Intermittent vibrations accelerate fracture healing in sheep

Mu, Degong; Lin, Junhao; Li, Chen; Hao, Baocheng; Gu, Feng; Liu, Chao; Tan, Lianjiang; Zhu, Dong; Zhang, Xizheng

doi:10.1590/s0102-865020190070000002

Cited by 2 publications

(2 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In large animals like sheep, several studies confirmed that LMHFV can improve fracture healing in a metatarsal osteotomy model ( Table 7). Li et al (2018) and Mu et al (2019) compared the efficacy of intermittent and continuous vibration and showed that LMHFV had the greatest effect in the 7day interval group (71.4% recovery with grade 3 healing vs. 42.9% in the continuous treatment group and 14.3% in the natural healing group without vibration. Callus volumes were also significantly increased in the 7-day interval group (Li et al, 2018), confirming the results in rodents.…”

Section: Influence Of Lmhfv On Cartilaginous and Bony Callus Formationmentioning

confidence: 99%

Influence of Low-Magnitude High-Frequency Vibration on Bone Cells and Bone Regeneration

Steppe

Liedert

Ignatius

et al. 2020

Front. Bioeng. Biotechnol.

View full text Add to dashboard Cite

Bone is a mechanosensitive tissue for which mechanical stimuli are crucial in maintaining its structure and function. Bone cells react to their biomechanical environment by activating molecular signaling pathways, which regulate their proliferation, differentiation, and matrix production. Bone implants influence the mechanical conditions in the adjacent bone tissue. Optimizing their mechanical properties can support bone regeneration. Furthermore, external biomechanical stimulation can be applied to improve implant osseointegration and accelerate bone regeneration. One promising anabolic therapy is vertical whole-body low-magnitude high-frequency vibration (LMHFV). This form of vibration is currently extensively investigated to serve as an easyto-apply, cost-effective, and efficient treatment for bone disorders and regeneration. This review aims to provide an overview of LMHFV effects on bone cells in vitro and on implant integration and bone fracture healing in vivo. In particular, we review the current knowledge on cellular signaling pathways which are influenced by LMHFV within bone tissue. Most of the in vitro experiments showed that LMHFV is able to enhance mesenchymal stem cell (MSC) and osteoblast proliferation. Furthermore, osteogenic differentiation of MSCs and osteoblasts was shown to be accelerated by LMHFV, whereas osteoclastogenic differentiation was inhibited. Furthermore, LMHFV increased bone regeneration during osteoporotic fracture healing and osseointegration of orthopedic implants. Important mechanosensitive pathways mediating the effects of LMHFV might be the Wnt/beta-catenin signaling pathway, the estrogen receptor (ER) signaling pathway, and cytoskeletal remodeling.

show abstract

Section: Influence Of Lmhfv On Cartilaginous and Bony Callus Formationmentioning

confidence: 99%

Influence of Low-Magnitude High-Frequency Vibration on Bone Cells and Bone Regeneration

Steppe

Liedert

Ignatius

et al. 2020

Front. Bioeng. Biotechnol.

View full text Add to dashboard Cite

show abstract

“…Most fracture healing processes follow the stages above. According to the characteristics of each stage of fracture healing, various methods and drugs are adopted to accelerate the process of fracture healing ( Chen and Luan, 2019 ; Li et al, 2019 ; Mu et al, 2019 ; Nakata et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Exogenous PTH 1-34 Attenuates Impaired Fracture Healing in Endogenous PTH Deficiency Mice via Activating Indian Hedgehog Signaling Pathway and Accelerating Endochondral Ossification

Liu

Wei

et al. 2022

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Fracture healing is a complicated, long-term, and multistage repair process. Intermittent administration of parathyroid hormone (PTH) has been proven effective on intramembranous and endochondral bone formation during the fracture healing process, however, the mechanism is unclear. In this study, we investigated the role of exogenous PTH and endogenous PTH deficiency in bone fracture healing and explored the mechanism by using PTH knockout (PTH-/-) mice and ATDC5 cells. In a mouse femur fracture model, endogenous PTH deficiency could delay endochondral ossification whereas exogenous PTH promotes accumulation of endochondral bone, accelerates cartilaginous callus conversion to bony callus, enhances maturity of bony callus, and attenuates impaired fracture healing resulting from endogenous PTH deficiency. In fracture callus tissue, endogenous PTH deficiency could inhibit chondrocyte proliferation and differentiation whereas exogenous PTH could activate the IHH signaling pathway to accelerate endochondral ossification and rescue impaired fracture healing resulting from endogenous PTH deficiency. In vitro, exogenous PTH promotes cell proliferation by activating IHH signaling pathway on ATDC5 cells. In mechanistic studies, by using ChIP and luciferase reporter assays, we showed that PTH could phosphorylate CREB, and subsequently bind to the promoter of IHH, causing the activation of IHH gene expression. Therefore, results from this study support the concept that exogenous PTH 1-34 attenuates impaired fracture healing in endogenous PTH deficiency mice via activating the IHH pathway and accelerating endochondral ossification. Hence, the investigation of the mechanism underlying the effects of PTH treatment on fracture repair might guide the exploration of effective therapeutic targets for fracture.

show abstract

Intermittent vibrations accelerate fracture healing in sheep

Cited by 2 publications

References 21 publications

Influence of Low-Magnitude High-Frequency Vibration on Bone Cells and Bone Regeneration

Influence of Low-Magnitude High-Frequency Vibration on Bone Cells and Bone Regeneration

Exogenous PTH 1-34 Attenuates Impaired Fracture Healing in Endogenous PTH Deficiency Mice via Activating Indian Hedgehog Signaling Pathway and Accelerating Endochondral Ossification

Contact Info

Product

Resources

About