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Articular cartilage

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Articular cartilage

  1. 1.  Type of hyaline cartilage covers the bone ends and makes smooth movements possible.  It distributes the load across joints,minimizing the peak stress on subchondral bone.
  2. 2.  Relatively acellular.  No vascular,neural or lymphatic supply  Has little capacity to heal after injury.  Wear resistant  Low frictional  Lubricated surface  Slightly compressible and elastic
  3. 3.  Differs from hyaline cartilage in that it is not covered by perichondrium.  Collagen fibres of articular cartilage matrix are of type-II which exhibit characteristic cross banding of collagen fibres exsist.
  4. 4.  Young cartilage – typically white,smooth, glistening and compressible  Aged – thinner,less cellular,firmer and more brittle with less regular surface and yellowish opacity.  Thickness –  Bony end plate
  5. 5.  ZONES OF ARTICULAR CARTILAGE 1) SUPERFICIAL ZONE Not smooth,layer of hyaluronic acid LAMINAR SPLENDENS –most superficial Elongated chondrocytes,relatively inactive 2) TRANSITIONAL ZONE Thicker ,cells rounded & larger, arranged pairs Actively engaged in matrix component synthesis
  6. 6. DEEP ZONE - Largest zone - Largest collagen fibrils,highest proteoglycan content, lowest water ZONE OF CALCIFIED CARTILAGE - Irregular cells pyknotic nuclei /stability - TIDE MARK - Continuous with subchondral plate
  7. 7.  PERICELLULAR MATRIX - CHONDRON - Modulate the pressure transmission - regulation of chondrocyte response to pressure,prevent squashing  TERRITORIAL MATRIX - Fibrillar basket - surrounds the pericellular matrix
  8. 8.  INTERTERRITORIAL MATRIX - Largest matrix compartment - parellel arrangement of collagen fibrils - responsible for mechanical properties.
  9. 9.  Less than 1% of tissue volume  Rarely divide normally / cell density decreases with age  Synthesize matrix components- proteoglycans constantly renewed,collagen slow turnover  CILIUM – Regulation of matrix turnover
  10. 10.  COLLAGEN - Type II ,major (90%) - Characteristic cross banded fibrils - Type IX,X,XI minor  NON-COLLAGENOUS PROTEINS - Link protein /binding GAG to hyaluronic acid - Chondronectin and anchorinCII
  11. 11.  PROTEOGLYCANS - Family of glycoproteins large protein core attached to GAG side chains. - Form of large aggregates - Provide the resilience to A.C under load
  12. 12.  Mature A.C – diffusion from synovial fluid  Immature A.C – vascular channels in sub chondral bone,base of cartilage,S.F  Energy – anerobic pathway  Microenviroment:high CO2 & low O2  Survive for more than 2 days after death
  13. 13.  CHONDROMALACIA: A.C damage or degeneration  OUTER BRIDGE Classification: Based on arthroscopic exam
  14. 14.  GRADE O- Normal  GRADE I- Swelling & softening of intact A.C  GRADE II-Fissuring & fibrillation over small area < .5 inch  GRADE III- Same over larger area > .5 inch  GRADE IV- Erosion of subchondral bone
  15. 15.  Mitosis induced by laceration,compression,  Superficial lacerations – doesn’t cross tidemark donot heal.  Penetrates the subchondral bone- reach S.C vessels initiate healing process  Fibrinous arcade – scaffold that directs the mesenchymal cells to form F.C matrix  Repaired tissue – intermediate between H.C & F.C / poor biomehanical properties.
  16. 16.  Biphasic material – solid & liquid phase  Fibre reinforced gel- mutually repellant macromolecules binds water-osmotic P.  Water resides in microscopic pores and flow of the water induced by pressure gradient or matrix contraction.Flow pressure provides load support & minimize stress on matrix.
  17. 17.  JT loading & motion required to maintain normal adult A.C  Immobilisation of JT cause rapid loss of proteoglycans so deformation in response to load will increase.  Excessive use or increased loading affect
  18. 18.  Debridement of chondral flaps and removal of loose chondral fragments.  Abrasion chondroplasty  Microfracture
  19. 19.  Periosteal & Perichondrial grafting  Autologous cartilage implantation  Osteochondral autograft  Osteochndral allograft

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