In recent decades innovations in total knee arthroplasty (TKA) biomaterials, design and surgical techniques have increased the rate of patient satisfaction. However, 11–25 % of patients report a noticeable improvement with respect to preoperatively but are still not satisfied with their TKA [
1,
2]. It has been reported that even one year after surgery, a relevant percentage of patients (37 %) have not attained complete recovery [
3] and indicates unfavourable long-term pain outcome (10 %–34 %) [
4]. It has been suggested that early pain control and joint inflammation resolution following TKA may prevent long-term pain and functional limitations in uncomplicated TKAs [
5]. Indeed, the strong local inflammatory component, which is present for some weeks after TKA surgery, may affect soft-tissue healing, leading to excess fibrous tissue, hypertrophic synovitis and heterotopic ossification that sustains chronic inflammation of the joint [
6]. Pro-inflammatory mediators are directly responsible for several clinical symptoms that reflect the structural progression of osteoarthritis [
7]. In particular, a significant correlation between interleukin-6 (IL-6) concentrations in joint fluid and functional scores was found one month after TKA, demonstrating that an intense inflammatory response is associated with a slow recovery [
8]. It has also been demonstrated that high pre-operative synovial fluid concentrations of tumor necrosis factor-α (TNF-α), metalloproteinase-13 (MMP-13) and IL-6 in the knee are predictive of delayed pain resolution two years following TKA [
9]. Moreover, a significant increase of IL-1β levels in the synovial fluid has been observed following TKA [
10]. Therefore, the synovial membrane appears to be a promising target for novel strategies to control inflammation, prevent structural joint alterations and treat clinical symptoms, such as pain and swelling, after knee surgery [
7]. Varani et al. [
11], after having demonstrated the presence of A
2A or A
3 adenosine receptors in human-fibroblast-like synoviocytes, showed that their modulation could be used to control inflammatory joint diseases [
12]. Indeed, pulsed electromagnetic fields (PEMFs) show agonist activity for A
2A and A
3 adenosine receptors, indicating that they can be used to control local inflammation and manage joint diseases [
11,
12]. In human osteoarthritic fibroblasts, PEMFs increase the activation of these receptors reducing the synthesis of inflammatory mediators such as prostaglandin E
2 (PGE
2) and IL-6 and -8 [
13].
The primary objective of this randomised controlled trial in patients undergoing TKA stimulated with PEMF was to evaluate pain relief during follow-up; the secondary aim of the study was to determine whether PEMF could reduce joint swelling and accelerate functional recovery. A phone survey was performed to evaluate the number of patients still experiencing pain and functional limitation three years post-TKA.