Download Free Medical Regeneration-Healing PowerPoint Presentation

Regeneration-Healing PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

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 : 1321 | Downloads : 1

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

REGENERATION HEALING (repair)
Slide 2-

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
Slide 3-

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
Slide 4-

REGENERATION Replacement of lost structures Is dependent on the type of normal turnover the original tissue has Can be differentiated from “compensatory” growth
Slide 5-

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
Slide 6-

ppt slide no 6 content not found
Slide 7-

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
Slide 8-

ECTODERM, ep. MESODERM, str. ENTODERM, ep.
Slide 9-

ppt slide no 9 content not found
Slide 10-

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)
Slide 11-

CELL TYPES Labile: eg., marrow, GI Quiescent: liver, kidney NON-mitotic: neuron, striated muscle
Slide 12-

STEM CELLS(TOTIPOTENTIAL*) EMBRYONIC ADULT
Slide 13-

EMBRYONICSTEM CELLS DIFFERENTIATION “KNOCKOUT” MICE (mice raised with specific gene defects) REPOPULATION OF DAMAGED TISSUES, in research
Slide 14-

ADULTSTEM CELLS MARROW (HEMOCYTOBLAST) (hematopoetic stem cells) NON-MARROW (RESERVE)
Slide 15-

MARROW STROMAL CELL
Slide 16-

ADULT TISSUE DIFFERENTIATION and REGENERATION PARALLELS EMBRYONIC DEVELOPMENT
Slide 17-

Growth Factors (GFs) Polypeptides Cytokines LOCOMOTION CONTRACTILITY DIFFERENTIATION ANGIOGENESIS
Slide 18-

Growth Factors (GFs) Epidermal Transforming (alpha, beta) Hepatocyte Vascular Endothelial Platelet Derived Fibroblast Keratinocyte Cytokines (TNF, IL-1, Interferons)
Slide 19-

ppt slide no 19 content not found
Slide 20-

CELL PLAYERS (source AND targets) Lymphocytes, especially T-cells Macrophages Platelets Endothelial cells Fibroblasts Keratinocytes “Mesenchymal” cells Smooth muscle cells
Slide 21-

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
Slide 22-

T (Transforming) GF-alpha Made in macrophages, T-cells, keratinocytes Similar to EGF, also effect on hepatocytes
Slide 23-

H (Hepatocyte) GF Made in “mesenchymal” cells Proliferation of epithelium, endothelium, hepatocytes Effect on cell “motility”
Slide 24-

VE (Vascular Endothelial) GF Made in mesenchymal cells Triggered by HYPOXIA Increases vascular permeability Mitogenic for endothelial cells KEY substance in promoting “granulation” tissue
Slide 25-

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
Slide 26-

F (Fibroblast) GF Made in MANY cells Chemotactic and mitogenic, for fibroblasts and keratinocytes Re-epithelialization Angiogenesis, wound contraction Hematopoesis Cardiac/Skeletal (striated) muscle
Slide 27-

T (Transforming) GF-beta Made in MANY CELLS Chemotactic for PMNs and MANY other types of cells Inhibits epithelial cells Fibrogenic Anti-Inflammatory
Slide 28-

K (Keratinocyte) GF Made in fibroblasts Stimulates keratinocytes: Migration (motility) Proliferation (mitogen) Differentiation
Slide 29-

I (Insulin-like) GF-1 Made in macrophages, fibroblasts Stimulates: Sulfated proteoglycans Collagen Keratinocyte migration Fibroblast proliferation Action similar to GH (Pituitary Growth Hormone)
Slide 30-

TNF (Tumor Necrosis Factor)α and β Made in macrophages, mast cells, T-cells Activates macrophages KEY influence on other cytokines
Slide 31-

Interleukins Made in macrophages, mast cells, T-cells, but also MANY other cells MANY functions: Chemotaxis Angiogenesis REGULATION of other cytokines
Slide 32-

INTERFERONS Made by lymphocytes, fibroblasts Activates MACROPHAGES Inhibits FIBROBLASTS REGULATES other cytokines
Slide 33-

SIGNALING Autocrine (same cell) Paracrine (next door neighbor) (many GFs) Endocrine (far away, delivered by blood, steroid hormones)
Slide 34-

ppt slide no 34 content not found
Slide 35-

TRANSCRIPTION FACTORS HEPATIC REGENERATION TNF IL6 HGF
Slide 36-

ExtraCellular Matrix (ECM) Collagen(s) I-XVIII Elastin Fibrillin CAMs (Cell Adhesion Molecules) Immunoglobulins, cadherins, integrins, selectins Proteoglycans Hyaluronic Acid
Slide 37-

ECM Maintain cell differentiation “Scaffolding” Establish microenvironment Storage of GF’s
Slide 38-

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
Slide 39-

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
Slide 40-

DEFINITIONS: REGENERATION: Growth of cells to replace lost tissues HEALING: A reparative tissue response to a wound, inflammation or necrosis
Slide 41-

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
Slide 42-

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”
Slide 43-

ppt slide no 43 content not found
Slide 44-

ppt slide no 44 content not found
Slide 45-

ppt slide no 45 content not found
Slide 46-

WOUND HEALING 1st INTENTION Edges lined up 2nd INTENTION Edges NOT lined up Ergo…. More granulation More epithelialization MORE FIBROSIS
Slide 47-

ppt slide no 47 content not found
Slide 48-

“HEALTHY” Granulation Tissue
Slide 49-

FIBROSIS/SCARRING DEPOSITION OF COLLAGEN by FIBROBLASTS With time (weeks, months, years?) the collagen becomes more dense, ergo, the tissue becomes “STRONGER”
Slide 50-

Wound RETARDING factors(LOCAL) DECREASED Blood supply Denervation Local Infection FB Hematoma Mechanical stress Necrotic tissue
Slide 51-

Wound RETARDING factors(SYSTEMIC) DECREASED Blood supply Age Anemia Malignancy Malnutrition Obesity Infection Organ failure