pathogenesis of perio Flashcards
1
Q
inflammation
A
local response to cellular injury that marked by capillary dilation, leukocytic infiltration, redness, heat, pain
2
Q
healthy periodontium
A
color–light pink
contour–thin, scalloped ging margins–tightly adapted to tooth–fills interproximal space
consistency–firm on palpation
texture–stippled
3
Q
unhealthy periodontium
A
- color–red to blue
- contour–ging margins become edematous–interdental papilla enlarged
- consistency–soft and friable and may become fibrotic over time
- texture–smooth
4
Q
healthy stratified squamous epithelium
A
- intact
- no rete peg into CT
- clinically shallow
- few inflammatory cells, bacteria
- tight intercellular junctions
5
Q
healthy junctional epithelium
A
- arterioles and venules form loop patterns seen along lining surfaces
- stratified, nonkeratinizing
- 2 mm x .15 mm
- hemidesmosomal attachment to tooth
- turnover q 4-6 d
6
Q
vessels of healthy perio
A
- distinct in form
- capillaries within gingiva in form of terminal loops
- afferent and efferent
- in sulcus, arranged in flat, anastomosing plexus parallel to enamel
7
Q
stage 1
A
initial lesion
- 2-4 days
- vasculitis (dilated blood vessels)
- PMNs migration into JE and sulcus (polymorphs/WBCs)
- collagen loss (perivascular)–increased ging crevicular fluid GCF flow (transudate)
- not clinically detectable
- mostly neutrophils
8
Q
stage II
A
early lesion 4-7 days -gram + aerobic microbiota -JE alteration -vascular dilation/proliferation -rete pegs formation -PMNs migration -lymphocytes (t cells) -increased fibroblast/collagen -edema
9
Q
stage III
A
established lesion
- gram + and - aerobic/anaerobic microbiota
- increased JE permeability
- PMNs + T cells (CD4/8) + B cells (IgG)
- numerous macrophages
- obvious gingivitis and BOP
- initial pocketing but NO attachment loss (CT on CEJ and epithelium on enamel)
- affects all ages
- 7-21 days
10
Q
vascular changes of inflammation
A
- normal loop patten become obliterated
- increased number and density of vessels
- pocket epithelium is ulcerated
- edema increases hydrostatic pressure within gingiva-therefore, it bleeds spontaneously or upon stim
11
Q
whats an excellent predictor of perio stability?
A
absence of BOP
12
Q
presence of BOP indicates what not what?
A
indicates local inflammation not necessarily disease progression
13
Q
supragingival plaque is almost always present in–
A
gingivitis (calculus may or may not be present)
14
Q
gingivitis has no evidence of?
A
radiographic evidence of bone loss
15
Q
treatment of gingivitis
A
- plaque control or scaling
- 50% of patients do not progress to perio
16
Q
components of advanced lesion (perio)
A
- G+
- G -
- leukocyte wall
- hyperplastic ep
- PGE2
- IL1 beta
- TNF alpha
- IL 6
- MMPs
- CT
- macrophages and lymphocytes
17
Q
advanced lesion/periodontitis
A
- mostly gram - anaerobic
- apical proliferation of JE, ulceration of lining
- predominance of plasma cells, possible copious exudate flow
- further loss of collagen, altered fibroblasts
- perio pocket
- sig pocketing, CAL, and bone resorption
- periods of quiescnece/exacerbation
18
Q
periodontal pocket
A
pathologically deepened sulcus
19
Q
gingival pseudo pocket in periodontitis
A
formed by gingival enlargement without destruction of underlying tissues
20
Q
periodontal defects in periodontitis
A
- suprabony: bottom of the pocket is coronal to underlying alveolar bone. Bone loss is horizontal
- infrabony: bottom of the pocket is apical to the level of the adjacent alveolar bone. Bone loss is vertical
21
Q
periodontits results when what
A
rate of breakdown exceeds rate of repair
22
Q
what migrates to the site of infection in periodontitis?
A
PMNs–large white blood cells with high amounts of collagenase
- collagenase destroys tissue
- mediators (IL-1beta) activate more white blood cells to enter area of infection and activate bone destroying cells
23
Q
most of the destructive collagenase that breaks down tissues and bone comes from what?
A
infiltrating cells–PMNs
24
Q
PMNs
A
- neutrophils/first responders
- first at site
- multilobulated
- short-lived cells
- pus formed at site of infection is filled with dead or dying neutrophils
- effectively phagocytoses most periodontal pathogens
25
macrophages
the big mac
- one lobed kidney shaped nucleus
- delayed arrival
- long lived and most numerous in chronic inflamm
- highly phagocytic
- coordinates immune response with T-lymph in chronic inflamm
26
complement system
- activated when pathogens evade cellular defenders
- work with both innate and adaptive defenders to neutralize pathogens
- lysis, opsonization, activation of inflamm response
27
t cells
increase response of other immune cells by releasing cytokines
types: T helper, cytotoxic, suppressor
28
b cells
- antibody production (principle function)
- stimulate immature B cells to differentiate into plasma cells
- opsonization--coat bacteria to make it more sus to phagocytosis by PMNs or macrophages
- activating complement system
- 5 major types of antibodies --IgG, IgM, IgA, IgD, IgE
29
which immunoglobulin is predominant in periodontal tissue?
IgG
30
IL 1 and 6
increased vascular permeability, t cell and b cell activation, fever
-in chronic inflamm--stim osteoclastic activity, induces breakdown of collagen in perio
31
IL-8
increased attraction of PMNs to infection site
| -in chronic inflamm--stimulates bone resorption and CT destruction
32
leukotrienes
facilitates leukocyte transendothelial migration and migration to infection site
-in chronic inflamm--stimulates bone resorption
33
prostaglandins
vasodilation, fever, pain
| -in chronic inflamm--stimulates bone resorption, stim collagen destruction
34
TNF-alpha
increased vascular permeability, chemotaxis, T cell and B cell activation, fever
-in chronic inflamm--stimulates bone resorption, induces collagen breakdown
35
chronic inflammation pathway
1. invasion of pathogens into tissue
2. acute inflamm
3. persistent bacterial infection longer than 2 weeks
4. chronic inflammation
5. exaggerated host inflamm response
36
what triggers inflammation?
bacteria and its byproducts
37
what triggers irreversible tissue destruction?
-host-derived pro-inflamm mediators (IL-1, 6, 8, TNF a, PGE2)
38
advanced lesion
develops later but not always
corresponds to frank and overt periodontitis
plasma cells mostly
pocket formation, BOP, bone loss, attachment loss
39
oral systemic link
- diabetes
- stress
- obesity
- cardiovascular conditions
40
hypothesis of diabetes and periodontitis
hyperglycemia and hyperlipidemia result in metabolic alterations, which may exacerbate bacteria induced inflamm perio--> advanced glycated endproducts--receptor for advanced glycated end products (AGE-RAGE interaction)
41
AGE-RAGE
AGE: accumulate during normal aging but accelerates with DM
RAGE: receptor for advanced glycation endproducts: member of IG fam and present in increased levels on cells in DM like fibroblasts, endothelial cells, and monocytes
-activates NF-KB pathway which increases transcription of proinflamm mediators
42
obesity with perio
adipocytes--> adipokines--> insulin resistence
43
CRP
- C-reactive protein
- liver-produced, non-specific acute phase reactant that serves as a systemic marker of inflamm
- elevated in ischemia and myocardial infarction
- elevated in perio disease
- reflects amount of inflammation in your body
- elevated CRP is a direct risk for CVD
44
smoking and perio
- microbiologic differences
- impairs innate and immune response
- neutrophil migration and chemotaxis are negatively affected
- gingival and perioodntal ligament fibroblast recruitment may be negatively affected in smokers
- collagen production is decreased while collagenolytic activity increased
