodysplastic phenotype (CDPA)

CFA18-FGF4 mutation (autosomal dominant)

Dysproportionate dwarfism - shortened, malformed limbs (standard in certain breeds)

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7
Q

K9 Chondrodystrophy

A

Chondrodystrophic phenotype (CDDY)

CFA12-FGF4 mutation (incomplete autosomal dominant)

Shortened, malformed limbs (additive effect), IVDD (premature degeneration —> IVD herniation —> neurologic signs)

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8
Q

Generalized osteodysplasias

A

Skeletal defects in which cartilage cells/matrix are ok
Bone cell/matrix affected (generalized deformities, monostotic or polyostotic malformations

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9
Q

Osteogenesis imperfecta

A

Osteopenic disease (puppies, calves, lambs, humans)
Decreased bone density, excessive bone fragility

Mutation in both Type I collagen synthesis (BOTH osteoblasts and odontoblasts affected = bone + teeth affected)

Thin, weak bone matrix —> increased fragility, thin dentin, joint laxity + “blue” sclera (thinning)

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10
Q

Focal chondrodysplasia

A

Developmental defects in ECO at focal, repeatable sites

Osteochondrosis + Osteochondritis dissecans

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11
Q

Osteochondrosis + osteochonritis dissecans

A

Heterogenous lesion(s) in GROWTH cartilage (dogs, horses, pigs, cattle, poultry); epiphyseal > metaphyseal

Focal defect in endochondral ossification

~50% of lesions bilaterally symmetrical

Secondary OA common

Common joints: stifle, shoulder, elbow (pig), hock

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12
Q

Etiopathogenesis of OC/OCD

A

Damage to vasculature within growth cartilage (cartilage canals)

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13
Q

Pathogenesis of OCD

A

Focal interruption of endochondral vascular invasion or ischemic necrosis —> ECO failure —> retained cartilage core —> pressure induced fissure —> OCD

Retention of growth cartilage at AEC or metaphyseal growth plate —> defect if large retainined and heals or fissure —> dissecting cartilage flap (OCD) —> secondary DJD

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14
Q

Factors affecting bone response to injury

A

Etiology/inciting cause
Point at which injury occurs (pre/post natal development, mature skeleton)

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15
Q

Osteodystrophy due to failure of normal growth/development

A

Nutritional, endocrine, metabolic imbalance
Both trabecular and compact bone

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16
Q

Osteodystrophy due to abnormality during remodeling of mature bone or in repair

A

Nutritional, endocrine, metabolic imbalance

trabecular&raquo_space; compact bone

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17
Q

Causes of osteodystrophy

A

Temporal imbalances:
Nutritional (protein, vitamins, minerals)
Endocrine/hormonal
Toxic origins (drugs)

GI/renal/hepatobiliary dysfunction
Affect all bone!

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18
Q

Important factors / hormones in bone control

A

Endocrine: PTH (parathyroid), Calcitonin (thyroid)

Kidneys: Ca/phosphate

Kidney/liver/skin/intestine: Vitamin D3

Local factors: RANKL

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19
Q

Bone modeling

A

Primary trabeculae removed/replaced with STRONGER/FEWER trabeculae WITHOUT cartilage template core —> less radioopaque

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20
Q

Function of bone remodeling

A

Maintain bone mass

Replace old bone / repair microfracture

Respond to metabolic/nutritional changes

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21
Q

Regulators of OCLs

A

RANKL (from osteoblasts —> OCL activation / diff)
PTH (indirect inc in OCL activation)
Calcitonin (dec bone resorption systemic)

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22
Q

Common metabolic osteodystrophies

A

Osteoporosis
Rickets/Osteomalacia
Fibrous osteodystrophies (Renal failure —> secondary hyperparathyroidism)

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23
Q

Osteopenia

A

Decreased bone density / mass

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24
Q

Osteoporosis

A

Clinical syndrome
Bone pain / pathologic fractures (due to osteopenia)

Bone shape is normal, but reduced trabecular&raquo_space; cortical bone (i.e. QUALITY is reduced)

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25
Causes of osteoporosis
Protein calorie malnutrition Calcium deficiency Copper deficiency Severe GI parasitism or IBD Physical inactivity (disuse/immobilization)
26
Lesions of osteoporosis
Dec osteoblast activity Dec trabecular bone —> dec compact bone —> dec bone density + inc porosity Pathologic fractures and infractions (micro fractures) —> reduced bone length
27
Rickets and osteomalacia
Defective mineralization —> affect bone and growth cartilage —> bone deformities (angular limb deformities, scoliosis, flared physes) —> pathological fractures + subchondral collapse —> bone pain
28
Rickets
soft/weak bones + growth plate cartilage (Young, growing animals)
29
Osteomalacia
Softening of bones In ADULT animals, cartilage not affected
30
Causes of rickets/osteomalacia
Nutritional deficiencies: Vitamin D deficiency (typically with unconventional diet) Phosphorous deficiency (herbivores with P deficiency diet) Calcium deficiency NOT a cause (except in birds)
31
Phases of bone formation
1. Osteoid formation 2. Mineral deposition (lacking in rickets/osteomalacia)
32
Rickets / osteomalacia pathogenesis
Reduced mineralization in bone (or bone + growth plate - young) —> deposition of large soma of osteoid along endosteal bone surfaces + osteomalacia canals —> dec OCL resorption —> inability to bind / resort old bone; growth plate deformities (in young) (unmineralized growth cartilage —> dec primary trabeculae)
33
Lesions of rickets
Flared metaphyses and retained cartilage core at growth plate Compact bone: bowed legs, catastrophic fractures Trabecular bone: infractions Bone surfaces lined by large seams of unmineralized osteoid (any site of remodeling, trabecular >> cortical bone)
34
Lesions of osteomalacia
Bone surfaces lined by large seams of unmineralized osteoid (any site of remodeling, trabecular >> cortical bone) Weaked trabeculae: microfractures Weakened compact bone: catastrophic fracture
35
Fibrous ostrodystrophy pathogenesis
Persistent + extreme inc PTH Primary hyperparathyroidism —> inc OCL activity/bone resorption —> dec OB diff —> dec bone formation —> inc fibroblast diff —> fibrosis Renal insufficiency or High P diet —> inc phosphate —> inc Ca precipitation —> secondary hyperparathyroidism —> inc PTH —> inc OCL —> bone resorption / replace with fibrous
36
Clinical fibrous osteodystrophy
K9: Rubber jaw EQ: big head syndrome
37
Renal osteodystrophy can cause components of rickets/osteomalacia AND FOD due to …
Decreased Vitamin D3
38
Dynamic response of bone
Respond to: Physiologic homeostatic process Mechanical stress Metabolic stress Inflammatory stress
39
Osteoblasts
immature cells that “build bone”
40
Osteocytes
Mature cells that maintain bone
41
Osteoclasts
Macrophage like cells that resorb bone
42
Woven bone
Immature bone Temporary, high cellularity, poorly organized, rapid formation, poorly mineralized Acts as a bandaid (weak)
43
Lamellar bone
Mature bone Low cellularity, organized, slow formation, STRONG, well-mineralized
44
Sites of bone repair
Periosteum - outer surface of bones Endosteum - lines inner surface of bone (interface between hematopoietic marrow and bone)
45
Mechanisms of bone formation
Cutting cones - compact bone, “miners in tunnels”; slow and limited Intramembranous ossification - FAST Endochondral ossification - slow conversion
46
Intramembranous ossification
Bone formed directly from mesenchyme WITHOUT cartilage template (fast) Condensation of mesenchyme —> OB differentiation —> osteoid + HA —> ossification centers —> woven bone island —> remodeled to lamellar bone
47
Reaction of joint to injury
Joint cartilage + soft tissue supports (tendon, ligament, menisci) have POOR REGENERATIVE RESPONSE + limited healing capacity Final common pathway = degeneration
48
Common etiologies of joint injury
Congenital instability/incongruence Traumatic instability Repetitive stress injury Infection / inflammation Common end-stage pathway = DJF
49
Degenerative joint disease
Incorporates all anatomic components Articular cartilage; subchondral bone; synovium; soft tissue structures (joint capsule, ligaments, menisci)
50
End-points of DJD
Ankylosis (self fusion) Arthrodesis (surgical fusion) Arthroplasty (surgical reconstruction / replacement)
51
Features of early cartilage degeneration
Gross: surface dullness/roughness, thinning (focal, regional, or diffuse) Histo: PG loss with matrix contraction + clefts (less pink on histo); chondrocyte necrosis + loss
52
Progressive cartilage degeneration
Gross: severe thinning + score lines, yellow discoloration Histo: chondrocyte loss/dropout, chondrocyte clones
53
Advanced cartilage degeneration
Gross: erosions—> full thickness ulcers —> subchondral bone hemorrhage —> hemarthrosis —> subchondral bone lysis —> collapse divots Histo: matrix fraying/vertical fissures, erosions/ulcers, +/- fibrocartilage repair
54
End-stage cartilage degeneration
Gross: full-thickness cartilage ulcers, subchonral bone hemorrhage Histo: full thickness cartilage ulcer with horizotonal fissure; deep excavation/collapse of subchondral bone with subchondral hemorrhage
55
Progressive lesions of DJD
“Adaptive” remodeling —> pathologic inc bone density from decrease in cartilage shock absorption —> excessive compressive forces —> sclerosis —> dec vascular access —> dec OCL remodeling —> bone failure —> catastrophic fractures
56
Subchondral bone failure
Repetitive stress injury (overuse / obesity) —> subchondral failure + collapse —> catastrophic fractures
57
Sequeale of subchondral bone failure
DJD characterized by Subchondral “bone cysts” from synovial herniation Eburnation (polishing of bone cartilage ulcers —> bone on bone contact)
58
Osteophytosis
Progressive articular bone proliferation of DJD Growth of osteophytes on bone
59
Progressive lesions to synovium and joint capsule in DJD
Synovitis: (histo) increased layers and large cells in intima; increased vascularity, fibrosis, inflammation in subintima Gross: hypertrophied (thickened), hyperemia (red) synovial membrane, effusions from intimal/subintimal changes
60
Severe chronic lesions of synovium/joint capsule in DJD
Thickened synovium with subintimal neovascularization / fibrosis; superficial erosion; Proteinaceous exudate Gross: super-thick synovial hypertrophy + hemosiderin from chronic hemorrage —> yellow-brown discoloration
61
Canine hip dysplasia
Congenital joint laxity; large/giant breed dogs predisposed Factors: genetics, obesity, excessive exercise
62
Pathogenesis of canine hip dysplasia
Excessive joint laxity with instability —> chronic subluxation of coxofemoral joint —> secondary DJD with modeling of femoral head/acetabular cup + arthritis
63
Fracture classifications
Traumatic vs pathologic
64
Traumatic fracture
Normal bone broken by excessive force
65
Pathologic fracture
Abnormal bone broken by Minaj trauma or during normal weight bearing forces (Repetitive stress injury, congenital/metabolic bone disease), osteomyelitis, primary/metastatic neoplasia
66
Fracture configurations
Closed vs open Simple vs comminuted Transverse vs Sagittal/parasagital Avulsion Articular
67
Salter-Harris fractures
Involve growth plates (occur in young) Type I, II, III, IV, V
68
Type II Salter-Harris Fracture
Fracture extends across physis —> breaks out metaphysis
69
Consequences if in growth plate fracture bone heals, but growth plate cartilage does not
Limb shortening or angular limb deformity
70
Types of fracture healing
Direct (primary) healing —> rigid fracture stabilization Indirect (secondary) healing —> biomechanical environment dictates how healing occurs, limited intervention (?)
71
Stages of indirect bone healing
1 - Inflammation 0-7 d 2 - Repair A - Soft callus 1-3 w. (Early callus - granulation tissue + woven bone + cartilage islands) B - Bony callus 3-6 w 3 - Remodel > 8 w to yrs
72
Response to a fracture
1 - tearing of periosteum + displacement of fracture ends —> trauma to adjacent soft tissue 2 - hemorrhage with hematoma + clot formation by fibrin polymerization 3 - Imparied blood flow —> necrosis of fracture ends + bone fragments 4 - release of cytokines + growth factors by platelets, macrophages in clot 5 - influx / proliferation of MSCs and granulation tissue formation 6 - OB differentiation, woven bone 7 - bridging callus —> soft callus —> hard callus
73
Soft callus
Woven bone +/- cartilage with periosteal vessels forming within 1-3 w of fracture healing Low O2 tension —> hyaline cartilage formation (radiolucent!) —> EO —> eventually radioopaque (hard callus)
74
Primary fracture callus
Provides some stability to allow some degree of limb function until healing complete
75
Complications of fracture healing
Mal-union / fibrous non-union Inadequate blood supply Infection (osteomyelitis, septic arthritis)
76
Mal-union / fibrous non-union
Caused by poor or delayed healing Permanent + painful If articular —> early degenerative OA
77
Impact of inadequate blood supply on fracture healing
Necrotic bone (sequestrum) Poor healing / necrotic tissue —> substrate for infection
78
Osteomyelitis / septic arthritis
Occurs at time of injury or delayed Bacterial “squatters” in sequestrum / bone biofilms Inhibits neovascularization / callus formation (delayed healing —> mal-union / fibrous non-union)
79
Synovitis
Inflammation of synovial membrane and synovial fluid compartment
80
Arthritis
Inflammation/degeneration of all components of joint (synovial membrane + joint capsule, cartilage, subchondral bone)
81
Osteomyelitis
Inflammation of bone, including endosteum + medullary spaces
82
Osteitis
Inflammation of cortex only
83
Acute arthritis
Inflammatory cells + pro-inflammatory cytokines - synovial hyperemia + edema - reduced PG of synovial fluid + cartilage - reduced synovial viscosity - chondrocyte necrosis + loss of ECM Orange, red, brown synovial fluid (if hemorrhage) Increased turbidity (fibrin, neutrophils - if septic)
84
Chronic arthritis
Cartilage lesions progressive thinning/erosions/ulcers Stiffening of joint Subchondral bone involvement Reduced joint function + DJD
85
Routes of joint infection
Septicemia (neonates > adults) : umbilicus, respiratory tract, GI Direct penetration (more common in adults) - trauma, injection, surgery Extension from local wound/septic epiphysitis
86
Acute changes in synovium
Decreased viscosity (digestion of GAG + dilution by edema) Turbid (fibrin / neutrophil) Red/orange/brown discoloration Hyperemic joint
87
Chronic changes to synovium / joint
Suppurative —> lymphoplasmacytic inflammation Synovial villus hypertrophy Joint capsule fibrosis + Osteophytosis
88
Acute changes to articular cartilage / subchondral bone
Yellowing + thinning cartilage surface Fissures / collapse from ECM degeneration + chondrocyte necrosis
89
Chronic changes to articular cartilage + subchondral bone
Focal or diffuse thinning, erosions, ulcers Pannus formation “red velvet” surface Subchondral bone sclerosis / disuse osteopenia
90
Bacterial causes of infectious arthritis / osteomyelitis
G -: coliforms, Salmonella G+: Strep, Staph, Actinomyces bovis, T pyogenes Mycoplasma
91
Fungal causes of infectious arthritis / osteomyelitis
Opportunistic fungi (Aspergillus, Candida) Coccidiomycoides, Blastomyces
92
Septic physitis/epiphysitis
In young growing animals - bacteria within vessels in ossification front of growth plates Thrombosis / infarcts of intramedullary fat, marrow, bone —> sequestrum —> septic arthritis
93
Sequestrum / sequestration
Necrotic bone islands —> will hypermineralize —> radioopaque; also resorption of surrounding bone (radiolucent rim)
94
Occurrence of primary bone tumors in animals
Dogs > cats >>> farm animals
95
Most common primary bone tumors in SA
Osteosarcoma (appendicular > axial) Chondrosarcoma (cartilage; flat bone predilection)
96
Behavior of bone tumors
In dogs - most malignant In cats - benign ~ malignant In horses/cattle/other domestic - benign >> malignant
97
Osteosarcoma
80% of primary bone tumors in dogs Large, giant breed dogs 75% appendicular skeleton; 2/3 in forelimbs, 1/3 hind
98
K9 osteosarcoma
Malignant neoplasm of osteoblasts Aggressive, invasive neoplasm Frequent + RAPID metastasis (LN, lungs, bones) Poor prognosis Site of origin: central (most common), parosteal, periosteal, extraskeletal Radiographic appearance: lyric to sclerotic, proliferative Doesn’t directly cross joints! Pathologic fractures
99
Diagnostic features of osteosarcoma
1 - osteolysis (destruction of bone architecture) 2 - osteoproliferation 3 - histology - neoplastic osteoblasts producing tumor osteoid (biopsy)
100
Feline osteosarcoma
Malignant + locally in vases / aggressive Slower metastasis + longer survival than in dogs
101
Histiocytic sarcoma
Round cell neoplasm (interstitial dendritic cell or macrophage) Locally invasive (joints) - often CROSSES joint! Rottweiler (and black + tan) dogs Stifle + elbow (elbow uncommon for OSA) Hemophagocytic subtype —> anemia Poor prognosis ~5.3 mo survival Metastasis to liver, lung, lymph nodes

Pathology (21 decks)

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