Influence of Pulsed Electromagnetic Field on human tendon-derived cells response using an induced model of inflammation

Tendons are mechano-responsive tissues[1] highly prone to injury, and tendon lesions are a considerable cause of morbidity and disability. Upon injury, the healing is slow and results in poor biomechanical quality of healed tendons that often require surgical interventions and rehabilitation[2]. Inflammation is known to have a pivotal role in tendon healing and failed healing responses contribute to the progression of tendinopathies. Thus, studying tendon inflammation may provide a target for managing injuries and stimulate tendon regeneration. Recently, pulsed electromagnetic field (PEMF) has shown potential to modulate inflammation[3], however, PEMF implications in tendons within an inflammation-relevant context remain largely unknown. Thus, this work aims to investigate PEMF potential to modulate human tendon resident cells (hTDCs) behavior using an IL-1b induced inflammation model.

In this model, hTDCs were stimulated with IL-1b, a well described pro-inflammatory cytokine, and their response assessed for tenogenic and inflammatory markers. Afterwards, the effect of PEMF in hTDCs cells treated with IL-1b (1ng/ml) was investigated varying the magnetic field strength (15-50Gauss) and the frequencies (5-200Hz) within clinical therapeutic ranges [4,5] using a magneto therapy equipment. After IL-1b stimulation, and immediately before and after 1h exposure to PEMF, hTDCs were characterized for cell viability, proliferation and expression of inflammatory cytokines. Cells response was also investigated 24h, 48h and 7 days after PEMF stimulation.

The results showed that a low frequency (5Hz) and high magnetic field intensity (40G) with a 50% duty cycle decreases IL-6, a cytokine active in the initial stage of inflammation, without affecting hTDCs viability and proliferation.

Data suggest that the application of PEMF with 5Hz frequency contributes for the modulation of hTDCs response to inflammation induced by IL-1b treatment. Ongoing studies on a wider range of inflammatory mediators will complement IL-6 results and abnormal pro/anti-inflammatory profiles will be further investigated. 

References:

1. Subramanian, A. et al, Development, 2015. p.4191-204;
2. Komatsu, I. et al, Acta Biomater, 2016. p.136-46;
3. Girolamo, L. et al, Knee Surg Sports Traumatol Arthrosc, 2014. p.3443-3453;
4. Dakin, S.G. et al, Vet Immunol Immunopathol, 2014. p.121-7;
5. Santos, L.J. et al, Trends Biotechnol, 2015. p.471-9.