Abstract

under investigation are therefore of fundamental importance. OA can have biomechanical (injury) and biochemical origins. From the biochemical point of view, OA is a degenerative disease of the articular cartilage. Cartilage is a dense connective tissue that consists of a small population of chondrocytes within a large extracellular matrix made of type II collagen fibers (15–20% of the volume), proteoglycans (PG; 3–10%) and water (65–80%). PGs further consist of a protein core and negatively charged glycosaminoglycan (GAG) side chains, which endow the cartilage with a negative fixed charge density (FCD). This FCD attracts free-floating positive counter-ions, such as sodium (Na), which in turn attract water molecules within the cartilage through osmotic pressure. The negative charge from the GAG side chains also provides a strong electrostatic repulsive force between the PG molecules and is responsible for the compressive stiffness of cartilage. The collagen molecules aggregate into fibers that serve to immobilize the PG and provide a tensile force opposing the tendency of the PG to expand the cartilage. Early OA is mainly characterized by a reduction of FCD (or GAG) concentration, possible changes of size and organization of the collagen fibers, aggregation of the PG and increased water content. These changes lead to an alteration of the mechanical properties of the cartilage, which can therefore lose its loadand shear-bearing functions [5,6].

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call