Host defences against microbial plaque Flashcards

1
Q

The balance between what 4 things prevents the formation of periodontal diseases?

A
  1. Presence of pathogen
  2. Absence of beneficial species
  3. Host response
  4. Conducive environment around the oral cavity
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2
Q

What are the functions of the host defences?

A
  1. To keep bacteria out out of the periodontium| 2. Destroy any foreign microbes which succeeded in entering the system
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3
Q

What are the stages of plaque formation

A
  1. Pioneer species attach to the pellicle surface of a clean tooth2. These multiply to form micro colonies 3. Resulting in confluent growth of biofilm 4. This increases species diversity
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4
Q

Name the 5 things that help defend us from plaque

A
  1. Saliva
  2. Gingival epithelium
  3. Inflammation
  4. Immune system
  5. Mediators
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5
Q

What are the functions of saliva?

A

Washing effect – remove bacterial and food debris

Protects the oral mucosa w mucin and glycoproteins

antimicrobial effects, contains:
Peroxidase/hypothiocyanite
lysozymes/lactoferrin
antibodies (IgA)

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6
Q

What occurs if there is a lack of saliva?

A

Xerostomia

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7
Q

What are some factors that may cause Xerostomia?

A
  1. Patients who are mouth breathers
  2. Drugs/ alcohol
  3. Radiotherapy
  4. Patients who have had their salivary glands removed surgically
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8
Q

What are people with xerostomia more susceptible to?

A

Gingivitis| Cervical caries

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9
Q

What is the gingival epithelium’s role

A

effective barrier against micro-organisms, however it is permeable to
many small molecules. epithelium of the outer or oral surface of the gingiva is keratinized or para-keratinized, while the
sulcular/crevicular epithelium is thinner and not keratinized

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10
Q

What is the junctional epithelium permeable to?

A
  1. Bacterial products that need to go in2. Crevicular fluid and neutrophils that need to go out3. It becomes more permeable in disease
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11
Q

Describe the junctional epithelium in periodontal health. what are the 2 way movements of the bacteria ?

A

lies against enamel and extends up to CEJ

two way movement; connective tissue
to crevice/sulcus and sulcus/crevice to connective tissue.

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12
Q

Describe what happens to the junctional epithelium as periodontal health deteriorates

A

Junctional epithelium migrates apically| This eventually forms a pocket between the junctional epithelium and root surface

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13
Q

What is associated with the formation of a pocket between the junctional epithelium and root surface

A

Loss of connective periodontal attachment and loss of alveolar bone

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14
Q

What is inflammation?

A

It is a response of living tissue to injury and provides a rapid first line of defence

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15
Q

What are the 2 types of inflammation?

A
  1. Acute| 2. Chronic
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16
Q

What is acute inflammation?

A

inflammation has a relatively rapid onset and neutrophil polymorphs are the most abundant cells

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17
Q

Describe chronic inflammation

A

inflammation has a relatively insidious onset, prolonged course, slow resolution and lymphocytes, macrophages and plasma cells are the most abundant cells

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18
Q

What are the functions of the inflammatory response?

A
  1. To dilute by increasing crevicular fluid
  2. To wall off the inflammatory cells
  3. Destroy the inflammatory cells and the damaging pathogens
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19
Q

Describe the sources of the fluid response of inflammation

A
  1. Vasodilation
  2. Increased permeability of endothelial cells
  3. Fluid and plasma proteins are release into the tissues and through GCF
  4. inflammatory exudate
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20
Q

What is the inflammatory exudate

A

plasma proteins like antibodies and compliment that are released into the tissues and through GCF

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21
Q

How many proteins are involved in the compliment system?

A

9

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22
Q

Why does the compliment system play an important role in the fluid response of inflammation?

A
  1. It is responsible for mass cells producing histamine
  2. Chemotaxis for neutrophils
  3. Responsible for lysis and inhibition of a few species off bacteria
  4. Can lead to opsonisation for phagocytosis
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23
Q

What do we expect to see as the fluid response of inflammation is occurring ?

A
  1. Increased crevicular fluid flow
  2. Gingival erythema
  3. Oedema and selling of the gingiva
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24
Q

Name the key components of the cellular response of inflammation

A
  1. Neutrophils| 2. Macrophages
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25
Q

Why are neutrophils important?

A

Critical in preventing periodontal diseases

Enters gingival crevice

forms a layer on the surface of plaque biofilm

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26
Q

Describe the function of neutrophils in response to UNATTACHED bacteria

A

recognizes and binds bacteria (opsonisation)

Phagocytosis – Process by which ingestion of solid particles by
throwing pseudopodia around it

production of antibacterial agents

digest micro-organisms within lysosomes (Phagosomes)

expel remnants

Causes bystander damage

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27
Q

What can bystander damage cause?

A

A little bit of damage to the surrounding tissues

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28
Q

Describe the function of neutrophils in response to bacteria in the plaque matrix

A

-attach to plaque matrix

-secrete antibacterial enzymes
hydrogen peroxide
hypochlorous acid

-Kill bacteria

-dissolve plaque matrix

-Causes bystander damage

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29
Q

What is a recognised side effect to the host defence system?

A

Bystander damage

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30
Q

Where do macrophages develop?

A

They develop from monocytes in the blood

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31
Q

What do macrophages play an important role in?

A

Both immunity and inflammation

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32
Q

Where do macrophages emigrate too?

A

They emigrate to inflamed gingival tissue| Few of them enter the gingival crevice

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33
Q

What role do macrophages have in inflammation?

A
  1. Phagocytosis 2. Secrete tissue degrading enzymes 3. They secrete compliment components 4. They secrete mediators
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34
Q

Name some functions macrophages secrete in relation to inflammation

A

-tissue degrading enzymes
-complement components (plasma proteins killing pathogens)
-mediators e.g IL-1 TNF, Prostaglandins

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35
Q

What type of inflammation is periodontal disease implicated by?

A

Both acute and chronic

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36
Q

What is gingivitis usually characterised by biochemically?

A

An increase in leukotriene B4 in the gingival crevicular fluid

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37
Q

What is leukotriene B4 a product of?

A

Degranulating neutrophils in the sulcus

38
Q

What is periodontitis usually characterised by biochemically?

A

increase in prostaglandin E2. IL-1β and tumor necrosis factor α which represent an activation of macrophages and lymphocytes within the tissue

39
Q

Describe the acquired immune response

A

It is stimulus specific and has memory It is initiated by antigens Antigens are recognised by lymphocytes

40
Q

What are the 2 aspects of the immune responses?

A
  1. Humoral| 2. Cell mediated
41
Q

Which cells are involved in the humeral response?

A

B lymphocytes undergo differentiation to give:1. Plasma cells 2. Immunoglobulins

42
Q

Which cells are involved in the cell mediated response?

A

T lymphocytes there are 2 types:| 1. T helper cells 2. T cytotoxic cells

43
Q

What activates the humoral response?

A
  1. Bacteria 2. Toxins3. Other plaque antigens
44
Q

Describe the humoral response

A
  1. Antigen presented by the macrophages 2. B lymphocytes recognise foreign antigens and undergo clonal expansion 3. B lymphocytes differentiate into plasma cells under T lymphocytes are initiated 4. Antibodies are produced
45
Q

What type of antibodies make up the majority of the humoral response?

A

IgG makes up 75% of the antibodies in the humoral response

46
Q

Describe the antibody production in the saliva

A
  1. Bacteria is swallowed in the saliva 2. Antigens recognised in the gut 3. IgA secreted into the saliva
47
Q

Describe the antibody production in the gingiva

A
  1. Antigens penetrate gingiva 2. Antigens carried to lymph node outside the ginigva 3. Antibodies IgG and IgM are secretes into the plasma pass to GCF
48
Q

What are the 2 mechanism by which antibodies fight off antibodies?

A

-Binding to bacteria
Inhibiting attachment
opsonisation
activating complement
inhibiting metabolism

-Binding to soluble factors
neutralizing toxins
inhibiting enzymes

49
Q

What does the cell mediated immune response regulate?

A

Regulates plasma cell differentiation and role in periodontal disease

50
Q

What are some defects in the host response?

A
  1. Quantitative defect: Reduction in neutrophil number
  2. Qualitative defect: Defective neutrophil function
51
Q

What can a reduction in neutrophil number cause?

A
  1. Cyclic neutropenia 2. Agranulocytosis these can have a clinical effect on gingiva and periodontal tissues
52
Q

Name some genetic conditions that can result in defective neutrophil function

A

Downs syndrome Diabetes
Papillon- Levfevre syndrom
Chediak-Higashi syndrom
Leucocyte adhesion deficiency

53
Q

Name some mediators?

A
  1. Histamine
  2. Bradykinin
  3. Cytokines
  4. Prostaglandins
  5. Metalloproteinases (e.g collagenase, gelatinase, stromolysins)
54
Q

What are histamine and bradykinin associated with?

A

Vasodilation| Increased vascular permeability

55
Q

Describe Cytokines

A

They are soluble proteins
They are secreted by cells
They transmit signals
The inflammatory and immune response

56
Q

Give examples of Cytokines

A

IL-1 , TNF

57
Q

What is the role of Cytokines?

A

To amplify inflammatory response

58
Q

How do Cytokines amplify the inflammatory response

A
  1. They activate macrophages
  2. Activate lymphocytes
  3. Causes cells to release prostaglandins and more Cytokines
  4. Causes endothelial cels and fibroblast proliferation
  5. Causes fibroblasts to release collagenase
  6. Indices bone resorption
59
Q

What do Prostaglandins do?

A
  1. They cause capillary dilation
  2. Increase endothelial permeability
  3. PGE2 causes bone resorption
60
Q

What are Prostaglandins produced by

A

arachidonic acid in cell membranes of inflammatory cells

61
Q

Give examples of metalloproteinases

A
  1. Collagenase
  2. Gelatinase
62
Q

What are metalloproteinases involved in?

A

Connective tissue destruction

63
Q

What are metalloproteinases produced by?

A

Fibroblasts, Monocytes, Neutrophils

64
Q

What are metalloproteinases induced by?

A

IL-1

65
Q

What are the major regulators of immunoinflammatroy responses that categorise periodontitis?

A

Cytokines Chemokine Prostaglandins

66
Q

What is bystander damage a prominent feature of?

A

Of chronic inflammatory disease

67
Q

How can we identify risk patients

A
  1. Medical history
  2. Social history
  3. Family history
  4. Smokers
  5. Host response based diagnostics kits
68
Q

How does bystander damage happen?

A

Bacteria initiates disease by activating host mechanism that destroys supporting structure. Subsequent damage of crestal alveolar bone.

69
Q

How can we tailor treatment to high risk patients

A
  1. Liaison with there GP
  2. Give the oral hygiene aids
  3. Give them smoking advice
  4. Be selective about our use of adjunctive antibiotics
  5. Prognosis of periodontal surgery
  6. regular maintainence
70
Q

What do Cytokines, Chemokine ,Prostaglandins have a major role in

A

They are major regulators of immunoinflammatroy responses that categorise periodontitis

71
Q

what causes damage in periodontist, bacteria or the host response?

A

Periodontitis is an inflammatory disease initiated by bacteria but it is the host response that causes the majority of the damage to the periodontium

72
Q

name the 2 host responses triggered by plaque

A

innate immunity & aquired immunity

73
Q

describe innate immunity

A

innate:
First line of defence mechanism

Rapid response

Non-specific and lack memory

When not controlled or when
dysregulated causes collateral tissue
damage

E.g., Saliva, gingival epithelium, GCF,
complement system, PMNLs
(Polymorphonuclear neutrophils) and
Pattern recognition receptors

74
Q

describe acquired immunity

A

Takes longer to develop

Slow response

Specific and has memory

More efficient

E.g., T lymphocytes, B lymphocytes,
immunoglobulins – IgG
(Predominantly seen in GCF), IgA
(Predominantly seen in saliva)

75
Q

what is a compliment activation pathway?

A

complex series of interacting plasma proteins which form a
major effector system for antibody- mediated immune reactions.

76
Q

what do many complement components exist ?

A

inactive precursors;

77
Q

once the complement component is activated, what happens?

A

component may behave as an enzyme which cleaves several molecules of the next component in the sequence. Each precursor is cleaved into two or more fragments: major ‘b’, minor ‘a’

78
Q

what is the major fragment made of?

A

has two biologically active sites: one for binding to cell membranes or the triggering complex, and the other for
enzymatic cleavage of the next complement component.

79
Q

what is the minor fragment made of?

A

have important biological properties in
the fluid phase.

80
Q

what is the primary purpose of the complement pathway?

A

remove or destroy antigen, either by direct lysis or by opsonisation.

81
Q

what is classical pathway activated by?

A

binding of IgM or IgG to antigen causes a conformational change in the Fc region of the antibody to reveal a binding site for the first component in the classical pathway, C1.

82
Q

what is the central reaction in alternate pathway?

A

likewise to classical one, is the activation of C3. The alternative pathway, however, generates a C3 convertase without the need for antibody, C1, C4 or C2.

83
Q

What is the most important activators of alternate pathway ?

A

bacterial cell walls and endotoxin. Thus, the alternative pathway is responsible for innate defence against dental biofilm.

84
Q

2 components of gingivitis?

A

fluid (increased crevicular fluid flow and gingival oedema)
cellular (neutrophils and (later) macrophages)

85
Q

the pro inflammatory cytokines IL-1 and TNF are strongly associated with what?

A

periodontitis lesions

86
Q

different cytokines patterns at diff sites suggest what?

A

specific regulatory patterns may be involved in stable and active lesions.

87
Q

do disease active sites have a characteristic of either a predominant TH-1 or TH-2 lymphocyte response?

A

naauuuuur

88
Q

primary mediators of tissue destruction in periodontitis

A

Prostaglandin E2, possibly COX 2

89
Q

people with severe diseases have elevated levels of what?

A

PGE2

90
Q

PGE2 levels are determined by what

A

cyclooxgenase2 enzyme and cytokines esp IL-1 & TNF