Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease where the body’s immune system mistakenly attacks its own healthy tissues and organs, leading to widespread inflammation. The skeletal system, which provides the body’s structure, protection, and support, is a frequent target of this systemic inflammatory process. Lupus often causes damage throughout the musculoskeletal structure, affecting joints, cartilage, and bone tissue. The resulting conditions can range from painful joint inflammation to severe bone deterioration.
Inflammatory Impact on Joints and Cartilage
Musculoskeletal involvement is one of the most common manifestations of SLE, affecting nearly 90% of patients at some point. This involvement presents as arthralgia (joint pain without swelling) or true arthritis, characterized by synovitis (inflammation of the joint lining). Lupus arthritis is typically symmetrical, affecting the small joints of the hands, wrists, and knees.
Chronic inflammation attacks the synovial lining, leading to swelling, tenderness, and stiffness. Unlike rheumatoid arthritis, lupus arthritis is generally non-erosive, meaning it does not typically cause destructive damage to the underlying bone. However, the inflammation can severely affect surrounding soft tissues, such as the tendons and ligaments.
Damage to these soft tissues can lead to joint deformities, known as Jaccoud’s arthropathy. This deforming, non-erosive condition results in misalignment, such as ulnar deviation in the fingers. A defining feature of Jaccoud’s arthropathy is that these deformities are often passively correctable, indicating laxity in the soft tissue structures rather than bone or cartilage destruction.
The Risk of Osteoporosis and Bone Loss
People with Lupus face a significantly accelerated risk of developing low bone mineral density, leading to osteopenia and osteoporosis. This condition is driven by two main factors.
The chronic systemic inflammation inherent to Lupus directly disrupts the natural bone remodeling process. Inflammation increases the activity of osteoclasts (cells that break down mature bone tissue) while simultaneously reducing the activity of osteoblasts (cells that form new bone). This imbalance leads to a net loss of bone mass over time.
Additionally, the necessary treatment for Lupus often involves the frequent and prolonged use of corticosteroids, such as prednisone, which are a major contributor to bone loss. Corticosteroids interfere with the body’s ability to absorb calcium and inhibit the function of bone-forming osteoblast cells. Even relatively low daily doses (2.5 mg to 7.5 mg) can increase the risk of fractures when taken for extended periods.
This accelerated bone demineralization significantly increases the risk of fragility fractures, particularly in the vertebrae and hips. Monitoring bone mineral density through a Dual X-ray Absorptiometry (DEXA) scan is essential for Lupus patients, often recommended within six months of starting corticosteroid therapy.
Avascular Necrosis: Bone Tissue Death
A severe structural complication associated with Lupus is Avascular Necrosis (AVN), also known as osteonecrosis. AVN is the death of bone tissue caused by an interruption of the blood supply to a section of the bone. The lack of blood flow deprives bone cells of oxygen and nutrients, causing the tissue to die.
While Lupus-related vasculitis can sometimes contribute, the most significant risk factor for AVN in Lupus patients is the high-dose, long-term use of corticosteroids. The proposed mechanism suggests that high steroid doses may cause fat cells to swell within the bone marrow or lead to the formation of small fat emboli that block the tiny arteries supplying blood to the bone. This circulatory failure causes the bone to weaken and eventually collapse.
The most commonly affected sites are the ends of long bones, particularly the femoral head in the hip, followed by the knee and shoulder joints. This condition causes severe pain, especially when bearing weight, and can rapidly lead to the destruction of the joint surface. In advanced stages, the collapse of the bone structure necessitates surgical intervention, often requiring total joint replacement to restore function and alleviate chronic pain.