1 / 31

Host Reactions to Biomaterials

Effect of the Implant on the Host. LocalBlood material interactionsProtein adsorptionCoagulationFibrinolysisPlatelet adhesion, activation, releaseComplement activationLeukocyte adhesion, activationHemolysisToxicity. Modification of normal healingEncapsulationForeign body reactionPannus f

varana
Download Presentation

Host Reactions to Biomaterials

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

    1. Host Reactions to Biomaterials

    2. Effect of the Implant on the Host Local Blood material interactions Protein adsorption Coagulation Fibrinolysis Platelet adhesion, activation, release Complement activation Leukocyte adhesion, activation Hemolysis Toxicity

    3. Modification of normal healing Encapsulation Foreign body reaction Pannus formation Infection Tumorgenesis Systemic and remote Embolization Hypersensitivity Elevation of implant elements in the blood Lymphatic particle transport

    4. Effect of the Host on the Implant Physical – mechanical effects Abrasive wear Fatigue Stress corrosion, cracking Corrosion Degeneration and dissolution Biological effects Absorption of substances from tissues Enzymatic degradation Calcification

    5. Inflammation Reaction of vascularized living tissue to local injury Contain, neutralize, dilute or wall off injurious agent or process Sets into motion series of events that heal and reconstitute wound site through replacement of injured tissue by: Regeneration of native parenchymal cells Formation of fibroblastic scar Combination of above

    6. Local Events Following Implantation Injury (due to device placement, tissue manipulation) Acute inflammation Chronic inflammation Granulation tissue Foreign body reaction Fibrosis

    7. Extent of reactions depends on Size, shape chemical and physical properties of material Degree of insult to tissues Tissue Organ Species

    8. Temporal Variation of Inflammatory Response

    9. Activated by injury to vascularized connective tissue Series of reactions Various cells Controlled by endogenous and autocoid mediators

    10. Acute Inflammation Relatively short duration – minutes to days Exudation of fluid and plasma proteins Emigration of leukocytes (predominantly neutrophils) Margination Adhesion Emigration Phagocytosis Release of leukocyte products

    12. Chemotaxis Unidirectional migration of cells along a chemical gradient Variety of endogenous and exogenous substances identified as chemotactic agents Receptor mediated phenomenon

    14. Models to Predict Cell Response

    15. Neutrophils phagocytose foreign organisms and materials Recognition (IgG and C3b) Attachment Neutrophil engulfment Degradation, killing Degradation may or may not occur depending on properties of biomaterial – “frustrated phagocytosis”

    17. Release of neutrophil products to degrade product Lysosomal enzymes Oxygen derived active metabolites Products of arachidonic acid metabolism Direct extrusion or exocytosis Amount of enzyme released depends on size of polymer particle – larger particles – greater release

    18. Complement 20 proteins Mediates a series of biologic reactions – defense against microbial agents Increased vascular permeability Chemotaxis Opsonization Lysis of target organisms

    20. Functions of Complement Components C3a increases vascular permeability C5a increases vascular permeability and is chemotactic for neutrophils, eosinophils, basophils and monocytes C3b important opsonin for neutrophils, macrophages and eosinophils C5b-9 – MAC – final lytic component

    21. Outcomes of Acute Inflammation Complete resolution Healing by scarring Abscess formation Progression to chronic inflammation

    22. Chronic Inflammation Less histologically defined Generally characterized by presence of Macrophages (process and present antigen to immune competent cells) Monocytes Lymphocytes (mediator of ab production) Proliferation of blood vessels and connective tissue

    23. Macrophages Most important cell in chronic inflammation due to production of a large number of biologically active products Neutral proteases Chemotactic factors Arachidonic acid metabolites Reactive oxygen metabolites Complement components Coagulation factors Growth factors and cytokines Initiation of wound healing response

    25. Granulation Tissue “Normal wound healing response” to biomaterials 3-5 days after implantation of biomaterial Initiated by action of monocytes and macrophages Fibroblasts, vascular endothelial cells at site of injury proliferate Pink tissue, granular in appearance

    26. Endothelial cells – production of new blood vessels Fibroblasts – synthesis of collagen and proteoglycans Formation of fibrous capsule

    28. Foreign Body Reaction Foreign body giant cells Components of granulation tissue Form and topography of material determines composition of foreign body reaction Foreign body reaction consisting of macrophages and foreign body giant cells may persist for lifetime of implant

    29. Fibrosis and Fibrous Encapsulation End stage healing response to biomaterials Regeneration – replacement of injured tissue by cells of same type Replacement by fibrous capsule Controlled by Proliferative capacity of tissue receiving implant (labile, stable, permanent) Persistence of tissue framework at implant site

    32. Given our current inability to control the sequence of events following injury in implantation, restitution of normal tissue structure with function is rare.

More Related