Abstract
Severe traumatic spinal cord injury (SCI) results in a devastating and permanent loss of function, and is currently an incurable condition. It is generally accepted that future intervention strategies will require combinational approaches, including bioengineered scaffolds, to support axon growth across tissue scarring and cystic cavitation. Previously, we demonstrated that implantation of a microporous type-I collagen scaffold into an experimental model of SCI was capable of supporting functional recovery in the absence of extensive implant–host neural tissue integration. Here, we demonstrate the reactive host cellular responses that may be detrimental to neural tissue integration after implantation of collagen scaffolds into unilateral resection injuries of the adult rat spinal cord. Immunohistochemistry demonstrated scattered fibroblast-like cell infiltration throughout the scaffolds as well as the presence of variable layers of densely packed cells, the fine processes of which extended along the graft–host interface. Few reactive astroglial or regenerating axonal profiles could be seen traversing this layer. Such encapsulation-type behaviour around bioengineered scaffolds impedes the integration of host neural tissues and reduces the intended bridging role of the implant. Characterization of the cellular and molecular mechanisms underpinning this behaviour will be pivotal in the future design of collagen-based bridging scaffolds intended for regenerative medicine.
Highlights
Severe traumatic spinal cord injury (SCI) causes a devastatingly rapid and permanent loss of function, largely due to destruction of spinal tissue, including long-distance projecting axons in white matter tracts, resulting in the effective separation of projection neurons from their target neurons [1]
We demonstrated that implantation of a microporous type-I collagen scaffold into an experimental model of SCI was capable of supporting functional recovery in the absence of extensive implant–host neural tissue integration
The transition zone was generally composed of tightly packed cells with oval-shaped nuclei (Fig. 2E and J) and was associated with a more intense eosin staining in the haematoxylin and eosin (H&E)-stained sections (Fig. 2E)
Summary
Severe traumatic spinal cord injury (SCI) causes a devastatingly rapid and permanent loss of function, largely due to destruction of spinal tissue, including long-distance projecting axons in white matter tracts, resulting in the effective separation of projection neurons from their target neurons [1]. Experimental and post-mortem studies have shown that such injury-induced primary and secondary degenerative events include apoptotic cell death, inflammation and oedema, resulting in the formation of cystic cavitation as well as glial and connective tissue scarring [2,3,4,5,6] These events lead to the development of molecular and physical barriers that are hostile to axon regeneration and prevent any significant functional recovery [7,8,9,10]. The roles played by cells involved in the ( important) fibroadhesive component of scarring seem to have been largely over-looked
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