Beyond Skin and Joints: The Challenges of Enthesitis and Dactylitis in PsA

Enthesitis is a challenging aspect of psoriatic arthritis (PsA) management. Caused by the inflammation of tendons and ligaments inserting into bone, enthesitis is one of the key aspects of the CASPAR (Classification Criteria for Psoriatic Arthritis) criteria, and can be particularly uncomfortable and distressful for patients. Dactylitis is another common feature of PsA that can be challenging for patients. Both are frustrating for rheumatologists to manage. Dr. Elaine Husni, from the Cleveland Clinic, tackled the issues of enthesitis and dactylitis in her talk, "Your Patients with Enthesitis and Dactylitis: Let's Take a Closer Look."

Both dactylitis and enthesitis are clinical signs under the umbrella of peripheral manifestations of PsA. Regarding enthesitis, animal studies have shown that the areas in which tendons attach to bone tend to be high stress areas. Stress can promote new bone formation, and can be associated with proliferation of bone and entheseal inflammation. Stress may also be associated with increased IL-23 levels that can cause activation of resident entheseal Th-17 cells, which can lead to further enthesitis and osteoproliferation that is seen in PsA. What is so interesting about the pathophysiology of this process is that dysregulation of bone can lead to erosions as well as new bone formation in the same PsA patient. This is very different from what is found in RA patients.

Dactylitis may be acute (painful) or chronic (painless), and is usually asymmetrical in PsA. If tender, it is often associated with erosive disease and radiographic progression at that digit.

Management of enthesitis and dactylitis can be challenging. Local injection is often ineffective. The GRAPPA guidelines include options such as NSAIDs, DMARDs, and biological agents. However, the use of DMARDs is not largely supported by clinical trials. Positive results have been reported in clinical trials for anti-TNFs including adalimumab, etanercept, certolizumab, golimumab, and infliximab, but these trials have limitations (e.g., not all were placebo-controlled and in many, enthesitis and dactylitis were part of secondary outcome analyses).

Newer agents include PDE4 inhibitors (apremilast), IL-12/23 inhibitors (ustekinumab) and IL-17A inhibitors (secukinumab). Many reports show improvement with these agents. It is important to note that an improvement in dactylitis symptoms does not always ensure improvement in enthesitis.

Dr. Husni offered some expert opinion regarding the management of PsA patients with enthesitis and/or dactylitis: she recommended starting with physiotherapy and oral NSAIDs, and said she was unlikely to use methotrexate or sulfasalazine. She would use local steroid injections and topical NSAIDs as necessary, and would then proceed to anti-TNF agents, ustekinumab, secukinumab, or apremilast depending on factors such as focal vs diffuse involvement, recalcitrant or disabling disease, availability, as well as patient preference.

A major issue for rheumatologists in certain areas of the world, including Canada, is access to biologic agents for dactylitis and enthesitis only, without evidence of erosions on x-rays or axial disease. In addition, the dismissal of the use of oral DMARDs is interesting. One wonders if the trials and reports looking at methotrexate or sulfasalazine under-dosed these drugs, which may have lead to reduced responses?

More reports from ACR 2015