Host Response to Biomaterials for Cartilage Tissue Engineering: Key to Remodeling

Abstract

Biomaterials play a core role in cartilage repair and regeneration. The success or failure of an implanted biomaterial is largely dependent on host response following implantation. Host response has been considered to be influenced by numerous factors, such as immune components of materials, cytokines and inflammatory agents induced by implants. Both synthetic and native materials involve immune components, which are also termed as immunogenicity. Generally, the innate and adaptive immune system will be activated and various cytokines and inflammatory agents will be consequently released after biomaterials implantation, and further triggers host response to biomaterials. This will guide the constructive remolding process of damaged tissue. Therefore, biomaterial immunogenicity should be given more attention. Further understanding the specific biological mechanisms of host response to biomaterials and the effects of the host-biomaterial interaction may be beneficial to promote cartilage repair and regeneration. In this review, we summarized the characteristics of the host response to implants and the immunomodulatory properties of varied biomaterial. We hope this review will provide scientists with inspiration in cartilage regeneration by controlling immune components of biomaterials and modulating the immune system.

Local Inflammatory Response after Intramuscularly Implantation of Anti-Adhesive Plasma-Fluorocarbon-Polymer Coated Ti6AI4V Discs in Rats

“…In contrast to those findings, other studies indicate a direct correlation between an activation of the host immune system and the hydrophobicity of metallic alloys [ 6 , 29 ]. Seong and Matzinger hypothesise that exposed hydrophobic structures trigger a DAMP activated immune response [ 19 ].…”

“…After immediate surface adsorption of blood proteins, the interaction of cells and the implant as well as the characteristics of the metallic surface have a great influence on the initial attachment process. This is mediated by integrin receptors, leading to adhesion as well as a primary immune response of the body [ 5 , 6 ]. It is well established in the literature that the surface microtopography such as roughness or micro-discontinuities, hydrophilicity/-phobicity, chemistry and charge influence molecular adhesion processes [ 7 , 8 , 9 ].…”

“…Although this is important to initiate the natural wound healing process, it can lead to tissue damage in cases of prolonged activation. M1-type macrophages, identified by expression of markers such as CD68 and CD80 [ 6 ], can differentiate into M2-type tissue macrophages, known for their anti-inflammatory modulation. Among other markers, M2 macrophages express CD163.…”

A Comparison of the Capacity of Mesenchymal Stromal Cells for Cartilage Regeneration Depending on Collagen-Based Injectable Biomimetic Scaffold Type

“…Apparently, the scaffold MCH induces the secretory activity of MSCs to a greater extent than the tissue-specific scaffold DPC, whereas DPC is a stimulator for the formation of cartilage-like structures. It can be assumed that the differences in the functional activity of DPC and MCH scaffolds are based on the dependence of cell behavior on the elasticity, topography, and chemical composition of the carrier [27][28][29]. Interestingly, in a comparative study of gelatin gels with different rigidity, it was demonstrated that the gel with high rigidity promoted osteogenic differentiation of MSCs yet polarized macrophages towards the M1 phenotype, which is characterized by the production of proinflammatory cytokines [30].…”

Decellularized Avian Cartilage, a Promising Alternative for Human Cartilage Tissue Regeneration

“…One major setback in tissue graft or organ transplant, from a donor of a different species from that of the recipient, is the possibility of zoonosis and immunological rejection [ 49 , 50 , 51 , 52 ]. The major concerns have been diseases, such as herpesviruses, retroviruses, Toxoplasma gondii [ 53 , 54 ], Mycobacterium tuberculosis, encephalomyocarditis virus [ 55 ].…”