China
Africa
Explore chapters and articles related to this topic
Biomaterials and Immune Response in Periodontics
Published in Nihal Engin Vrana, Biomaterials and Immune Response, 2018
Sivaraman Prakasam, Praveen Gajendrareddy, Christopher Louie, Clarence Lee, Luiz E. Bertassoni
The activation of these macrophages and the subsequent release of degrading agents result in the resorption and remodelling of regenerative biomaterials including collagen. Macrophages and foreign body giant cells release reactive oxygen species, degradative enzymes and acids into a privileged zone that exists between the cells and the biomaterial surface.36–38 Thus, the surface of the biomaterial in the immediate vicinity of the inflammatory cells, macrophages and giant cells becomes susceptible to degradation. The rate and chemistry of this degradation depends on the chemistry of the biomaterial in use. At the minimum, the inflammatory response elicited by the material should not detrimentally affect the regenerative outcome intended for the use of the material.
Introduction to Host-Biomaterial Interactions
Published in Nina M. K. Lamba, Kimberly A. Woodhouse, Stuart L. Cooper, Polyurethanes in Biomedical Applications, 2017
Nina M. K. Lamba, Kimberly A. Woodhouse, Stuart L. Cooper
The typical foreign body response is characterized by the formation of granulation tissue and the presence of giant cells. The granulation tissue and granulatomous reactions associated with implants contain both epithelioid cells (flattened cells believed to be derived from macrophages), macrophages themselves, fibroblasts, and capillaries surrounded by a “cuff” of lymphocytes. Giant cells are believed to be formed from the fusion of many macrophages and/or epithelioid cells.49,80 Macrophages and foreign body giant cells have been found attached to the surfaces of implanted materials.82
Mechanical Effects of Cardiovascular Drugs and Devices
Published in Michel R. Labrosse, Cardiovascular Mechanics, 2018
The classic soft tissue injury response is the acute inflammation phase, which is relatively brief (minutes to a few days). Capillary constriction produces hemostasis, which is followed by fluid leakage and neutrophil migration into the tissue. The neutrophils remove the injury debris by phagocytosis of microorganisms and small foreign particles. The classic symptoms of redness, swelling, heat, and pain accompany this phase of normal wound healing. This initial response usually resolves during the formation of granulation tissue, which replaces the injured native tissue with a provisional matrix consisting of a fibrin scaffold. Fibroblasts migrate to the injured site and use the scaffold as a framework for collagen deposition. Angiogenesis aids the progression of this process, during which the fibrin scaffold is degraded and the remaining collagen is organized and crosslinked to form a fibrous capsule. The capsule surrounds and isolates the implant from the immune system and, if no inflammation persists at the site, provides a stable tissue–biomaterial interaction. However, if chronic inflammation is present, tissue macrophages frustrated by the inability to phagocytose the foreign material, coalesce into large, multinucleated foreign body giant cells, which may persist at the tissue–implant interface for the implant’s lifetime. The resultant response to tissue injury depends on both the regenerative capacity of the cells and the degree of preservation of the stroma framework (i.e., it is the part of a tissue that has connective and structural roles but does not carry out the specific functions of an organ) at the injury site. Tissue cells can be labile (continually proliferating), stable (can but do not normally replicate), and permanent (cannot reproduce after differentiation). Preservation of stroma framework leads to better restitution of tissue structure, whereas its destruction leads to fibrosis. These factors are also affected by local blood supply, and systemic conditions such as nutrition and disease. In general, an implant is a hindrance to healing and tissue regeneration and should be designed to best mitigate the body’s natural healing responses.
In vitro anti-inflammatory potential of marine macromolecules cross-linked bio-composite scaffold on LPS stimulated RAW 264.7 macrophage cells for cartilage tissue engineering applications
Published in Journal of Biomaterials Science, Polymer Edition, 2021
A. S. Sumayya, G. Muraleedhara Kurup
Inflammation plays a key role in the rejection of biomaterial implants. The initial immune response to an implanted biomaterial determines whether the implant will be accepted or rejected as a foreign body by the immune system [20]. The immune reaction to a biomaterial implant begins with an acute inflammatory response with innate recognition of foreign materials, which can eventually lead to the rejection of the implant [21]. The foreign body reaction is characterized by the presence of different immune cells including neutrophils, macrophages, dendritic cells and lymphocytes at the implantation site and subsequent formation of granulation tissue, foreign body giant cells and a fibrous capsule around implanted biomaterials [20]. Modulation of inflammation is an important component to enable a favorable healing result associated with functional tissue formation, reduction of tissue damage due to inflammation, minimizing chronic inflammation and improving tissue regeneration [22]. Thus anti-inflammatory signals are compulsory to prevent rejection by the host immune system. Therefore, the choice of biomaterial is of the greatest importance, with an obvious preference for materials that cause a minimal acute response [23].