Ortopedik ve Dental Malzemeler

Yard. Do. Dr. Feride Sermin Utku

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Biocompatibility
Success of implant operation depends on the kind of tissue response to the surgical procedure and any interaction between tissues and implants. Biocompatibility entails
mechanical, chemical, pharmacological and surface compatibility.
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Biocompatibility entails local and systemic response of tissues.

Systemic Effects by Implants

biodegradable implants such as absorbable suture and surgical adhesives,
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PMMA lowers blood pressure due to the reaction toward MMA monomers. Systemic effects of:
biodegradable polymer scaffolds large number of wear and corrosion particles released by metallic and polymeric implants.
Various organs have different affinities for different metallic elements. Corrosion-resistant metal alloys release some elements into the body.
Interfere with physiologic activities. Divalent ions may inhibit enzymes.

Systemic Effects by Implants

Rupture. Autoimmune diseases, i.e. Systemic sclerosis and chronic connective tissue inflammation were claimed to have developed after mammary augmentation with silicon. T cell memory to silica was observed in the off-spring of women after receiving silicone breast implants.
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Mammary augmentation with silicone gel in a silicone rubber envelope. Median 16 years of use.

Carcinogenicity
Chemical structure and function structural or pharmacological similarity to known carcinogenic agents (aromatic amines, polynuclear aromatic hydrocarbons with multiple ring structures, alkylating agents, aflatoxins, halogenated hydrocarbons, chloroform, polychlorinated biphenyls, pesticides, metallic nickel, cadmium and cobalt) Carcinogenecity studies
Short-term Long-term
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Response to Implants
Type of cell metals Description (except noble metals) evoke a severe tissue reaction. Less reaction with Titanium due to oxide layer Co-cr and SS must be passivated Biocompatible, minimal tissue reaction, sometimes a thin layer of encapsulation Some glass-ceramics showed direct bonding between implant and bone Quite inert if there are no unbound additives antioxidants, fillers, anti-discoloring agents, plasticizers, etc., and free monomers
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Ceramic, carbon Glass-ceramic polymers

tissue response
implant : tissue
Minimal response Thin collagenous membrane encapsulation Chemically induced response Acute, mild inflammatory response Chronic, severely inflammatory response Necrotic response Layer of necrotic debris 7 Physically Induced Response nflammatory response to particulate Tissue growth into porous materials
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Biyomateryallerin Olas Etkileri

Uyguland blgede snrl fibrz bir doku ile evriliyorsa

B) biyoinert etki
Uygulanan kemik dokuyla arada snrl fibrz bir doku olmadan birleir. Dokuyla biyomateryal arasnda herhangi bir etkileim olmamaktadr.

C) Biyoaktif etki
Biyomateryal uyguland dokuda benzer hcrelerin oluumunu aktive etmektedir.

D) Toksik etki
Biyomalzemelerin alerjik, immn, nonimmn, mutajenik, karsinojenik ve enflamatuvar etkileri grlr.
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A) biyotolere etki

Biyouyumluluk
Baz aratrmaclar gerekten tam anlamyla biyouyumlu ve biyoinert malzeme olmadn sylemektedirler. Bu yzden biyouyumluluk materyal seiminin en nemli parametresidir. Biyolojik ortam iin malzeme tasarm, birbiriyle etkileen ayr dinamik unsurun varlndan dolay son derece zordur. Bunlar:
1. Biyomateryal yzeyinin kimyasal yaps 2. Aradaki pellikl (arayz) tabakas 3. Konak hcre yantdr.
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Biyomateryale tutunan pellikl tabakas evreyle fizyolojik etkileime araclk eder. Bu yzden yzey kimyasnn, pellikl komponentlerinin ve adsorbsiyon mekanizmasnn tanmlanmas, oluacak yant kontrol etmede birincil neme sahiptir.

The Defense System/Immune Response

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Immunity: Resistance of the body to microbes Elimination of worn-out or damaged body cells Destruction of abnormal or mutant cell The body reacts to foreign materials in ways to get rid of them. Either moved, extruded or walled-off. If particulate or fluid, it can be ingested by giant cells and removed.

Immune response is a stimulus-response sequence of events. Immune response: Non-specific defense (during the initial exposure to a foreign organism) Specific defense Humoral (antibodies) Cell-mediated (sensitized lymphocytes).
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Effector cells of immune system

White-blood cells (leukocytes colorless blood corpuscles capable of ameboid movement) Polymorphonuclear granulocytes Neutrophils (50-70%) bone marrow- phagocytosis of bacteria, cell debris and antibody-primed foreign matter Eosinophils (1-4 %) bone marrow. Unknown function Basophils (0.1 %) bone marrow release of histamine and other chemicals (similar to tissue mast cells) Lymphocytes (20-40%) bone marrow and lymphoid tissue. B cells: production of antibodies after transformation into plasma cells. T cells : responsible for cellmediated immunity Monocytes (2-8%) bone marrow. Transformed into tissue macrophages with phagocytic activity. Macrophages - major function is phagocytosis of bacteria, cell debris and antibodyprimed foreign matter. Found scattered throughout the tissues of the body. In liver, spleen, lymph nodes and bone marrow they form part of the lining of vascular and lymphatic channels. Plasma cells - derived from B-lymphocytes in lymphoid tissue and are responsible for humoral immunity
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1. 2. 3.

Neutrophils are short lived. They disintegrate and disappear after 24-48 hours. Monocytes differentiate into macrophages and these cells are very long-lived. (up to months) Monocytic emigration may continue for day to weeks, and chemostatic factors are activated over longer periods of time. 14

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Inflammation- clotting and provisional matrix formation

Injury to vascularized tissue in the implantation procedure: immediate development of provisional matrix at the implant site. occur early, in minutes to hours following implantation of a device. Provisional matrix consists:
fibrin, produced by activation of the coagulation and thrombosis systems, Inflammatory products released by the complement system, activated platelets, inflammatory cells and endothelial cells.
to provide structural and biochemical components to the process of wound healing. Provisional matrix may be viewed as a naturally derived, biodegradable, sustained release system in which mitogens, chemo-attractants, cytokines and growth factors are released to control subsequent wound-healing processes.
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 Neutrophils (polymorphonuclear leukocytes, PMNs) and other motile white cells emigrate or move from the blood vessels to the perivascular tissues and the injury site. Specific receptors for chemostactic agents on the cell membranes of leukocytes are important in the emigration or movement of leukocytes. Following the localization of leukocytes at the injury (implant) site, phagocytosis and the release of enzymes occurs following activation of neutrophils and macrophages. The major role of the neutrophil in acute inflammation is to phagocytose microorganisms and foreign materials. Acute inflammation normally resolves quickly, usually less than 1 week, depending on the extent of injury at the implant site. The presence of acute inflammation (PMNs Polymorphonuclear Granulocytes) at the tissue/implant interface at time periods beyond 1 week suggests the presence of an infection. (fig 2)

Acute inflammation

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Acute inflammation
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Chronic inflammation
Persistent inflammatory stimuli lead to chronic inflammation. Characterized by: Presence of macrophage, monocytes and lymphocytes (production of antibodies) Proliferation of blood vessels and connective tissue. Factors: Chemical and physical properties of the materials in themselves Motion in the implant site by the materials Infection Short duration and confined to implant site.
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Chronic inflammation
If destructive inflammation persists and no healing process occurs in 3-5 days, chronic inflammation process commences. Marked by presence of macrophages and coalesced macrophages MNGCs. Sometimes the mononuclear cells evolve into histiocytes, which regenerate collagen. This generated collagen is used to close the wound or to wall-off unremoveable foreign materials by encapsulation with a thin membrane. The macrophage is probably the most important cell in chronic inflammation because of the great number of biologically active products it can produce. Important classes of products produced and secreted by macrophages include
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neutral proteases, chemotactic factors, arachidonic acid metabolites, reactive oxygen metabolites, complement components,coagulation 20 factors, growth-promoting factors, and cytokines.

Chronic inflammation necrotic abscess

Extensive tissue injury or irritants cause prolonged reaction with tissue destruction by collagenase, derived from granulocytes, which are lysed by the lower pH (below 5.2) at the wound site. If there is no drainage for necrotic debris, lysed granulocytes, formed blood elements, etc., then the site becomes a severely destructive inflammation resulting in necrotic abscess.
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Cellular response to repair

Mesenchymal cells evolve into migratory fibroblasts that move into the injured site while the necrotic debris, blood clots, etc., are removed by the granulocytes and macrophages. The inflammatory exudate contains fibrinogen, converted to fibrin by enzymes released through blood and tissue cells. On the fibrin scaffold, collagen is deposited. New capillaries are formed. Fibrin scaffold is removed by enzymes activated by endothelial cells, which along with fibroblasts secrete collagenase to digest away excess collagen.
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Granulation tissue
After this stage, following implantation of a biomaterial, the healing response may be initiated by reaction of monocytes and macrophages. Fibroblasts and vascular endothelial cells in the implant site proliferate and begin to form granulation tissue. Granulation tissue: form pink, soft granular appearance on the surface of healing wounds, and its characteristic histologic features include proliferation of new small blood vessels and fibroblasts (Fig 4). The new small blood vessels formation: angiogensis (neovascularization). This process involves: proliferation, maturation and organization of endothelial cells into capillary vessels.
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Remodelling
After 2 to 4 weeks of fibroblastic activities the wound undergoes remodelling, during which the glycoprotein and polysaccharide content decreases and the number of fibroblasts decrease. There is a latent period for collagen molecules (procollagen is deposited by fibroblasts) to polymerize to maturity. The collagen maturation and restructuring period requires >6 mo to complete. However, the wound strength never reaches the original value.
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Foreign body giant cell formation

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Foreign-body-type giant cells may surround nonphagocytosable particulate materials in granulomas. Foreign-body giant cells are formed by the fusion of monocytes and macrophages in an attempt to phagocytose the material. (Fig 5)

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The foreign body reaction to biomaterials is composed of foreign-body giant cells (FBGCs) and components of granulation tissue (macrophages, fibroblasts, and capillaries). (fig 6)

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Fabric materials generally have a surface response composed of macrophages and foreign body giant cells, with varying degrees of granulation tissue subjacent to the surface response. (fig 7)

Foreign-body reaction
The foreign-body reaction consisting mainly of macrophages and/or foreign-body giant cells may persist at the tissue-implant interface for the lifetime of the implant (Fig 1). Generally, fibrosis (i.e. fibrous encapsulation) surrounds the biomaterial with its foreign body reaction from the local tissue environment. Fig 8 demonstrates the sequence of events involved in inflammation and wound healing when medical devices are implanted. In general, the PMN predominant acute inflammatory response and the lymphocyte/monocyte predominant chronic inflammatory response resolve quickly depending on the type and location of implant. If the implant is chemically and physically inert to the tissue, the FBGC may not form. Only a thin layer of collagenous tissue encapsulates the implant.
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If the implant is chemically and physically inert to the tissue, the FBGC may not form. Only a thin layer of collagenous tissue encapsulates the implant.

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Fibrosis/fibrous encapsulation

The end-stage healing response to biomaterials is generally fibrosis or fibrous encapsulation. (fig 9) Repair of implant sites can involve two distinct process:
- Regeneration, which is replacement of injured tissue by parenchymal cells. - Replacement by connective tissue.
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