The aetiology of periodontal diseases - aspects of host defence Flashcards

1
Q

Role of saliva in defence of periodontal diseases

A
Contains IgA
Contains antibacterial substances 
-lactoferrin
-thiocynate
-hydrogen peroxide
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2
Q

Role of epithelium

A
  1. Surface epithelium shed together with any attached bacteria
  2. Permeability barrier
  3. JE may be more permeable than oral epithelium
  4. Epithelium can stimulate inflammatory and immune response by releasing cytokines e.g. IL-1
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3
Q

The inflammatory response

A
Crevicular fluid
Tissue damage
> blood flow
Oedema
Neutrophils, macrophages
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4
Q

Crevicular fluid

A

Inflammatory exudate
Contains complement: C1-9
May contain antibodies which act as an ‘opsonin’ & aid phagocytosis
Contains clotting cascade and kininogens

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5
Q

Complement C3a, C5a, C9

A
  • C3a & C5a: vascular changes, stimulate histamine release, promote formation of leukotrienes and prostaglandins; attract phagocytes and aid phagocytosis
  • C9: membrane attack complex, destroys micro-organisms
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6
Q

Clotting cascade

A

Fibrin forms a barrier to spread of infection

-thrombin and Hageman factor promote the inflammatory response

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7
Q

Kininogens

A

Converted to kinins by proteases

Bradykinin - similar to histamine, promotes inflammatory response

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8
Q

What happens to crevicular fluid in the crevice

A

Becomes modified
Bacteria in plaque can metabolise some components
Complement, immunoglobulin and other components partly consumed and degraded in crevice
Up to 1ml fluid may be lost per day

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9
Q

Functions of neutrophils

A

Production of NETS - neutrophil extracellular traps
Kill microbes by antimicrobial peptides
Neutrophils themselves die in the process

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10
Q

Functions of macrophages

A

Phagocytosis
Antigen presentation - simulate immune response
Growth factors
-stimulation of fibroblasts and endothelial cells to promote healing
Cytokines and chemokines attract inflammatory cells and regulate inflammatory response
-IL-1 & TNF important

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11
Q

The inflammatory response: neutrophils

A

Neutrophils cannot phagocytose - secrete enzymes and NETS
Kill bacteria and solublizes plaque
Washed out by crevicular fluid
Some neutrophils inhibited

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12
Q

Evidence that neutrophils are important

A

Pxs with < neutrophils have > periodontal destruction e.g. cyclic neutropenia
Pxs with defective neutrophil function have > periodontal destruction e.g. Papillon Lefevre syndrome
Impaired neutrophil function may contribute to periodontitis in diabetes and Downs’ syndrome

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13
Q

What are macrophages derived from?

A

Blood monocyte

+IFN-γ T cells

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14
Q

The inflammatory response: macrophages

A

Stimulate immune response
Release cytokines
Phagocytose
Stimulate healing

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15
Q

Humoral immunity

A

B cells

Production of antibody by plasma cells

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16
Q

Cell mediated immunity

A

T cells

Immune regulation and cytotoxic T cell killing of virally infected and neoplastic cells

17
Q

What leads to IgA being secreted in saliva?

A

Bacteria swallowed and antigens recognised in gut MALT

18
Q

What does IgA secretion lead to?

A

Antigen penetrates epithelium
Carried to lymph nodes
Initiates immune response
Antibody secreted in plasma
Antibody enters crevice in crevicular fluid
Some antibody produced locally in tissues by plasma cells

19
Q

Role of antibody in defence

A
Bind to bacteria
-acts as opsonin
-activates neutrophil enzyme secretion
-prevents bacterial attachment
-activates complement
-directly inhibits bacterial metabolism
Bind to soluble factors
-neutralises toxins
-inhibits enzymes
20
Q

Chronic marginal gingivitis

A

Bleeding on probing

False pocketing

21
Q

What is the cause of the tissue damage and bone loss in periodontal disease?

A

Bacterial products

Host response

22
Q

Bacterial products

A

Endotoxins
-may damage epithelium, fibroblasts
Bacterial enzymes e.g. collagenase, hyaluronidase
-break down CT
LPS, capsular material, peptidoglycans, muramyl dipeptide, proteases
-may cause resorption

23
Q

Host products

A

Release of enzymes from neutrophils
Complement
Production on IL-1, IL-6 by macrophages
-stimulates bone resorption and epithelial proliferation
Inflammatory mediators
-prostaglandins, other cytokines, leukotrienes also stimulate bone resorption

24
Q

Summary of tissue destruction

A

Some caused by bacteria but effects are limited by host response
Some due to host response - so called bystander cell damage
-IL-1 may be particularly important
Inflammation results in disturbance of normal tissue turnover
Mostly periodontal disease is stable, with tissue damage = repair
Progression when balance altered by host response or bacterial factors