PMID- 34580378
OWN - NLM
STAT- MEDLINE
DCOM- 20211228
LR  - 20240404
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 11
IP  - 1
DP  - 2021 Sep 27
TI  - Electromagnetic stimulation increases mitochondrial function in osteogenic cells 
      and promotes bone fracture repair.
PG  - 19114
LID - 10.1038/s41598-021-98625-1 [doi]
LID - 19114
AB  - 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.
CI  - (c) 2021. The Author(s).
FAU - Hollenberg, Alex M
AU  - Hollenberg AM
AD  - Center for Musculoskeletal Research, University of Rochester School of Medicine & 
      Dentistry, Rochester, NY, USA.
FAU - Huber, Aric
AU  - Huber A
AD  - Center for Musculoskeletal Research, University of Rochester School of Medicine & 
      Dentistry, Rochester, NY, USA.
FAU - Smith, Charles O
AU  - Smith CO
AD  - Center for Musculoskeletal Research, University of Rochester School of Medicine & 
      Dentistry, Rochester, NY, USA.
FAU - Eliseev, Roman A
AU  - Eliseev RA
AD  - Center for Musculoskeletal Research, University of Rochester School of Medicine & 
      Dentistry, Rochester, NY, USA. roman_eliseev@urmc.rochester.edu.
AD  - University of Rochester Medical Center, 601 Elmwood Ave, Rm 1-8541, Rochester, 
      NY, 14642, USA. roman_eliseev@urmc.rochester.edu.
LA  - eng
GR  - P30 AR069655/AR/NIAMS NIH HHS/United States
GR  - R01 AR072601/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20210927
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
SB  - IM
MH  - Animals
MH  - Cell Differentiation/radiation effects
MH  - Cell Line
MH  - Fracture Healing/*radiation effects
MH  - Fractures, Bone/pathology/*therapy
MH  - Humans
MH  - Magnetic Field Therapy/*methods
MH  - Membrane Potential, Mitochondrial/radiation effects
MH  - Mice
MH  - Mitochondria/physiology/*radiation effects
MH  - Osteoblasts/physiology/radiation effects
MH  - Osteogenesis/radiation effects
MH  - Oxidative Phosphorylation/radiation effects
PMC - PMC8476611
COIS- The study was in part sponsored by Sanabit Technologies Inc (Rochester, NY), a 
      developer of electromagnetic therapy for bone repair. Dr Eliseev's work has been 
      funded in part by Sanabit Technologies Inc. Mr Hollenberg, Mr Huber, and Dr. 
      Smith declare no potential conflict of interest. Sanabit Technologies played no 
      role in the conceptualization, design, data collection, analysis, decision to 
      publish, or preparation of the manuscript.
EDAT- 2021/09/29 06:00
MHDA- 2021/12/29 06:00
PMCR- 2021/09/27
CRDT- 2021/09/28 06:22
PHST- 2021/02/22 00:00 [received]
PHST- 2021/08/25 00:00 [accepted]
PHST- 2021/09/28 06:22 [entrez]
PHST- 2021/09/29 06:00 [pubmed]
PHST- 2021/12/29 06:00 [medline]
PHST- 2021/09/27 00:00 [pmc-release]
AID - 10.1038/s41598-021-98625-1 [pii]
AID - 98625 [pii]
AID - 10.1038/s41598-021-98625-1 [doi]
PST - epublish
SO  - Sci Rep. 2021 Sep 27;11(1):19114. doi: 10.1038/s41598-021-98625-1.