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perio exam 2 > pathogenesis of perio > Flashcards

pathogenesis of perio Flashcards

1
Q

inflammation

A

local response to cellular injury that marked by capillary dilation, leukocytic infiltration, redness, heat, pain

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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

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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
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4
Q

healthy stratified squamous epithelium

A
  • intact
  • no rete peg into CT
  • clinically shallow
  • few inflammatory cells, bacteria
  • tight intercellular junctions
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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
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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
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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
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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
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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
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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
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11
Q

whats an excellent predictor of perio stability?

A

absence of BOP

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12
Q

presence of BOP indicates what not what?

A

indicates local inflammation not necessarily disease progression

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13
Q

supragingival plaque is almost always present in–

A

gingivitis (calculus may or may not be present)

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14
Q

gingivitis has no evidence of?

A

radiographic evidence of bone loss

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15
Q

treatment of gingivitis

A
  • plaque control or scaling

- 50% of patients do not progress to perio

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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
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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
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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
Q

macrophages

A

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
Q

complement system

A
  • activated when pathogens evade cellular defenders
  • work with both innate and adaptive defenders to neutralize pathogens
  • lysis, opsonization, activation of inflamm response
27
Q

t cells

A

increase response of other immune cells by releasing cytokines
types: T helper, cytotoxic, suppressor

28
Q

b cells

A
  • 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
Q

which immunoglobulin is predominant in periodontal tissue?

A

IgG

30
Q

IL 1 and 6

A

increased vascular permeability, t cell and b cell activation, fever
-in chronic inflamm–stim osteoclastic activity, induces breakdown of collagen in perio

31
Q

IL-8

A

increased attraction of PMNs to infection site

-in chronic inflamm–stimulates bone resorption and CT destruction

32
Q

leukotrienes

A

facilitates leukocyte transendothelial migration and migration to infection site
-in chronic inflamm–stimulates bone resorption

33
Q

prostaglandins

A

vasodilation, fever, pain

-in chronic inflamm–stimulates bone resorption, stim collagen destruction

34
Q

TNF-alpha

A

increased vascular permeability, chemotaxis, T cell and B cell activation, fever
-in chronic inflamm–stimulates bone resorption, induces collagen breakdown

35
Q

chronic inflammation pathway

A
  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
Q

what triggers inflammation?

A

bacteria and its byproducts

37
Q

what triggers irreversible tissue destruction?

A

-host-derived pro-inflamm mediators (IL-1, 6, 8, TNF a, PGE2)

38
Q

advanced lesion

A

develops later but not always
corresponds to frank and overt periodontitis
plasma cells mostly
pocket formation, BOP, bone loss, attachment loss

39
Q

oral systemic link

A
  • diabetes
  • stress
  • obesity
  • cardiovascular conditions
40
Q

hypothesis of diabetes and periodontitis

A

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
Q

AGE-RAGE

A

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
Q

obesity with perio

A

adipocytes–> adipokines–> insulin resistence

43
Q

CRP

A
  • 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
Q

smoking and perio

A
  • 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

perio exam 2 (4 decks)

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