Joints allow movement while providing mechanical stability. They are classified as solid (nonsynovial) and cavitated (synovial). The solid joints, also known as synarthroses, provide structural integrity and allow only minimal movement. They lack a joint space and are grouped according to the type of connective tissue (fibrous tissue or cartilage) that bridges the ends of the bones. Fibrous synarthroses include the cranial sutures and the bonds between roots of teeth and the jawbones. Cartilaginous synarthroses (synchondroses) are represented by the symphyses between the sternum and the ribs and between bones of the pelvis. Synovial joints, in contrast, have a joint space that allows for a wide range of motion. Synovial membranes enclose these joints. The membranes are lined by type A synoviocytes that are specialized macrophages with phagocytic activity and type B synoviocytes that are similar to fibroblasts and synthesize hyaluronic acid and various proteins. The synovial lining lacks a basement membrane, which allows for efficient exchange of nutrients, wastes, and gases between blood and synovial fluid. Synovial fluid is a plasma filtrate containing hyaluronic acid produced by synovial cells that acts as a viscous lubricant and provides nutrition for the articular cartilage.
Hyaline cartilage is a unique connective tissue ideally suited to serve as an elastic shock absorber and wear-resistant surface. It lacks a blood supply, lymphatic drainage, and innervation. Hyaline cartilage is composed of water (70%), type II collagen (10%), proteoglycans (8%), and chondrocytes. The collagen resists tensile stresses and transmits vertical loads. The water and proteoglycans resist compression and limit friction. The chondrocytes synthesize the matrix as well as enzymatically digest it. Chondrocytes secrete degradative enzymes in inactive forms and enrich the matrix with enzyme inhibitors.
Osteoarthritis (OA), also called degenerative joint disease, is characterized by degeneration of cartilage that results in structural and functional failure of synovial joints. It is the most common disease of joints. Although the term osteoarthritis implies an inflammatory disease, it is considered an intrinsic disorder of cartilage in which chondrocytes respond to biochemical and mechanical stresses resulting in the breakdown of the matrix and failure of its repair. Nevertheless there is little doubt that inflammatory mediators (described later) whose release is triggered by joint injury perpetuate and worsen the damage.
In most instances OA appears insidiously, without apparent initiating cause, as an aging phenomenon (idiopathic or primary osteoarthritis). In these cases the disease is usually oligoarticular (affects few joints). In about 5% of cases, OA appears in younger individuals with some predisposing condition, such as joint deformity, a previous joint injury, or an underlying systemic disease that places joints at risk. In these settings the disease is called secondary osteoarthritis. The prevalence of OA increases exponentially beyond the age of 50, and about 40% of people older than 70 are affected.
The lesions of OA stem from degeneration of the articular cartilage and its disordered repair. Articular cartilage serves as a low-friction surface that transmits loads to the underlying bone. Cartilage resists compression through the viscoelastic properties of the extracellular matrix (principally type II collagen, proteoglycans, and water) secreted by chondrocytes. Repeated biomechanical stress contributes to development of OA, but genetic factors, including genes encoding components of the matrix and signaling molecules, also play a role. These factors are thought to predispose to chondrocyte injury, which in turn leads to alteration of the extracellular matrix (