Cardiovascular biomaterials: when the inflammatory response helps to efficiently restore tissue functionality?

Abstract

The evaluation of biological host response to implanted materials permits the determination of the safety and biocompatibility of biomedical devices, prostheses and biomaterials. Once a biomaterial is introduced into the body to a corresponding implant site, a sequence of events occurs promoting the activation of inflammatory mediators such as leukocytes and the release of signaling molecules such as cytokines and growth factors, evoking an inflammatory and wound healing process. This review examines the cellular and molecular mechanisms involved in the foreign body reaction, especially how cytokines impact the overall inflammatory response to devices. It also reviews how these events can be modulated by the physical and chemical properties of the biomaterials such as wettability, chemistry and geometry of surface. Particular attention is dedicated to the cardiovascular field, where the use of synthetic polymers has several limitations such as thrombogenicity and risk of infection. New materials and strategies to improve biomaterial characteristics are discussed. Copyright © 2012 John Wiley & Sons, Ltd.

Inflammation in intervertebral disc degeneration and regeneration

“…However, no evidence for a beneficial role of inflammation in maintaining homeostasis has been presented, owing to the difficulty in studying IVD tissue homeostasis. In other tissues, such as bone [218,219] or cardiovascular tissue [220], the control of inflammation has already proven to be critical in shifting the degeneration/ regeneration balance towards regeneration. In particular, our group has focused on modulating inflammation in bone [5,[221][222][223][224].…”

Endothelialization mechanisms in vascular grafts

“…These conditions trigger the endothelial lining to secrete adhesive factors such as von Willebrand factor, tissue factor, fibronectin, coagulation factor, cytokines, and surface adhesion molecules. The secreted adhesion receptors and chemokines recruit leukocytes and thereby initiate the inflammatory cascade (Boccafoschi, Mosca, & Cannas, ; Hahn & Schwartz, ). Different characteristics of the graft‐like composition, diameter ratio between the graft and native vessel, and the suture strength influence the outcome of the inflammatory response.…”

A hypothesis-driven parametric study of effects of polymeric scaffold properties on tissue engineered neovessel formation

“…[11,15]). For the purposes herein, we first reduced this extensive list of parameters to a focused list consisting of those scaffold parameters that have been most frequently investigated experimentally (Table 1).…”

“…Motivated in part by experimental findings that reveal the particular importance of scaffold pore size and degradation rate [cf. 12,15], we selected the following scales: L s = r min , $T_s={false(k_q^{p}false)}^{-1}$, and $M_s=c^p{r}_{\mathit{\text{min}}}/{false(k_q^{p}false)}^2$, where r min is the minimum pore size that admits cellular infiltration (having units of microns), $k_q^p$ is the rate of degradation (having units of days −1 ), and c p is the shear modulus of the scaffold (having units of Pa). Using this set of scales, the Buckingham Pi analysis suggested a reduction in parameters from 6 to 4 (Table 2), namely $$ffalse(k_q^p,\epsilon ,c^p,\omega ,r,{\varphi }^{k}false)\to \mathrm{f̌}true(\epsilon ,\frac{\omega }{r_{\text{italicmin}}},\frac{r}{r_{\text{italicmin}}},{\varphi }^{k}true)$$ where ε represents scaffold porosity, ω is the diameter of the polymeric fibers composing the scaffold, r is the mean pore size, and ϕ k describes the alignment of the fibrous scaffold (cf.…”