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Modulation of the Inflammatory Response and Bone Healing
Masahiro Maruyama1, Claire Rhee1, Takeshi Utsunomiya1
1Department of Orthopaedic Surgery, Stanford University, Stanford, CA, United States.
Frontiers in Endocrinology
|July 14, 2020
Summary
Optimizing bone healing requires a transient, acute inflammatory phase. Immunomodulation, particularly using preconditioned mesenchymal stromal cells (MSCs), shows therapeutic potential for complex fractures and non-unions.
Area of Science:
- Orthopedics
- Regenerative Medicine
- Immunology
Background:
- Complex fractures and large bone defects present significant orthopedic challenges, with 5-10% of fractures resulting in non-unions.
- Bone healing involves inflammatory, repair, and remodeling phases, with initial inflammation being critical for success.
- Mesenchymal stromal cells (MSCs) and immune cells crosstalk is vital for bone healing; disruptions lead to impaired healing.
Purpose of the Study:
- To review the principles of inflammation and bone healing.
- To update on cellular interactions and immunomodulation strategies for enhancing bone healing.
- To highlight the therapeutic potential of immunomodulation in orthopedic regenerative medicine.
Main Methods:
- Review of current literature on bone healing, inflammation, and cellular interactions.
- Summary of immunomodulation techniques, including MSC preconditioning and cytokine therapy.
- Analysis of the role of acute inflammation and its resolution in fracture repair.
Main Results:
- Optimal bone healing depends on a transient, acute inflammatory phase.
- Preconditioned MSCs (primed/licensed/activated) demonstrate therapeutic potential by enhancing immunosuppressive properties.
- Both pro-inflammatory and anti-inflammatory cytokine approaches are being explored for bone healing modulation.
Conclusions:
- Understanding and modulating the inflammatory phase is key to improving bone healing outcomes.
- Immunomodulation strategies, especially involving MSCs, offer promising avenues for treating non-unions and large bone defects.
- Targeting cellular crosstalk and inflammation resolution can optimize fracture repair.
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