Inflammatory Response Part 1 Acute Inflammation DTH23 PDF

Inflammatory Responses Part 1 Sarah Balian Biomedical Science Intended Learning Outcomes By the end of this session students should be able to: Describe the classical signs of acute inflammation and their relevance. Explain significance of the formation of a cellular and a fluid exudate and...

Inflammatory Responses Part 1 Sarah Balian Biomedical Science Intended Learning Outcomes By the end of this session students should be able to: Describe the classical signs of acute inflammation and their relevance. Explain significance of the formation of a cellular and a fluid exudate and how they are formed. Discuss the assorted ways by which acute inflammation can be generated. Explain the processes of phagocytosis and bacterial killing. Recognise the effects and action of chemical mediators involved with acute inflammation on tissues. Inflammation What does inflammation mean to you? Purpose? Swelling and a way of the body trying to protect when an injury or something happens Armed with your writing utensils Friend or Foe? Jot down bullet points to the following questions Friend And foe What does it ‘look’ like? Swelling /puffy Relevance of inflammation in dentistry? Gingivitis / periodontal disease Define Inflammation What key words would you use? Local response of tissue to injury Stimulus can be variable: 1. Microbial Bacteria - 2. Immunological imunesystem -. 3. Physical 4. Chemical agents Will inflammation & its chemicals really stay local? No moves everything in the body everywhere - Types of Inflammation as Rest Inflammation standing Long quick& - Acute Chronic Inflammation Inflammation -Langer response first Features comparing Acute & Chronic Inflammation Feature Acute Chronic Onset Fast Slow Cellular infiltrate Mainly neutrophils Monocytes/macrophages & lymphocytes Tissue injury / fibrosis Usually mild and self-limited Local & systemic factors Prominent Presence of cardinal signs Likely to be present No cardinal signs Presence of stimulus Long term exposure Response Fibrosis & angiogenesis Tissues are "create own blood supply -  Infections Tissue necrosis Bacteria, viruses, fungi, Physical / chemical injuries parasites Heart attack Collection of dead tissue in confined space Trauma Foreign bodies Blunt & penetrating trauma Splinters, sutures, bones, Burns, frostbite, chemicals finger nails Popcorn kernels Immune (hypersensitivity reactions) Triggered by environmental factors Or autoimmune diseases Cardinal Signs of Acute Inflammation Five Cardinal Signs of Inflammation Rubor (redness) Calor (heat) Tumor (swelling) Dolor (pain) Loss of function Event in Acute Inflammation Linked with Immunology Lectures  Events Vascular changes - changes to the blood vessels(capillaries) - Vascular Events Increased white b'lood cells or trying to flush out problem ↑ 1. Persistent vasodilation More blood flow = increased pressure 2. Elevation of hydrostatic pressure Allow more in and out thought cell wall 3. Increase in vascular permeability A fluid that is released when a lot of hydrostatic pressure is present 4. Transudation of fluid into extracellular space Plasma proteins and fluid 5. Slowing of or statis of micro circulation  Allow more in and out thought cell wall Causes of increased vascular permeability Endothelial cell contraction Endothelial injury 1. Direct white bod e O - 2. Leucocyte induced Increased transcytosis fluid Leakage from new blood vessels Image from Researchgate Feb 2021  Chain reaction Leucocyte recruitment to site – Cellular Events chemotaxsis & Chemical gradient occurs when injury happens Injury occurs - chemotaxsis occurs (recruitment of wbc) which says to leukocytes to come to area. Phagocytosis of particles – engulfment of particles chemical messenger system. Phagocytosis - Process which a cell es engulfs Large bacteria microorganisms.. 2 types of phagocytic cells 1. PMN’s part of early inflammatory response 2. Monocytes & macrophages cels Iphagocytic Opsonisation – ‘marker’ optimisation coating of an antigen, so you get an antigen which is the foreign body. The tissues mark those antigens.Those antigens and foreign bodies and they are marked when the white blood cells in the PMN leucocytes polymorphonucleocytes come along and please take this one so they get opsonised. They basically get marked to get engulfed.  white blood cells. - Neutrophils and macrophages Phagocytosis when at inflamed tissue site release proteolytic enzymes: In the mouth the wbc release enzyme (collagenase ) which break down collagen in the gingiva Protease Collagenase Elastase Lipase So the ‘host’ is calling upon the immune cells to ‘come and fight’ against an ‘insult’. The immune response arrives however as well as impacting the ‘insult’, who else is it impacting? Host.  Patterns of Inflammation ecome con Pranic ↑ Suppurative Serous Fibrinous Ulcerative (purulent) I I I % Serous fluid Scaring Puss/ Breac in neucrotic tissue. epithelium Chemical Mediators  Image from Nature Feb 2021 chain of events. 18 Chemical Mediators – a chemical messenger that acts upon a blood vessel, inflammatory cells or other cells to cause a inflammatory response Exogenous Endogenous - From body. Endotoxins - From bacteria Plasma Coming from where? Leucocytes Endothelial cells Fibroblasts Image from pinterest website Feb 2021  chemicals in Lots of the body. - Chemical Mediators - CYTOKINES Chemical proteins produced by many cells E.g. Produced by PMN’s 1. Macrophages 2. B Lymphocytes 3. Epithelial cells 4. Gingival Fibroblasts 5. Osteoblasts Mediate & regulate immune & inflammatory reactions Cytokines – be pro-inflammatory & anti- inflammatory Interleukin (IL-1, IL-6 & IL-8) Tumor Necrosis Factor (TNF) Produced by leucocytes & many Immune cell recruitment, other cells, role in activation & produced by macrophages, TNF differentiation, neutrophil is able to induce fever recruitment  a Releasei rea - Cytokines – Vasoactive amine - Histamine Histamine comes from mast cells Acts on blood vessels Histamine causes dilation of arterioles & increase permeability Image from Wikipedia website Feb 2021 Prostaglandins Type of Cytokine. - Produced by mast cells, macrophages & endothelial cells Lipid compound fat based -. Involved in vascular & systemic reactions of inflammation Causes vasodilation Fever Pain I pro Inflamotry Leukotrienes - Type of Cytokine 'Anti-inflamatory. Produced by leucocytes and mast cells by the action of lipoxygenase & Act as chemotactic for Group of enzymes that introduce oxygen into neutrophils fatty acids. Usually accompanied by histamine & prostaglandins Releases lysosomal enzymes Vasoconstriction Chemokines Small Protein. Family of small proteins that act as primarily chemo-attractants for specific types of leukocytes. Enhancing chemotaxis Site. Drows WBC to Injury Image from Wikipedia website Feb 2021 Summary Causes of inflammation Chemical mediators Difference between in inflammation acute & chronic Patterns of acute Sign of inflammation Inflammation Events occurring in acute inflammation Where does this become relevant? Pathogenesis of Periodontal Disease Note down key words from today Inflammation friend or foe? Reading recommendations Ross & Wilson Anatomy and Physiology in Health and Illness, 13e Paperback – 6 Jun. 2018 Acute Inflammation - TeachMePhysiology