Inflammation PDF

Inflammation Dr. Heba Elhendawy Associate Professor of Oral Pathology  Definition: Inflammation is the local vascular, lymphatic and cellular reactions of living tissues to irritant (injurious agent). Inflammation is a protective mechanism with the purpose of localization and removal of the irr...

Inflammation Dr. Heba Elhendawy Associate Professor of Oral Pathology  Definition: Inflammation is the local vascular, lymphatic and cellular reactions of living tissues to irritant (injurious agent). Inflammation is a protective mechanism with the purpose of localization and removal of the irritant. Inflammation is designated by adding the suffix (itis) to the name of organ ( pulpitis, osteomyelitis). Causes of inflammation: 1. Living irritant: bacteria and their toxins, viruses, parasites, and fungi. 2. Non-living irritant: Physical irritants as excessive heat and cold, irradiation. Chemical irritants as acids, alkalis, poisons. Mechanical irritants as trauma, mechanical friction. 3. Antigens: cause allergic inflammation due to antigen antibody reaction as bronchial asthma.  Types of inflammation: Acute inflammation Chronic inflammation irritant of a short duration of action irritant of a prolonged duration of action tissue response is rapid (Sudden onset) tissue response is slow (Gradual onset) last for minutes, several hours or few days. last for months to years. excess inflammatory exudate (marked tissue edema). scanty inflammatory exudate (mild tissue edema). Productive (+++ granulation tissue formation) Cells: PNLs (mainly), macrophages. Lymphocytes, plasma cells, eosinophils, basophils, macrophages Prominent cardinal signs of inflammation. Less prominent cardinal signs of inflammation. Prominent vascular changes. Less prominent vascular changes.  Acute inflammatory cells (PMNLs) PMNL= polymorph nuclear leucocytes. Eosinophilis Basophilis Neurophilis Chronic inflammatory cells lymphocytes Plasma cells Events of acute inflammation: 1. Local tissue damage (necrosis of tissue). 2. Local vascular reaction (vasodilatation of blood vessels, increase capillary permeability. 3. Local reaction of tissue histocytes to clean the tissue from tissue debris. Macrophage work like the cleaner. 2. Local vascular reactions ( vascular phenomenon) Increase Bl. flow Inrease blood viscosity dt fluid exudate formation. 3. Local reaction of the tissue histocytes Late in acute inflammation the macrophages replace PMNLs (why?) 1. Clean the site of inflammation. 2. Prepare for tissue repair process. Fluid inflammatory exudate Composition: High protein (4-8 gm%) Mainly fibrinogen that transform to fibrin. - Formed by release of plasma proteins from the dilated blood vessels due to increased capillary permeability. Function: 1. Dilute toxins, poisons, chemicals to minimize their effect. 2. Bring antibodies to the site of infection. 3. Supply nutrition to cells and carry out the waste products. 4. Supply fibrinogen that changes to fibrin…. - That form fibrin network for PMNLs, macrophages to move toward the irritants. - Form network upon which fibroblasts proliferate to start repair. - Localize infection by surrounding the inflamed area and blocking the interstitial tissue spaces and lymphatics. Inflammatory exudate(fluid+ cellular exudate)  2. Cellular exudate Composition: neutrophils and macrophage(phagocytic cells). Phagocytosis: ingestion and destruction of bacteria, necrotic debris, and foreign bodies by phagocytic cells.  Types of acute inflammation: Suppurative (pyogenic or septic) Non suppurative Sever acute inflammation characterized by No pus formation pus formation. pyogenic microorganisms as staphylococci, streptococci. Types: Types: 1. localized (e.g. Abscess, furuncle, 1. Catarrhal inflammation. carbuncle). 2. pseudomembranous inflammation. 2. Diffuse (Facial cellulitis). 3. Sero-fibrinous inflammation. 4. Serous inflammation. 5. Hemorrhagic inflammation. 6. Necrotizing inflammation. 7. Allergic inflammation. 1. Suppurative inflammation  Abscess Def: localized suppurative inflammation resulting in formation of irregular cavity containing pus. Cause: staphylococcus aureus. Pathology: Early stage: the abscess is formed of two zones (central necrotic tissue, and inflammed tissue at periphery). Then PMNLs die and release proteolytic enzymes that liquify the margins of necrotic area forming the pus three zones (necrotic core, pus cavity, inflamed zone). The abscess enlarges in size by further necrosis and liquefaction of the surrounding inflamed zone until the release of coagulase enzyme by staph. aureus that help fibrin formation to localize inflammation.  Cellulitis Def: acute diffuse suppurative inflammation. Cause: streptococcus haemolyticus that produces two enzymes 1. Fibrinolysin enzyme that dissolve fibrin. 2. Hyaluronidase enzyme→ dissolves hyaluronic acid in ground substance→Spread of bacteria and toxins. Sites: loose subcutaneous tissue, fascial planes, areolar tissue of orbit. Pathology: as abscess with the following changes: 1. Failure of localization due to absence of fibrin. 2. Necrosis is extensive. 3. Pus formation is slow.  1. Definition & causes of inflammation. 2. Difference between acute & chronic inflammation. 3. Cells of inflammation (acute & chronic). 4. Events occur in inflammation (tissue damage, vascular change, final histocytes action). 6. Fluid inflammatory exudate (composition and function). 7.Cellular inflammatory exudate (composition, chemotaxis, Phagocytosis). 8. Types of acute suppurative inflammation (localized, Diffuse). 9. Forms of localized acute suppurative inflammation (Abscess, furuncle, carbuncles). 10. Facial cellulitis (definition, causative organisms, mechanisms, common affected tissues). The End