Acute v Chronic inflammation Flashcards
What is Acute inflammation
Response to infection/damage
Rapid onset, yet short-term
Involves only the innate immune system (e.g., neutrophils)
Response is localized
Complete restoration of tissues
What can cause acute inflammation
Microbial infection
Physical agents
Irritants e.g., corrosive chemicals
Tissue necrosis
What causes chronic inflammation
Persistent exposure to
-microbial infection
-physical agents
-irrantants e.g. corrosive chemicals
-tissue necrosis
What makes it chronic inflammation
Long-term, can last up to years
Involves both the innate and adaptive immune system
Associated with tissue damage (e.g., fibrosis- formation of scar tissue) – no restoration
Symptoms may be less pronounced, but more persistent
What are the signs of inflammation
Redness (rubor) – Dilation of small blood vessels
Heat (calor) – Increased blood flow (hyperaemia)
Swelling (tumor) – Accumulation of fluid in extra vascular space (oedema)
Pain (dolor) – Stretching of tissues and due to release of chemical mediators
Loss of function
What causes redness (rubor) and heat (calor)
Small blood vessels adjacent to site of damage become dilated - excessive bloodflow
Endothelial cells swell and retract
Exudation – the vessels become ‘leaky’ and allow passage of fluids
Endothelial cells activated to promote immune cells passage to damaged/infected tissues
What isswelling
Defined as an excess of watery fluid collecting in tissues of the body
Increased blood and lymph flow
What does inflammatory exudate (watery fluid) consist of
Fluids and salts – dilute the microorganisms
Glucose and oxygen – support response and immun cells
Soluble mediators
Fibrin
What causes pain with inflammation
Stretching of tissues and due to release of soluble mediators
What are the main types of soluble mediatorss
Histamine
Prostaglandins
Leukotrienes
Serotonin
Bradykinin
What are the main roles of prostaglandins in inflammation
Causes vascular dilation
Acts of nerve fibres – itching
Role in tissue remodelling
What produces prostaglandins
Produced by macrophages and neutrophils (with leukotrienes)
Product of fatty acid metabolism (arachidonic acid - (red meat, fish)
Most abundant is Prostaglandin E2
What is coagulation factor 7
Hageman factor
-A serine protease found circulating inactive in blood
What are the main plasma factor systems activated by the hageman factor
Kinin system
Fibrinolytic system
Coagulation system
Complement system
What is the kinin system
Kinin System
Involves plasma proteins
Kallikrein (plasma protein) is generated by Hageman factor
Neutrophils also engage in the kinin-kallikrein system.
Kallikrein converts kininogens to kinins (e.g., bradykinin – widespread effect, can stimulate the changes in the vascular (inflammation))
What does the coagulation system consist of
Intrinsic (internal trauma)
Initiated by contact with collagen
Extrinsic (external trauma)
Each pathway converges into:
Common pathway – formation of stable blood clot (fibrin) through action of thrombin
What is the purpose of the fibrinolytic system
Results in activation of plasmin
Kallikrein and Hageman factor play a role in its conversion
Involved in breakdown of fibrin
Prevents excess clotting
Activates complement (plasmin cleaves C3 complement protein)
How is plasminogen converted to plasmin
Kallikrein
Urokinase (thrombolytic drug)
Hageman factor
Tissue plasminogen activator (tPA found in endothelial cells)
What is haemostasis
To stop the flow of blood
What is the balance between the coagulation and fibrinolytic system called
Haemostasis
What are the two balancing factors in haemostasis
Bleeding to death - Trauma, major surgery,hemophilia
Clotting to death - thrombosis, MI, stroke
What are the disordered of the plasma factor systems
Von Willebrand disease
Haemophilia A
Haemophilia B
Warfarin
Heparin
What drugs are used to combat excessive bleeding
Warfarin
Heparin
-promote antithrombin acitivity preventing excessive clot formation
What are examples of acute inflammation
Gingivitis
Abscess formation
Pericoronitis
Cellulitis
Angular Cheilitis
Ludwig’s Angina
What is abscess formation
Pus forms in a pyogenic membrane
What are the different types of dental abscesses
Gingival - gum tissue
Periodontal - Infection deeper in the gum
Periapical - infection of the pulp
What are the two classes of chronic inflammation
Non-specific
Persistent acute inflammation
Excessive suppuration
Specific
Arises de novo
Persistent exposure to agent
Can be granulomatous
What is non-specific chronic inflammation
Infiltrate dominated by tissue macrophages, T cells and B cells (more adaptive immune cells)
Characterized by tissue destruction vs repair
Whar is the most relevant non-specific chronic inflammation
Periodontitis
What is specific chronic inflammation
Induced by non-immunological or immunological agents
Autoimmune diseases
Can be granulomatous (involving the formation of granulomas)
Characterized by excessively activated tissue macrophages
What are the most prevelant dental related autoimmune diseases
Rheumatoid arthritis - loss of tolerance to citrullinated proteins in synovial fluid
Sjogren’s syndrome - host T and B cells attack the cells of the salivary and lacrimal
What is OFG (orofacial granulomatosis)
Characterized by excessively activated tissue macrophages
Epithelioid macrophages
Giant cells consist of these macrophages fused together
B and T cells also present
Granulomas form in the soft tissue
What does the kinin system lead to the production of
bradykinins
How does the fibrinolytic system prevent excessive clotting
Involves plasmin which degrades fibrin
