SEMINAR PRESENTATION
ACUTE INFLAMMATION
PRESENTED BY:
SHREYA SINGH
MDS II year
Dept of Prosthodontics
MMCDSR
INTRODUCTION
• “Inflame”- to set fire.
• Inflammation is the “Dynamic response of vascularised tissue to
injury.”
• Hose Response to get rid of damaged or necrotic tissues and foreign
invaders.
• Is a protective response.
• Serves to bring defense and healing mechanism to the site of injury.
ACUTE INFLAMMATION
• It is a complex reaction to injurious agents such as microbes and
damaged, usually necrotic cells, that consists of vascular responses,
migration and activation of leukocytes and systemic reactions.
• The unique feature of the inflammatory process is the reaction of
blood vessels, leading to the accumulation of fluid and leukocytes in
extravascular tissues.
• It is divided into 2 patterns:
1. Acute
2. Chronic
ACUTE INFLAMMATION
• Rapid in onset (seconds or minutes)
• Is of relatively short duration, lasting for minutes, several hours or a few
days
• It has 3 major components:
Alterations in vascular caliber that lead to an increase in blood flow
Structural changes in the microvasculature that permit plasma
proteins and leukocytes to leave the circulation
Emigration of the leukocytes from the microcirculation, their
accumulation in the focus of injury, and their activation to eliminate
the offending agent
STIMULI FOR ACTIVE INFLAMMATION
• Infections: bacterial, viral, parasitic & microbial toxins
• Trauma (blunt and penetrating)
• Physical & chemical agents (thermal injury, irradiation, environmental
chemicals)
• Foreign bodies (splinters, dirt, sutures)
• Immune reactions (also called hypersensitivity rxn)
LEWIS TRIPLE RESPONSE
• FLUSH: Capillary dilatation
• FLARE: Arteriolar dilation
• WHEAL: Exudation, Edema
CARDINAL SIGNS OF INFLAMMATION
Classical 5 Signs: Celsius 1st c. B.C. &Virchow 19th c. A.D.
• RUBOR : Redness – Hyperemia
• CALOR : Warmth/Heat – Hyperemia
• DOLOR : Pain - Nerve, Chemical Mediators
• TUMOR: Swelling – Exudation
• LOSS OF FUNCTION: Functio laesa
THE 5 CARDINAL SIGNS OF
INFLAMMATION
INFLAMMATION –
MECHANISM
1. Vasodilatation
2. Exudation – Edema
3. Emigration of Cells
4. Chemotaxis
5. Phagocytosis
ACUTE INFLAMMATION
Physiological Responses Symptoms
• Release of soluble mediators
• Vasodilatation • Heat (calor)
• Increased blood flow • Redness (rubor)
• Extravasation of fluid (permeability) • Swelling (tumor)
• Cellular influx (chemotaxis) • Pain (dolor)
ACUTE INFLAMMATION
Physiological Responses Symptoms
• Release of soluble mediators
• Vasodilatation • Heat (calor)
• Increased blood flow • Redness (rubor)
• Extravasation of fluid (permeability) • Swelling (tumor)
• Cellular influx (chemotaxis) • Pain (dolor)
ACUTE INFLAMMATION
Physiological Responses Symptoms
• Release of soluble mediators
• Vasodilatation • Heat (calor)
• Increased blood flow • Redness (rubor)
• Extravasation of fluid (permeability) • Swelling (tumor)
• Cellular influx (chemotaxis) • Pain (dolor)
ACUTE INFLAMMATION
Physiological Responses Symptoms
• Release of soluble mediators
• Vasodilatation • Heat (calor)
• Increased blood flow • Redness (rubor)
• Extravasation of fluid (permeability) • Swelling (tumor)
• Cellular influx (chemotaxis) • Pain (dolor)
RED, WARM & SWOLLEN (FLARE, FLUSH &
WHEAL)
CALOR, RUBOR, DOLOR, TUMOR, LOSS OF
FUNCTION.
SURGICAL WOUND INFLAMMATION
RED, WARM & SWOLLEN (FLARE, FLUSH &
WHEAL)
CALOR, RUBOR, DOLOR, TUMOR, LOSS OF
FUNCTION.
MOUTH APHTHUS ULCER
ACUTE ENTERITIS
RED, WARM & SWOLLEN (FLARE, FLUSH &
WHEAL)
CALOR, RUBOR, DOLOR, TUMOR, LOSS OF
FUNCTION.
VASCULAR EVENTS
VASCULAR CHANGES
VASODILATATION
• Increased permeability of vessels due to widened intercellular
junctions and contraction of endothelial cells (Histamine, VEGF,
Bradykinin)
HAEMODYNAMIC CHANGES
Transient vasoconstriction
Persistent progressive vasodilatation
Elevation in local hydrostatic pressure resulting in transudation of fluid
into the extracellular space
Slowing or stasis
Leukocytic margination
VASODILATION
• Brief arteriolar vasoconstriction followed by vasodilation
• Accounts for warmth and redness
• Opens microvascular beds
• Increased intravascular pressure causes an early transudate
(protein-poor filtrate of plasma)into interstitium.
VASCULAR LEAKAGE
• Vascular permeability (leakiness) commences
• Transudate gives way to exudate (protein-rich)
• Increases interstitial osmotic pressure contributing to edema
(water and ions)
MECHANISM OF INFLAMMATION
VASCULAR CHANGES
EXUDATION
LEUKOCYTE CELLULAR EVENTS
CELLULAR EVENTS
• Leukocytes Margination → Adhesion (Pavementing) → Rolling →
Emigration
• Emigration of:
• Neutrophils (1-2 Days)
• Monocytes (2-3 Days)
• Chemotaxis
• Endogenous Signaling Molecules – Lymphokines
• Exogenous – Toxins
• Phagocytosis - Lysosomal Enzymes, Free Radicals, Oxidative Burst
NEUTROPHIL MARGINATION
EMIGRATION OF LEUCOCYTES
CHEMOTAXIS
• Migration of leukocytes towards site of inflammation.
• Stimuli for movement- Chemo-attractants.
• Most commonly exogenous substances(bacterial proteins)
CHEMOTAXIS
The chemotactic factor mediated transmigration of
leukocytes after crossing several barriers to reach the
interstitial tissues is called chemotaxis
• The agents acting as potent chemotactic substances for
different leukocytes called chemokines are:
• Leukotriene B4 (LTB4)
• Platelet factor 4 (PF4)
• Components of complement system (C3, C5)
• Cytokines (IL-1,IL-5,IL-6)
• Soluble bacterial products (formylated peptides)
• Monocyte chemo-attractant protein (MCP-1)
PHAGOCYTOSIS
• It is the process of engulfment of solid particulate material
by the cells
• There are 2 types of phagocytic cells:
• Polymorphonuclear neutrophils called as microphages
• Circulating monocytes and fixed tissue mononuclear phagocytes
called as macrophages
• It involves the following steps-
PHAGOCYTOSIS
• Recognition and attachment mannose and scavenger
receptors on WBC’s
• Engulfment- formation of phagocytic vacuole: Pseudopod
formation due to Actin polymerization
• Killing and degradation
PHAGOCYTOSIS
RECOGNITION AND ATTACHMENT
ENGULFMENT
KILLING AND DEGRADATION
• Recognition and attachment /Opsonization stage
• Ig G opsonin
• C3b opsonin
OPSONIZATION
MAKING IT TASTY AND ATTRACTIVE
PARTICLE- microbes or bacterial products or toxins
Opsonins: IgG antibody, proteinC3, mannose binding lectin,
fibronectin,fibrinogen and C-reactive protein
KILLING AND DEGRADATION
• Oxygen Dependent Systems: formation of reactive oxygen species
• NADPH oxidase enzyme complex
• Hydrogen Peroxide – MPO - Halide system
Most potent bactericidal system of neutrophils
Polymorphs after phagocytosis undergo apoptotic cell death
CHEMICAL MEDIATORS
• Plasma-derived
• Complement
• Kinins
• Coagulation factors
• Cell-derived:
• Mast cell- histamine
• Prostaglandins
SPECIFIC MEDIATORS
• Vasoactive amines
• Histamine:
• Causes vasodilatation and venular endothelial cell
contraction, Junctional widening
• Released by mast cells, basophils, platelets in response to
injury (trauma, heat), immune reactions (IgE-mast cell)
SPECIFIC MEDIATORS
Serotonin:
• Vasodilatory effects similar to those of histamine;
• Platelet dense - body granules;
• Release triggered by platelet aggregation
Arachidonic acid metabolites
(eicosanoids)
Prostaglandins and leukotrienes are derived from arachidonic
acid metabolism through:
• Cyclo-oxygenase and
• Lipoxygenase pathway
PATHWAY OF ARACHIDONIC ACID
METABOLISM
Cyclooxygenase pathway produces:
• Thromboxane: Aggregates platelets & causes vasoconstriction
• Prostacycline: Inhibit platelets aggregation and dilates blood vessels.
• Prostaglandin: Increases vasodilation and increases vascular
permeability.
Lipoxygenase pathway produces
Leukotrienes:
• Causes vasoconstriction and increases vascular permeability.
• Stimulates leukocytes adhesion to the endothelium.
• Are chemotaxins
Plasma derived: Plasma proteases
• Clotting factors
• Complement factors
• Kinins
KENIN SYSTEM
Leads to formation of bradykinin from cleavage of
precursor (HMWK)
• Vascular permeability
• Arteriolar dilatation
• Non-vascular smooth muscle contraction (e.g., bronchial
smooth muscle)
• Causes pain
COMPLEMENT SYSTEM
Components C1-C9 present in inactive form
• Activated via classic (C1) or alternative (C3) pathways to
generate MAC (C5 - C9) that punch holes in microbe
membranes
• In acute inflammation
• Vasodilatation, vascular permeability, mast cell degranulation: C3a,
C5a
• Leukocyte chemotaxis :C5a
• As an opsonin, increases phagocytosis: C3b
SPECIFIC MEDIATORS
PAF (platelet activating factor:
Derived also from cell membrane phospholipid
• causes vasodilatation,
• increased vascular permeability,
• increases leukocyte adhesion
SPECIFIC MEDIATORS
Cytokines
• Polypeptide products of many cell types but mainly lymphocytes and
macrophages that act on same cell autocrine, as a message to other
cells paracrine effect or systemically endocrine effect.
• Increase endothelial cell adhesion molecule expression and activation
and aggregation of PMNs.
• IL-1, TNF-a and -B, IFN-y are especially important in inflammation.
SPECIFIC MEDIATORS
Nitric Oxide
• Short-acting soluble free-radical gas.
• Produced by endothelial cells, macrophages, causes:
• Vascular smooth muscle relaxation and vasodilatation
• Kills microbes in activated macrophages
SPECIFIC MEDIATORS
Lysosomal components
• Leak from PMNs and macrophages after demise,
attempts at phagocytosis.
• Acid proteases (only active within lysosomes).
• Neutral proteases such as elastase and collagenase
are destructive in ECM.
Increased vascular permeability:
• Histamine
• Prostaglandin
• Leukotrienes
• Serotonin
• Bradykinin
• PAF (Platelet Activating Factor)
• NO (Nitric Oxide)
FACTORS DETERMINING VARIATION
IN INFLAMMATORY RESPONSE
1. Factors involving the organisms
• type of injury
• Virulence
• Dose
2. Factors involving the host
• general health of host
• immune state of host
• leukopenia
• local host factors
MORPHOLOGY OF ACUTE
INFLAMMATION
PSEUDOMEMBRANOUS INFLAMMATION
• It is inflammatory response of mucous surface (oral, bowel,
respiratory) to toxins of diphtheria or irritant gases.
ULCER:
• it is local defect on the surface of an organ produced by inflammation
• common sites are stomach, duodenum, typhoid, intestinal
tuberculosis, bacillary and amoebic dysentery
SUPPURATION (ABSCESS FORMATION)
• Contains purulent exudate or pus and the process of abscess
formation is known as suppuration -boil,carbuncle
CELLULITIS
• It is a diffuse inflammation of soft tissues resulting from spreading
effects of substances like hyaluronidase released by some bacteria
BACTERIAL INFECTION OF THE
BLOOD
• Bacteraemia
• Septicaemia
• Pyaemia
SYSTEMIC EFFECTS OF ACUTE
INFLAMMATION
1. FEVER
2. LEUKOCYTOSIS
3. LYMPHANGITIS-LYMPHADENITIS
4. SHOCK
FATE OF ACUTE INFLAMMATION
• Resolution
• Healing by scarring
• Progression or suppuration
• Progression to chronic inflammation
INFLAMMATION OUTCOME
• Chronic Inflammation
INJURY • Acute Inflammation Resolution/Healing
• Abscess
• Ulcer
• Fistula
• Sinus
THANK YOU
PRESENTED BY:
SHREYA SINGH
MDS II year
Dept of Prosthodontics
MMCDSR
