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ODDR > Host Responces > Flashcards

Host Responces Flashcards

1
Q

what are the cells involved in bone loss?

A
  • Osteoclost
  • Osteoblast
  • fibroblasts
  • Macrophage.
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2
Q

what is the function of Osteoclasts?

A

bone resorbing.

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3
Q

what is the function of osteoblast?

A

bone forming

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4
Q

what is thefunction of fibroblasts?

A

form and maintain collagenous matrix.

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5
Q

what is the function of macrophages?

A

active member of the tissues defense.

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6
Q

what do monocytes form one they have fused together?

A

osteoclasts.

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7
Q

what growth factors control monocytes?

A

RANKL

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8
Q

what cells produce RANKL?

A

Osteoblasts.

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9
Q

how does RANKL bind to a monocyte?

A

binds to a specific receptor on the monocyte membrane.

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10
Q

how do osteoclasts degrade bone?

A

through pumping protons (H) ito the adjacent bone to dissolve mineral and then potent enzymes (Cathepsin K) to break down bone matrix,

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11
Q

what is the function of Cathepsin K?

A

to break down bone matrix.

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12
Q

what is meat when the bone is dynamic?

A

it responds to changes in loading - so that the ratio of bone formation / removal is dependent on the applied stress.

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13
Q

what is bone removal/ formation dependent on?

A

the applied stress.

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14
Q

what cells mediate bone removal/formation? and how?

A

osteoblasts.

via the production of RANKL.

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15
Q

How is stress in bone detected? (both directly and indirectly)

A

directly = by osteocytes and osteoblasts detecting it mechanically
indirectly - macrophages which respond to loading by producing cytokines (IL-1)

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16
Q

what does the production of IL-1 increase?

A

increases the production of RANKL by osteoblasts.

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17
Q

what exogenous plaque bacterial derived materials can cause bone destruction?

A

lipo-polysaccharide LPD.

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18
Q

What are the effects of plaque to bone loss?

A
  • LPD (plaque bacteria derived materials) act on osteoblasts - increasing production of RANKL.
  • LPD causes macrophages to increase IL-1 production.
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19
Q

what are the effects of IL-1 increase to bone loss?

A
  • triggers fibroblasts to produce IL-1
  • stimulates fibroblasts to produce IL-6
  • acts on fibroblasts to produce collagenase
  • act on osteoclasts to up-regulate Cathespisin K production.
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20
Q

what are the effects of IL-6 in bone loss?

A

increases the effectiveness of RANKL.

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21
Q

what are the effects of Cathepsin K production in bone loss?

A

increases the effectiveness of individual cells in degrading bone matrix

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22
Q

what are some examples of local factors in perio disease?

A
  • anatomical factors (morphology, PRS, enamel pearls etc)
  • Pt habits (mouth breathing, smoking)
  • latrogenic factors (ortho appliances +denture, restorations)
  • microbiological factors (colonisation of crevice+root surface.)
  • pre-existing deposits and disease.
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23
Q

what are some examples of systemic factors in perio disease?

A
  • environmental factors + metabolic factors (drugs, gingival overgrowth, sex hormones, diabetes)
  • Genetic /inherited factors (down symdrime, papillon lefevre sysdrom, hypophatasia, ehlers-Danlos syndrome)
  • Behavioural (smoking)
  • Lifestyle (stress)
  • Haemoatological (Chediak-Higashi, Neutropenia, Leukaemia)
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24
Q

what effects can having diabetes cause in regards to perio disease?

A
  • increase susceptibility to perio disease - related to level of glucose control.
  • decreased neutrophil function
  • decreased collagen synthesis
  • increased collagenolytic activity
  • increase periodontal pathogens in sub-gingival biofilm
    Perio disease can also effect diabetic control.
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25
Q

what are the effects of down syndrome in regards to perio disease?

A
  • increase susceptibility due to defect of neutrophil chemotoxis.
  • Oh is poor and they tend to be mouth breathers.
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26
Q

what are the effects of Papillon Lefevre syndrime in regards to perio disease?

A
  • defect of neutrophil chemotaxis and phagocytosis.

- rapid perio destruction.

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27
Q

what are the effects of Ehlers-Danlos syndrome in regards to perio disease?

A
  • disorder of collagen formation.
  • Type 8 associated with severe perio distruction
  • hyperextensible skin etc
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28
Q

wwhat are the effects of hypophatasia in regards to perio disease?

A
  • low levels of enzyme alkaline phosphatase
  • defective mineralisation and formation of cementum
  • teeth exfoliate and get rickets.
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29
Q

what are the effects of smoking in regards to perio disease?

A
  • result in fibrotic gingivae with rolled margins
  • increase pockets / recession anteriorly, bone loss, calculus, furcation.
  • decrease in gingival bleeding and BOP.
  • effects composition of bacterial flors, increasing cytokine release and so increasing the destruction of matrix.
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30
Q

what are the effects of stress in regards to perio disease?

A
  • depresses immune system.
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31
Q

how does an individual get chediak-Higashi?

A

through genetics.

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32
Q

what are the effects in the mouth of acute leukaemias?

A
  • slightly like gingival overgrowth.

- gingival swelling, excessive random bleeding, and gngival ulcerations.

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33
Q

what age group is most likely to be effects by Actue leukaemias?

A

under 20’s - often children.

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34
Q

what age group is most likely to be effects by chronic leukaemias?

A

older age groups.

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35
Q

what are the 3 histopathological stages of gingivitis?

A
  • Initial
  • Early
  • Established.
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36
Q

what are the initial features of plaque-induced gingivitis?

A
  • inflammation begins 24/48 hours after plaque accumulation begins.
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37
Q

what are the effects of inflammation during initial gingivitis?

A

causes vasodilation of tissues and causes an increas

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38
Q

how soon after plaque accumulation starts does inflammation begin?

A

24/48 hours.

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39
Q

what happens after approx 1 week after plaque accumulation?

A
  • increase inflammatory infiltrate
  • increase lymphocytes/ macrophages/ neutrophil migration.
  • fibroblasts start to show sign s if cell damage.
  • early loss of gingival collagen
  • gingival swelling, resulting in deepening of the gingival crevis.
  • rete peg proliferation
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40
Q

when do fibroblasts start to show signs of cell damage?

A

during early gingivitis (after 1 week of plaque accumulation)

41
Q

what happens to the PDL during established gingivitis?

A
  • increases inflammatory infiltrate (alot of plasma cells)
  • PMN (neutrophils) predominates
  • fibroblasts start to show signs of cell damage
  • early loss of gingival collagen (but no loss of connective tissue)
42
Q

what % of plasma cells make up the inflammatory infiltrate in established gingivitis?

A

10-30%

43
Q

in what stage of peio disease do fibroblasts start to show signs of cell damage?

A
  • during established gingivitis.
44
Q

what happens to the PDL during periodontitis?

A
  • inflammatory infiltrate extends
  • plasma cells dominate (over 50%)
  • loss of perio connective tissue attachment
  • perio pockets.
  • alveolar bone loss.
45
Q

how is tissue damage in the epithelium during perio diseas?

A
  • bacterial enzymes cause damage to keratinocytes.
  • release of enzymes from neutrophils cause damage to keratinocytes.
    -complement activation can cause cell dmaage.
    -
46
Q

how is tissue damage i connective tissue during perio disease?

A
  • bacterial toxins are toxic to fibroblasts
  • bacterial enzymes cause degradation of extra-cellular matrix components.
  • enzymes from neutrophils cause break down of extra-cellular matrix component.
  • complement activation causes damage to fibroblasts.
    production of IL-1 +TNF increase secretion of collagenase + proliferation by fibroblasts.
  • ## production of TGfb and PDGF causes stimulation of fibroblast chematoxis.
47
Q

what are some examples of bacterial -derived bone resorbing agents>?

A
  • capsular (from Aa)
  • Lipopolysaccharides
  • Lipoteichoic acids
  • Actinomyce resorbing factors
  • Peptidoglycan
  • Muramyl dipeptide
  • bacterial lipoproteins
48
Q

what are host derived cytokines that are bone resorbing agents?

A
  • IL-1
  • tumour necrosis factor (TNF)
  • transforming growth factor beta
  • platelet derived growth factor
  • IL-6
49
Q

what are other host0derived bone resorbing agents (thats are not cytokines)?

A
  • Prostaglandins

- Leukotrienes.

50
Q

what are some kep features of periodontal breakdown?

A
  • apical migration of epithelium
  • breakdown of PDL
  • bone resorption.
51
Q

In periodontitis what % of the cells are plasma cells in the inflammatory infiltrate?

A

over 50%

52
Q

what are the effects of Perio tx after 1 week?

A
  • reduction of neutrophils in gingival crevice
  • inflammatory infiltrate starting to diminish
  • reduction in gingival swelling
  • some pocket epithelial lining will begin to heal
  • begin to get fibroblast proliferation
53
Q

what are the effects of perio tx after 1 month?

A
  • maybe evidence of gingival recession
  • new fibroblast tissue forming
  • inflammatory infiltrate diminishing
  • long epithelial attachment beginning to form
  • alveolar bone re-models by not regeneration coronally.
54
Q

what are the effects of perio tx 3-6 months after?

A
  • lesion can become stable
  • healing could result in recession
  • only small number of neutrophils in gingival crevice
  • junctional epithelial re-established with formation of long epithelial attachment.
  • gingival connective tissue is mature with minimal inflammatory infultrate
  • bone remodelling almost complete.
55
Q

what are the clinical signs of healing of perio disease?

A
  • reduced probing pocket depths
  • reduced bleeding on probing
  • gain in clinical attachment (reduced mobility)
  • maybe recession
  • possible bony infil in angular defects.
56
Q

How does saliva protect us against microbial plaque?

A
  • has antimicrobial effects: peroxidase / phothiocyanata / lysozymes / lactoferrin / antibodies (IgA)
57
Q

what does the gingival epithelium consist of?

A
  • oral sulcular epitherlium
  • junctional epithelium
  • oral gingival epithelium
58
Q

what type of protection does the gingival epithelium give?

A

physical barrier.

59
Q

what is the function of the inflammatory response?

A
  • dilute (by increasing crevicular fluid)
  • wall off (inflammatory cells)
  • destroy/ damage pathogens (inflammatory cells)
60
Q

what cells are involved in the inflammatory response?

A
  • Neutrophils

- Macrophages.

61
Q

what do neutrophils do to bacteria in a plaque matrix?

A

attach and secrete antibacterial enzymes that kill bacteria and dissolve plaque matrix.

62
Q

what do neutrophils do to unattached bacteria in the mouth?

A
  • phagocytosis
63
Q

what is the function of a macrophage in inflammation?

A
  • phagocytosis
  • secrete tissue-degrading enzymes
  • secrete complement components
  • secrete mediators (IL-1 ad TNF)
64
Q

what is the function of a macrophage in immunity?

A
  • process and prevent antigens

- secrete IL-1

65
Q

what is the product of degranulating neutrophils in the sulcus?

A

leukotriene B4 in GCF

66
Q

what is the process of the humoral immune response?

A

B cells undergo proliferation into plasma cells that secrete Ig.

67
Q

what cells are involved in the cell mediated immune response?

A

T cells that are either T helper cells, or T cytotoxic cells.

68
Q

Oncean antigen enters the body how does it get carried to the lymph nodes?

A

via macrophages

69
Q

what % of antibodies produced are from the IgG family?

A

75%

70
Q

what are the functions of antibodies?

A
  • bind to bacteria (inhibitig attachment)

- binding to soluble factors (neutralizing toxins, inhibiting enzymes)

71
Q

what are the defects in out host responses?

A
  • reduced neutrophil number

- defective neutrophil functions (in some patients with conditions eg down syndrome, diabetes)

72
Q

what are the effects of HIV on perio?

A

reduction in the number and function of T helper cells - so more susceptible.

73
Q

what medication are aid in perio disease?

A
  • Histamine + Bradykinin
  • Cytokines
  • Prostaglandins
  • Metalloprotienases
74
Q

what is the function of Histamine and Bradykinin?

A

vasodilation, they increase vascular permeability.

75
Q

what is the function of cytokines?

A

they are soluble proteins that are secreted by cells. They transmit signals, and coordinate inflammatory and immune responses.
- amplify inflammatory responce (eg IL-1)

76
Q

what is the function of prostaglandins?

A

produced from arachidonic acid in the cell membrane of inflammatory cells, they cause capillary dilation, endotherthial permeability and can cause bone resorption.

77
Q

what cells produce metalloproteinsases?

A

fibroblasts, monocytes and neutrophils.

78
Q

what is an example of a metalloproteinsase?

A

collagenase, gelatinase.

79
Q

what happens during a Type 1 hypersensitivity reaction?

A
  • IgE binds to common harmless antigens.

- narrowing airways

80
Q

what happens during a Type ll hypersensitivity reaction?

A
  • small molecules bind to cell surfaces and modify thier structure.
  • then IgG binds to that
  • Can be cause by drugs.
  • can result in activation of complement, phagocytic cell or NK cells.
  • can result in anaemia or abnormal bleeding.
81
Q

what happens during a Type lll hypersensitivity reaction?

A
  • soluble antigens + mediated by IgG
  • antibody + antigen cluster together. This triggers immune effector functions and cells - causing tissue damage and pathology.
  • smaller complexes are deposited on blood vessel walls attracting complement and leukocytes causing damage to blood vessels and tissues.
82
Q

what happens during a Type lv hypersensitivity reaction?

A
  • delays reaction
  • mediated by antigen-specific effector T cells.
  • foreign molecules will bind to host proteins, altering their structure and making them look different so they will be seen as foreign and nonself by the immune system.
83
Q

why does autoimmune disease develop?

A
  • genetic susceptibility
  • Tolerance breakdown
  • infection/ environmental exposure.
84
Q

how can infections trigger autoimmunity?

A
  • damage to a cell or tissue barrier.

- releasing perviously sequestered self antigens, rendering them accessible to self-reactive lymphocytes that may exist.

85
Q

what is molecular mimicry?

A

where a pathogen may produce a molecule that resembles a host protein. Them once in the immune system and raised an immune response, the effector cells and antibodies produced may then recognise and attack the similar host structures.

86
Q

what is organ specific autoimmune disease?

A

tissue damage is limited to the few organs that express the target autoantigen

87
Q

what is an example of organ specific autoimmune disease?

A

Type 1 diabetes.

88
Q

what is systemic autoimmune disease?

A

tissue damage that can happen at multiple site i the body - wherever the autoantigen is present.

89
Q

what is an example of a systemic autoimmune disease?

A

Rheumatoid Arthritis

Systemic Lupus erythemastosus (SLE)

90
Q

what cells does HIV-1 kill?

A

CD4 positive cells (T-Helper Cells)

91
Q

How can opportunistic infection kill due to AIDs?

A
  • CD4 levels have dropped below critical level - immune system collapses and pt has AIDs
  • so opportunistic pathogens will cause severe disease.
92
Q

why without any tx will HIV result in AIDs?

A
  • CD4 cells are needed to control infection.
  • antibodies produced in an immune response dont bind well to intact virus particles of infected cells
  • HIV rapidly mutates, so they can escape recognition.
93
Q

why is HIV drug resistant?

A

rapidly mutates.

but can be successful if taken in combinations.

94
Q

what is the anti-HIV drug? and when does it need to be taken?

A

PEP.

needs to be taken up to 73 hours post exposure.

95
Q

where in the mouth is HIV most likely to be found?

A

in GCF

96
Q

what happens to the rate of HIV in GCF during perio disease?

A

increases.

97
Q

Why in saliva is HIV non-infectious.

A

because saliva contains anti-HIV factors that block it from being infectious.

98
Q

what id found in saliva that meant HIV non-infectious?

A
  • Mucins - clump viral particles together.
  • Mucins and agglutinin - may strip HIV of gp120.
  • Secretory Leulocyte protease inhibitor produced by salivary glands binds to T helper cells and blocks HIV-1 gaining access and infecting the cell.

ODDR (5 decks)

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