The Aging Joint and Osteoarthritis
Osteoarthritis (OA) is a condition involving the degeneration of articular cartilage, remodeling of subchondral bone, and inflammation of the joint space (synovitis). This disease is age-related and is twice as prevalent in women as in men. Idiopathic OA results from changes that occur over a 15 to 20 year time span, particularly as the joint ages. The changes that lead to the development of idiopathic OA are insidious and gradual. There is an increased incidence of this form of OA following some type of joint trauma and injury. The most common site of idiopathic OA is the knee, but the condition can develop in any joint.
In contrast, familial osteoarthritis usually presents early, often after growth stops, mainly due to changes in the cartilage matrix that cause joint degeneration. This form of OA is less common and is associated with a mutation in the type II collagen gene.
Risk Factors of Osteoarthritis
According to researchers Loeser & Shakoor (2003), OA is not just an inevitable consequence of aging, but the changes associated musculoskeletal system aging increase the risk of developing this condition. OA occurs only if other risk factors are present in addition to advancing age, such as those factors associated with underuse or misuse of the joints and musculoskeletal system. In order for OA to develop, there must be complex interactions concerning balance, strength, and proprioception (how the body itself senses stimuli). Many older adults experience loss of joint function and pain but do not have radiographic evidence of OA disease.
Direct Correlation with Age
In 2002, researchers Martin & Buckwalter found that the incidence of OA was directly correlated with age. These scientists reported a strong association between advancing age and OA development. The articular aging changes that occur include softening and fraying of the articular surface, loss of matrix tensile stiffness and strength, and decrease in size and aggregation of proteoglycan aggrecans (a component of cartilage).
Because there is a decrease in ability of special cells called chondrocytes to maintain and repair tissue, OA results are manifested by decreased synthetic and mitotic activity (cell division), loss of anabolic growth factor response, and less functional link proteins. The progressive chondrocyte aging is evident because of expression of a particular enzyme called beta-galactosidase, as well as evidence of erosion of the cell length, and mitochondrial degeneration (mitochondria are essential for producing energy for the cell). These factors lead to age related loss of function.
The Pathophysiology of Osteoarthritis
OA is a complex disease caused by the contribution of metabolic and biomechanical factors that alter the tissue balance of subchondral bone and articular cartilage. A primary role in the pathophysiology of the cartilage is played by cellular and extracellular matrix interactions that are facilitated by cell surface receptors, or integrins.
These integrins are essential for the regulation of growth and the differentiation and maintenance of cartilage. With the osteoarthritis process, abnormal integrin molecule expression changes the cell signaling, modifies chondrocyte synthesis, and causes imbalance of cytokine molecules and regulatory factors. The cytokines activate the enzymatic degeneration of the cartilage structure. The main enzymes involved in this process are metalloproteinases (MMPs). Growth factors repair tissue damage when available in adequate quantities. The lack of growth factors can lead to OA pathogenesis.
General Changes in the Bone and Cartilage
OA involves not just degeneration of the cartilage, but also extensive remodeling of the subchondral bone. As the bone changes, there is formation of cysts from focal bone resorption. Scientific evidence also shows changes in bone metabolism with this disease. Bone cells alter chondrocyte metabolism in many people, leading to osteoporosis – a disease where bone density is reduced.
Osteophytes (bone spurs) develop from an endochondral process in the sites at the edges of the injured
cartilage. These osteophytes have a cap of articular cartilage and an actively remodeling bone base to provide some stability to the unstable joint. Bone proteins are produced excessively with joint inflammation. Degenerative changes occur with matrix turnover, and this process is detectable just days following a joint injury, such as damage to the meniscus (cartilage) of the knee. This remarkable interplay between cartilage and bone reflects the complexity of OA development. These changes occur years prior to the clinical disease onset, and the changes in bone metabolism suggest a systemic disease nature.
The classic loss of articular cartilage observed in OA often is used for diagnosis of the condition. Focal lesions enlarge and involve the joint compartments causing changes in the articulating surfaces by producing alterations in loading. With post-traumatic OA, there are alterations in the cartilage matrix detectable within days or weeks following the injury.
In idiopathic OA, degeneration is detected first at the articular surface of the cartilage, in the form of fibrillation. This involves splits or clefts developing between groups of cartilage cells that later penetrate the damaged superficial cartilage. Progressive cartilage erosion follows, and apoptosis (cell death) is enhanced. This process is generally very slow but may accelerate where there is significant joint injury and inflammation.
The Inflammatory Process of Osteoarthritis
With synovitis (inflammation of the synovium), there is an early increase in MMPs (enzymes) within the synovial fluid. This causes the synovial cells to synthesize and secrete hyaluronic acid. Hyaluronic acid is the substance that cushions the joint and serves as a shock absorber. In addition, cartilage oligomeric protein is increased in patients with synovitis. This is because of pro-inflammatory cytokine generation. For this reason, a lab test (C-reactive protein) is elevated in patients with OA. These changes define the inflammatory process of OA.
Osteoarthritis and Injury
Injury to a joint at any point can result in development of OA, especially in the aging joint. Other risk factors include obesity, aging, and heredity. For knee OA, the risk of disease development appears to increase as the amount of meniscal tissue removed increases. This is why doctors recommend special knee strengthening exercises and maintenance of body weight.
Researchers recently found that women who sustained anterior cruciate ligament (knee) injuries while playing soccer had changes that were visible by radiography within 12 years of the injury, and men with the same injury developed OA within 14 years. Repetitive use of the knee, such as jobs requiring heavy labor, increases the risk of knee OA with advancing age. Current research also suggests that sports enthusiasts and manual laborers are at the greatest risk for knee OA.
References
- Felton, D.T. (1988). Epidemiology of hip and knee osteoarthritis. Epidemiologic Reviews, 10, 1-28.
- Hutton, C. (1994). Osteoarthritis revisited and revised. Annals of Rheumatic Diseases, 53, 85-86.
- Loeser, R.F. & Shakoor, N. (2003). Aging or osteoarthritis: which is the problem? Rheumatic Diseases Clinics of North America, 29(4): 653-673. DOI: 10.1016/S0889-857X(03)00062-0
- Martin, J.A. & Buckwalter, J.A. (2002). Aging, articular cartilage chondrocyte senescence and osteoarthritis. Biogerontology, 3(5): 257 – 264.
- Poole, A.R. (1999). An introduction to the pathophysiology of osteoarthritis. Frontiers in Bioscience 4. Retrieved on December 7, 2012 from: http://www.bioscience.org/1999/v4/d/poole/fulltext.htm
- Roos, E. (2005). Joint injury causes knee osteoarthritis in young adults. Current Opinions in Rheumatology, 17(2), 195-200.
Last reviewed 26/Feb/2014
Dr Merlin Thomas
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