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Infection and Immunity BDS2 > Pathogenesis and Aetiology of Periodontal Disease > Flashcards

Pathogenesis and Aetiology of Periodontal Disease Flashcards

1
Q

what is gingivitis

A

inflammation localised to gingival tissues, acute inflammation, normal physiological response to infection or injury

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2
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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3
Q

what type of plaque has saliva as a major immune defence strategy?

A

supragingival

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4
Q

what contents of saliva target and inhibit microbial growth?

A

antimicrobials, peptides and antibodies

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5
Q

what is the most successful intervention for preventing caries and periodontal disease?

A

mechanical intervention (brushing)

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6
Q

what types of barriers do the oral mucosa provide?

A

physical and functional

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7
Q

how does the oral mucosa provide a physical barrier?

A

prevents microbes accessing underlying tissues

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8
Q

how does the oral mucosa provide a functional barrier

A

by detecting and responding to microbial challenge through activation of TLR which activates inflammatory pathways

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9
Q

where does gingival crevicular fluid have a predominant effect?

A

subgingival portion of tooth

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10
Q

what is the primary aetiological factor for periodontal diseases?

A

poor oral hygiene

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11
Q

what is the unique biofilm profile determined by?

A

interactions by microbiomes and host factors and interactions amongst bacteria

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12
Q

what are the first species to colonise the tooth surface?

A

gram+ streptococcal

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13
Q

what do gram+ streptococcal species do on the tooth surfaces?

A

modify the environment and create new attachment sites for different species and bind directly or provide metabolites to support other species

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14
Q

what are the early colonisers of the oral biofilm?

A

aerobic gram+ species

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15
Q

what are the late colonisers of the oral biofilm?

A

gram- anaerobic species

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16
Q

what is the red complex?

A

triad of periodontal pathogens

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17
Q

what species are in the red complex?

A

porphyromonas gingivalis, tannerlla forsythia, treponema denticola

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18
Q

do all periodontal patients have the red complex?

A

no

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19
Q

what does periodontitis need to occur?

A

bacteria

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20
Q

comment on the presence of periodontal pathogens?

A

present at low numbers in healthy sites, increased numbers in diseased sites or can be absent from diseased sites

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21
Q

what is polymicrobial dysbiosis?

A

periodontitis associated with community of microorganisms which work together to disrupt the homeostasis of health

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22
Q

how does gingivitis occur?

A

the homeostatic relationship is disrupted through the accumulation of plaque or transition of periodontal pathogens leading to modest inflammation

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23
Q

what is the effect of persisting inflammatory reactions in the oral biofilm?

A

it exerts an ecological pressure on species present in biofilm and gives some species a competitive advantage allowing them to exist while others succumb to inflammation

24
Q

what type of species succumb to inflammation and are eliminated

A

commensal species

25
Q

what type of species can persist and adapt in inflammatory environments

A

accessory pathogens and periodontal pathogens

26
Q

what is periodontitis associated with?

A

a shift to dysbiotic biofilm which actively disrupts homeostasis for its own benefit which damages host tissues

27
Q

what are the virulence factors of P gingivalis?

A

asaccharolytic, gingipains, atypical LPS, inflammophilic, drives dysbiosis

28
Q

what does asaccharolytic mean?

A

it takes nutrients from the breakdown or proteins and peptides

29
Q

what are gingipains

A

proteases with broad specificity

30
Q

what does the atypical LPS of p. gingivalis do?

A

it is a TLR4 antagonist so it blocks inflammatory signalling

31
Q

what does inflammophilic mean?

A

inflammatory environment favours expression of virulence

32
Q

what do virulence factors do?

A

give immune system something to attack and alerts the immune system to the presence of microbes

33
Q

how are virulence factors regulated

A

in response to environmental conditions

34
Q

how does p. gingivalis persist in the oral environment

A

atypical LPS is used to hide from the immune system and persist in oral health, plaque accumulation stimulates inflammation and then P. gingivalis can express full virulence factors

35
Q

name some factors which cause dysbiosis in the oral environment

A

smoking, salivary flow rates, diet, oral hygiene, innate/adaptive immune factors

36
Q

what is the aetiology of periodontitis associated with?

A

accumulated plaque bacteria, presence of periodontal pathogens, polymicrobial dysbiosis, in susceptible hosts, host-pathogen interactions

37
Q

what is the false pocket in gingivitis due to?

A

inflammation and swelling, no attachment loss

38
Q

how does periodontitis have attachment loss?

A

PDL has came away from tooth surface so larger pocket, exposes more tooth surface available for biofilm accumulation deeper into the pocket and degradation of alveolar bone

39
Q

what are the 2 hallmark signs of periodontitis

A

attachment loss and alveolar bone loss

40
Q

what is the pathogenesis of gingivitis?

A

1 - increased TLR stimulation
2 - increased pro-inflammatory mediators (cytokines, peptides, chemokines)
3 - acute inflammatory response
4 - neutrophils remain predominant cell type
5 - monocytes recruited and differentiate to macrophages
6 - lymphocytes recruited to fine-tune the immune response (T cells coordinate and B cells release antibodies)

41
Q

what do neutrophils do in the pathogenesis of gingivitis?

A

phagocytose, degranulate and release enzymes into GCF which bathes the attachment surface

42
Q

how does increased vasodilation help immune cell defence?

A

it allows immune cells to migrate and control infection

43
Q

what can you see histologically with periodontitis in the PDL?

A

large aggregates of granular cells which overwhelm and destruct the integrity of the tissue

44
Q

what is the role of neutrophils in periodontal destruction?

A

they are crucial for maintaining healthy periodontium so when gingivitis occurs there is excessive infiltration which is associated with chronic inflammation (microbial subversion, degradative enzymes, inflammatory cytokines and oxygen radicals make a hypoxic environment, connective tissue destruction)

45
Q

what does a loss of neutrophil function present like at a young age?

A

aggressive periodontitis as neutrophils are not available to control bacterial growth in a healthy gingivae

46
Q

what is excessive infiltration of neutrophils associated with?

A

inflammation but is ineffective at controlling periodontal pathogens so it starts to contribute to periodontal tissue destruction

47
Q

what is the role of adaptive immunity in periodontal destruction?

A

T and B lymphocytes present , aggregates rich in CD4 T cells and B cells evident as lesion progresses, unable to regulate dysbiotic biofilm, B cells predominant in advanced lesions, IgG fails to regulate dysbiotic biofilm, inflammation induced alveolar bone loss

48
Q

what is the protective role of the adaptive immunity in periodontal destruction?

A

it prevents systemic infection by creating a barrier between pathogens and blood vessels

49
Q

what do osteoblasts do?

A

synthesis and secrete bone tissue and contribute to bone formation

50
Q

what do osteoclasts do?

A

resorbs bone, derived from monocyte/macrophage lineage

51
Q

what is bone formation and resorption regulated by?

A

RANK/RANKL/OPG triad

52
Q

how does inflammation lead to bone loss?

A
  1. T and B cells in gingival tissues are activated
  2. Lymphocytes release cytokines with RANKL and secrete into periodontal lesion
  3. RANKL binds to RANK on pre-osteoclast e.g., monocyte
  4. monocyte turns into osteoclasts
  5. OPG binds to RANKL to prevent RANKL binding to RANK and further osteoclast production - HEATH
  6. high levels of RANKL due to lots of T and B cells, low levels of OPG so it cannot inhibit RANKL binding
  7. large numbers of monocytes recruited
  8. osteoclast differentiating
  9. resorbed bone, alveolar bone resorption, tooth loss
53
Q

on a cellular level how does bacterial induced inflammation and pathologic tissue destruction occur?

A

1 - bacterial products bind TLR on epithelium which stimulates cytokines, chemokines and AMPs
2 - vasodilation and recruitment of leukocytes (neutrophils)
3 - bacterial products activate neutrophils and further release of pro-inflammatory mediators
4 - activated lymphocytes express RANKL so RANKL/OPG balance disrupted
5 - RANKL binds RANK on osteoclast precursors (monocytes) so osteoclastogenesis activated and alveolar bone resorption occurs
6 - pro-inflammatory cytokines contribute to bone resorption by inhibiting bone formation
7 - elevated and dysregulated MMP activation contributes to connective tissue destruction

54
Q

what is the outcome of the initial infection determined by?

A

host/biofilm interactions

55
Q

what is the nature of interactions between host and biofilm modified by?

A

environmental and genetic risk factors

Infection and Immunity BDS2 (7 decks)

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