Tendon disorders are frequent and are responsible for substantial morbidity both in sports and in the workplace [1]. Although the mechanisms that weaken the tendon are poorly understood, most tendon disorders are caused by an abnormal/failure regenerative process. However, the involvement of inflammatory cues in the development of tendon injuries is expected since overuse or repetitive stretching are known to trigger the release of pro-inflammatory mediators, which can induce expression of metalloproteinases and leads to collagen degradation [2]. In previous studies, magnetotherapy has shown to impact biological processes as proliferation and differentiation [3] and to modulate the inflammatory response by controlling the mast cell infiltration and healing in a rodent model upon implantation of magnetically responsive starch-PCL membranes (magSPCL) [4].

In this study we propose to establish an in vitro model by exogenous supplementation of interleukin 1β (IL-1β) to tendon resident cells (TDCs) isolated from tendon samples obtained of arthroplasty surgeries, in order to study TDCs response to inflammation with or without the actuation of a low frequency magnetic field (MF, 1h/day). Cells were collected after IL-1b stimulation (0.01 – 1ng/ml), immediately before and after MF stimulation, and at 24h, 48h and 7 days after MF and characterized for cell viability, proliferation, mRNA transcriptional levels of inflammatory cytokines and ECM remodeling proteins.

Preliminary results showed that treatment with 1ng/ml concentration of IL-1b had a positive effect on cell viability and proliferation 7 days after treatment. Although MF properties do not particularly impact cellular response, treatment with 1 ng/ml of IL-1b also influences the expression of inflammation and matrix degradation genes.

Since we also envision investigating the anti-inflammatory properties of magSPCL membranes in the modulation of TDCs response with or without IL-1B treatment (1ng/ml), ongoing studies with magnetic actuation are being performed with TDCs seeded onto these membranes.