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basic oral and dental care > acute inflammation > Flashcards

acute inflammation Flashcards

1
Q

What is inflammation?

A

Response of vascular living tissue to injury

Protective, destroys, walls off, dilutes and initiates repair

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2
Q

What are features of acute inflammation?

A 
Red
Hot
Swollen
Pain
Loss of function
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3
Q

What is acute inflammation?

A 
Immediate onset
Short lived
Usually single episode
Neutrophils and granulocytes
Vascular response
Eg. Dental abscess, acute pulpitis, lacerations, acute herpetic ginigivostomatitis, parotitis, piercing reaction
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4
Q

What are causes of acute inflammation?

A 
Infection (bacterial, viral, parasitic)
Trauma
Physical and chemical agents
Tissue necrosis- lack of blood supply
Foreign bodies
Immune reactions- hypersensitivity
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5
Q

What are 4 vascular events?

A
  1. Vasoconstriction of arterioles- affected area becomes white (local axon reflex)
  2. Arteriolar capillary and venues dilation- affected area and warm
    (histamine, serotonin, nitric oxide and prostaglandins)
  3. Increased vascular permeability- swelling due oedema, movement of fluid and proteins into tissues (histamine, C3a, C5a and leukotrienes)
  4. Vascular stasis- loss of fluid in circulation slows blood flow

All occurs within minutes

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6
Q

What causes vasodilation?

A

Trauma, C’ and cytokines cause mast cells to release HISTAMINE

Platelet aggregation causes release of SEROTONIN (5HT)

NITRIC OXIDE from WBCs

PROSTAGLANDINS

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7
Q

What causes increased vascular permeability?

A
  1. Retraction of endothelial cells due to histamine and bradykinin
  2. Endothelial injury (trauma or microbial action)
  3. Increased transport of fluid and proteins through endothelial cells (transcytosis)
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8
Q

What is an oedema?

A

Excess of fluid in tissues- and helps dilute bacterial and other toxins

Exudate- extra vascular fluid w HIGH protein content (plasma proteins and WBCs)

Transudate- extra vascular fluid w LOW protein content

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9
Q

Why is complement important in oedema?

A

C’- collection of soluble proteins and their membrane receptors (innate immunity)
C1-C9 (more than 20)
Inactive form in plasma, when activated become proteolytic enzymes causing enzyme cascade

Classical pathway- antibodies bound to antigen
Alternative pathway- C1 binds directly to pathogen (microbial surface molecule eg. LPS)
Lectin pathway- plasma manase binding lectin binds to microbes to activate C1)

C3->C3a and C3b
C3b (stays on cell) C3b converts to C5->C5a and C5b
C5b (stays on cell) and attracts C6-C9 and forms membrane attack complex MAC
MAC- drill hole into cell wall for fluids to rush into cell

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10
Q

How does complement contribute to inflammation?

A

C3a- dilation and increased vascular permeability
C3a and C5a- stimulate histamine release, promote formation of leukotrienes and prostaglandins and attract phagocytes
C3b- binds to pathogens and phagocytes w a C3b receptor (opsonisation)

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11
Q

What is the Membrane Attack Complex?

A

C5-C9
Destroys microorganisms
Forms transmembrane channels which disrupt phospholipid bilayer
Fluids rush in
Leads to cell lysis and death (important in killing microbes/bacteria)

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12
Q

How do antibodies contribute to oedema?

A

Antibodies act as opsonin and aid phagocytosis

WBC tries to engulf microbe
Microbe evades this
Opsonin (C3b/antibody) can bind to microbe and WBC uses surface receptors to bind to opsonin
This leads to engulfment for phagocytosis

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13
Q

How does the clotting cascade contribute to oedema?

A

Fibrin forms barrier to spread of infection (fibrinogen->fibrin via thrombin
Coagulation may promote inflammation

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14
Q

How do kininogens contribute to oedema?

A

Kininogens->kinins via proteases (eg. Thrombin) such as Bradykinin which is v similar to histamine

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15
Q

What is the cellular response?

A
  1. Margination- due to vascular stasis (slow blood flow so WBCs move to edge of vessel)
  2. Pavementation- neutrophils adhere weakly using adhesion molecules (selectins) on vessel wall and therefore roll which slows down. When stopped- bind strongly using integrins (eg. ICAM, LFA1 which are promoted by IL-1 and TNF alpha) onto endothelial cells
  3. Emigration- movement of neutrophils between endothelial cells via chemotaxis via chemotactic gradient (eg. IL-8, C5a)
  4. Aggregation of WBCs
  5. Phagocytosis- neutrophils/macrophages engulf and destroy
    Engulf via pseudopodia (projection) to form phagosome and destroyed by ROS and hydrolytic enzymes
    Occurs within hours
    Neutrophils (6-24hr) followed by macrophages (24-48hr)
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16
Q

What are purulent/pyogenic bacteria?

A

Bacteria that causes pus

17
Q

What is pus?

A 
Mainly neutrophils (granulocyte-basophils,eosinophil) 50-75% of WBCs (small cells w bi/tri lobed nuclei)
Some macrophages (larger, paler stained cells)
Small amount of necrotic tissue)
18
Q

What is a neutrophils mechanisms to destroy pathogens?

A
  1. Phagocytosis
  2. Degranulation (release defensins, lysozyme, lactoferrin to surrounding tissue for destruction- should contain anti-proteases so not too much damage)
  3. NETS (neutrophil extracellular traps)- released as neutrophil dies, DNA acts as meshwork containing proteases, increases conc of antimicrobials, limits surrounding tissue damage
    3.
19
Q

Why is there pain during inflammation?

A 
Increase in tissue pressure due to oedema
Inflammatory mediators (eg. Bradykinin, prostaglandins) stimulate pain fibres
Encourages rest of the area by loss of function
20
Q

What are the outcomes of acute inflammation?

A

Complete resolution
Healing by fibrosis
Progression to chronic inflam

21
Q

What is complete resolution?

A

Common response to trauma in oral cavity eg. Ulceration

Injury, WBCs, remove bacteria, oedema drains away in lymphatics, return to normal tissue

22
Q

What is healing by fibrosis?

A

Common on skin and specialised tissue eg. Heart and brain

Injury, WBC, remove bacteria, tissue can’t return to normal, replaced by granulation tissue (fibroblasts making collagen, endothelial cells making blood vessels) maturing into scar tissue

23
Q

Why might acute inflam progress into chronic inflam?

A
  1. Inflam response fails to rid injurious agent eg. Foreign body

Often at apex of non vital tooth- abscess, resolved due to antibiotics or drain, however agent still present, so cause isn’t resolved

  1. Interference w normal process of healing eg. Neutropenia, radiotherapy

basic oral and dental care (49 decks)

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