Bone and Joints 3

Question 1

What is the makeup of articular (hyaline) cartilage

Answer 1

->70% water
-chondrocytes (produce matrix)
-Type 2 collagen fibers (tensile strength and have looped arrangement)
-Proteoglycan aggregates (bind/tap water component)

Question 2

What is the capacity for cartilage to heal/repair/remodel

Answer 2

Cartilage has minimal capacity for repair, little remodeling/turnover of hyaline cartilage. Mature cartilage is avascular with no undifferentiated cells.

Question 3

Can chondrocytes synthesize new matrix

Answer 3

Yes, the can synthesis new matrix to replace lost/degraded matrix. This capacity is reduced asa the animal ages

Question 4

What are the zones of the articular surface

Answer 4

-Superficial/gliding zone (C): resists shear forces during motion, fibers parallel to surface
-Middle zone (D): resists compressive forces, shock absorption, fibers perpendicular to surface
-Calcified/base zone (E): anchors cartilage to subchondral bone
Subchondral bone 10 times more deformable than cortical bone

Question 5

What is the difference between mature and growing cartilage

Answer 5

Mature articular cartilage: no nerves or blood vessels
Growing cartilage: blood vessels within canals, get nutrition from synovial fluids. In growing animals articular cartilage overlies growth epiphyseal cartilage

Question 6

Within the joint capsule, what are the make ups of the outer fibrous capsule and inner synovial membrane

Answer 6

-Outer fibrous capsule: blood vessels and nerve endings (pain receptors). Dense- limits spread of infection/neoplasms
-Inner synovial membrane: inner intimal lining is discontinuous and well vascularized.
Both encourage bacterial invasion of joint space from emboli trapped in sub-synovial blood vessels

Question 7

What is the make up of fibrocartilage

Answer 7

-Glycosaminoglycan content less than hyaline articular cartilage
-Contains type 1 and 2 collagen
-Avascular: no direct participation in inflammation but inflammation in adjacent synovium impacts on cartilage
-Biochemically less able to tolerate long-term mechanical loading/trauma
-No pain unless synovium or subchondral bone involved due to nerve endings in these locations

Question 8

What are the steps of the Degenerative Joint Disease/Osteoarthritis side of the Final Common Pathway of Joint injury

Answer 8

-Direct structural injury to normal/abnormal cartilage
-Chondrocytes release MMPs

Question 9

What are the steps of the Arthritis side of the Final Common Pathway of Joint injury

Answer 9

-Bacteria/immune complexes in synovial capillaries
-Inflammation triggered- leukocytes release

Question 10

What are the steps of the final part of the Final Common Pathway of Joint injury

Answer 10

-Lysosomal enzymes
-Degeneration of proteoglycans/collagen
-Water-binding capacity altered
-Chondromalacia
-Mechanical injury (fibrillation, ulceration, eburnation)
-Debris phagocytose by sub-synovial macrophages

Question 11

What is fibrillation

Answer 11

Vertical fissures following direction of collagen fiber alignment
(Chondromes form adjacent to fissures)

Question 12

What is pannus formation

Answer 12

-Fibrovascular/histiocytic tissue from transitional zone/subchondral bone
-Spreads across articular surface, interferes with nutrition
-Collagenolytic: erodes surface, can result in fibrous ankylosis

Question 13

What is osteophyte formation

Answer 13

-Irregular outgrowths of bone
-Stresses on joint capsule leads to proliferation of cells in osteogenic layer of attached periosteum causing EO leading to osteophyte formation

Question 14

What is villous hypertrophy-hyperplasia

Answer 14

-Part of synovitis with a velvety appearance
-Hypertrophy-hyperplasia of the synoviocytes with inflammatory cell infiltration. This impedes drainage which leads to swelling. The infiltration of neutrophils and neutrophil radicals cause a decrease in lubricative properties of joint fluid
-No basement membrane or tight junctions so debris from the degenerating joint are phagocytosed in capsule leading to fibrous thickening (fixation), cartilagenous-osseous meta plasma, and joint mice.

Question 15

What is an end stage joint

Answer 15

-The end result of a long-standing inflammation due to DJD or arthritis
-Irreversible changes with no possibility of return to normal structure or function
-Often difficult to determine what started the process in the first place as lesion loses its specific features and becomes more chronic

Question 16

What is hip dysplasia and what are some consequences of it

Answer 16

-An inherited lack of conformity between the shape of femoral head and the acetabulum commonly seen in large and giant breed dogs. There is an increased joint laxity and inadequate pelvic muscle mass causing joint instability with abnormal forces acting on the craniodorsal acetabulum and a more malformed joint. This disorder is both a malformation and a deformity
-It leads to osteophyte formation, rupture of ligament of femoral head, and can lead to DJD

Question 17

What is osteochondrosis, what does it result in, and what causes it

Answer 17

-It is a developmental disease that is a focal failure of EO due to localized ischemia
-Results in fragile cartilage and physeal and epiphyseal growth plates and infarcts
-Caused by trauma, genetics, and nutrition, and most common in rapidly growing males

Question 18

What is the pathogenesis of osteochondrosis

Answer 18

-Growing cartilage is vascularized via blood vessels within canals. There is necrosis of these vessels due to compression/pinching, leading to zones of necrotic cartilage. These zones fail to undergo EO and persist as cones of fragile necrotic cartilage in subchondral bone. These zones are susceptible to fragmentation and can form a cartilaginous flap or ‘joint mouse’. These may interfere with joint movement and trigger synovitis

Question 19

How does the bacteria get into the joint to cause bacterial arthritis

Answer 19

-Hematogenous: neonatal farm animals (poly articular)
-Direct extension: soft tissue/bone
-Penetrating wound

Question 20

What is the localization of bacterial arthritis favored by and what results from this

Answer 20

-Inner synovial lining (basement membrane) discontinuous
-Rich sub-synovial vasculature where emboli become trapped
-Results in a fibrinous or purulent arthritis depending on the nature of the bacteria

Question 21

Describe the changes seen in fibrinous bacterial arthritis

Answer 21

-Synovial fluid increases in volume and turbidity
-Periarticular oedema present
-Proliferation of villi and pannus
-Chronic stage: periarticular fibrosis
-Typically caused by E. coli, mycoplasmas, hemophilus

Question 22

Describe the changes seen in purulent/suppurative bacterial arthritis

Answer 22

-More severe and destructive
-Joint cavity fills with pus
-More destruction to cartilage by neutrophil enzymes
-Extend into periarticular tissues leading to enlargement/fistulation
-Ankylosis may result especially low motion joints (carpus/tarsus)
-Typically caused by T. Pyogenes, S. Aureus

Question 23

Describe immune-mediated arthritis and what are the two classifications

Answer 23

-Immune reaction in synovial capillaries
-Lesions somewhat similar to bacterial arthritis
-Cytology of joint fluid may help to differentiate
-Toxic/degenerate neutrophils in joint aspirate may mean there is bacteria present
-Two classifications: erosive and non-erosive

Question 24

What do dogs affected with erosive/rheumatoid-like immune mediated arthritis have antibodies to, and what does this disease cause

Answer 24

-Antibodies to altered endogenous Igs, heat shock proteins, type 2 collagen in their collagen. These form immune complexes in the synovium which activate complement and attract leucocytes which initiate joint lesions.
-These lesions form a persistent reaction, triggering pannus, and causing erosions, shifting lameness, and joint swelllings in the stifle, carpus, and digits

Question 25

Describe the pathogenesis of non-erosive immune mediated arthritis and where in the body this disease affects

Answer 25

-Primary immunological disease elsewhere leading to circulatin complexes in synovial capillaries. Inflammation is thus not as persistent, pannus is not triggered, and no erosions occur.
-Small joints of distal limbs and some evidence in other organs are seen, clinical signs wax and wane

Question 26

What is the process of DJD and what are some other names for this disease

Answer 26

—Process is degeneration of proteoglycans/collagen in articular cartilage. It is primarily degenerative while arthritis is primarily inflammatory
-Other names include arthropathy, degenerative arthritis, osteoarthritis, osteoarthrosis

Question 27

What causes DJD

Answer 27

-Trauma, developmental defects, abnormal joint function, aging, or inherent metabolic defect in the cartilage can trigger degeneration. Chondrocytes are central to degeneration and normally maintain balance between degradation and repair of matrix.
-Under the influence of cytokines, growth factors, and physical stimuli lead to the release of degradative enzymes (MMPs)