Inflammation Types and Causes

Inflammation

• A local response of tissue to injury
• Stimulus can vary; microbial, immunological, physical, or chemical agents
• Inflammation and its chemicals may not remain localized

Types of Inflammation

• Acute Inflammation: Fast onset, mainly neutrophils as cellular infiltrate, usually mild and self-limited tissue injury, prominent local and systemic factors, likely to have cardinal signs
• Chronic Inflammation: Slow onset, monocytes/macrophages and lymphocytes as cellular infiltrate, long-term exposure to stimulus, fibrosis and angiogenesis as a response

Causes of Inflammation

• Infections: Bacteria, viruses, fungi, parasites
• Tissue Necrosis: Physical or chemical injuries, heart attack, collection of dead tissue in a confined space
• Trauma: Blunt and penetrating trauma, burns, frostbite, chemicals
• Foreign Bodies: Splinters, sutures, bones, finger nails, popcorn kernels
• Immune (Hypersensitivity Reactions): Triggered by environmental factors or autoimmune diseases

Cardinal Signs of Acute Inflammation

• Rubor (Redness): Caused by vasodilation
• Calor (Heat): Caused by increased blood flow
• Tumor (Swelling): Caused by fluid exudation
• Dolor (Pain): Caused by pressure on nerve endings
• Loss of Function: Caused by swelling and pain

Events in Acute Inflammation

• Vascular Events: Vasodilation, increased hydrostatic pressure, increased vascular permeability, transudation of fluid, slowing of microcirculation
• Cellular Events: Leucocyte recruitment (chemotaxis), phagocytosis of particles (engulfment)

Causes of Increased Vascular Permeability

• Endothelial cell contraction
• Endothelial injury (direct or leucocyte induced)
• Increased transcytosis
• Leakage from new blood vessels

Phagocytosis

• Two types of phagocytic cells: PMNs (early inflammatory response) and monocytes/macrophages
• Opsonization: ‘marker’ that helps phagocytosis

Phagocytosis at Inflamed Tissue Site

• Neutrophils and macrophages release proteolytic enzymes: protease, collagenase, elastase, lipase
• Immune response impacts the ‘insult,’ but also impacts the surrounding tissues.

Patterns of Inflammation

• Serous: Thin, watery fluid
• Fibrinous: Thick, sticky fluid containing fibrin
• Suppurative (purulent): Pus, containing neutrophils and bacteria
• Ulcerative: Erosion of the surface

Chemical Mediators

• Chemical messengers that act on blood vessels, inflammatory cells, or other cells to cause an inflammatory response
• Exogenous: Endotoxins
• Endogenous: Plasma, leukocytes, endothelial cells, fibroblasts
• Cytokines: Chemical proteins produced by many cells, including PMNs, macrophages, B lymphocytes, epithelial cells

White Blood Cells and Inflammation

• White blood cells (WBCs), or leukocytes, are crucial for the inflammatory response and immune defense.
• WBCs like neutrophils and macrophages are the first line of defense against pathogens.
• WBCs release enzymes like protease, collagenase, and elastase that can break down pathogens but also damage healthy tissue.
• WBCs release cytokines (e.g., TNF-alpha, interleukins) to recruit more immune cells and amplify inflammation.
• Macrophages play a role in healing by clearing debris and stimulating tissue repair.
• Chronic inflammation, fueled by continuous WBC activation, can cause widespread tissue damage.

Inflammation

• Inflammation is a localized tissue response to injury caused by various stimuli, including microbial, immunological, physical, or chemical agents.
• It serves as a protective mechanism, eliminating harmful agents and initiating tissue repair.

Types of Inflammation

• Acute inflammation:
  • Rapid onset, primarily involves neutrophils.
  • Characterized by redness, heat, swelling, pain, and loss of function.
• Chronic inflammation:
  • Slow onset, involves monocytes, macrophages, and lymphocytes.
  • Leads to fibrosis and tissue remodeling.

Cardinal Signs of Acute Inflammation

• Rubor (redness): Caused by vasodilation.
• Calor (heat): Resulting from increased blood flow.
• Tumor (swelling): Due to fluid exudate.
• Dolor (pain): From chemical mediators stimulating nerve endings.
• Loss of function: Due to swelling and tissue damage.

Vascular and Cellular Events in Acute Inflammation

• Vascular events:
  • Persistent vasodilation: Leads to increased blood flow.
  • Increased hydrostatic pressure: Pushes fluid into tissue.
  • Vascular permeability: Endothelial cells contract, allowing fluid and proteins to move into tissues.
  • Transudation: Fluid moves into extracellular space.
  • Slowing of microcirculation: Enables immune cells to reach the injury site.
• Cellular events:
  • Leukocyte recruitment: Immune cells (mainly neutrophils) migrate to the inflammation site via chemotaxis.
  • Phagocytosis: Neutrophils and macrophages engulf pathogens and debris, enhanced by opsonization.
  • Release of proteolytic enzymes: Enzymes like protease, collagenase, and elastase break down pathogens but can also cause tissue damage.

Patterns of Inflammation

• Serous: Clear, watery fluid from mild inflammation.
• Fibrinous: Thick, sticky exudate indicating more severe inflammation.
• Suppurative (Purulent): Pus-filled, common with bacterial infections.
• Ulcerative: Involves tissue loss, creating an open sore.

Chemical Mediators of Inflammation

• Exogenous mediators: Substances from outside the body, such as endotoxins from bacterial infections.
• Endogenous mediators: Produced within the body, affecting blood vessels and immune cells.
• Key chemical mediators:
  • Cytokines: Proteins produced by cells like macrophages and fibroblasts, regulating immune responses, including:
    • Tumor Necrosis Factor (TNF): Promotes inflammation and can induce fever.
    • Interleukins (IL-1, IL-6, IL-8): Attract immune cells and aid in their activation.
  • Histamine: Released from mast cells, dilates arterioles and increases vascular permeability.
  • Prostaglandins: Lipid compounds from mast cells that cause vasodilation, pain, and fever.
  • Leukotrienes: Produced by leukocytes, act as chemotactic agents, promote vasoconstriction, and release lysosomal enzymes.
  • Chemokines: Small proteins that attract leukocytes to inflammation sites, enhancing chemotaxis.

Summary

• Causes of Acute Inflammation: Infection, trauma, necrosis, foreign bodies, and immune reactions.
• Differences Between Acute and Chronic Inflammation: Acute is fast and temporary, while chronic is prolonged and associated with tissue remodeling.
• Key Events in Acute Inflammation: Vascular changes, leukocyte recruitment, and phagocytosis.
• Chemical Mediators: Essential for coordinating the immune response and promoting tissue repair.

Relevance to Dentistry

• Understanding the inflammatory response is crucial for dental professionals as it plays a key role in periodontal disease pathogenesis.
• Recognizing and managing inflammation helps in treating conditions like gingivitis and periodontitis.