Pathology of Joints

Types of Joints
1. Fibrous
2. Osseous
3. Cartilaginous
4. Synovial
  1. Most clinically significant
  2. Anatomy
    1. Composed of two bone ends bound together by a fibrous capsule & ligaments
    2. Inner surface of capsule is lined by synovial cells & the joint space contains synovial fluid
  3. Functions
    1. Absorb force of impact (Cartilage & synovial fluid)
    2. Allow a variable degree of movement
    3. Articular cartilage
      1. Minimizes friction
      2. Transmits force to underlying bone (Distributes weight)
      3. Composition:
        Proteoglycan (PG)
        Collagen
        Cells
        Water
        Provides turgor & elasticity to articular cartilage
        Traps water (lubrication, flow of nutrients - joint flushing)
  4. Causes of Injury:
    1. Trauma
      1. Joint instability
        Lubrication failure
        Infection
        Immune mediated
  5. Response to Injury:
    1. 1st line of defense: Articular cartilage
      1. Limited response to injury
      2. Avascular, reinforced gel
      3. Little reparative capacity
        Chrondrocytes can't move very far
        Little remodeling occurs
        Few cells which can actually respond
      4. Only proteoglycan is continually turned over
Degenerative Joint Disease (DJD)
1. = Osteoarthritis
2. Destructive disease leading to loss of articular cartilage in one or multiple joints
3. Incorporates a variety of diseases with a common end stage
4. Initiating changes may be caused by: Trauma, Joint instability, synovial inflammation, ageing, etc.
5. Gross lesions identical: Cartilage breakdown & loss
6. Pathogenesis (Not entirely clear):
  1. Primary event: Proteoglycan loss
    1. => Loss of lubrication
      1. => Collagen disruption
        Fibrillation of cartilage, Frays, clefts, Ulcers, Exposure of Bone, Eburnation, +/- Osteophytes & joint mice, brown/yellow discoloration, linear grooves, synovial hypertrophy & capsular fibrosis
    2. => Decrease in Tugor & Elasticity of Articular Cartilage
  2. Failure of chrondrocytes to maintain balance b/w matrix break down & repair
    1. Degradative enzymes play a role:
      1. Matrix metalloproteinases (MMPs)
        Inhibitors normally control these enzymes
        Inhibitors are decreased in DJD => Activation
        Results in decreased proteoglycan => adverse effect on elastic properties of cartilage
        Release of cartilage breakdown products induces inflammation via local irritation
        Enzymes include:
        Gelatinases (digest type I & BM collagens)
        Collagenases (digest collagen)
        Stromelysins (digest non-collagenous proteins)
      2. Produced by chondrocytes, synoviocytes & inflammatory cells
Joint Inflammation
1. Arthritis
  1. Classifications:
  2. Infectious
    1. Farm animals & Horses (esp. young)
    2. Portals of entry include navel & GI tract => Bacteraemia
      1. Bacteria reach joints Haematogenously => Polyarthritis
        Multiple joints
        Other portals of entry:
        Traumatic inoculation
        Extension from bone or periarticular soft tissue
    3. (Dogs & Cats - One joint - trauma related)
    4. Acute
      1. Fibrinous
        Fibrinogen in blood vessels -> leaks -> fibrin
        Oedema, synovial villi thickened
        Early resolution is common, but fibrin may be converted to fibrous tissue (enlarged joint w/ restricted movement)
      2. Suppurative
      3. Fibrinosuppurative
      4. Outcomes:
        Infection cleared -> complete resolution
        Infection cleared -> healing by fibrosis
        Continued inflammation:
        Persistent, subclinical or intermittent
        Re-seeding of joint
        Failure to get rid of irritant bacterial products
    5. Chronic
      1. Lymphoplasmacytic
        Proliferative
  3. Non-infectious
    1. Dogs & Cats
    2. Immune mediated disease
      1. Trauma
        Foreign material (urate crystals = gout (birds))
      2. Often polyarthritis
      3. Two forms:
        1) Erosive
        Immune process is JOINT centered
        Instability & luxation of multiple joints
        Ex. Rheumatoid arthritis: Small & toy breed Dogs (rare in Cats)
        Polyarthritis: Grey hounds
        Feline progressive polyarthritis
        Pathogenesis:
        Animal forms Abs against endogenous (unknown) Ag
        Abs IgG & IgM = Rheumatoid factor
        Complexes form & are depositied on articular surfaces
        Pannus formation (granulation tissue) => Cartilage erosion
        2) Non-Erosive
        Joint NOT the primary target
        Immune complexes form elsewhere & settle in the joint
        Ex. Systemic lupus erythematosus (SLE)
        Dogs
        Anaemia, thrombocytopaenia, polymyositis, glomerulonephritis
        Chronic diseases (such as pyometra, otitis externa, IBD, endocarditis, UTI, fungal infections) can lead to immune complex deposition in joints
        No pannus & no villous hyperplasia of lining
        No cartilage destruction
        Idiopathic
        Drug associated
    3. Results from:
      1. Persistent antigenic material in the synovium
      2. Deposition of Ag/Ab complexes in the synovium
Developmental Disorders
1. Athrogryposis
  1. Persistent congenital flexure of a joint in conjunction w/ muscle contraction
  2. Causes:
    1. Inactivity or paralysis (in utero)
      1. Spinal dysraphism
        Intrauterine viral infections
        Toxic plants (poison hemlock)
2. Hip dysplasia
  1. Common in Dogs (large/giant breeds)
  2. Inherited disease in which joint laxity (instability) results in secondary degenerative joint disease (DJD)
  3. Joint laxity -> Subluxation -> flattening of dorsal rim of acetabulum -> modeling of the acetabulum & femoral head
  4. Contributing factors:
    1. Heredity, weight, over-exercise, low pelvic mass
  5. Gross lesions:
    1. Articular cartilage (femoral head & acetabulum)
      1. Erosion &/or Ulceration
    2. Joint capsule/synovium
      1. Subchondral bone
        Shallow, wide acetabulum, Eburnation: Osteophyte formation
      2. Capsule stretched & thickened, w/ cartilage & bone formation w/in; round ligament may be ruptured
3. Osteochondrosis
  1. A disorder of growth cartilage occurring in growing animals
  2. Most species
  3. Failure of Endochondral Ossification
  4. Really a defect in cartilage growth (i.e. chrondrodysplasia)
  5. Growth cartilage is not mineralized so is focally or multifocally retained
    1. An area of growth cartilage fails to undergo matrix calcification or vascular invasion, & therefore does not become converted to bone
  6. Manifestations include thickened articular cartilage/cartilage flaps (osteochondritis dissecans or OCD), retained cartilage cores, bone cysts, angular limb deformity & DJD
  7. Endochrondral ossification takes place at the:
    1. Physis
      1. Subarticular epiphyseal growth cartilage
  8. Multifactorial: Trauma, genetic, rapid growth, ischaemia, nutritional
  9. Idiopathic
  10. Giant breeds: humoral head ( 4-8 months old)
    1. Horses: Distal tibia
  11. Lesions bilateral in 70% of cases (But lameness often unilateral)
4. IVDD (Intervertebral Disk Disease)
  1. Chrondrodystrophic Dogs:
    1. Predisposed to degenerative disk change from early age
    2. The nucleus pulpsus is replaced by chondroid tissue which mineralizes & fragments
      1. Annulus fibrosus secondarily degenerates
  2. Non - Chondrodystrophic Dogs:
    1. Degeneration begins in the Annulus fibrosis
      1. Fibrosis of the nucleus (vs. chondroid degneration)
        Middle-aged Dogs affected & thoracolumbar area predisposed
  3. Disk can herniate (if Annulus is intact - more common Non-chondrodystrophics) or Rupture through the Annulus (More likely in Chondrodystrophics)
    1. Extruded material is gritty. haemorrhagic or "cheesy"

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Pathology of Joints

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	Created by melian.yates over 10 years ago