Osteoarthritis: Effects on Cartilage, Bone, and Joint Function

How does osteoarthritis affect the skeletal system?

Osteoarthritis (OA) primarily affects the skeletal system by progressively degrading articular cartilage within joints, leading to friction, pain, and subsequent detrimental changes in the underlying subchondral bone, synovial tissues, ligaments, and surrounding musculature, ultimately compromising joint integrity and function.

Understanding Osteoarthritis: A Primer

Osteoarthritis is the most common form of arthritis, characterized as a chronic, degenerative joint disease. Unlike inflammatory arthritides such as rheumatoid arthritis, OA is primarily a mechanical breakdown of the joint's protective tissues. It is not simply "wear and tear" but a complex interplay of mechanical stress, biochemical changes, and cellular responses that lead to the gradual deterioration of the entire joint structure. While it can affect any joint, it most commonly impacts weight-bearing joints like the knees, hips, and spine, as well as the hands and feet.

The Primary Target: Articular Cartilage

The initial and most significant impact of osteoarthritis on the skeletal system is the breakdown of articular cartilage. This smooth, slippery connective tissue covers the ends of bones within a joint, providing a low-friction surface that allows bones to glide effortlessly over each other during movement. It also acts as a shock absorber, distributing mechanical loads across the joint.

In OA, the chondrocytes (cartilage cells) begin to lose their ability to repair the cartilage matrix effectively. This leads to:

• Softening and Fissuring: The cartilage becomes less resilient, developing cracks and erosions.
• Thinning and Erosion: Over time, the cartilage thins dramatically, eventually exposing the underlying bone.
• Increased Friction: With the loss of the smooth cartilage surface, bone-on-bone friction increases, leading to pain, stiffness, and further joint damage.
• Reduced Shock Absorption: The joint's ability to cushion impacts is severely compromised, transmitting greater stress directly to the subchondral bone.

Subchondral Bone Changes

The bone located directly beneath the articular cartilage is known as subchondral bone. As the overlying cartilage degenerates and loses its protective function, the subchondral bone experiences increased mechanical stress. In response to this altered loading, the bone undergoes significant changes:

• Subchondral Sclerosis: The bone becomes denser and thicker (sclerotic) as the body attempts to reinforce the stressed area. This increased rigidity can further impair the joint's ability to absorb shock.
• Subchondral Cysts: Fluid-filled sacs can form within the subchondral bone, often communicating with the joint space through microscopic defects in the bone. These cysts can contribute to pain and structural weakening.
• Bone Marrow Lesions (BMLs): These are areas of increased fluid and inflammation within the bone marrow, visible on MRI. BMLs are strongly associated with pain and progression of OA.

Osteophyte Formation (Bone Spurs)

As the joint attempts to stabilize itself and repair the damaged areas, the body often responds by forming osteophytes, commonly known as bone spurs. These bony outgrowths develop along the joint margins, where the cartilage has eroded and the bone is exposed.

• Mechanism: Osteophytes are believed to be the body's attempt to increase the surface area of the joint and reduce stress, or to stabilize the joint in the face of cartilage loss.
• Consequences: While seemingly a reparative process, osteophytes can
  • Restrict joint movement, limiting range of motion.
  • Impinge on surrounding soft tissues, nerves, or blood vessels, causing pain and neurological symptoms (especially in the spine).
  • Contribute to joint stiffness and crepitus (grinding sensation).

Synovial Membrane and Fluid Alterations

Within a joint capsule, the synovial membrane lines the joint and produces synovial fluid, which lubricates the joint and provides nutrients to the cartilage. In OA, these components are also affected:

• Synovitis: The presence of cartilage debris and inflammatory mediators within the joint space can irritate the synovial membrane, leading to inflammation (synovitis). This causes joint swelling, warmth, and pain.
• Altered Synovial Fluid: The quality and quantity of synovial fluid can change, becoming less viscous and less effective as a lubricant and shock absorber, further accelerating cartilage degradation.

Ligament and Tendon Involvement

The structural integrity of a joint is also maintained by ligaments (connecting bone to bone) and tendons (connecting muscle to bone). As OA progresses, these surrounding soft tissues can be affected:

• Ligament Laxity or Contracture: The instability caused by cartilage loss and bone changes can lead to stretching and laxity of ligaments, further destabilizing the joint. Conversely, chronic pain and disuse can lead to ligamentous contractures, reducing joint mobility.
• Tendon Strain and Tendinopathy: Altered joint mechanics and compensatory movements due to pain can place abnormal stresses on surrounding tendons, leading to inflammation (tendinitis) or degeneration (tendinopathy).

Muscle Atrophy and Weakness

The skeletal system's functionality is intrinsically linked to the muscular system. In OA, pain, stiffness, and reduced physical activity frequently lead to muscle inhibition and atrophy around the affected joint.

• Impact on Joint Stability: Weakened muscles provide less dynamic support to the joint, exacerbating instability and increasing stress on the already damaged structures.
• Vicious Cycle: Muscle weakness contributes to poor biomechanics, which can accelerate OA progression, leading to more pain and further disuse, creating a debilitating cycle.

Systemic Effects on the Skeletal System

While OA is localized to specific joints, its chronic nature and impact on mobility can have broader systemic effects on the skeletal system:

• Altered Gait and Posture: Pain and stiffness in weight-bearing joints often lead to compensatory changes in walking patterns and posture, which can place abnormal stress on other joints and the spine, potentially leading to secondary musculoskeletal issues.
• Reduced Bone Density (Localized): While subchondral bone often becomes sclerotic, disuse and reduced weight-bearing due to pain can lead to localized bone mineral density loss in other parts of the affected limb or even generalized bone loss if overall activity levels significantly decrease.
• Increased Fall Risk: Impaired balance, muscle weakness, pain, and joint instability significantly increase the risk of falls, leading to fractures.

In conclusion, osteoarthritis is a multifaceted disease that profoundly impacts the skeletal system, initiating with cartilage degradation and cascading into a series of detrimental changes affecting every component of the joint and its surrounding structures. Understanding these mechanisms is crucial for developing effective management strategies aimed at preserving joint function and improving quality of life.