Osteoarthritis

Overview

Osteoarthritis (OA) is the most common cause of arthritis in adults, especially the elderly, and is fundamentally the result of articular cartilage degeneration. The primary cause of this cartilaginous degeneration is long-term mechanical stress, leading to dysregulation of cartilage homeostasis and ultimately its destruction. Bony changes characteristic of OA are a purely secondary feature that follows increased stress on bone due to cartilage degeneration. In the average patient the joints of the hand, C/L-spine, hips, and knees are especially prone to OA although atypical joints can be involved if previously injured.

Etiology and Pathogenesis

Chronic mechanical stress is the ultimate cause of OA; however, joints can show variable levels of vulnerability depending on the stresses placed upon them and their architecture. A healthy joint with little stress is unlikely to develop OA. In contrast, the joints of the hands and large weight-bearing joints of the legs and spine are frequently involved, representing high-use, high-stress joints in the average human body. The hips, knees, and L-spine may develop OA earlier in the obese due to increased loads. Additionally, certain individuals with specialized occupations may see atypical joints involved due to their occupational over use. Joints that have undergone deformity or damage due to previous injury are much more likely to develop secondary OA due to derangements in the distribution of load within the injured joint. As a point of interest, one question is why certain joints of the lower extremities such as the knee and hips are frequently involved while the ankles are spared. This may represent non-ideal morphological changes that occurred during evolution which adapted joints originally optimized for knuckle-walking to upright walking.

Articular Cartilage helps to spread the force load at a joint across the entire articular surface of the bone and with the aid of the lubricating synovial fluid acts as a near frictionless surface. Cartilage is an avascular tissue and is maintained by chondrocytes which remodel the tissue by resorbing degenerating cartilage and synthesizing fresh cartilage. The balance between resorption and synthesis must be finely maintained to avoid cartilaginous overgrowth or excess loss.

The trigger for osteoarthritic changes appears to be long-term mechanical stress; however, the cartilaginous degeneration appears to be compounded by factors beyond simply wear-and-tear. Mechanically stressed cartilage becomes more metabolically active and chondrocytes not only proliferate but appear to increase their remodeling activity likely in an attempt to repair damage. Over time, this response appears to yield imbalances in cartilage remodeling that accelerates degeneration by rendering cartilage weaker and more prone to injury. In the end stage chondrocytes appear to undergo apoptosis, leading to their loss from the cartilage.

Long-term degeneration of overlying cartilage exposes the bone to abnormal mechanical stresses that can activate osteoblasts and osteoclasts to increase bone remodeling. This bone remodeling activity may also be stimulated by cytokines released from activated chondrocytes in the overlying cartilage. Whatever the cause, bone underlying degenerating cartilage undergoes thickening and sclerosis visible on radiography. At the edges of affected cartilage where mechanical loads are minimal, the cartilage proliferates and becomes slowly ossified, yielding the progressive development of bony outgrowths, termed "osteophytes".

Morphology

In the early stages the surface of affected cartilage shows fibrillation with initially small defects gradually extending down to the underlying bone. Eventually these focal defects coalesce and the underlying bone can become completely exposed. The chondrocytes in damaged cartilage initially proliferate and increase their metabolic activity which is associated with swelling of the surrounding cartilage and its mechanical softening. Eventually, chondrocytes can be seen to undergo apoptotic loss.

Subchondral bone in affected joints undergoes sclerosis which can be observed on radiography. At the edges of affected cartilage, proliferating cartilage undergoes progressive ossification, developing into bony outgrowths termed "osteophytes". These osteophytes can grow to become quite large, easily observed as bony nodules at affected joints on physical exam.

Clinical Consequences

OA is typically a disease of the elderly with acceleration in the obese or in joints that have undergone previous injury. In the average patient the hips, knees, lumbar spine, cervical spine, PIPs, DIPs of the hands can be classically involved as well as the MTP and carpometacarpal (CMC) joint of the thumb.
Initially, patients will report transient self-resolving pain after periods of increased activity but over time pain in the affected joint can become constant, often increasing over the course of the day. Stiffness is often present in the morning but usually resolves rapidly, within less than 30min. Additionally, development of OA is often asymmetric. The progression of pain throughout the day, the rapid resolution of morning stiffness, and the asymmetric distribution are all important features that distinguish OA from rheumatoid arthritis.
The presence of osteophytes are also diagnostically useful and can be frequently observed grossly as the characteristic hard, bony hypertrophy of OA-affected joints. Osteophytes at the DIPs are termed "Heberden's Nodes" while those at the PIPs are termed "Bouchard's Nodes". Osteophytes as well as subchondral sclerosis are features of OA on radiography and contrast with the subchondral erosions of RA. Finally, the irregular degeneration of affected cartilage can be indirectly observed as "crepitation" in affected joints as they are passively moved on physical exam.

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