histo/pathogensis of perio diseas :) Flashcards

1
Q

normal periodontoum

A

bone
PDL
Gingiva
cementum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what lines the root surace

A

cementum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

gingival epithelium histology

A

long rate ridges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

junctional epithelium

A

thinner and more porous
forms barrier against dentinal plaque
attaches at the CEJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

healthy periodontium

A

junctional epithelium attaches at the ACJ

PDL attaching to alveolar bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

protective features of the host against PDD

A

barrier effect of intact junctional epithelium
factors in saliva
gingival crevicular
activation of T/B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

gingival crevicular fluid

A

originates from gingival capillaries

contains neutrophils and complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

risk factors of PDD

A

poor oral hygiene
smoker
genetic
systemic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

gingivitis symptoms

A
vasodilation
increased blood flow
damage to fibroblasts
oedema
increase in crevicular fluid
still in tact at ADJ
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

histological changes at gingivitis

A
hyperplasia of JE
increased inflammatory cells
no migration of JE or bone loss
increased blood flow
loss of gingival collagen fibres 
development of deeper rate ridges
more inflammatory cells
junctional epithelium still attaches to ADJ
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

clinical changes of gingivitis

A

bleeding on probing
false pocketing
pain, redness, swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

pre disposing factors to gingivitis

A
  • Pregnancy/puberty
  • Orthodontic appliances
  • Dentures
  • Restorations with overhangs
  • Effects of medications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

periodontist symtoms

A

JE has moved apically
plaque has moved more apically bone loss
more inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

clinical changes of periodontitis

A
tooth mobility 
true pocket over 4mm
bleeding on probing
recession 
tooth loss
halitosis
calculus 
junctional epithelium may ulcerate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

periodontisis histology

A

junctional epithelium ends more apically than at ADJ
true pockett formed
more inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

BPE scoring

A

code 0-4

* furcation involvement

17
Q

where can growth of plaque be

A

supra or sub gingival

18
Q

what is growth on the tooth called

A

biofilm

19
Q

what is a biofilm

A

3D structure of heterogenous bacterial and the material produced as a product of growth

20
Q

subginigval plaque

A

heterogenous
firmly attached bacteria at tooth surface
many different cocci and bacilli
channels can run in the 3D structure allowing nutrients to flow

21
Q

bacteria in a periodontal pocket

A

contains mainly gram positive Layer attached to hard tissue
overlying gram - layer
many motile and anaerobic bacteria

22
Q

progression to periodontist

A

not always precede by gingivitus

early lesion can take many years to progress to advanced lesion, signifies change from gram + to gram - bacteia

23
Q

what changes a quiescent site to an active one

A

change in host

change in microbial challenge

24
Q

dysbiosis

A

healthy to disease

25
Q

what do gram - and aerobic bacteria produce

A

short fatty acids

26
Q

keystone pathogens

A

red complex bacteria can alter the community to move it to a disease causing community
produce virulence factors

27
Q

what do the red complex bacteria do

A

produce virulence factors
change in complement levels changes immune repsonce
bacteria grow, leading to more inflammation

28
Q

rapidly processing periodontal disease

A

produces LtA leukotoxin that targets neutrophils

CDT toxin that targets epithelial cells

29
Q

acute necoritising ulcerative gingivitis

A

true infection with tissue invasion

associated with identifiable predisposing factors

30
Q

what causes acute necrotising ulcerative gingivitis

A

small selection of specific bacteria by host derive nutrients
fuso-spirochaetal complex

31
Q

pathogenic community at host interface

A

removes sugars from human cells
cytokines being produced by antigens produced by bacteria
community stick together, communicate with each other
produce different virulence factors

32
Q

what are all the community pathogenic factors leading to a disease community

A
  • LPS and capsule
  • fibronectin
  • toxins
  • anaerobic growth proceeds butyric acid
  • phospholipase digests lipids, glucosidases digest glycoproteins removing sugar so organisms can grow
33
Q

what do LPS and capsule do to contribute to the disease coomunit

A

cause immune responce stimulating cytokine production

34
Q

what does fibronectin do in contributing for community pathogenic factors

A

allows sticking to surfaces