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
2
Q
pathogens inmplicated in periodontitis
(gram-negative anaerobic)
A
- porphyromonas gingivalis
- prevotella intermedia
- bacteroides forsythus
- campylobacter restus
3
Q
pathogens implicated in periodontitis
(gram-negative facultative)
A
- actinobacilus actinomycetemcomitans (Aa)
(implicated in aggressive periodontitis)
4
Q
is plaque sufficient to develop periodontitis
A
necessary bu not sufficient
5
Q
what is the principal cause of initial inflammatory lesion leading to ginigivitis
A
bacteria
6
Q
what dictates uncontrolled inflammatory immune response driving the tissue destruction and periodontitis ?
A
the host response
(not the type of bacteria)
7
Q
ginigivitis is concdered a _____ to non-specific accumulation of ____
A
non-specific reaction, plaque
8
Q
is bacteria the major determinate of the progression of ginigivitis to periodontitis
A
nope, despite universal presence of plaque
9
Q
what is responisble for initiation of ginigivitis lesions?
A
host-parasite interaction
10
Q
bacteria respnisble for progresson to advanced periodonitis?
A
no definitive evidence
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
12
Q
what factors promote a good dingival health ?
A
- plaque reduction
- decreased inflammation
- low GCF flow
- higher eh
- mainly gram + faculative anaerobes
13
Q
what is the only etiology of periodontal disease ?
A
Bacrerial plaque
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)
15
Q
direct effects of periodontal disease
A
- invasion
- release of exotoxins
- cell constituents
- enzymes (proteases)
16
Q
indirect effects of periodontal diseases onss
A
- immunological and other host responses (destructive)
- loss of periodontal tissue
- gingiva
- periodontal ligament
- alveolar bone
17
Q
periodontitis is an
A
inflammation-based infection of the supporting supporting structures of the teeth
18
Q
two forms of periodontits occurs
A
- chronic periodontitis
- aggressive periodontitis
19
Q
periodontitis modified by systemic Diseases
A
- Chronic periodontitis
- aggressive periodontitis
- periodontitis modified by systemic diseases
20
Q
less common types of periodintitis
A
manifestation of systemic diseases
necrotizing peridontitis
21
Q
which is the most commone periodontitis in adults?
A
chronic
22
Q
chronic perioditis features
A
- can be localized or generalized
- red or purpleish tissue
- loss of attachment and bone
23
Q
which disease has severity consistent with amount of plaque?
A
chronic periodontitis
(variable microbiota)
24
Q
which disease is the plaqye not consitant with severity of the diease ?
A
aggressive periodontitis
25
aggressive periodontitis progression of the disease?
tissue destruction in rapid
(whereas chronic progression is moderate)
26
Most common baccteria associated with aggressive periodontitis
g(-) Actinobacillus actinomycetemcomintans (Aa)
27
In aggressive periodontitis there is an abnormality in
PMN function and hyperresponsive macrophages
28
what is secreted in aggressive periodontisis ?
* prostaglandins
* IL-1ß
29
What are the two forms of aggressive periodontitis ?
* Localized Aggressive Periodontitis (LAP)
* strong Ab respnose
* Generalized Aggressive periodontitis (GAP)
* poor Ab response
30
which form of periodontitis has a strong Ab response
which form of periodontitis has a weak Ab response
Localized aggressive periodontitis
generalized aggressive periodontitis
31
Localized aggressive periodontitis associated with ?
actinobacillus actinomycetemocomitas (Aa)
32
localized aggressive periodontitis is associtaed with abnormal
Neutrophil function
33
where is dectrction usuallt found in localized aggressive periodontitis?
around first molars and incisors
(preveriosly known as localized juvenile periodontitis)
34
Generalized aggressive periodontits
| (3)
* rapid attachment and bone loss
* no systemic disease
* genetic factor
35
for generalized aggressove periodontitis is the amount of destruction proportional to amount of plaque?
no
36
major virulence traits of periodontal pathogens
5
1. Proteases
2. Hemagglutinins
3. LPS
4. Fimbriae
5. Polysaccharide capsule
37
proteases
degrade host proteins disrtupt host defenses
38
P.gingivalis proteases are
Arg- and Lys- specifiv proteases
39
Hemagglutinins
responsible for bacterial biding to host cell receptors
40
P. ginigivalis hemagglutinins
HagA, HagB, HagC
41
LPS
surface Ag releative lack of endotoxicity compared to enteric LPS
42
Fimbriae
role in adherence colonization and periodontal dectruction
43
polysaccharide capsule
highly encapsulated strains inhibit phagocytosis and AC mediated cytolysis
44
Polysaccharide capsule
hihgly encapsulatd strains inhibit phagocytosis and MAC- mediated cytolysis
45
Virulent oral pathogens induce
destructive immune responses and impair protective hosot immune system
46
P.gingivalis induce
* inflammation and bleeding
* use hemagglutinins and proteases to lyse RBCs to extract nutrients for rapid growth
47
bacterial virulence overwhelms innate immune system cells
PMNs release tissue damaging substances
48
proteases degrade
serum AG
complement proteins
leukocyte-derived cytokines
49
Bacteria (Aa) enhances virulence by releaing
4
* Proinflammatory virulence factors
* peptides
* poplysaccharide Ag
* LPS
50
Aa enhacing virulence leads to
enhnaced cytokine selction
| (change in immune homeostatsis)
51
Aa produce most important secretion
leukotoxin-toxic to PMNs and monocytes
52
stains of AA can produce factors that
* inhibit PMN chemotaxis,
* resistance to phaocytosis
* inhibition of H2O2 production and killing by PMNs
53
evasion of immune components permits
pathogen and host tissue destruction
54
bacteria attract ____ to the site of infection
leukocyte to the site of infection
55
bacteria attract leukocyted directly via
bacterial peptides
56
bacteria attrat leukocytes to the site of infection indirectly via
cytokines secreted bacterial LPS binds to monocyte/macrophage via CD14 and TLR-4
57
secretion of inflammatory cytokines
IL-1ß
TNF-alpha
58
which is the main prostaglandin secreted ?
PGE2
found in high conc. on GCF
59
what is responsible for bone resorption and induction of bone destruction by P. ginigivalis infection
secretion of PGE2
| (in GCF)
60
inhibition of PGE2 production by...
NSAIDs and dexamethasone
(result= decreases loss of alveolar bone )
61
early periodontal lesion are characterized by
T cells and machrophages
| (cellular immune response)
62
established and advanced lesions contain
B cells and plasma cells
| (humoral immune response )
63
progression of lesions are controlled by
host Th cell-derived cytokines
64
cytokine patern lease to
protective immune response
alternatively a pathological/destructive response
65
early clinical gingivitis correlates with
Th1-type with IL-12 and IFN-gamma
66
Th1-typenof immune response with IL-12 and IFN-gamma
leading to macrophage activataion
increased phagocytosis and protective immunity
67
in established and advaced lesions with clinical periodontitis ...
TH2 response, production of IL-4, IL-10 and IL-13
68
TH2 response, production of IL-4, IL-10 and IL-13 leads to
Ab production
69
despite hihg conc of systemic and local Ab
periodontitis may persist and progress
70
persisting periodontitis indicates
* inappropriate production of cytokines
* over production of IL -1 and inflammation
71
chronic periodontitis associated with
Th2 type response
72
aggressive periodontitis associated with which response ?
* Th1 dependent Ab production
* high IgG2 Ab
73
IgG2 Ab specific to
carbohydrate Ags
74
IgG2 Ab production is dependent on
Th1-type cytokine
controlled by genetic factors
75
patients with localized aggressive periodontitis (LAP) are characterized with
elevated levels of IgG2 Ab
76
in periodontitis the generation of \_\_\_(many)\_\_\_\_ are associated with inflammatory cell recuitment matrix destruction and bone resorption
lipid mediators prostaglandins
thromboxanes
leukotrienes
77
resolution of inflammation via release of
lipoxins
resolvins
protectins
78
resolution of inflammation leads to
tissue repair
regeneration of subgingibal microflora population
79
combining what will lead to resolution of inflammation and tissue homeostasis
antibacterial and anti-inflammatory
80
Rx for inflammation control
azithromycin (bacteriostatic)
anti-inlammatory and immunodulatory properties
81
mechanism for Rx that resolve inflammaiton
* Inhibit synthesis of reactive oxygen species and inflammatory cytokines
* reduce the level of IL-1ß, GMCSF and prostaglandin E2
82
revised treatment for management of periodontitis
* 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
plausible mechanism that links periodontitis to
* systemic inflammatin and disease
* induce pregnancy complications
* promotion of atherosclerosis
* liver
* gut
84
induction of anti-citrullinated proteind Ab in
RA patients via P.gingivalis- mediated citrullination
