Basic Mechanism Involved in Process of Inflammation and Repair

Inflammation and
repair
Inflammati
on
Causes of inflammation
• Inflammation is defined as the local response of living mammalian
tissues to injury due to any agent. It is a body defense reaction in order to
eliminate or limit the spread of injurious agent, followed by removal of the
necrosed cells and tissues.
• Causes of inflammation
– Infective agents like bacteria, viruses and their toxins, fungi, parasites.
– Immunological agents like cell-mediatedand antigen-antibody reactions.
– Physical agents like heat, cold, radiation, mechanical trauma.
– Chemical agents like organic and inorganic poisons.
– Inert materials such as foreign bodies.
Signs of inflammation
• Signs of inflammation
Five cardinal signs of inflammation as
• rubor (redness)
• tumor (swelling)
• calor (heat)
• dolor (pain)
• functio laesa (loss of function)
Types of inflammation
• Depending upon the defense capacity of the host and duration of
response, inflammation can be classified as
Acute inflammation
• Causes of acute inflammation:
• Infection, trauma, physical and chemical agents, necrosis, foreign bodies, and immune
reactions.
• Stages of acute inflammation:
– Vasodilation
– Increased vascular permeability
– Movement of white blood cells from blood vessels into soft tissue at the site of inflammation
Stages of acute inflammation
–Movement of white blood cells from blood vessels into soft tissue at the site of inflammation: The steps
required are rolling, pavementing, and transmigration.
Fate of acute inflammation
• The acute inflammatory process can culminate in one of the following
outcomes:
– Resolution: complete return to normal tissue following acute inflammation.
– Healing: Fibrosis takes place when the tissue destruction in acute
inflammation is extensive so that there is no tissue regeneration. But when
tissue loss is superficial, it is restored by regeneration.
– Ulcer: Loss of the mucosa and deeper tissues.
– Fistula: Anomalous patent connection between two organs; most commonly
organs with a lumen.
Fate of acute inflammation
– Suppuration: When the pyogenic bacteria causing acute inflammation result
in severe tissue necrosis, the process progresses to suppuration. Subsequently,
mixture of neutrophils, bacteria, fragments of necrotic tissue, cell debris and
fibrin comprise pus which is contained in a cavity to form an abscess.
– Scar formation: Replacement of lost parenchyma with disorganized
connective tissue (e.g., collagen).
– Chronic inflammation
Chronic inflammation
• Prolonged inflammation consisting of active inflammation and tissue
destruction and repair, all occurring simultaneously.
• Causes of Chronic inflammation:
– Chronic inflammation following acute inflammation.
– Recurrent attacks of acute inflammation.
– Chronic inflammation starting de novo.
Types of chronic inflammation
• Based on histological features, chronic inflammations are classified as
following 2 corresponding types
– Chronic non-specific inflammation: It is characterised by non-specific
inflammatory cell infiltration e.g. chronic osteomyelitis(bone infection), lung
abscess. e.g. actinomycosis.
– Chronic granulomatous inflammation: It is characterised by formation of
granulomas e.g. tuberculosis, leprosy, syphilis, actinomycosis, sarcoidosis etc.
Histology of lung Histology of lung with

Actinomycosis pulmonary tuberculosis
Cells involved in chronic inflammation
• Macrophages: Activated macrophages produce proteases, IL-1, TNF,
arachidonic acid metabolites.
• angiogenesis(new blood vessels formation)
• growth factors such as platelet- derived growth factor (PDGF) or
fibroblast growth factor (FGF).
• Lymphocytes : Activated lymphocytes produce
– FGF stimulates fibroblasts to produce collagen, which results in scarring.
– PDGF and transforming growth factor-β (TGF-β)(antibody synthesis).
– Interferon-γ (activates macrophages).
Systemic effects of chronic inflammation
• Chronic inflammation is associated with following systemic
features:
– Fever
– Anaemia
– Leucocytosis(high WBC count)
– ESR (Erythrocyte sedimentation rate)(elevated in all cases of chronic
inflammation}
– Amyloidosis (long-term, chronic suppurative inflammation may
develop secondary systemic (AA) amyloidosis)
Granulomatous inflammation
• Granuloma is defined as a circumscribed,
tiny lesion, about 1 mm in diameter,
composed predominantly of collection of
modified macrophages called epithelioid
cells, and rimmed at the periphery by
lymphoid cells.
Repair and healing
Healing of Tissues
• Healing is the body response to injury in an attempt to restore normal

structure and function. Healing involves 2 distinct processes:
 Regeneration: healing takes place by proliferation of parenchymal cells and
usually results in complete restoration of the original tissues.
 Repair: healing takes place by proliferation of connective tissue elements
resulting in fibrosis and scarring.
Both the processes take place simultaneously

Healing of Tissues
 Regeneration:
 Some parenchymal cells are short-lived while others have a longer lifespan.
 In order to maintain proper structure of tissues, these cells are under the
constant regulatory control of their cell cycle. These include growth factors
such as Epidermal growth factor (EGF), Vascular endothelial growth factor
(VEGF), Platelet-derived growth factor (PDGF), Fibroblast growth factor
(FGF), Transforming growth factor-β (TGF-β).
Healing of Tissues
 Repair:
 Repair is the replacement of injured tissue by fibrous tissue. Two
processes are involved in repair:
• Granulation tissue formation.
• Contraction of wounds.
 Repair response takes place by participation of mesenchymal cells(stem
cells), endothelial cells, macrophages, platelets, and the parenchymal
cells of the injured organ.
Wound healing
• Healing of skin wounds provides a classical example of combination of
regeneration and repair. Wound healing can be accomplished in one of the
following two ways:
– Healing by first intention (primary union)
• Characteristics: clean and uninfected, surgically incised, without much loss of
cells and tissue and edges of wound are approximated by surgical sutures.
– Healing by second intention (secondary union)
• Characteristics: open with a large tissue defect (at times infected), having
extensive loss of cells and tissues and the wound is not approximated by
surgical sutures but is left open.
Wound healing
 Healing by first intention (primary union)
 Sequence of events in primary union: Initial haemorrhage, Acute
inflammatory response, Epithelial changes, Organisation and Suture tracks.
Wound healing
– Healing by second intention (secondary union)
– Sequence of events in secondary union: Initial haemorrhage,
Inflammatory phase, Epithelial changes, Granulation tissue, Wound
contraction and Presence of infection.
Stages of wound
healing
• The stages of wound healing are linear, wounds can progress backward or forward
depending on internal and external patient conditions.
Four stages of wound healing
Four stages of wound healing
• Hemostasis Phase:
Hemostasis starts when blood leaks
Blood vessels constrict to restrict the blood flow
Platelets stick together in order to seal the break

in the wall of the blood vessel
Coagulation occurs and reinforces the platelet

plug with threads of fibrin
Platelets adhere to the sub-endothelium surface

within seconds of the rupture of a blood
vessel's epithelial wall
First fibrin strands begin to adhere (release of

prothrombin)
• Inflammatory Phase
 Inflammation is the second stage of wound healing.
 Inflammatory Phase is right after the injury when the injured blood
vessels leak transudate (made of water, salt, and protein) causing
localized swelling.
 Inflammation both controls bleeding and prevents infection.
 During the inflammatory phase, damaged cells, pathogens, and
bacteria are removed from the wound area
• Proliferative Phase
 In Proliferative Phase, wound is rebuilt with new tissue made up of
collagen and extracellular matrix.
 In addition, a new network of blood vessels is constructed so that the
granulation tissue can be healthy and receive sufficient oxygen and
nutrients.
 Myofibroblasts (cell that is in between a fibroblast and a smooth muscle
cell) cause the wound to contract by gripping the wound edges and
pulling them together using a mechanism similar to that of smooth
muscle cells.
• Maturation Phase
– Also called the remodeling stage of wound healing
– Maturation phase is when collagen is remodeled from type III to type
I and the wound fully closes.
– During the maturation phase, collagen fibers can lie closer together and cross-link.
– Cross-linking of collagen reduces scar thickness and also
makes the skin area of the wound stronger.
*Type I is the predominant collagen type in a wound scar

*The initial collagen in wounds is type III
Failure of wound healing
• The stages of wound healing are a complex and fragile process. Failure to
progress in the stages of wound healing can lead to chronic wounds.
• Factors that lead up to chronic wounds are venous disease, infection,
diabetes and metabolic deficiencies of the elderly.

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Inflammation and

Histology of lung Histology of lung with

• Healing is the body response to injury in an attempt to restore normal

Both the processes take place simultaneously

Blood vessels constrict to restrict the blood flow

Platelets stick together in order to seal the break

Coagulation occurs and reinforces the platelet

Platelets adhere to the sub-endothelium surface

First fibrin strands begin to adhere (release of

*Type I is the predominant collagen type in a wound scar

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