Foreign Body Response and Biocompatibility - The Body Synthetic | BMES 212, Exams of Biology

Download Foreign Body Response and Biocompatibility - The Body Synthetic | BMES 212 and more Exams Biology in PDF only on Docsity! • A few milliseconds after the implant is inserted into the body, a biolayer of water, proteins and other biomolecules from the physiological liquid forms on the implant surface •Cells from the surrounding tissue migrate to the area around the implant stimulated by cytokines and growth factors in the biolayer. http://www.inano.dk/sw2495.asp Foreign Body Response • Anything inserted into the body elicits this response • First on the scene are the neutrophils or polymorphonuclear leukocytes (most common white cells) attracted by chemicals released by damaged cells – Produce proteases, and H2O2 and other small molecules Biocompatibility • The ability of a material to perform an appropriate host response in a specific application - not always required to be completely inert • Biomaterials are of 4 types, – Inert, Interactive, Viable and Replant Biocompatibility • Inert – No host response (but always a wound response) • Interactive – Elicit specific response e.g., ingrowth • Viable – May contain cells, host treats as normal tissue,matrix, modifies it etc. • Replant – Native tissue from self or donor – Should have same MHC markers as host Major Histocompatibility Complex Group of genes which codes for proteins found on the cell surfaces (antigens) in higher vertebrates. Differ slightly on different individuals. All genes linked and found on chromosome 6 (in humans). In humans MHC is called the HLA, human leukocyte antigen -system or group determined by 5 genes, all polymorphic (i.e. multiple alleles at each locust in any population). Only twins have the same HLA, and therefore the same antigens. Tissues with the same HLA antigens are compatible. Because of the polymorphism (multiple alleles) of HLA genes a donor and a host could differ and the immune system will regard the graft as foreign and cause rejection. Histo (greek for tissue) Biocompatibility Requirements • No irritation of surrounding structures • Elicit little or no inflammatory response • No allergic reaction • Not cause cancer Biological Environment • Very aggressive • Highly chemically reactive • Variable degrees of mechanical stress • Very constant conditions maintained pH  1.0 Gastric  6.8 Intracellular  7.0 interstitial  7.15-7.35 Blood Temperature  37oC Core  20-42.5 oC Disease  0-45 oC Skin extremities Mechanical Cycles  3 x 105 Peristalsis  3 x 106 Swallowing  0.5-4 x 107 Heart contraction  0.1-1 x 106 Finger joint  2 x 106 Walking Host vs. Material Response • Host response – effect of material on the tissue • Material response – effect of biological environment on the implant Both are linked Inflammation • First phase acute inflammation – Polymorphonuclear lymphocyte invasion • attach to invader, attempt to kill or degrade it • most gone in 24-48 hours • Tissue injury involves coagulation factor XII – Fibrous clot forms from blood platelets and fibrinogen at site of injury – Local capillaries dilate increasing blood flow – Kinins react with nerve endings and together with swelling, cause pain Cellular Response • Second phase chronic inflammation (cellular invasion) – Monocytes move in and become macrophages – Engulf debris 0.1–1 micron – Particles > 50 microns no response. Toxic particles ⇒ cell death and pus (not infected) – Release growth factors to trigger tissue rebuilding Cellular Response • Remodeling if no infection or adverse FBR – Foreign body giant cells cover implant – Neovascularization (granular appearance) – Fibrous encapsulation • Different tissue remodel to different extents – Bone • complete – Skin • Nearly complete, scar formation,not hair follicles – Cartilage • Never complete, replaced by fibrocartilage which degrades under repeated load Blood Compatible Surfaces • Surface Roughness • Surface charge • Shear Stress (laminar flow better) • Surface tension (low less likely to adhere) • Coatings (heparine etc.) • Must avoid platelet activation Platelet Adhesion and Activation Platelets adhering to Aggregation Normal platelets damaged endothelium of platelets into a in flowing blood and undergoing activation thrombus Platelet thrombus Platelets adherin: \ to subendothelia Platelets space 2003 Dia-Prasentation von Sanofi-Synthelabo - Bristol-Myers Squibb aus dem Jahr 2002 © eaten e ma v4 s ce al bar iclimeslsiccs till) Clotting Hemostatic og SECONDARY —& Thrombin —> alt an Urls R eM MU Re ae eee Cele ee oe Chronos N, Harrington RA (Eds). Antiplatelet Therapy in Clinical Practice. London: Martin Dunitz; 2000: pp, 15-35 2003 Dia-Prasentation von Sanofi-Synthelabo - Bristol-Myers Squibb aus dem Jahr 2002 ©