The bones of the human skeletal system are connected by a complex series of joints, which connect two or more bones and allow for a wide variety of movements that would otherwise be impossible (Briant 2008).

In order to facilitate smooth joint movement, the surfaces of joints are lined by a low-friction, load-distributing, wear-resistant tissue called articular cartilage, which is composed of 65 to 80 percent water, collagen (fibrous proteins), proteoglycans, and chondrocytes (cells that produce cartilage) (Pearle 2005). In adults, damaged cartilage has a very limited capacity for self-healing due to blood supply limitations, and the relatively poor capacity of resident chondrocytes to migrate and proliferate (Henrotin 2009).

Joints can be classified as synovial, fibrous, or combination joints, based on the presence or absence of a synovial membrane and the amount of motion that occurs in the joint.
Normal synovial joints allow a significant amount of motion the articular surface. These joints are composed of the following:
Articular cartilage
Subchondral bone
Synovial membrane
Synovial fluid
Joint capsule

Normal articular surface of synovial joints consists of articular cartilage surrounded by proteoglycans and collagen. The cartilage protects the underlying subchondral bone by distributing large loads, maintaining low contact stresses, and reducing friction.
Synovial fluid supplies nutrients to the articular cartilage; it also absorbs shock from slow movements, as well as the elasticity required to absorb shock from rapid movements.

Osteoarthritis (OA) can occur in any freely moving joint in the body, but it most commonly affects load- and stress-bearing joints like the knees, lumbar spine, and hips (Lawrence 2008).
At the onset of OA, where cartilage cells depart from their normal pattern of growth and differentiation, the outermost layer of articular cartilage begins to soften as its protein structure degrades. As OA progresses, this loss of protein content becomes more rapid, affecting deeper and deeper layers of cartilage (Pearle 2005). Eventually, the entire protective layer of cartilage is destroyed as the chondrocytes become completely overwhelmed and unable to reverse the tissue damage.

Because cartilage does not contain free nerve endings, joint destruction is typically not associated with pain until it is considerably advanced. This is a major reason why OA tends to be diagnosed so late in the disease process (Bijlsma 2011; Felson 2005).
With a majority of the protective cartilage now gone, the raw surfaces of the bones become exposed to gradual bone-on-bone erosion. This process inevitably leads to the destruction/deformation of nearly all the joint structures involved in movement, and is often accompanied by chronic inflammation in and around the joint space (i.e., synovial membrane) (Pearle 2005).
In many cases, the bone destruction caused by OA is followed by “remodeling”, which is characterized by bone spurs that grow along the joint margins. Although these bony outgrowths are believed to stabilize the injured joint by increasing bone surface area, they are also a significant source of pain, as joint movement causes them to rub against adjacent bones, nerves, and/or soft tissue (Mayo Clinic 2009; Pearle 2005). The intensity of symptoms can vary significantly, ranging from mild to severe (Strand 2011).
The pain caused by OA is typically worsened upon physical activity. As the disease progresses, however, patients may begin to report pain even when resting. Complaints of stiffness tend to occur more frequently in the morning, and often resolve shortly after awakening. However, any period of prolonged inactivity can cause this stiffness, which is sometimes referred to as “inactivity gelling” (Kalunian 2012b).
In cases of advanced OA, patients often report both physical and psychosocial disability. In fact, along with cardiovascular disease, OA causes more disability than any medical condition among the elderly (Hunter 2009).

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