Inflammation and wound healing

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Introduction

Inflammation is a protective response of vascularized tissues against harmful stimuli such as infections, trauma, toxins, and tissue injury. The main purpose of inflammation is to:

  • Eliminate the injurious agent
  • Remove damaged tissue
  • Initiate healing and repair

Inflammation may be:

  • Acute inflammation → short duration with predominant neutrophils
  • Chronic inflammation → prolonged inflammation with lymphocytes, macrophages, fibrosis, and tissue destruction

The outcome of inflammation may include:

  • Complete regeneration
  • Scar formation
  • Fibrosis
  • Chronic tissue damage

Understanding inflammation and tissue repair is important for UG and PG students because these processes form the basis of many pathological diseases.

Acute Inflammation

Acute inflammation is an immediate and early response to tissue injury. It usually lasts for:

  • Few minutes
  • Few hours
  • Few days

Characteristics

  • Exudation of plasma proteins
  • Vascular changes
  • Migration of neutrophils

Etiology of Acute Inflammation

Common causes include:

1. Infections

  • Bacterial
  • Viral
  • Fungal
  • Parasitic

2. Physical Agents

  • Trauma
  • Burns
  • Radiation
  • Frostbite

3. Chemical Agents

  • Acids
  • Alkalis
  • Toxic chemicals

4. Tissue Necrosis

  • Ischemia
  • Infarction

5. Immune Reactions

  • Hypersensitivity reactions
  • Autoimmune diseases

Pathogenesis of Acute Inflammation

Acute inflammation mainly involves:

  1. Vascular changes
  2. Cellular events

1. Vascular Changes

Vascular changes are the earliest events in acute inflammation.

A. Vasodilation

  • First vascular response
  • Caused by:
    • Histamine
    • Nitric oxide

Effects

  • Increased blood flow
  • Redness (rubor)
  • Heat (calor)

B. Increased Vascular Permeability

Leads to leakage of protein-rich fluid into tissues.

Causes

  • Endothelial cell contraction
  • Endothelial injury

Results

  • Edema formation
  • Swelling (tumor)

C. Stasis

  • Slowing of blood flow due to fluid loss
  • Leads to concentration of RBCs

D. Leukocyte Margination

  • WBCs move toward endothelial surface

2. Cellular Events

A. Margination

Leukocytes move to the periphery of blood vessels.

B. Rolling

Transient adhesion of leukocytes to endothelium.

C. Adhesion

Firm attachment mediated by:

  • Integrins
  • Selectins

D. Diapedesis (Transmigration)

Leukocytes pass through endothelial gaps.

E. Chemotaxis

Movement of leukocytes toward site of injury.

Chemotactic agents:

  • C5a
  • IL-8
  • Bacterial products

F. Phagocytosis

Neutrophils and macrophages ingest and destroy pathogens.

Steps:

  1. Recognition and attachment
  2. Engulfment
  3. Killing and degradation

Chemical Mediators of Acute Inflammation

Important mediators include:

  • Histamine
  • Serotonin
  • Prostaglandins
  • Leukotrienes
  • Cytokines
  • Complement system

These mediators produce:

  • Vasodilation
  • Pain
  • Fever
  • Chemotaxis

Cardinal Signs of Acute Inflammation

Sign Cause
Redness (Rubor) Vasodilation
Heat (Calor) Increased blood flow
Swelling (Tumor) Edema
Pain (Dolor) Chemical mediators
Loss of function Tissue injury

Chronic Inflammation

Chronic inflammation is prolonged inflammation characterized by:
  • Tissue destruction
  • Fibrosis
  • Mononuclear cell infiltration

Predominant cells:

  • Macrophages
  • Lymphocytes
  • Plasma cells

Etiology of Chronic Inflammation

1. Persistent Infections

  • Tuberculosis
  • Fungal infections

2. Autoimmune Diseases

  • Rheumatoid arthritis
  • Systemic lupus erythematosus

3. Prolonged Exposure to Toxic Agents

  • Silica
  • Asbestos

4. Persistent Acute Inflammation

Failure of resolution of acute inflammation.

Pathogenesis of Chronic Inflammation

Role of Macrophages

Macrophages are the key cells in chronic inflammation.

Functions:

  • Phagocytosis
  • Cytokine production
  • Tissue destruction
  • Fibrosis stimulation

Activated macrophages release:

  • IL-1
  • TNF
  • Growth factors

Granulomatous Inflammation

A special type of chronic inflammation characterised by:

  • Granuloma formation

Granuloma contains:

  • Epithelioid macrophages
  • Giant cells
  • Lymphocytes

Examples:

  • Tuberculosis
  • Leprosy
  • Sarcoidosis

Tissue Regeneration and Repair

After tissue injury, healing occurs by:
  1. Regeneration
  2. Repair by fibrosis

1. Regeneration

Replacement of damaged cells by:

  • Same type of cells

Occurs in:

  • Liver
  • Skin
  • Bone marrow

Requires:

  • Intact extracellular matrix (ECM)

Role of Extracellular Matrix (ECM)

ECM provides:

  • Structural support
  • Cell adhesion
  • Tissue organization

Major components:

  • Collagen
  • Elastin
  • Fibronectin
  • Proteoglycans

ECM plays an important role in:

  • Cell migration
  • Regeneration
  • Scar formation

2. Repair by Healing

Occurs when tissue damage is severe and regeneration is incomplete.

Healing involves:

  • Granulation tissue formation
  • Angiogenesis
  • Fibrosis

Scar Formation and Fibrosis

Fibrosis occurs due to excessive collagen deposition.

Steps

  1. Angiogenesis
  2. Fibroblast proliferation
  3. Collagen synthesis
  4. Remodeling

Major mediator:

  • TGF-β

Cutaneous Wound Healing

Wound healing occurs by:

1. Healing by First Intention

Occurs in:

  • Clean surgical wounds

Characteristics:

  • Minimal tissue loss
  • Minimal scar formation
  • Rapid healing

2. Healing by Second Intention

Occurs in:

  • Large wounds
  • Infected wounds

Characteristics:

  • Extensive granulation tissue
  • Large scar formation
  • Wound contraction

Factors Affecting Wound Healing

Wound healing is a complex biological process influenced by several local and systemic factors. These factors may delay healing, impair scar formation, or increase the risk of infection and fibrosis.

Factors affecting wound healing are broadly classified into:

  1. Local factors
  2. Systemic factors

1. Local Factors

Local factors act directly at the wound site.

A. Infection

  • Most important cause of delayed wound healing
  • Causes prolonged inflammation and tissue destruction
  • Prevents proper collagen formation

B. Poor Blood Supply

Reduced blood flow decreases:

  • Oxygen supply
  • Nutrient delivery
  • Removal of waste products

Common in:

  • Peripheral vascular disease
  • Atherosclerosis

C. Foreign Bodies

Presence of:

  • Dirt
  • Sutures
  • Necrotic tissue

may prolong inflammation and delay healing.

D. Mechanical Stress and Movement

Excessive movement may:

  • Disrupt newly formed tissue
  • Cause wound dehiscence
  • Delay collagen deposition

E. Size and Location of Wound

  • Large wounds heal slowly
  • Areas with poor vascularity show delayed repair

F. Edema

Accumulation of fluid around wound:

  • Increases tissue pressure
  • Reduces oxygen diffusion
  • Delays healing

2. Systemic Factors

Systemic factors affect the body’s overall healing capacity.

A. Nutrition

Adequate nutrition is essential for tissue repair.

Important nutrients:

  • Protein → collagen synthesis
  • Vitamin C → collagen maturation
  • Zinc → cell proliferation

Malnutrition delays healing.

B. Diabetes Mellitus

  • Causes poor blood circulation
  • Increases susceptibility to infection
  • Delays collagen formation and repair

Diabetic wounds heal slowly.

C. Age

  • Healing is slower in elderly individuals
  • Reduced cell proliferation and collagen synthesis occur with aging

D. Anemia

Reduced hemoglobin decreases oxygen delivery to tissues, impairing repair.

E. Hormonal Factors

Glucocorticoids (steroids):

  • Suppress inflammation
  • Inhibit collagen synthesis
  • Delay wound healing

F. Immunosuppression

Conditions such as:

  • HIV/AIDS
  • Cancer therapy
  • Chemotherapy

reduce body defense mechanisms and impair healing.

G. Smoking

Smoking causes:

  • Vasoconstriction
  • Reduced oxygen supply
  • Impaired collagen synthesis

leading to delayed wound repair.

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