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Mandal > Immunopathology of gingivitis, periodontists and host immunity > Flashcards

Immunopathology of gingivitis, periodontists and host immunity Flashcards

1
Q

Specific plaque hypothesis

A
  • Plaque bacteria not equally pahtogenic
  • certian bacteria in plaque are respopnisble for destructive periodontitis
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2
Q

pathogens inmplicated in periodontitis

(gram-negative anaerobic)

A
  • porphyromonas gingivalis
  • prevotella intermedia
  • bacteroides forsythus
  • campylobacter restus
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3
Q

pathogens implicated in periodontitis

(gram-negative facultative)

A
  • actinobacilus actinomycetemcomitans (Aa)

(implicated in aggressive periodontitis)

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4
Q

is plaque sufficient to develop periodontitis

A

necessary bu not sufficient

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5
Q

what is the principal cause of initial inflammatory lesion leading to ginigivitis

A

bacteria

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6
Q

what dictates uncontrolled inflammatory immune response driving the tissue destruction and periodontitis ?

A

the host response

(not the type of bacteria)

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7
Q

ginigivitis is concdered a _____ to non-specific accumulation of ____

A

non-specific reaction, plaque

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8
Q

is bacteria the major determinate of the progression of ginigivitis to periodontitis

A

nope, despite universal presence of plaque

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9
Q

what is responisble for initiation of ginigivitis lesions?

A

host-parasite interaction

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10
Q

bacteria respnisble for progresson to advanced periodonitis?

A

no definitive evidence

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11
Q

ecological plaue hypothesis

A
  • subginival environment dictates/selects specific microbial composotion (drives health or disease)
  • accumulation of plaque triggers inflammatory host response
  • favors growth of gram - bacteria
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12
Q

what factors promote a good dingival health ?

A
  • plaque reduction
  • decreased inflammation
  • low GCF flow
  • higher eh
  • mainly gram + faculative anaerobes
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13
Q

what is the only etiology of periodontal disease ?

A

Bacrerial plaque

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14
Q

Role of bacterial plaque

A

colonization of subgingical regions be specic groups of organisms

(attach above and bellow the ginigival margin, need it to initiate disease)

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15
Q

direct effects of periodontal disease

A
  • invasion
  • release of exotoxins
  • cell constituents
  • enzymes (proteases)
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16
Q

indirect effects of periodontal diseases onss

A
  • immunological and other host responses (destructive)
  • loss of periodontal tissue
    • gingiva
    • periodontal ligament
    • alveolar bone
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17
Q

periodontitis is an

A

inflammation-based infection of the supporting supporting structures of the teeth

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18
Q

two forms of periodontits occurs

A
  • chronic periodontitis
  • aggressive periodontitis
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19
Q

periodontitis modified by systemic Diseases

A
  • Chronic periodontitis
  • aggressive periodontitis
  • periodontitis modified by systemic diseases
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20
Q

less common types of periodintitis

A

manifestation of systemic diseases

necrotizing peridontitis

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21
Q

which is the most commone periodontitis in adults?

A

chronic

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22
Q

chronic perioditis features

A
  • can be localized or generalized
  • red or purpleish tissue
  • loss of attachment and bone
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23
Q

which disease has severity consistent with amount of plaque?

A

chronic periodontitis

(variable microbiota)

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24
Q

which disease is the plaqye not consitant with severity of the diease ?

A

aggressive periodontitis

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25
Q

aggressive periodontitis progression of the disease?

A

tissue destruction in rapid

(whereas chronic progression is moderate)

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26
Q

Most common baccteria associated with aggressive periodontitis

A

g(-) Actinobacillus actinomycetemcomintans (Aa)

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27
Q

In aggressive periodontitis there is an abnormality in

A

PMN function and hyperresponsive macrophages

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28
Q

what is secreted in aggressive periodontisis ?

A
  • prostaglandins
  • IL-1ß
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29
Q

What are the two forms of aggressive periodontitis ?

A
  • Localized Aggressive Periodontitis (LAP)
    • strong Ab respnose
  • Generalized Aggressive periodontitis (GAP)
    • poor Ab response
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30
Q

which form of periodontitis has a strong Ab response

which form of periodontitis has a weak Ab response

A

Localized aggressive periodontitis

generalized aggressive periodontitis

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31
Q

Localized aggressive periodontitis associated with ?

A

actinobacillus actinomycetemocomitas (Aa)

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32
Q

localized aggressive periodontitis is associtaed with abnormal

A

Neutrophil function

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33
Q

where is dectrction usuallt found in localized aggressive periodontitis?

A

around first molars and incisors

(preveriosly known as localized juvenile periodontitis)

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34
Q

Generalized aggressive periodontits

(3)

A
  • rapid attachment and bone loss
  • no systemic disease
  • genetic factor
35
Q

for generalized aggressove periodontitis is the amount of destruction proportional to amount of plaque?

A

no

36
Q

major virulence traits of periodontal pathogens

5

A
  1. Proteases
  2. Hemagglutinins
  3. LPS
  4. Fimbriae
  5. Polysaccharide capsule
37
Q

proteases

A

degrade host proteins disrtupt host defenses

38
Q

P.gingivalis proteases are

A

Arg- and Lys- specifiv proteases

39
Q

Hemagglutinins

A

responsible for bacterial biding to host cell receptors

40
Q

P. ginigivalis hemagglutinins

A

HagA, HagB, HagC

41
Q

LPS

A

surface Ag releative lack of endotoxicity compared to enteric LPS

42
Q

Fimbriae

A

role in adherence colonization and periodontal dectruction

43
Q

polysaccharide capsule

A

highly encapsulated strains inhibit phagocytosis and AC mediated cytolysis

44
Q

Polysaccharide capsule

A

hihgly encapsulatd strains inhibit phagocytosis and MAC- mediated cytolysis

45
Q

Virulent oral pathogens induce

A

destructive immune responses and impair protective hosot immune system

46
Q

P.gingivalis induce

A
  • inflammation and bleeding
  • use hemagglutinins and proteases to lyse RBCs to extract nutrients for rapid growth
47
Q

bacterial virulence overwhelms innate immune system cells

A

PMNs release tissue damaging substances

48
Q

proteases degrade

A

serum AG

complement proteins

leukocyte-derived cytokines

49
Q

Bacteria (Aa) enhances virulence by releaing

4

A
  • Proinflammatory virulence factors
  • peptides
  • poplysaccharide Ag
  • LPS
50
Q

Aa enhacing virulence leads to

A

enhnaced cytokine selction

(change in immune homeostatsis)

51
Q

Aa produce most important secretion

A

leukotoxin-toxic to PMNs and monocytes

52
Q

stains of AA can produce factors that

A
  • inhibit PMN chemotaxis,
  • resistance to phaocytosis
  • inhibition of H2O2 production and killing by PMNs
53
Q

evasion of immune components permits

A

pathogen and host tissue destruction

54
Q

bacteria attract ____ to the site of infection

A

leukocyte to the site of infection

55
Q

bacteria attract leukocyted directly via

A

bacterial peptides

56
Q

bacteria attrat leukocytes to the site of infection indirectly via

A

cytokines secreted bacterial LPS binds to monocyte/macrophage via CD14 and TLR-4

57
Q

secretion of inflammatory cytokines

A

IL-1ß

TNF-alpha

58
Q

which is the main prostaglandin secreted ?

A

PGE2

found in high conc. on GCF

59
Q

what is responsible for bone resorption and induction of bone destruction by P. ginigivalis infection

A

secretion of PGE2

(in GCF)

60
Q

inhibition of PGE2 production by…

A

NSAIDs and dexamethasone

(result= decreases loss of alveolar bone )

61
Q

early periodontal lesion are characterized by

A

T cells and machrophages

(cellular immune response)

62
Q

established and advanced lesions contain

A

B cells and plasma cells

(humoral immune response )

63
Q

progression of lesions are controlled by

A

host Th cell-derived cytokines

64
Q

cytokine patern lease to

A

protective immune response

alternatively a pathological/destructive response

65
Q

early clinical gingivitis correlates with

A

Th1-type with IL-12 and IFN-gamma

66
Q

Th1-typenof immune response with IL-12 and IFN-gamma

A

leading to macrophage activataion

increased phagocytosis and protective immunity

67
Q

in established and advaced lesions with clinical periodontitis …

A

TH2 response, production of IL-4, IL-10 and IL-13

68
Q

TH2 response, production of IL-4, IL-10 and IL-13 leads to

A

Ab production

69
Q

despite hihg conc of systemic and local Ab

A

periodontitis may persist and progress

70
Q

persisting periodontitis indicates

A
  • inappropriate production of cytokines
  • over production of IL -1 and inflammation
71
Q

chronic periodontitis associated with

A

Th2 type response

72
Q

aggressive periodontitis associated with which response ?

A
  • Th1 dependent Ab production
  • high IgG2 Ab
73
Q

IgG2 Ab specific to

A

carbohydrate Ags

74
Q

IgG2 Ab production is dependent on

A

Th1-type cytokine

controlled by genetic factors

75
Q

patients with localized aggressive periodontitis (LAP) are characterized with

A

elevated levels of IgG2 Ab

76
Q

in periodontitis the generation of ___(many)____ are associated with inflammatory cell recuitment matrix destruction and bone resorption

A

lipid mediators prostaglandins

thromboxanes

leukotrienes

77
Q

resolution of inflammation via release of

A

lipoxins

resolvins

protectins

78
Q

resolution of inflammation leads to

A

tissue repair

regeneration of subgingibal microflora population

79
Q

combining what will lead to resolution of inflammation and tissue homeostasis

A

antibacterial and anti-inflammatory

80
Q

Rx for inflammation control

A

azithromycin (bacteriostatic)

anti-inlammatory and immunodulatory properties

81
Q

mechanism for Rx that resolve inflammaiton

A
  • Inhibit synthesis of reactive oxygen species and inflammatory cytokines
  • reduce the level of IL-1ß, GMCSF and prostaglandin E2
82
Q

revised treatment for management of periodontitis

A
  • inflammatory response can be controlled by mechanical debridement and adjunctive chemo
  • host immune and inflammatory reaction decrease
  • favorible genetic predispostion and absence of adverse enviornmental influence
  • infection will be contained and return toward normal commensal flora
83
Q

plausible mechanism that links periodontitis to

A
  • systemic inflammatin and disease
    • induce pregnancy complications
    • promotion of atherosclerosis
    • liver
    • gut
84
Q

induction of anti-citrullinated proteind Ab in

A

RA patients via P.gingivalis- mediated citrullination

Mandal (7 decks)

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