Osteoarthritis – Structure of Articular Cartilage

Cartilage is the layer covering a joint. Its main function is to produce smooth articulations among the joint surfaces. Type of cartilage in synovial  joint is hyaline cartilage. Hyaline cartilage is a hard, translucent material rich in Type II collagen and proteoglycan.

To reduce the friction, the cartilage is lubricated by various mechanisms.

Synovial  joints serve as mechanical bearings with  low coefficients of friction. Their three major sources of lubrication are:

Hydrodynamic lubrication

Loading of the articular cartilage causes compression that forces water out of the cartilage. This fluid forms an aqueous layer that separates and protects the opposing surfaces.

Boundary layer lubrication

A small glycoprotein called lubricin, which is produced by synovial lining cells, binds to articular cartilage where it retains a protective layer of water molecules.

Hyaluronic acid

It i s produced by synovial lining cells and lubricates the contact surface between synovium and cartilage.

The  cartilage is a highly organized into a structure and consists different molecular components consisting of  four zones include:

Superficial or tangential zone

This is the smallest zone that constitutes 10 percent of the cartilage. Collagen fibers are thin and are oriented horizontally to subchondral bone. Low glycan content. This zone is called the lamina splendens.

Middle or transitional zone

it is the largest zone that constitutes 50% of the cartilage. Collagen fibers are thicker and start to be arranged into radial bundles. It has got High proteoglycan and water content.

Deep or radial zone

It constitutes 20% of the cartilage. it carries  largest collagen fibers arranged perpendicular to subchondral bone and posseses many chondrocytes.

Calcified zone

This zone separates cartilage from subchondral bone. Collagen fibers penetrate into this zone and anchor the cartilage to the bone.

Adult cartilage is avascular, and chondrocytes obtain nutrients through diffusion. The nutrients are derived from the synovial fluid whose  diffusion is facilitated during joint loading. With joint loading, some of the water in cartilage is squeezed out into the synovial space. When the joint is unloaded, the hydrophilic properties of the cartilage proteoglycans cause the water to be sucked back into the cartilage. As the water returns to the cartilage, diffusion of nutrients from the synovial fluid is facilitated.

In normal articular cartilage, chondrocytes rarely divide. Chondrocytes synthesize and replace the extracellular matrix components. Proteoglycans have a faster turnover rate  compared with collagen. The degradation of these macromolecules is accomplished by proteolytic enzymes like Metalloproteases, such as collagenases , stromelysins  and gelatinases.

Cytokines such as interleukin-1 and tumor necrosis factor canincrease  upregulate the degradative process,whereas transforming growth factor and insulin-like growth factor-1 have an opposite effect on chondrocyte metabolism.

Cartilage breakdown can be detected by assays using monoclonal antibodies to measure type II collagen and proteoglycans  in bodily fluids.

In osteoarthritis, the patients experiences pain due to irritation of the subchondral bone, which gets exposed as the cartilage degenerates. Additionally, accumulation of synovial fluid can cause pain through distention of the innervated joint capsule and synovium. Accompanying mild synovial inflammation also causes pain.

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Related posts:

  1. Pathophysiology of Cartilage and Matrix Changes in OA
  2. Structure of A Synovial Joint
  3. Why Does Osteoarthritis Occur-A Look Into Pathophysiology
  4. What Are Risk Factors for Osteoarthritis
  5. Surgical Treatment For Osteoarthritis

Comments

  1. judith says:

    I recently read about ‘deep ulcerations’ at the joint sites (I am particularly refering to the hand) which impact the tissue of the fingers. This seems to be an infectious process.

    The reason for micobacterium lepre affecting certain nerves was before thought of as “\’idopathic’ until through autopsy investigation it was discovered the bacterium preferred cooler sites and thus the antiinflammatory process targeted the site and damaged the nerves irreparably. Also, lesions were thought to be a result of the ‘leprous process’. However, they were simply a result of injuries unfelt because of the absence of pain resulting from nerve death.

    What kind of research had been made into the ‘ideopathic’ nature of Osteoarthritis of the hand?

    Dr Arun Pal Singh Reply:

    @judith,

    There is an easy way to find that. Use Google Scholar

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