The rising importance of osteoimmunological aspects in bone healing supports the essential role of the initial haematoma as a source for inflammatory cells that release the cytokine pattern that directs cell recruitment towards the injured tissue.
The significant expression of osteopontin in wound healing supports the knowledge that it is has a broad yet critical role in injury site extracellular microenvironments containing highly proliferative cells and undergoing rapid remodeling.
Yet, strong depletion of monocytes only partially impairs skeletal muscle healing, supporting the existence of alternative mechanisms to palliate the loss of infiltrating macrophage progenitors.
Indeed, when powders of silica nanoparticle rather than solutions were spread, the particle agglomerates limit wound closure and healing (Supporting Information, Figure S2).
Our finding that both neutrophil depletion and CCR2 antagonism lead to impaired fracture healing supports the crucial role of neutrophil-derived CCL2 in fracture repair (Figs 2D, E and 4).
This ongoing presence of pain after healing supports the notion that a chronic pain condition may develop; possibly neuropathic in nature, due to potential nerve injury, but also potentially due to poorly managed acute nociceptive pain.
In-depth analysis of selected pathways and molecules was presented for the pro-fibrotic/wound healing supporting roles of TAK1, a downstream effector of non-Smad transforming GF β1 (TGFβ1) signaling, the β2 adrenoceptor, Trefoil family factor 2 (TFF2) and CCN2 (Connective tissue growth factor, CTGF).
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Human studies examining the effects of non-steroidal anti-inflammatory drugs on fracture healing support the conclusions from animal studies (Burd et al. 2003).
