Osteoarthritis Resources and Blog

How will it progress?

By on June 2, 2014 in Uncategorized

The Anatomy and Joint Disease of OSteoarthritis:

Although the disease process is degenerative over time, otherwise termed the Osteoarthrosis component, it can also present with low-grade inflammation in the periarticular tissues.  The disease presents asymmetrically and can affect a number of joints throughout the body. Osteoarthritis is most common in the distal interphalangeal joint (DIP) of the hand, base of the thumb-first carpometacarpal joint (CMC) (yellow and prurple area), intervertebral facet joints (IVFJ), as well as various joints of the knee, ankles, and hip.  OA can also affect the wrist, elbow, and shoulder, but these joints are less commonly affected. In joints afflicted with OA, all of the components within the joint and those structures surrounding and supportive of the joint are affected.  These include the cartilage, bone, soft tissue, synovium, joint capsule, periarticular ligaments, periosteum of the bone, and the periarticular muscles.  The function of articular cartilage is to absorb stress under a mechanical load and to provide a smooth surface for moving joints to course over.  The cartilage consists of cells called chondrocytes, which are embedded in a matrix, which consist of substances such as collagen and proteins that function, respectively, to provide strength, and to hydrate and sustain the chondrocytes.  The chondrocytes line the joint, creating a cellular layer, and produce a substance called synovial fluid, which provides lubrication between the smooth surfaces of the bones.  The joint capsule is a structure that encapsulates the joint space, or synovium.  The supporting ligaments and tendons of the joint lie external to the capsule. The matrix of the cartilage is in a constant state of break down and repair, referred to respectively as catabolism and anabolism. This process is ideally balanced or homeostatic and is mechanically driven and chemically mediated.

An Imbalance:

An imbalance in the homeostatic process of the degradation and rebuilding phases of cartilage is believed to be the primary cause of OA.  When joints engage in movement, the production of chondrocytes is stimulated in order to replace those cells lost in degradation.  Prolonged disuse of joints causes changes in the makeup of the matrix of cartilage, ultimately resulting in a loss of joint function.  Age-related changes in the composition of the matrix, decreased sensitivity of chondrocytes to stimulation and a loss of function of these cartilaginous cells all contribute to the development of OA in a joint.  Abnormal reparative processes and inflammation of the cartilage can lead to the formation of anomalous boney structures known as osteophytes or bone spurs, which replace normal flexible, functional cartilage.

Inflammation can occur through the formation of osteophytes and through swelling that is associated with the inflammatory process, contributes to patient pain and discomfort.


The most prominent inflammation, termed synovitis, presents in the form of warmth, swelling, and thickening of the fluid within the joint.  Though laboratory testing has identified common signs of inflammation in some Osteoarthritic patients, not all patients with OA present with the inflammatory component of the disease.

Pain involving one or more joints is the most common complaint made by osteoarthritic patients to their physicians.  The onset of pain in OA is insidious and its severity is mild to moderate.  OA pain in less-advanced disease states is generally worsened with joint use and relieved by joint rest.  However, patients exhibiting more advanced OA are more likely to complain of joint pain during rest and throughout the night.  The degradation and loss of cartilage in the joint causes pain, as the weight-bearing joints are no longer cushioned at the junction of the two bones.  The structural sources of pain include the synovial membrane, joint capsule, periarticular ligaments, periarticular muscle spasm, periosteum, and subchondral bone.  The pain mechanism can be the result of one of the many abnormal features that can occur in OA.  Possible mechanisms of pain in OA include: increased intracapsular pressure, pressure between bones, microfractures, effects of muscle wasting, and the structural changes within and around the joint.


In addition to pain, stiffness is also a common symptom of OA.  Stiffness associated with prolonged periods of immobility, as during sleep, often resolves within thirty minutes of joint use.  The stiffness associated with OA is the result of abnormal joint function, and the effect that it has on the structures surrounding the joint.  The duration of time for stiffness to resolve lengthens with progression of the disease.  In addition to stiffness, patients may also present with crepitus, which is an often audible and palpable grinding between the bones of a joint, secondary to the increased contact between boney surfaces.  Additional symptoms resulting from structural changes within the joint include a decreased range of motion in the affected joint, resulting in functional impairment.

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