Section editor: Paul Banaszkiewicz

Segment author: Christopher George Ghazala; Paul Banaszkiewicz

Document history :6/07/2019

• It is important to understand the structure and function of synovium as it is frequently altered in many disease processes such as rheumatoid arthritis.
• Synovial fluid mechanics may be covered as part of lubrication

• The internal epithelial lining of a joint capsule is covered by synovium, and secretes synovial fluid to lubricate the joint surfaces and provide nourishment to the articular cartilage and surrounding tissues.
• The synovium is formed by two to three layers of synovial cells, known as synoviocytes, that merge on the deep layer with loose fibrocollagenous tissue that contains a rich blood supply and numerous cell types including adipocytes, fibroblasts, mast cells and macrophages.
• Under light microscopy, synoviocytes appear as flat oval cells with dark-staining nuclei. Cells lining the lumen have ovid nuclei and extensive cytoplasmic processes that extend from the nucleus. These surface synoviocytes are known as type B cells and produce synovial fluid; whereas the deeper layer are known as type A cells. Type A cells are phagocytic and type B cells have numerous endoplasmic reticulum for protein synthesis.

A cells

• A cells are macrophages.

B cells

• B cells are exocrine/synthetic cells.
• Synthesise hyaluronic acid from protein and glycosaminoglycan.

C cells

• May exist as an intermediate cell type.
• Arranged into microvilli and villi resulting in a large surface area (knee = 100 m²; whole body = 1000 m²).

• Control diffusion
• Ingest debris
• Secrete immunoglobulins
• Secrete lysosomal enzymes
• Secrete hyaluronate
• Secrete lubricating glycoproteins
• Reduce friction in joint

• Synovial cells may transform into chondrocytes – occur at attachment site of the synovial membrane to periphery of articular cartilage.
• Synovial cells are capable of rapid and complete repair or regeneration.

• When challenged with an infectious inoculum, synovial membrane undergoes an acute inflammatory response with accumulation of polymorphonuclear leukocytes and monocytes.
• Complement activation produces chemotactic factors and other mediators of inflammation that enhance the inflammatory process.
• Lysosomal enzymes attack hyaluronate leading to loss of the diffusion barrier.
• Inflamed synovium contains large clefts which probably permit the passage of molecules of almost any size.
• Synovium becomes a “leaky sieve.”
• If infection is not quelled, synovium will necrose within 24 hours, followed by necrosis of chondrocytes and failure of glycosaminoglycan production.
• Acute inflammatory response along with cellular disintegration (with release of lysosomal enzymes and proteases) will further injure chondrocytes.
• Antibiotics can also easily get into the joint.
• But – lysosomal enzymes (collagenase, protease, galactosidase) damage the joint – therefore joint toilette required.
• Hydrocortisone blocks the release of lysosomal enzymes.

• Synovial fluid is an ultrafiltrate of blood plasma (by molecular sieving) plus hyaluronic acid and glycoproteins.
• Does not contain fibrinogen – thus no clotting.
• Exhibits non-Newtonianfluid characteristics – viscosity is not constant and inversely depends on shear rate. The relationship between viscosity and shear rate depends on amount of hyaluronate.

• Nourishes articular cartilage through diffusion.
• Lubricates via the following mechanisms:

1. Hydrodynamic (fluid separates the surfaces under load)
2. Boundary (slippery surfaces)
3. Weeping (fluid shifted to loaded areas)
4. Boosted (fluid entrapment)

• Lubricin (a glycoprotein) is a key lubricating component.