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Regeneration-Healing PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Regeneration - Healing (Repair)” by Ian Rice MD.

This medical PowerPoint presentation is about regeneration, the process of repairing or regrowing damaged or lost tissue or organs in living organisms. It is a natural biological process that occurs in many organisms, ranging from simple organisms like bacteria to complex organisms like humans.

In humans, regeneration is limited to certain tissues, such as the liver and skin, which can regenerate to a limited extent. Other tissues, like the heart and nervous system, have limited regenerative capabilities, and damage to these tissues is often permanent.

Healing is the process of repairing damaged tissues or organs, and it is closely related to regeneration. In some cases, healing involves regeneration, such as in the case of the liver or skin, where damaged tissue is replaced by new tissue.

In other cases, healing involves the formation of scar tissue, which is a type of connective tissue that replaces damaged tissue but does not have the same structure or function as the original tissue. Scar tissue is often weaker and less flexible than the original tissue, and it can limit the function of the affected area.

Overall, regeneration and healing are important biological processes that allow living organisms to repair damage and recover from injury or disease. While these processes are often limited in humans, ongoing research is focused on understanding and enhancing the regenerative capabilities of the body.

Tags : Regeneration, Healing, Orthopaedic Surgery, Orthopaedic Surgery PowerPoint presentation

Published on : Jun 23, 2023 | Views : 859 | Downloads : 1

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REGENERATION HEALING (repair)
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LEARNING OBJECTIVES Review the normal physiology and concepts of cell proliferation, cell growth, cell “cycle”, and cell differentiation Understand the basic factors of tissue regeneration Understand the relationships between cells and their ExtraCellular Matrix (ECM) Understand the roles of the major players of healing---angiogenesis, growth factors (GFs), and fibrosis Differentiate 1st & 2nd intention healing
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DEFINITIONS: REGENERATION: Growth of cells to replace lost tissues (no injury) HEALING: A reparative tissue response to a wound, inflammation or necrosis, often leads to fibrosis (injury) GRANULATION TISSUE “ORGANIZING” INFLAMATION NEOVASCULARIZATION
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REGENERATION Replacement of lost structures Is dependent on the type of normal turnover the original tissue has Can be differentiated from “compensatory” growth
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HEALING (repair) Needs a wound, inflammatory process, or necrosis Many disease appearances anatomically are the result of “healing” such as atherosclerosis Often ends with a scar Fibrosis, as one of the 3 possible outcomes of inflammation, follows “healing” Requires a connective tissue “scaffold” Fibrosis occurs in proportion to the damage of the ECM, ExtraCellular Matrix
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Cell Population Fates PROLIFERATION Hormonal, especially steroid hormones eg., EPO, CSF, GFs DIFFERENTIATION*, vs. “multiply” “UNI”-DIRECTIONAL, GAIN and LOSS APOPTOSIS *One of the most KEY concepts in neoplasia
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ECTODERM, ep. MESODERM, str. ENTODERM, ep.
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CELL CYCLE G0 Quiescent (not a very long or dominent phase) G1 PRE-synthetic, but cell GROWTH taking place S Cells which have continuous “turnover” have longer, or larger S-phases, i.e., DNA synthesis S-phase of TUMOR CELLS can be prognostic G2 PRE-mitotic, or, if you will, POST-synthetic M (Mitotic:, P,M,A,T, Cytokinesis)
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CELL TYPES Labile: eg., marrow, GI Quiescent: liver, kidney NON-mitotic: neuron, striated muscle
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STEM CELLS(TOTIPOTENTIAL*) EMBRYONIC ADULT
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EMBRYONICSTEM CELLS DIFFERENTIATION “KNOCKOUT” MICE (mice raised with specific gene defects) REPOPULATION OF DAMAGED TISSUES, in research
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ADULTSTEM CELLS MARROW (HEMOCYTOBLAST) (hematopoetic stem cells) NON-MARROW (RESERVE)
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MARROW STROMAL CELL
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ADULT TISSUE DIFFERENTIATION and REGENERATION PARALLELS EMBRYONIC DEVELOPMENT
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Growth Factors (GFs) Polypeptides Cytokines LOCOMOTION CONTRACTILITY DIFFERENTIATION ANGIOGENESIS
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Growth Factors (GFs) Epidermal Transforming (alpha, beta) Hepatocyte Vascular Endothelial Platelet Derived Fibroblast Keratinocyte Cytokines (TNF, IL-1, Interferons)
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CELL PLAYERS (source AND targets) Lymphocytes, especially T-cells Macrophages Platelets Endothelial cells Fibroblasts Keratinocytes “Mesenchymal” cells Smooth muscle cells
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E (Epidermal) GF Made in platelets, macrophages Present in saliva, milk, urine, plasma Acts on keratinocytes to migrate, divide Acts on fibroblasts to produce “granulation” tissue
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T (Transforming) GF-alpha Made in macrophages, T-cells, keratinocytes Similar to EGF, also effect on hepatocytes
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H (Hepatocyte) GF Made in “mesenchymal” cells Proliferation of epithelium, endothelium, hepatocytes Effect on cell “motility”
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VE (Vascular Endothelial) GF Made in mesenchymal cells Triggered by HYPOXIA Increases vascular permeability Mitogenic for endothelial cells KEY substance in promoting “granulation” tissue
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PD (Platelet Derived) GF Made in platelets, but also MANY other cell types Chemotactic for MANY cells Mitogen for fibroblasts Angiogenesis Another KEY player in granulation tissue
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F (Fibroblast) GF Made in MANY cells Chemotactic and mitogenic, for fibroblasts and keratinocytes Re-epithelialization Angiogenesis, wound contraction Hematopoesis Cardiac/Skeletal (striated) muscle
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T (Transforming) GF-beta Made in MANY CELLS Chemotactic for PMNs and MANY other types of cells Inhibits epithelial cells Fibrogenic Anti-Inflammatory
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K (Keratinocyte) GF Made in fibroblasts Stimulates keratinocytes: Migration (motility) Proliferation (mitogen) Differentiation
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I (Insulin-like) GF-1 Made in macrophages, fibroblasts Stimulates: Sulfated proteoglycans Collagen Keratinocyte migration Fibroblast proliferation Action similar to GH (Pituitary Growth Hormone)
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TNF (Tumor Necrosis Factor)α and β Made in macrophages, mast cells, T-cells Activates macrophages KEY influence on other cytokines
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Interleukins Made in macrophages, mast cells, T-cells, but also MANY other cells MANY functions: Chemotaxis Angiogenesis REGULATION of other cytokines
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INTERFERONS Made by lymphocytes, fibroblasts Activates MACROPHAGES Inhibits FIBROBLASTS REGULATES other cytokines
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SIGNALING Autocrine (same cell) Paracrine (next door neighbor) (many GFs) Endocrine (far away, delivered by blood, steroid hormones)
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TRANSCRIPTION FACTORS HEPATIC REGENERATION TNF IL6 HGF
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ExtraCellular Matrix (ECM) Collagen(s) I-XVIII Elastin Fibrillin CAMs (Cell Adhesion Molecules) Immunoglobulins, cadherins, integrins, selectins Proteoglycans Hyaluronic Acid
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ECM Maintain cell differentiation “Scaffolding” Establish microenvironment Storage of GF’s
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Collagen One - bONE (main component of bone) Collagen Two - carTWOlage (main component of cartilage) Collagen Three - reTHREEculate (main component of reticular fibers) Collagen Four - FLOOR - forms the basement membrane
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GENETIC COLLAGEN DISORDERS I OSTEOGENESIS IMPERFECTA, E-D II ACHONDROGENESIS TYPE II III VASCULAR EHLERS-DANLOS V CLASSICAL E-D IX STICKLER SYNDROME IV ALPORT SYNDROME VI BETHLEM MYOPATHY VII DYSTROPHIC EPIDERMOLYSIS BULLOS. IX EPIPHYSEAL DYSPLASIAS XVII GEN. EPIDERMOLYSYS BULLOSA XV, XVIII KNOBLOCH SYNDROME
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DEFINITIONS: REGENERATION: Growth of cells to replace lost tissues HEALING: A reparative tissue response to a wound, inflammation or necrosis
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HEALING FOLLOWS INFLAMMATION PROLIFERATION and MIGRATION of connective tissue cells ANGIOGENESIS (Neovascularization) Collagen, other ECM protein synthesis Tissue Remodeling Wound contraction Increase in wound strength (scar = fibrosis) LET’S MAKE THIS AS SIMPLE AS POSSIBLE: 1) NEUTROPHIL 2) ENDOTHELIAL CELL 3) FIBROBLAST
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ANGIOGENESIS(NEOVASCULARIZATION) From endothelial precursor cells From PRE-existing vessels Stimulated/Regulated by GF’s, especially VEGF Also regulated by ECM proteins aka, “GRANULATION”, “GRANULATION TISSUE”, “ORGANIZATION”, NEOVASCULARIZATION, “ORGANIZING INFLAMMATION”
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WOUND HEALING 1st INTENTION Edges lined up 2nd INTENTION Edges NOT lined up Ergo…. More granulation More epithelialization MORE FIBROSIS
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“HEALTHY” Granulation Tissue
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FIBROSIS/SCARRING DEPOSITION OF COLLAGEN by FIBROBLASTS With time (weeks, months, years?) the collagen becomes more dense, ergo, the tissue becomes “STRONGER”
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Wound RETARDING factors(LOCAL) DECREASED Blood supply Denervation Local Infection FB Hematoma Mechanical stress Necrotic tissue
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Wound RETARDING factors(SYSTEMIC) DECREASED Blood supply Age Anemia Malignancy Malnutrition Obesity Infection Organ failure