The pathology of the foreign body reaction against biomaterials

Abstract

The healing process after implantation of biomaterials involves the interaction of many contributing factors. Besides their in vivo functionality, biomaterials also require characteristics that allow their integration into the designated tissue without eliciting an overshooting foreign body reaction (FBR). The targeted design of biomaterials with these features, thus, needs understanding of the molecular mechanisms of the FBR. Much effort has been put into research on the interaction of engineered materials and the host tissue. This elucidated many aspects of the five FBR phases, that is protein adsorption, acute inflammation, chronic inflammation, foreign body giant cell formation, and fibrous capsule formation. However, in practice, it is still difficult to predict the response against a newly designed biomaterial purely based on the knowledge of its physical-chemical surface features. This insufficient knowledge leads to a high number of factors potentially influencing the FBR, which have to be analyzed in complex animal experiments including appropriate data-based sample sizes. This review is focused on the current knowledge on the general mechanisms of the FBR against biomaterials and the influence of biomaterial surface topography and chemical and physical features on the quality and quantity of the reaction. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 927-940, 2017.

Biomaterial‐induced multinucleated giant cells express proinflammatory signaling molecules: A histological study in humans

“…In this sense, none of the evaluated biomaterials were able to shift the inflammatory pattern of MNGCs toward an anti‐inflammatory type. This observation is plausible because MNGCs are formed in a proinflammatory microenvironment as a result of persistent chronic inflammation . Additionally, biomaterial‐induced MNGCs share morphological and biological properties with the pathological inflammatory giant cells observed in sarcoidosis and tuberculosis that are similarly formed in response to persistent chronic inflammation .…”

Generation and Evaluation of Novel Stromal Cell‐Containing Tissue Engineered Artificial Stromas for the Surgical Repair of Abdominal Defects

“…Once grafted in vivo, our results showed that SCTLAS were properly integrated in the host abdominal wall tissues with no signs of rejection, infection or other complications, thus suggesting that the bioengineered tissues were highly biocompatible, whereas control SM displayed some signs of inflammatory reaction mainly consisting of macrophage cells. Previous works demonstrated that synthetic SM may exert immediate and chronic inflammatory responses after in vivo implantation, although these responses depend on the properties of each individual mesh . In fact, a recent report suggests that the in vivo use of biomaterials could be associated to a foreign body reaction with several phases and stages that may include a chronic inflammation phase with the presence of abundant macrophages .…”

Effects of age-related shifts in cellular function and local microenvironment upon the innate immune response to implants

“…That is, following placement all materials – regardless of design or composition – are subject to some degree of protein adsorption, an early neutrophil response, and subsequent invasion of the site of implantation by mononuclear phagocytes. While this represents an oversimplification of a complex process (which has been reviewed at length elsewhere [1–3]), the view that these events – eventually leading to an inflammatory response at the implant surface – represent a negative occurrence has led to a number of approaches to evade the early host immune response including, tuning of surface topography [4–8], porosity [9–14], and chemistry [15–18] of the material, as well as the use of non-fouling surfaces and coatings [19–21] and decorating surfaces with matricellular proteins to prevent non-self recognition [22–24]. While these techniques have undoubtedly shown promise, prevention of long-term interaction of protein or cells with implants has yet to be demonstrated.…”