The knee joint is covered by cartilage, a resilient and smooth elastic tissue that protects the ends of long bones at the joints. It serves as a frictionless surface during movement. Cartilage is composed by a three-dimensional network of extracellular macromolecules called the extracellular matrix. The macromolecules that compose this matrix are proteins adorned with sugars (the proteoglycans), collagen ﬁbrils, that give structure, shape and tensile strength to the tissue, and water. The chondrocytes, the cartilage cells, are imbedded in this matrix, producing, maintaining, and renewing it. Optimal conservation of the matrix composition is crucial to preserve the biomechanical properties of articular cartilage, such as support, load distribution and to provide lubrication in the joints.
Albeit a resilient connective tissue, the constant weight-bearing and repeated trauma makes cartilage vulnerable to injury. Its structure has few to no blood vessels limiting its ability to regenerate and self-repair from some injuries, that usually heal through the formation of a fibrous scar tissue. Those scars’ tough, dense, and fibrous material fills the torn part of the cartilage, but have inferior biological and mechanical properties, degenerating with time. Eventually it will lead to a permanent loss of structure and properties that can cause pain, loss of function and disability, which represents a major problem in orthopaedic medicine. At that stage, it is no longer possible to revert back to the initial healthy properties and shape of the cartilage.
Articular cartilage injury is a continuum through our lives. Involving loss of components, rupture of cartilaginous matrix, ﬁnally leading to the rupture of the bone matrix. During this degenerative continuum, we can find defects in different stages that can be described as:
– Partial thickness defects or Mild Cartilage Injuries – macroscopically or examined by the unaided eye, they can be identified by softness and afterward by fibrillation of the cartilage, i.e., by the formation of some fibrous scar tissues. These scarred areas are thick with no access to bone marrow stem cells, which leads to a low ability to spontaneous or natural repair. Those defects evolve with time, being associated with swelling and mechanical symptoms caused by detachment of cartilage flaps that happens when cartilage separates from the bone and moves like a door with a hinge at one end;
– Full thickness defects or Severe cartilage injuries – macroscopic observation shows a complete erosion of the cartilage, leaving the underlying bone exposed in small or widespread areas. In these injuries, stem cells derived from the bone marrow, not from the cartilage, can form a ﬁbrocartilaginous tissue to compensate the loss, but are also associated with increased pain, limitation in activity and structural changes that lead to knee osteoarthritis.