Inflammation is the body's local response to injury, triggered by various agents such as bacteria, toxins, and physical trauma, characterized by the four cardinal signs: redness, swelling, heat, and pain. It can be acute, lasting less than two weeks, or chronic, where inflammation persists. Wound healing involves phases of hemostasis, inflammation, proliferation, and remodeling, regulated by various growth factors and the extracellular matrix.

1. Inflammation and Healing
Prepared by: Mrs. Deeksha gupta
Assistant Professor,
Krishna Institute of Pharmacy & Sciences, Kanpur

2. DEFINITION AND CAUSES:
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. The agents causing inflammation may be as under:
1. Infective agents like bacteria, viruses and their toxins, fungi, parasites.
2. Immunological agents like cell-mediated and antigen-antibody reactions.
3. Physical agents like heat, cold, radiation, mechanical trauma.
4. Chemical agents like organic and inorganic poisons.
5. Inert materials such as foreign bodies
SIGNS OF INFLAMMATION
The Roman writer Celsus in 1st century A.D. named the famous 4 cardinal signs of inflammation as:
 rubor (redness);
 tumor (swelling);
 calor (heat); and
 dolor (pain).
 To these, fifth sign functio laesa (loss of function) was later added by Virchow.

3. TYPES OF INFLAMMATION

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A. Acute inflammation is of short duration (lasting less than 2 weeks) and represents the early body reaction,
resolves quickly and is usually followed by healing.
The main features of acute inflammation are:
1. accumulation of fluid and plasma at the affected site;
2. intravascular activation of platelets; and
3. polymorphonuclear neutrophils as inflammatory cells.
Sometimes, the acute inflammatory response may be quite severe and is termed as fulminant acute
inflammation.
B. Chronic inflammation is of longer duration and occurs either after the causative agent of acute
inflammation persists for a long time, or the stimulus is such that it induces chronic inflammation from the
beginning.

5. MECHANISM OF INFLAMMATION
Acute inflammatory response by the host to any agent is a continuous process but for the purpose of
discussion, it can be divided into following two events:
I. Vascular events.
II. Cellular events.
Intimately linked to these two processes is the release of mediators of acute inflammation, discussed
just thereafter.
I. VASCULAR EVENTS
 Alteration in the microvasculature (arterioles, capillaries and venules) is the earliest response to
tissue injury.
 These alterations include: haemodynamic changes and changes in vascular permeability.
 In and around the inflamed tissue, there is accumulation of oedema fluid in the interstitial
compartment which comes from blood plasma by its escape through the endothelial wall of
peripheral vascular bed.
 In the initial stage, the escape of fluid is due to vasodilatation and consequent elevation in
hydrostatic pressure.
 This is transudate in nature.
 But subsequently, the characteristic inflammatory oedema, exudate, appears by increased vascular
permeability of microcirculation.

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II. CELLULAR EVENTS
The cellular phase of inflammation consists of 2 processes:
1. exudation of leucocytes; and
2. phagocytosis.
1. Exudation of Leucocytes
The escape of leucocytes from the lumen of microvasculature to the interstitial tissue is the most important
feature of inflammatory response. In acute inflammation, polymorphonuclear neutrophils (PMNs) comprise the
first line of body defense, followed later by monocytes and macrophages.
Fig. Sequence of changes in the exudation of leucocytes. A, Normal axial flow of blood with central column of cells and peripheral zone of cell-free plasma. B, Margination and pavement of neutrophils
with narrow plasmatic zone. C, Adhesion of neutrophils to endothelial cells with pseudopods in the intercellular junctions. D, Emigration of neutrophils and diapedesis with damaged basement
membrane.

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Phagocytosis
Phagocytosis is defined as the process of engulfment of solid particulate material by the cells (cell-eating). The cells
performing this function are called phagocytes. There are 2 main types of phagocytic cells:
i) Polymorphonuclear neutrophils (PMNs) which appear early in acute inflammatory response, sometimes called as
microphages.
ii) Circulating monocytes and fixed tissue mononuclear phagocytes, commonly called as macrophages.
Neutrophils and macrophages on reaching the tissue spaces produce several proteolytic enzymes like lysozyme,
protease, collagenase, elastase, lipase, proteinase, gelatinase, and acid hydrolases. These enzymes degrade collagen and
extracellular matrix. The microbe undergoes the process of phagocytosis by polymorphs and macrophages and involves
the following 3 steps:-
1. Recognition and attachment
2. Engulfment
3. Killing and degradation
Fig: Stages in phagocytosis of a foreign particle. A, Opsonization of the particle. B, Pseudopod engulfing the opsonized particle.
C, Incorporation within the cell (phagocytic vacuole) and degranulation. D, Phagolysosome formation after fusion of lysosome of the cell.

8. CHEMICAL MEDIATORS OF INFLAMMATION
The substances acting as chemical mediators of inflammation may be released from the cells, the
plasma, or damaged tissue itself. They are broadly classified into 2 groups:
i) mediators released by cells; and
ii) mediators originating from plasma.
Fig:- Chemical mediators of inflammation.

9. WOUND HEALING
Healing of skin wounds provides a classical example of combination of regeneration and repair described above.
Wound healing can be accomplished in one of the following two ways:
 Healing by first intention (primary union)
 Healing by second intention (secondary union).
Basic principles of wound healing:
Hemostasis: The process of wound healing begins with hemostasis, which is the immediate response to injury
aimed at stopping bleeding. Platelets aggregate at the site of injury to form a temporary plug, and blood vessels
constrict to reduce blood flow. This initial phase is crucial for preventing excessive blood loss and initiating the
healing process.
Inflammatory Phase: Neutrophils help to eliminate bacteria and debris through phagocytosis, while
macrophages play a key role in clearing cellular debris and secreting growth factors that promote tissue repair.
The inflammatory phase also involves the release of pro-inflammatory cytokines and chemokines, which recruit
additional immune cells to the site of injury.
Proliferative Phase: The proliferative phase is marked by the formation of new tissue and the restoration of the
wound bed. Fibroblasts migrate to the wound site and produce collagen, the main structural protein in
connective tissue, to form granulation tissue. This tissue provides a scaffold for new blood vessels and epithelial
cells to grow into the wound bed. Additionally, epithelial cells at the wound edges proliferate and migrate across
the wound surface to form a new epithelial layer, a process known as re-epithelialization.

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Remodeling Phase: The final phase of wound healing is the remodeling phase, during which the newly
formed tissue undergoes remodeling and maturation. Excess collagen is broken down by matrix
metalloproteinases (MMPs), and the collagen fibers undergo cross-linking to increase tensile strength. The
wound undergoes contraction, reducing its size, and the vascular network matures to restore blood flow.
This phase can last for months to years, depending on the size and severity of the wound.
Regulation by Growth Factors and Cytokines: Throughout the wound healing process, various growth
factors and cytokines play critical roles in coordinating cellular activities and modulating the immune
response.
Extracellular Matrix Deposition: The extracellular matrix (ECM) provides structural support for cells and
facilitates cell migration and signaling during wound healing. Components of the ECM, such as collagen,
fibronectin, and hyaluronic acid, are synthesized and deposited by fibroblasts to form the provisional matrix
and later the mature scar tissue.

11. Thank
You