Decoding Cold Therapy Mechanisms of Enhanced Bone Repair through Sensory Receptors and Molecular Pathways
Applying cold to a bone injury can aid healing, though its mechanisms are complex. This study investigates how cold therapy impacts bone repair to optimize healing. Cold was applied to a rodent bone model, with the physiological responses analyzed. Vasoconstriction was mediated by an increase in the...
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MDPI AG
2024-09-01
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| author | Matthew Zakaria Justin Matta Yazan Honjol Drew Schupbach Fackson Mwale Edward Harvey Geraldine Merle |
| author_facet | Matthew Zakaria Justin Matta Yazan Honjol Drew Schupbach Fackson Mwale Edward Harvey Geraldine Merle |
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| description | Applying cold to a bone injury can aid healing, though its mechanisms are complex. This study investigates how cold therapy impacts bone repair to optimize healing. Cold was applied to a rodent bone model, with the physiological responses analyzed. Vasoconstriction was mediated by an increase in the transient receptor protein channels (TRPs), transient receptor potential ankyrin 1 (TRPA1; <i>p</i> = 0.012), and transient receptor potential melastatin 8 (TRPM8; <i>p</i> < 0.001), within cortical defects, enhancing the sensory response and blood flow regulation. Cold exposure also elevated hypoxia (<i>p</i> < 0.01) and vascular endothelial growth factor expression (VEGF; <i>p</i> < 0.001), promoting angiogenesis, vital for bone regeneration. The increased expression of osteogenic proteins peroxisome proliferator-activated receptor gamma coactivator (PGC-1α; <i>p</i> = 0.039) and RNA-binding motif protein 3 (RBM3; <i>p</i> < 0.008) suggests that the reparative processes have been stimulated. Enhanced osteoblast differentiation and the presence of alkaline phosphatase (ALP) at day 5 (three-fold, <i>p</i> = 0.021) and 10 (two-fold, <i>p</i> < 0.001) were observed, along with increased osteocalcin (OCN) at day 10 (two-fold, <i>p</i> = 0.019), indicating the presence of mature osteoblasts capable of mineralization. These findings highlight cold therapy’s multifaceted effects on bone repair, offering insights for therapeutic strategies. |
| format | Article |
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| spelling | doaj-art-d04f8b18b07c4b1d8286b762804148752025-08-20T01:56:00ZengMDPI AGBiomedicines2227-90592024-09-01129204510.3390/biomedicines12092045Decoding Cold Therapy Mechanisms of Enhanced Bone Repair through Sensory Receptors and Molecular PathwaysMatthew Zakaria0Justin Matta1Yazan Honjol2Drew Schupbach3Fackson Mwale4Edward Harvey5Geraldine Merle6Surgical and Interventional Sciences Division, Faculty of Medicine, McGill University, Montreal, QC H3A 2B2, CanadaSurgical and Interventional Sciences Division, Faculty of Medicine, McGill University, Montreal, QC H3A 2B2, CanadaSurgical and Interventional Sciences Division, Faculty of Medicine, McGill University, Montreal, QC H3A 2B2, CanadaSurgical and Interventional Sciences Division, Faculty of Medicine, McGill University, Montreal, QC H3A 2B2, CanadaLady Davis Institute for Medical Research, Lady Davies Institute Jewish General Hospital, 3755 Cote-St. Catherine Road, Room 602, Montréal, QC H3T 1E2, CanadaSurgical and Interventional Sciences Division, Faculty of Medicine, McGill University, Montreal, QC H3A 2B2, CanadaSurgical and Interventional Sciences Division, Faculty of Medicine, McGill University, Montreal, QC H3A 2B2, CanadaApplying cold to a bone injury can aid healing, though its mechanisms are complex. This study investigates how cold therapy impacts bone repair to optimize healing. Cold was applied to a rodent bone model, with the physiological responses analyzed. Vasoconstriction was mediated by an increase in the transient receptor protein channels (TRPs), transient receptor potential ankyrin 1 (TRPA1; <i>p</i> = 0.012), and transient receptor potential melastatin 8 (TRPM8; <i>p</i> < 0.001), within cortical defects, enhancing the sensory response and blood flow regulation. Cold exposure also elevated hypoxia (<i>p</i> < 0.01) and vascular endothelial growth factor expression (VEGF; <i>p</i> < 0.001), promoting angiogenesis, vital for bone regeneration. The increased expression of osteogenic proteins peroxisome proliferator-activated receptor gamma coactivator (PGC-1α; <i>p</i> = 0.039) and RNA-binding motif protein 3 (RBM3; <i>p</i> < 0.008) suggests that the reparative processes have been stimulated. Enhanced osteoblast differentiation and the presence of alkaline phosphatase (ALP) at day 5 (three-fold, <i>p</i> = 0.021) and 10 (two-fold, <i>p</i> < 0.001) were observed, along with increased osteocalcin (OCN) at day 10 (two-fold, <i>p</i> = 0.019), indicating the presence of mature osteoblasts capable of mineralization. These findings highlight cold therapy’s multifaceted effects on bone repair, offering insights for therapeutic strategies.https://www.mdpi.com/2227-9059/12/9/2045coldbone healingtissue engineeringhypoxiavasculatureosteogenesis |
| spellingShingle | Matthew Zakaria Justin Matta Yazan Honjol Drew Schupbach Fackson Mwale Edward Harvey Geraldine Merle Decoding Cold Therapy Mechanisms of Enhanced Bone Repair through Sensory Receptors and Molecular Pathways Biomedicines cold bone healing tissue engineering hypoxia vasculature osteogenesis |
| title | Decoding Cold Therapy Mechanisms of Enhanced Bone Repair through Sensory Receptors and Molecular Pathways |
| title_full | Decoding Cold Therapy Mechanisms of Enhanced Bone Repair through Sensory Receptors and Molecular Pathways |
| title_fullStr | Decoding Cold Therapy Mechanisms of Enhanced Bone Repair through Sensory Receptors and Molecular Pathways |
| title_full_unstemmed | Decoding Cold Therapy Mechanisms of Enhanced Bone Repair through Sensory Receptors and Molecular Pathways |
| title_short | Decoding Cold Therapy Mechanisms of Enhanced Bone Repair through Sensory Receptors and Molecular Pathways |
| title_sort | decoding cold therapy mechanisms of enhanced bone repair through sensory receptors and molecular pathways |
| topic | cold bone healing tissue engineering hypoxia vasculature osteogenesis |
| url | https://www.mdpi.com/2227-9059/12/9/2045 |
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