Cartilage and Joint Pathology Flashcards

1
Q

Does inflammation play a part in cartilage injury?

A

No, but cartilage can be affected by inflammation in the synovium, subchondral bone or growth cartilage

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2
Q

How can repetitive stress damage cartilage?

A

It damages the matrix and chondrocytes leading to inappropriate cellular responses e.g. production of degradative enzymes, chondrocyte death and a cycle of injury.

Proteoglycan and collagen interactions are disrupted.

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3
Q

What is the response to injury?

A
  • Response to injury is limited due to cartilage having a minimal capacity for repair
  • If proteoglycans are lost, collagen fibres condense and fray (fibrillation)
  • Clefts and fissures form in the vertical axis - this allows synovial fluid to enter subchondral bone and cause inflammation
  • Fibrillation is accompanied by erosion
  • Erosion doesn’t penetrate into the subchondral bone but is persistent. It doesn’t heal but does not progress either
  • Necrosis of chondrocytes is subsequent to fibrillation and erosion (hypocellularity)
  • Limited regenerative hyperplasia of chondrocytes
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4
Q

How does eburnation occur?

A
  • Ulceration of cartilage causes the full thickness to be lost, gets filled with vascular fibrous tissue
  • Often undergoes metaplasia to fibrocartilage but rarely hyaline cartilage
  • Exposed subchondral bone develops an increased density due to increased mechanical use (eburnation)
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5
Q

What are the stages in degenerative joint disease?

A
  • Cellularity of cartilage declines with age and turnover of collagen and cells occurs at a lower rate
  1. Chondromalacia (softening)
  2. Erosion and fibrillation
  3. Ulceration
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6
Q

Define ‘periarticular osteophytes’

A
  • Bony outgrowths/spurs, initiated by mechanical instability of the joint and/or inflammatory cytokines.
  • Don’t grow continuously but persist once formed
  • Can form within joint cavity (perichondrium) or from the periosteum at the junction with the joint capsule
  • Often get secondary synovial inflammation and hyperplasia
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7
Q

Define ‘pannus’

A
  • Fibrovascular and inflammatory tissue that arises in the synovium and spreads over the articular cartilage, destroying it (macrophages and collagenases are responsible)
  • Happens with chronic infectious synovitis or immune mediated disease
  • Joint may be fused
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8
Q

Define ‘osteochondrosis’

A
  • Disease of the outgrowth plate of cartilage, focal or multifocal failure of ossification. Involves the metaphyseal growth plate (accumulation of viable hypertrophic chondrocytes) and articular-epiphyseal complex (necrosis of epiphyseal cartilage)
  • Basic lesion formed by failure of cartilage to become mineralised and replaced by bone
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9
Q

Describe osteochondrosis latens

A

Initial lesions due to necrosis of blood vessels in the epiphyseal cartilage of the articular epiphyseal complex. Overlying cartilage and underlying subchondral bone are not affected (microscopic lesion)

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10
Q

Describe osteochondrosis manifesta

A
  • Grossly visible area of necrotic epiphyseal cartilage
  • Lesion is highly vulnerable to further damage
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11
Q

What is the origin of synovial fluid?

A

From the synovium

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12
Q

Describe the structure of a synovial membrane

A
  • Not an epithelium as it doesn’t have a BM. Contains specialised CT which as a secretory component
  • Intima - 2-4 cells deep, Type A macrophages, Type B fibroblasts
  • Subintima - supportive tissue of loose CT and fatty tissue, capillaries which run just beneath the intima
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13
Q

What are the components of synovial fluid?

A
  • plasma dialysate
  • small number of cells - lymphocytes, monocytes, neutrophils
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14
Q

What is the function of synovial fluid?

A
  1. Lubrication
    * fluid squeezed out onto articular cartilage
    1. Nutrient transport
  • articular cartilage is avascular
  • most AC is in close apposition with synovial membrane
  • synovial fluid provides it with nutrition
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15
Q

What are the indications for arthrocentesis?

A
  • Joint effusion
  • If suspect and infection (sudden onset, pyrexia, pain)
  • Multiple joints are affected
  • Pyrexia of unknown origin
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16
Q

What are the general principles of arthrocentesis?

A
  • GA or sedation
  • Prep - hair clip, aseptic skin prep, ‘no touch’ or surgical gloves
  • Needle size - 23g 0.6mm (blue) or 21g 0.8mm (green)
  • Gentle flexion and extension can help aspiration
17
Q

What are the explanations for finding blood in a joint tap?

A
  • Latrogenic - distinctly defined area, sharp border
  • Pathogenic - homogenous appearance
18
Q

What volume of fluid should there be present in dogs and cats normally?

A
  • Dogs - 0.1-1.0ml
  • Cats - 0ml can be normal
  • Volume increased in most diseased joints
19
Q

What appearance should synovial fluid have?

A
  • Normal - egg white, won’t clot but will gel
  • Degenerative disease - clear to pale yellow
  • Inflammatory disease - increased turbidity
  • Septic - dark, bloody, smell bad
  • Viscosity is subjective, shouldn’t be watery. Inflammatory joint disease will be reduced
20
Q

How can synovial fluid be analysed?

A
  • Cell counts - microscope or haematology analyser (hyalluronidase can be used to prepare samples for machine counts to reduce viscosity)
  • Cytology - examine background, assess RBC no., platelet count, differential count (WBC), assess NCC
21
Q

What signs will be present in a synovial fluid sample that would indicate haemorrhage?

A
  • Streaks of blood at time of collection
  • Acute haemartrosis - differentials similar to peripheral blood, platelets will be seen
  • Longstanding haemorrhage - no platelets, increased WBC, erythrophagocytosis, haematiodin crystals in macrophages (golden crystals in cytosol), haemosiderin deposits in macrophages (RBC breakdown products)