The researchers found that mice lacking the gene that controls the production of type VI collagen developed osteoarthritis at a rate more than five times greater than mice with a functioning gene.
To examine structures within the cartilage of mouse joints, Leonidas Alexopoulos, Ph.D., developed a novel "micro-vacuuming" technique. With this device, Alexopoulos extracted key structures within the cartilage of mouse hip joints, which are the size of the ball in a ball-point pen, and analysed how they responded to the stresses of everyday life.
The researchers focused their attention on the narrow region of tissue that surrounds the cartilage cells on the surface of joints and is known as the pericellular matrix (PCM). Together with cartilage cells like chondrocytes, collagen types II, VI and IX, and other proteins, the PCM forms a structure called a chondron, which is believed to provide a "buffer" zone between the cells and the remainder of the cartilage tissue.
"The interesting thing is that type VI collagen occurs nowhere else in the cartilage but the PCM, and no one really understood why," Alexopoulos explained. "When we analysed the PCM of mice unable to produce type VI collagen, we found that the chondrons in these mice were much softer and the joints did not respond well to mechanical pressures. The joint looked as if it osteoarthritis had developed.
"It appears now that the type VI collagen acts like a scaffold that provides structure and stiffness to the PCM," Alexopoulos continued. "With this model for osteoarthritis, we have a better understanding of how changes in the mechanical forces on the cells may lead to degeneration of the cartilage."
The results of their experiments with mice provide new insights that could lead to potential treatments for a disease that afflicts more than 40 million Americans, said the researchers.
MEDICA.de; Source: Duke University Medical Center