Biomedical Engineering Reference
In-Depth Information
interactions,
provisional
matrix
formation,
acute
inflammation,
chronic
inflammation,
granulation
tissue,
foreign-body
reaction,
and
fibrous
encapsulment.
Figure 1 highlights the cascade of host response events depending on the
presence of the implant. The phases during wound healing without implant
versus with implant materials do not completely differ and often overlap. For
example, granulation tissue is not a response unique to wounds with implants and
can occur during normal tissue healing without implant.
Host interaction with biomaterials begins with the Vroman effect, where
blood protein adsorption on the biomaterial surface starts the development of the
provisional matrix. With the highly dynamic protein adsorption on the material
surface begins the host's coagulation and inflammation events. Clotting and
blood-material interaction involve the formation of bulk fibrin around the injured
site and the implant while inflammation brings the recruitment of cells including
platelets, leukocytes such as neutrophils and other white blood cells.
Inflammatory response to material serves as a normal event to wall off and
locally contain the material at the injury site. In acute inflammation, neutrophils
and monocytes enter the wound site as a part of exudation and begin to degrade
the material and release a myriad of proteases, cytokines and oxygen-derived free
radicals. However, depending on the physical and chemical properties of the
material, the acute inflammatory phase may be prolonged (i.e. beyond 1 week)
and lead to chronic inflammation. If wound healing proceeds normally, acute
inflammation leads into granulation tissue, a phase that is marked by a soft, pink,
granular appearance on the wound healing surface as well as signs of
neovascularization. The lysosomal agents and chemical mediators produced
during acute inflammation activate and trigger growth factor upregulation by
endothelial cells and fibroblasts, and these cells also lay down the matrix bed of
collagen and proteoglycans to resolve the tissue repair process.
When the persistent presence of the biomaterial in the host and the
incompatibility lead to chronic inflammation however, much of the cells
recruited during the acute inflammatory phase (i.e. monocytes, macrophage,
lymphocytes) remain and a foreign body reaction ensues. Chronic inflammation
can be a part of a foreign body reaction, which is characterized by the presence
of foreign body giant cells and the encapsulation of the foreign object at the local
implant site in the host's attempt to wall off the material. Macrophages attempt to
phagocytose the material and the material is too large to be phagocytosed, they
undergo “frustrated phagocytosis” and macrophages fuse to form foreign body
giant cells. When foreign body reaction leads to fibrous encapsulation, densely
packed avascular collagen around the material forms to locally contain the
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