Rheumatoid Arthritis (RA) is a chronic, systemic, autoimmune inflammatory disease that primarily attacks the lining of the joints. This persistent inflammation eventually destroys cartilage and bone, often requiring surgical replacement with an artificial joint (arthroplasty). Although the artificial joint provides a new mechanical structure, it is implanted within a body that harbors ongoing systemic inflammation. The primary concern is whether this persistent RA activity can compromise the integrity and longevity of the prosthetic device. This article addresses the specific risks and considerations when RA activity persists around an implanted artificial joint.
How Systemic Inflammation Interacts with the Prosthesis
The inflammatory environment characteristic of active RA directly affects the tissues surrounding the artificial joint components. This systemic disease maintains a high concentration of pro-inflammatory signaling proteins, known as cytokines, in the bloodstream and the local joint space. Cytokines such as Tumor Necrosis Factor-alpha (TNF-α), Interleukin-1 (IL-1), and Interleukin-6 (IL-6) are drivers of this damaging process. These molecules disrupt the natural balance between bone formation and bone resorption, a process called remodeling.
The cytokines activate specialized cells called osteoclasts, which are responsible for breaking down bone tissue. Specifically, they stimulate the RANKL/RANK signaling pathway, increasing the number and activity of these bone-resorbing cells. This leads to accelerated bone resorption, or osteolysis, in the bone bed immediately adjacent to the prosthesis. The artificial joint relies on a secure, stable interface with the patient’s bone, whether fixed with cement or designed to allow bone to grow directly onto its surface.
The chronic, cytokine-driven osteolysis compromises this bone-prosthesis interface, essentially dissolving the bone that holds the implant in place. This inflammatory destruction weakens the mechanical fixation of the artificial component over time. The result is a failure of the implant’s physical connection to the skeleton, driven by the ongoing inflammatory state of the patient, not mechanical wear.
Distinct Complications in RA Patients
Patients with RA face a significantly higher risk of two distinct complications following joint replacement surgery compared to those with non-inflammatory conditions like osteoarthritis. The first is aseptic loosening, which occurs when the implant’s fixation to the bone fails without an active infection. This complication is a direct consequence of the inflammatory mechanism described previously, where RA disease activity accelerates the breakdown of the periprosthetic bone.
Higher inflammatory disease activity, measured by indices like the Simplified Disease Activity Index, is directly associated with an increased risk for radiographic signs of loosening. The rate of loosening is measurably higher in RA patients compared to those undergoing arthroplasty for osteoarthritis. When the bone supporting the implant is continuously eroded by inflammation, the resulting instability necessitates revision surgery.
The second major complication is Periprosthetic Joint Infection (PJI), a severe infection surrounding the artificial joint. RA patients are considered an independent risk factor for PJI, with infection rates up to three times higher than in the general arthroplasty population. This elevated risk stems from the underlying systemic immune dysfunction caused by RA and the necessary use of immunosuppressive medications.
The medications used to control RA, such as Disease-Modifying Antirheumatic Drugs (DMARDs) and biologics, intentionally suppress the immune system to halt joint destruction. While effective at controlling the disease, this immunosuppression makes the patient more vulnerable to bacterial colonization during and after surgery. Furthermore, the use of corticosteroids has been strongly linked to an increased risk of post-operative infection. The challenge is managing the systemic disease without increasing the odds of this devastating infection.
Optimizing Medical Management for Joint Replacement Success
Long-term success for an artificial joint depends on maintaining stringent control over the systemic disease. This requires careful coordination between the rheumatologist, who manages the RA, and the orthopedic surgeon. Pre-operative planning focuses on ensuring the patient enters surgery with the lowest possible RA disease activity to minimize the inflammatory burden around the implant site.
Perioperative management of immunosuppressive medications is important. Most guidelines recommend temporarily pausing certain medications, particularly biologic DMARDs and some targeted synthetic DMARDs, before surgery. This temporary discontinuation is a calculated risk to allow the patient’s immune function to recover slightly, thereby reducing the risk of PJI. Anti-TNF-α biologics are often held for a period corresponding to their half-life before the operation.
The risk of infection must be balanced against the risk of an RA flare if medication is stopped for too long, which would increase the inflammatory threat to the new joint. Some conventional synthetic DMARDs, such as methotrexate, are often continued throughout the perioperative period, as evidence suggests they do not significantly increase infection risk. High doses of oral glucocorticoids are a known risk factor and should be reduced as much as possible before surgery.
Following the procedure, the goal is to restart the RA medications promptly once the surgical wound has healed, typically around two weeks post-operation. Continuous RA treatment is necessary to reduce the chronic inflammatory load that drives aseptic loosening. Minimizing systemic inflammation reduces the rate of bone resorption around the implant, offering the best chance for the long-term stability and function of the new joint.