§
Clinical guidelines:
• Triamcinolone acetonide for all indications, especially high motion joints
• Methylprednisolone only for advanced OA or when total triamcinolone
dose is insufficient for multiple joint therapy.
• Generally used with 20 mg of hyaluronic acid as combination therapy to
allow lower corticosteroid dosage, protect chondrocytes against
potential deleterious corticosteroid effects and enhance antiinflammatory effect. There is limited scientific evidence for synergism.
• Steroids are best reserved for cases of acute, severe, post traumatic
synovitis and capsulitis. Realistically they are used in all joint diseases.
• Avoid using when intra-articular fracture or instability is present.
• Combine with 1 to 2 weeks stall rest.
• The use of high, repeated doses is detrimental.
• Do not exceed 18-20 mg triamcinolone or 200 mg methylprednisolone
per treatment as total body dose.
Hyaluronic Acid (Hyaluronan)
Hyaluronan (HA) is a glycosaminoglycan composed of the disaccharides Dglucuronic acid and N-acetyl-D-glucosamine that is secreted by the type B
synoviocytes of the synovial membrane. HA determines the viscoelasticity of
synovial fluid and serves as the principal lubricant of synovial soft tissues. HA
also may influence the composition of synovial fluid through steric hindrance
of active plasma components and leukocytes from the joint cavity.
Furthermore, HA appears to modulate the chemotactic response within the
synovial membrane by reducing cell migration and decreasing rates of
diffusion and flow of solutes.
HA was initially developed as an intra-articular drug for the purpose of
viscosupplementation. A number of different mechanisms are currently
reported and include analgesia through reductions in the sensitivity of articular
nerve endings and anti-inflammatory effects based on inhibition of
inflammatory cells and mediators. Furthermore HA leads to suppression of
synthesis of inflammatory cytokines and cartilage-degrading proteinases,
regulation of PGE2 synthesis, scavenging of oxygen-derived free radicals and
degradative enzymes. In view of short half-life of exogenous HA (6 hours), the
mechanism of binding to the CD44 membrane receptor of synoviocytes has
been credited with extended pharmacodynamic effects of the drug. It has
been suggested also that this binding mechanism stimulates the synthesis of
high molecular weight HA by synoviocytes, and promotes proteoglycan
synthesis by chondrocytes.
Stearic hindrance by large molecular weight HA preparations (> 1.106 dalton)
has been credited with improved synovial membrane permeability control,
reduced leakage of large protein molecules from the circulation and reduced
joint distension.
There is controversy regarding efficacy and molecular weight of high (MW in
the range of 0.5 to 2.0 x 106 dalton) versus low (MW < 0.5 x 106 dalton)
molecular weight HA. Proponents of the visco-supplementation theory believe
15-‐18
February
2016
East
London
Convention
Centre,
East
Lo ndon,
South
Africa
156