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PEMF Stimulation Mitochondrial Function Osteogenic Cells


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Comprehensive review of Bemer and PEMF (Pulsed Electromagnetic Field). Explore scientific research, studies, and articles on the benefits and applications of Bemer and PEMF therapy for health and wellness.



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Electromagnetic stimulation increases mitochondrial function in osteogenic cells and promotes
bone fracture repair
Alex M. Hollenberg1, Aric Huber1, Charles O. Smith1 & Roman A. Eliseev1,2*
Bone fracture is a growing public health burden and there is a clinical need for non-invasive therapies to aid in the fracture healing process. Previous studies have demonstrated the utility of electromagnetic (EM) fields in promoting bone repair; however, its underlying mechanism of action is unclear. Interestingly, there is a growing body of literature describing positive effects of an EM field on mitochondria. In our own work, we have previously demonstrated that differentiation of osteoprogenitors into osteoblasts involves activation of mitochondrial oxidative phosphorylation (OxPhos). Therefore, it was reasonable to propose that EM field therapy exerts bone anabolic effects via stimulation of mitochondrial OxPhos. In this study, we show that application of a low intensity constant EM field source on osteogenic cells in vitro resulted in increased mitochondrial membrane potential and respiratory complex I activity and induced osteogenic differentiation. In the presence of mitochondrial inhibitor antimycin A, the osteoinductive effect was reversed, confirming that
this effect was mediated via increased OxPhos activity. Using a mouse tibial bone fracture model
in vivo, we show that application of a low intensity constant EM field source enhanced fracture repair via improved biomechanical properties and increased callus bone mineralization. Overall, this study provides supporting evidence that EM field therapy promotes bone fracture repair through mitochondrial OxPhos activation.
Bone fracture is a growing public health burden, with the incidence expected to rise as the world population ages1,2. In the United States, bone fracture is the most common musculoskeletal condition requiring hospitaliza- tion among Medicare patients (≥ 65 years of age) as a consequence of increased fall risk, osteoporosis, and bone fragility3. While most fractures heal without complications, approximately 5–10% result in delayed healing or nonunion4,5. The etiology of nonunion is not fully understood, but important systemic risk factors include smok- ing, diabetes, and cachexia6. Local factors, including inadequate fixation and poor vascularity, are also recognized as contributors to delayed fracture repair. Nonunions are currently managed definitively with surgery, however there remains a clinical need for non-invasive therapies to aid in the fracture healing process.
One therapeutic approach to improve bone healing is the use of electromagnetic (EM) field stimulation. First published in 1974, Basset et al. suggested that EM fields may promote bone formation and nonunion repair7. Many subsequent studies have confirmed the osteogenic potential of pulsed EM fields (PEMFs), which is cur- rently an approved therapy for nonunion fractures, congenital pseudoarthrosis, osteoporosis, and failed spinal fusions8–11. Several studies have established that PEMF therapy in vitro promotes bone formation by increasing osteoblast proliferation and expression of osteoblast marker genes (e.g., RUNX2/CBFA1, ALP)12–14, while also suppressing bone resorption activity by osteoclasts15. In addition, PEMF therapy has been shown to stimu- late differentiation of human bone marrow-derived stromal cells (BMSCs) into osteoblasts, thereby enhancing mineralization16. Although several cellular mechanisms by which PEMF regulates these osteogenic effects have been proposed17–23, our current understanding remains limited.
Interestingly, there is a growing body of literature describing positive effects of an EM field on mitochondria24–27. In our own work, we have previously shown that differentiation of osteoprogenitors into osteoblasts is an energy dependent process that requires activation of mitochondrial oxidative phosphorylation (OxPhos)28,29. We have also helped to establish that in the setting of mitochondrial dysfunction, osteoblast/
1Center for Musculoskeletal Research, University of Rochester School of Medicine & Dentistry, Rochester, NY, USA. 2University of Rochester Medical Center, 601 Elmwood Ave, Rm 1-8541, Rochester, NY 14642, USA.*email: roman_eliseev@urmc.rochester.edu
(2021) 11:19114 | https://doi.org/10.1038/s41598-021-98625-1 1 Vol.:(0123456789)
OPEN
www.nature.com/scientificreports
Scientific Reports |

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