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Periodontology > Pathology > Flashcards

Pathology Flashcards

1
Q

Describe the disease process of gingivitis

A

Bacterial products from plaque stimulate epithelial cells to produce inflammatory mediators.
This causes fluid accumulation in tissues.
This allows neutrophils infiltrate gingival tissues.
Neutrophils release destructive enzymes and other inflammatory mediators.
These mediators cause positive feedback cycles of the disease process

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2
Q

What happens in gingivitis if plaque remains on tooth surface and the host inflammatory response continues?

A

Inflammation and destruction spreads to all periodontal structures, bone resorption = periodontitis

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3
Q

Why does bone resorption occur in periodontitis?

A

Create more room for host defence cells

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4
Q

How does the bacterial population shift from health to periodontitis?

A

From aerobic, gram positive organisms (streptococcal bacteria) to more anaerobic gram negative organisms

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5
Q

How does periodontal disease develop?

A

Change in environmental conditions causing altered microbial population
Exaggerated inflammatory response
Damage to supporting tissues of teeth

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6
Q

What do environmental changes in periodontal pockets lead to?

A

Changes in homeostasis of sub gingival microbiota
Altered gene expression

Change in microbial population = dysbiosis

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7
Q

What kind of environmental changes can occur in periodontal pockets?

A

Sustained plaque = gingival inflammation =
Increased flow of GCF - crevice becomes pockets and environment changes =
Nutrition
Temperature
pH
Oxygen and oxidation-reduction potential
Change from aerobic to anerobic

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8
Q

Why doesn’t everyone get periodontal disease?

A

Depends on genetics and risk factors e.g. smoking

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9
Q

What 3 factors contribute to periodontal disease?

A

Microbial dysbiosis, hyper-inflammatory host response and individual patients

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10
Q

How can bacteria directly cause tissue destruction? virulence factors

A

Leukocyte killing/impairment by leukotoxin (A. actinomycetemcomitans)
Impairment of PMN function
Damage to crevicular epithelium (p. gingivialis, a.a, t. denticola
Breakdown of periodontal tissues by proteolytic enzymes = nutrients for G-ve bacteria

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11
Q

Describe A.A virulence factors

A

Leukotoxin production = leukocyte killing

Damage to crevicular epithelium

Production of collagenases to breakdown periodontal tissues and providing nutrients for G-ve bacteria

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12
Q

Describe P. gingivialis virulence factors

A

Damage to crevicular epithelium

Production of collagenases and proteases

Dysregulation of cytokine network

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13
Q

What structure do G-ve bacteria contain that can cause tissue destruction?

A

LPS = endotoxin - activate complement and bone resorption

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14
Q

Describe the events when plaque accumulates in gingival margin

A

Infiltration of inflammatory cells which migrate into gingival tissues
Vasodilation and increased capillary permeability to aid this
Increased GCF
Breakdown of collagen in gingival tissue

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15
Q

How soon does an initial periodontal lesion appear after plaque accumulation?

A

24-48 hours

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16
Q

Describe events involved in an initial periodontal lesion

A

Patient would appear healthy
Localised to gingival sulcus and adjacent periodontal tissue
Vasodilation and increased vascular permeability
Increased GCF flow
Neutrophils migrate to gingival crevice
Few lymphocytes and macrophages present

17
Q

How soon does an early lesions appear after plaque accumulation?

A

4-7 days

18
Q

Describe events involved in early lesion

A

Increasing vascularity
Further increased GCF
lymphocytes and neutrophils predominantly infiltrating
Fibroblasts degenerate = more leukocyte infiltration
Collagen destruction = more space
redness of gingival

19
Q

How soon does an established lesions appear after plaque accumulation?

A

2-3 weeks

20
Q

Describe events involved in established lesion

A 
Dense inflammatory cell infiltrate = neutrophils, lymphocytes and plasma cells
Further increased GCF
More fibroblast damage
Loss of gingival collagen
NO loss of attachement
Formation of pocket
21
Q

Does an established lesion always change to advanced lesion if plaque is not disrupted?

A

No - only in susceptible patients

22
Q

Describe an advanced lesion

A

Clinical recognised as periodontitis
= pocket, loss of attachments, bone resorption, mobility

Mostly plasma cells in pocket

23
Q

What mediates the majority fo tissue destruction in periodontitis?

A

Host immune response

24
Q

How does the innate immunity contribute to periodontitis?

A

Saliva
Epithelium
Inflammatory response

25
Q

How does the innate response present in saliva?

A

Prevents drying of gignva and teeth
Anti-microbial effects -
- IgA protects mucosal surfaces and prevent adherence
- Swallowing
- Peroxidase = kills bacteria
- lysozyme and lactoferrin weaken cell wall and stop iron binding

26
Q

How does the innate response present in epithelium?

A

Physical barrier
Inflammatory response via keratinocytes
Immune response via Langerhans cells (macrophage)
High rate of turnover
junctional epithelium = leaky = release cytokines

27
Q

How does innate response present in inflammatory response?

A

Fluid component - GCF

Cellular = neutrophils and macrophages

28
Q

What does GCF contain?

A 
immune cells
Antibodies - IgG, IgA, IgM
Complement components
Enzymes
proteins that activate innate and adaptive immune response at sight of bacterial change
29
Q

List 4 inflammatory mediators

A

Cytokines
Prostaglandins
Matrix metalloproteinases
Growth factors

30
Q

Role of prostaglandins

A

Bone resorption, neutrophil chemotaxis, vascular permeability and vasodilation

31
Q

Role of matrix metalloproteinases

A

Pro-inflammatory, degrade connective tissues

32
Q

Role of growth factors

A

Growth factors from osteoblasts which regular osteoclast recruitment

33
Q

How can adaptive immune response be divided?

A 
Humoral = antibody
Cellular = lymphocytes
34
Q

Role of adaptive immune response

A

Recognition of specific microbial agents
Release of cytokines
Activation of T and B cells

35
Q

How can tissue destruction be caused indirectly by host response?

A

Humeral immunity = activation of complement and increased inflammation, recruitment of inflammatory cells and release of destructive enzymes

T killer cells

Breakdown of bone and collagen = junctional epithelium migrates down

Positive feedback cycle

Periodontology (10 decks)

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