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BDS2 - periodontitis > host bacterial interactions in periodontal disease > Flashcards

host bacterial interactions in periodontal disease Flashcards

1
Q

what is included in the term periodontal diseases

A
  • gingivitis

- periodontitis

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2
Q

what is gingivitis

A
  • inflammation localised to gingival tissues
  • acute inflammation = normal, physiological response, if successful will repair to homeostasis
  • normal, physiological response to infection or injury
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3
Q

what is periodontitis

A
  • inflammation of the gingival tissues and supporting periodontal structures
  • chronic inflammation
  • pathological inflammatory response associated with tissue destruction
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4
Q

what do gums look like in health

A
  • pink gums

- knife edge gingival margins

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5
Q

what do gums look like in gingivitis

A
  • gingival swelling/inflammation

- triggered by plaque

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6
Q

what do gums look like in periodontitis

A
  • accumulated plaque and calculus, more severe

- very red and inflamed gums

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7
Q

what does the amount of plaque relate to

A
  • amount of plaque correlates to the amount of swelling
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8
Q

is plaque the only factor that affects the disease

A
  • no

- it does affect the disease, but it is not the only factor

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9
Q

is poor oral hygiene an aetiological factor in periodontitis

A
  • yes, but it’s not the whole picture
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10
Q

how many species have been identified in oral biofilm

A
  • there have been 1,000 different species identified in oral cavities
  • every person will have around 150
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11
Q

what species did late colonisers typically have in oral biofilm

A

gram-negative anaerobes

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12
Q

what species did early colonisers typically have in oral biofilm

A

commensal species

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13
Q

how many complexes are in sub-gingival plaque

A
  • 6
  • blue
  • yellow
  • orange
  • green
  • red
  • purple
  • within each complex were microbes that were found together
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14
Q

what is the red complex in sub-gingival plaque

A
  • bacterial species most commonly isolated form diseased sites = numbers correlated with pocket depth and bleeding on probing
  • these are the PERIODONTAL PATHOGENS
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15
Q

what is the orange complex

A
  • also correlated with periodontal disease but to a lesser extent than red
  • significantly associated with disease parameters but less than red
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16
Q

how does the presence of these complexes not necessarily mean disease

A
  • some of these complexes were isolated from healthy sites in the mouth as well so don’t mean disease
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17
Q

do specific bacterial species cause periodontal disease

A
  • periodontitis cannot occur int he absence of bacteria

- it is difficult to establish role of specific microbes

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18
Q

where are periodontal pathogens present

A
  • present at low levels in the mouth
  • increased numbers in diseased sites
  • can be absent from disease sites
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19
Q

what is the difference between colonisation and infection

A
  • colonisation does not mean disease whereas in infection they invade tissues and cause inflammation
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20
Q

what is colonisation

A
  • microbial pressure on a body surface without clinical signs of inflammation or disease
  • commensal
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21
Q

what is infection

A
  • microbial invasion of host tissues
  • pathogens
  • 1st stage of infection
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22
Q

can commensal organisms become pathogenic

A
  • yes
  • if conditions favour expression of virulence
  • if opportunity arises
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23
Q

can pathogens behave like commensals

A
  • yes

- if conditions do not favour expression of virulence

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24
Q

what is the outcome of host-bacterial interactions

A
  • microbial pathogenicity
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25
Q

what is the microbial challenges

A
  • antigens

- virulence factors

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26
Q

what is the host response

A
  • adaptive

- innate

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27
Q

what do microbes do

A
  • microbes actively suppress virulence factors

- some microbes are more virulent than others so it can be easier to overcome the body’s immune system

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28
Q

what are the virulence factors for P gingivalis

A
  • immune evasion and subversion
  • asacharolytic
  • gingipans
  • atypical LPS
  • inflammaphobic
29
Q

what are asacharolytic

A
  • nutrients from breakdown of proteins and peptides

- means can’t use carbs as an energy source

30
Q

what are gingipans

A
  • proteases with broad-specificity
  • degrade host proteins = to make them available as nutrients for bacteria
  • activate MMP’s to clear up tissue damage
31
Q

what is the atypical LPS

A

TLR4 antagonist

32
Q

what are inflammaphobic’s

A
  • inflammatory environment favours expression of virulence

- these like inflammation as can express all factors in this environment

33
Q

are virulence factors present in a healthy mouth

A
  • yes

- but these will not do anything until there is inflammation

34
Q

what can modify the host response

A
  • genetic risk factors

- environmental risk factors

35
Q

what factors trigger gingival inflammation

A
  • changes in orla biofilm
    = accumulation
    = composition
    = expression of virulence
36
Q

what factors determine whether inflammation resolves or progresses

A
  • period tonal pathogenesis is determined by host-bacterial interactions
37
Q

what makes teeth ideal for biofilm accumulation

A
  • they are the only hard non-shedding site exposed to the environment
38
Q

what makes saliva an important defence

A
  • S-IgA
  • lysozyme
  • perioxidase
  • lactoferrin
  • muffins
  • agglutinins
  • cystatins
  • histatins
39
Q

what do neutrophils do during periodontal disease

A
  • travel through the tissues to the gingival margin and then degranulate and release all components into the gingival margin
40
Q

what makes the oral mucosa an important defence

A
  • AMPs
  • cytokines
  • chemokine
41
Q

what does gingival crevicular fluid contain

A
  • AMPs
  • cytokines
  • chemokines
  • lactoferrin
  • IgG
42
Q

what type of biofilm exists in health

A
  • symbiotic biofilm

- exists along with the host immune response

43
Q

what occurs during gingivitis

A
  • altered microbial colonisation
  • increased flow of GCF
  • influx of neutrophils, increased lymphocytes and monocytes
44
Q

what is the process of gingivitis

A
  • any changes can trigger inflammation
  • increased TLR stimulation
  • increased production of pro-inflammatory mediators
  • trigger acute inflammatory response = redness, swelling, bleeding, increased vasodilation, cell migration
  • neutrophils number increased = remain predominant cell
  • monocytes activated by cytokine and bacterial components there = recruited, activated and differentiate into macrophages
  • lymphocytes are recruited to fine-tune the immune response
45
Q

what can happen after gingivitis

A
  • ca resolve back to health or progress into periodontitis
  • if disease eliminated then return back to health
  • if disease not eliminated then inflammation allows the inflammaphobics more of an advantage to survive than commensal
46
Q

what type of biofilm is formed in disease

A
  • dysbiotic biofilm

- works against the host

47
Q

what are the environmental and genetic risk factors that can alter the ecological pressure exerted on the oral biofilm

A
  • disease
  • genetic differences
  • activity of salivary gland
  • salivary flow
  • innate/adaptive immune factors
  • oral hygiene
  • diet
  • smoking
  • antimicrobial agents
48
Q

what pressure can alter the competitiveness of bacteria within biofilm

A
  • ecological pressure
49
Q

what species are more susceptible to inflammatory response

A
  • symbiotic (avirulent)

- have a competitive advantage

50
Q

what type of pocket is in gingivitis

A
  • bigger pocket but there is not a true pocket
51
Q

what type of pocket is in periodontitis

A
  • attachment loss and formation of a true pocket allowing bacteria and biofilm to descend deeper into pocket
  • host immune response to the biofilm causes destruction
52
Q

how does the host immune reason change as disease progresses

A
  • changes drom protective to destructive
53
Q

what is the role of neutrophils in periodontal tissue destruction

A
  • crucial for maintaining healthy periodontium
  • in these patients the neutrophils are trapped and can’t enter the tissues so can have periodontitis from a young age
  • number of neutrophils increase during gingivitis = if it can contain the infection then will return to health, if not then periodontitis
54
Q

what is aggressive periodontitis associated with

A
  • leukocyte-adhesion deficiency

- immune under reaction

55
Q

what is excessive infiltration of neutrophils associated with

A
  • chronic inflammation
  • degradative enzyme
  • inflammatory cytokines and oxygen radicals contribute to hypoxic environment
56
Q

what does connective tissue destruction manifest as clinically

A
  • attachment loss
57
Q

what can adult chronic periodontitis be caused by

A
  • an immune over reaction

- the neutrophils are ineffective in controlling

58
Q

what can happen if you don’t get the balance of neutrophils right

A
  • if there is not enough then it can contribute to disease

- if there is too many neutrophils then it can contribute to tissue destruction and attachment loss

59
Q

what is the role of adaptive immunity in periodontal destruction

A
  • T and B lymphocytes are present in early lesion = present in gingivitis and help eliminate pathogen
  • aggregates rich in CD4 T cells, B cells and dendritic cells evident as lesion progresses
  • goes from innate to adaptive
  • unable to regulate dysbiotic biofilm
  • B cell preodominate advanced lesions
  • IgG fills to regulate dysbiotic biofilm
  • protective = prevents systemic infection
  • destructive = inflammation induced alveolar bone loss
60
Q

what are osteoblasts

A
  • synthesises and secretes bone tissue

- boen formation

61
Q

what are osteoclasts

A
  • resorbs bone

- derived from monocyte/macrophage lineage

62
Q

what happens in health for bone

A
  • bone formation and resorption are coupled

- regulated by RANKL/RANK/OPG triad

63
Q

what is RANKL

A

it is a cytokine and RANK is expressed on cytokines and OPG regulates

64
Q

what are the stages leading to bone loss

A

activated T and B cells in periodontal lesion secrete RANKL into the environment t

  • RANKL binds to RANK to induce osteoclast differentiation = RANKL binds to RANK on pre-osteoclasts which then become osteoclasts by differentiation
  • OPG prevents RANKL binding to RANK = OPG is a decoy receptor
  • OPG inhibits osteoclast differentiation
65
Q

how inflammation leads to bone loss

A
  • high levels of RANKL
  • low levels of OPG
  • inflammation induced bone resorption
  • pathological bone destruction
66
Q

what are the cellular and molecular events linking bacterial-induced inflammation with pathological tissue destruction

A
  • bacterial products bind TLR’s on epithelium, stimulating secretion of cytokines, chemokine and AMPs= perio pathogens
  • vasodilation and selective recruitment of leukocytes mainly neutrophils = swelling
  • bacterial products activate neutrophils, further release of pro-inflammatory mediators = amplification loop of neutrophil
  • activated lymphocytes express RANKL = RANKL/OPG balance disrupted
  • RANKL binds to RANK on osteoclast precursors = activate osteoclastogeneis (bone resorption)
  • pre inflammatory cytokines contribute to bone resorption by inhibiting bone formation
  • elevated and dysregulated MMP activation contributes to connective tissue destruction
67
Q

interaction between what determines the pathogenesis and severity of the disease

A
  • interaction between the host and microbes
68
Q

what governs patient susceptibility of the disease

A
  • regulation of immune-inflammatory mechanisms governs patient susceptibility
  • modified by environmental factors
69
Q

what is the aetiology of periodontal disease

A
  • bacteria

BDS2 - periodontitis (4 decks)

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