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SECONDARY OA: Appears at any age in a
previously damaged or congenitally abnormal
joint . OA is a “wear and tear” phenomenon.
Indeed the vertebrae , hips and knees are most
affected . OA can be superimposed upon
RHEUMATOID ARTHRITIS.
Two main theories:
1)BIOMECHANICAL THEORY
2)BIOCHEMICAL THEORY
   This maintains the wear and tear leads
    to deranged function,focal death, and
    reactive proliferation of chondrocytes.
   Collagen breakdown , fissuring and
    flaking and osteophyte formation
    occurs.
maintains that aging leads to lessened
matrix maintenance and excess of
lytic enzymes , which in turns lead to
synovitis . Synovitis further results in
a release of inflammatory mediators
and cytokines(especially IL-1) ,
degradative enzymes and free
radicals and eventually chondrocyte
death.
   Primary abnormality is thinning and
    fragmentation of the articular
    cartilage.
   Loss of articular cartilage leads to exposure of
    subchondral bone , which appears as shiny
    foci on the articular surface( enburnation ).
   New bone formation , usually in the form of
    nodules (spurs).
   Formation of osteocartilagenous loose bodies
    (“joint mice”).
   Inflammation is absent.
CLINICAL FEATURES:
Although OA may be asymptomatic,most
  patients experience morning stiffness in
  affected joints . There is usually no local
  heat or tenderness , but affected joints
  often show restricted range of motion ,
  small efusions and crepitus. A slowly
  progressive disease characterized by joint
  disability.It is associated with
  ALKAPTONUREA and FOOTBALL
  PLAYERS.
OSTEOARTHRITIS IN KNEE JOINT.
OSTEOARTHRITIS.
Osteoarthritis

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Osteoarthritis

  • 1.
  • 2.
  • 3.
  • 4.
  • 5.
  • 6. SECONDARY OA: Appears at any age in a previously damaged or congenitally abnormal joint . OA is a “wear and tear” phenomenon. Indeed the vertebrae , hips and knees are most affected . OA can be superimposed upon RHEUMATOID ARTHRITIS.
  • 7. Two main theories: 1)BIOMECHANICAL THEORY 2)BIOCHEMICAL THEORY
  • 8. This maintains the wear and tear leads to deranged function,focal death, and reactive proliferation of chondrocytes.  Collagen breakdown , fissuring and flaking and osteophyte formation occurs.
  • 9. maintains that aging leads to lessened matrix maintenance and excess of lytic enzymes , which in turns lead to synovitis . Synovitis further results in a release of inflammatory mediators and cytokines(especially IL-1) , degradative enzymes and free radicals and eventually chondrocyte death.
  • 10. Primary abnormality is thinning and fragmentation of the articular cartilage.  Loss of articular cartilage leads to exposure of subchondral bone , which appears as shiny foci on the articular surface( enburnation ).  New bone formation , usually in the form of nodules (spurs).  Formation of osteocartilagenous loose bodies (“joint mice”).  Inflammation is absent.
  • 11. CLINICAL FEATURES: Although OA may be asymptomatic,most patients experience morning stiffness in affected joints . There is usually no local heat or tenderness , but affected joints often show restricted range of motion , small efusions and crepitus. A slowly progressive disease characterized by joint disability.It is associated with ALKAPTONUREA and FOOTBALL PLAYERS.

Editor's Notes

  1. We will focus on adaptive responses. All these feature of an adaptive response require very specific interactions of molecules. Will describe B and T cells and their roles. Immunological memory - vaccination
  2. The important difference between B and T cells is how they can recognize antigens.
  3. • Antibody producing, have membrane bound antibodies, proliferation......., memory – plasma, point out the molecular interactions.
  4. • Has a T-cell receptor – only recognition of antigens together with MHC molecules. Explain how this work and the difference between class I and class II molecules. Point out the importance of molecular interaction. Explain how Th cells can help B cells - drawing
  5. Draw the pictures!!!!