host bacterial interactions in periodontal disease Flashcards
(69 cards)
1
Q
what is included in the term periodontal diseases
A
- gingivitis
- periodontitis
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
3
Q
what is periodontitis
A
- inflammation of the gingival tissues and supporting periodontal structures
- chronic inflammation
- pathological inflammatory response associated with tissue destruction
4
Q
what do gums look like in health
A
- pink gums
- knife edge gingival margins
5
Q
what do gums look like in gingivitis
A
- gingival swelling/inflammation
- triggered by plaque
6
Q
what do gums look like in periodontitis
A
- accumulated plaque and calculus, more severe
- very red and inflamed gums
7
Q
what does the amount of plaque relate to
A
- amount of plaque correlates to the amount of swelling
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
9
Q
is poor oral hygiene an aetiological factor in periodontitis
A
- yes, but it’s not the whole picture
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
11
Q
what species did late colonisers typically have in oral biofilm
A
gram-negative anaerobes
12
Q
what species did early colonisers typically have in oral biofilm
A
commensal species
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
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
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
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
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
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
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
20
Q
what is colonisation
A
- microbial pressure on a body surface without clinical signs of inflammation or disease
- commensal
21
Q
what is infection
A
- microbial invasion of host tissues
- pathogens
- 1st stage of infection
22
Q
can commensal organisms become pathogenic
A
- yes
- if conditions favour expression of virulence
- if opportunity arises
23
Q
can pathogens behave like commensals
A
- yes
- if conditions do not favour expression of virulence
24
Q
what is the outcome of host-bacterial interactions
A
- microbial pathogenicity
25
what is the microbial challenges
- antigens
| - virulence factors
26
what is the host response
- adaptive
| - innate
27
what do microbes do
- microbes actively suppress virulence factors
| - some microbes are more virulent than others so it can be easier to overcome the body's immune system
28
what are the virulence factors for P gingivalis
- immune evasion and subversion
- asacharolytic
- gingipans
- atypical LPS
- inflammaphobic
29
what are asacharolytic
- nutrients from breakdown of proteins and peptides
| - means can't use carbs as an energy source
30
what are gingipans
- proteases with broad-specificity
- degrade host proteins = to make them available as nutrients for bacteria
- activate MMP's to clear up tissue damage
31
what is the atypical LPS
TLR4 antagonist
32
what are inflammaphobic's
- inflammatory environment favours expression of virulence
| - these like inflammation as can express all factors in this environment
33
are virulence factors present in a healthy mouth
- yes
| - but these will not do anything until there is inflammation
34
what can modify the host response
- genetic risk factors
| - environmental risk factors
35
what factors trigger gingival inflammation
- changes in orla biofilm
= accumulation
= composition
= expression of virulence
36
what factors determine whether inflammation resolves or progresses
- period tonal pathogenesis is determined by host-bacterial interactions
37
what makes teeth ideal for biofilm accumulation
- they are the only hard non-shedding site exposed to the environment
38
what makes saliva an important defence
- S-IgA
- lysozyme
- perioxidase
- lactoferrin
- muffins
- agglutinins
- cystatins
- histatins
39
what do neutrophils do during periodontal disease
- travel through the tissues to the gingival margin and then degranulate and release all components into the gingival margin
40
what makes the oral mucosa an important defence
- AMPs
- cytokines
- chemokine
41
what does gingival crevicular fluid contain
- AMPs
- cytokines
- chemokines
- lactoferrin
- IgG
42
what type of biofilm exists in health
- symbiotic biofilm
| - exists along with the host immune response
43
what occurs during gingivitis
- altered microbial colonisation
- increased flow of GCF
- influx of neutrophils, increased lymphocytes and monocytes
44
what is the process of gingivitis
- 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
what can happen after gingivitis
- 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
what type of biofilm is formed in disease
- dysbiotic biofilm
| - works against the host
47
what are the environmental and genetic risk factors that can alter the ecological pressure exerted on the oral biofilm
- disease
- genetic differences
- activity of salivary gland
- salivary flow
- innate/adaptive immune factors
- oral hygiene
- diet
- smoking
- antimicrobial agents
48
what pressure can alter the competitiveness of bacteria within biofilm
- ecological pressure
49
what species are more susceptible to inflammatory response
- symbiotic (avirulent)
| - have a competitive advantage
50
what type of pocket is in gingivitis
- bigger pocket but there is not a true pocket
51
what type of pocket is in periodontitis
- 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
how does the host immune reason change as disease progresses
- changes drom protective to destructive
53
what is the role of neutrophils in periodontal tissue destruction
- 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
what is aggressive periodontitis associated with
- leukocyte-adhesion deficiency
| - immune under reaction
55
what is excessive infiltration of neutrophils associated with
- chronic inflammation
- degradative enzyme
- inflammatory cytokines and oxygen radicals contribute to hypoxic environment
56
what does connective tissue destruction manifest as clinically
- attachment loss
57
what can adult chronic periodontitis be caused by
- an immune over reaction
| - the neutrophils are ineffective in controlling
58
what can happen if you don't get the balance of neutrophils right
- 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
what is the role of adaptive immunity in periodontal destruction
- 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
what are osteoblasts
- synthesises and secretes bone tissue
| - boen formation
61
what are osteoclasts
- resorbs bone
| - derived from monocyte/macrophage lineage
62
what happens in health for bone
- bone formation and resorption are coupled
| - regulated by RANKL/RANK/OPG triad
63
what is RANKL
it is a cytokine and RANK is expressed on cytokines and OPG regulates
64
what are the stages leading to bone loss
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
how inflammation leads to bone loss
- high levels of RANKL
- low levels of OPG
- inflammation induced bone resorption
- pathological bone destruction
66
what are the cellular and molecular events linking bacterial-induced inflammation with pathological tissue destruction
- 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
interaction between what determines the pathogenesis and severity of the disease
- interaction between the host and microbes
68
what governs patient susceptibility of the disease
- regulation of immune-inflammatory mechanisms governs patient susceptibility
- modified by environmental factors
69
what is the aetiology of periodontal disease
- bacteria
