1. Acute Inflammation 2. Chronic Inflammation.
Neutrophils and leukocytes.
Fibroblast activation, where fibroblasts migrate to the injury site and produce extracellular matrix.
1. Recognition of the Foreign Antigen 2. Migration of macrophages and plasma cells 3. Production of chemokines and cytokines 4. Removal of invaders.
Endothelial retraction causes proteins and cells to leak out of blood vessels, unlike a normal immune response.
A localized collection of purulent inflammation accompanied by liquefactive necrosis.
They activate the complement system and help recognize the body's own substances, promoting inflammation.
Increased hydrostatic pressure and decreased colloid osmotic pressure, resulting in pure edema.
It results from a microbiological process, leading to necrotic cells, edema, and pus formation.
A complex reaction inside the cell that activates caspase, producing IL-1 and triggering acute inflammatory reactions.
The causative agent is removed, and new tissue forms with the same functionality as the initial tissue.
Cytokines promote selectins and integrins that facilitate the interaction with circulating leukocytes.
Due to sloughing of inflamed necrotic tissue, leading to the rupture of the epithelium.
Mannose-binding lectin and collectins, which aid in phagocyte migration and recognition.
Blood vessel permeability increases, leading to edema, swelling, and leakage of blood vessels.
Large amounts of fibrinogen pass out of blood vessels, forming fibrin in the fluid exudate.
They recognize foreign cells and trigger a response that contributes to damage, vasodilation, and recruitment of more cells.
TNF, IL-1, chemokines, C3a, C5a, and leukotrienes B4.
Cytokines produced during the inflammatory response.
The accumulation of a large amount of fibrinogen and persistent inflammatory response.
Destruction of essential tissue components leads to degeneration and replacement with scar tissue.
Polymorphonuclear Neutrophils are activated by cytokines and are responsible for phagocytosis at the inflammation site.
A local accumulation of polymorphonuclear cells in the oral epithelium after acute inflammation, resembling small abscesses.
IL-1 and TNF (tumor necrotic factors), along with prostaglandins.
Transudate and Exudate.
Accumulation of clear, watery fluid with variable protein content, often beneath epithelial tissues.
Cellular receptors for microbes found on plasma membranes and endosomes that trigger a cellular response by releasing cytokines.
Histamine and prostaglandins.
Leukocytes roll along the endothelium through weak temporary bindings until they reach the damage area.
A canal that allows debris to exit from an abscess, often found in the gums and teeth.
Histamine, C3a, C5a, and leukotrienes C4, D4, E4.
Increased vascular reaction leading to enhanced blood circulation and edema.
Infections, tissue necrosis, foreign bodies, and autoimmune diseases.
White blood cells assume a peripheral position and touch the endothelium.
Characterized by purulent acute inflammation involving the accumulation of debris and fluids in soft tissues of the oral cavity.
It induces vasodilation, contributing to redness (rubor) and heat (calor).
Lysosomal enzymes of leukocytes and reactive oxygen species (ROS).
The body's response in all vascularized tissues to an injury, originating from a foreign invader or necrotic tissue.
They are involved in generating further inflammation and are used in the degranulation of neutrophils.
Fluid rich in proteins leaking from blood vessels due to endothelial retraction, often caused by histamine.
Neutrophil Extracellular Trap (NET) is a second response mechanism where neutrophils create an extracellular trap.
An abscess, with or without pustules, often caused by Staphylococcus aureus, typically found in areas with hair.
1. Rubor (Redness) 2. Calor (Heat) 3. Tumor (Swelling) 4. Dolor (Pain).
Cytokines and growth factors.
Collagen fibers provide tensile strength to the healing tissue and form a network in the injured area.
Mouth, digestive tract, intestines, genitourinary system, and skin.
Hoofed animals such as sheep, cattle, and goats.
Prostaglandins, histamine, and bradykinin.
A local defect or excavation on the surface of an organ that exposes internal tissue to the exterior cavity.
A disease caused by Bacillus anthracis, characterized by the formation of a black ulcer indicating necrosis of the skin.
