Pathology

Question 1

Describe the disease process of gingivitis

Answer 1

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

Question 2

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

Answer 2

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

Question 3

Why does bone resorption occur in periodontitis?

Answer 3

Create more room for host defence cells

Question 4

How does the bacterial population shift from health to periodontitis?

Answer 4

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

Question 5

How does periodontal disease develop?

Answer 5

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

Question 6

What do environmental changes in periodontal pockets lead to?

Answer 6

Changes in homeostasis of sub gingival microbiota
Altered gene expression

Change in microbial population = dysbiosis

Question 7

What kind of environmental changes can occur in periodontal pockets?

Answer 7

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

Question 8

Why doesn’t everyone get periodontal disease?

Answer 8

Depends on genetics and risk factors e.g. smoking

Question 9

What 3 factors contribute to periodontal disease?

Answer 9

Microbial dysbiosis, hyper-inflammatory host response and individual patients

Question 10

How can bacteria directly cause tissue destruction? virulence factors

Answer 10

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

Question 11

Describe A.A virulence factors

Answer 11

Leukotoxin production = leukocyte killing

Damage to crevicular epithelium

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

Question 12

Describe P. gingivialis virulence factors

Answer 12

Damage to crevicular epithelium

Production of collagenases and proteases

Dysregulation of cytokine network

Question 13

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

Answer 13

LPS = endotoxin - activate complement and bone resorption

Question 14

Describe the events when plaque accumulates in gingival margin

Answer 14

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

Question 15

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

Answer 15

24-48 hours

Question 16

Describe events involved in an initial periodontal lesion

Answer 16

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

Question 17

How soon does an early lesions appear after plaque accumulation?

Answer 17

4-7 days

Question 18

Describe events involved in early lesion

Answer 18

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

Question 19

How soon does an established lesions appear after plaque accumulation?

Answer 19

2-3 weeks

Question 20

Describe events involved in established lesion

Answer 20

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

Question 21

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

Answer 21

No - only in susceptible patients

Question 22

Describe an advanced lesion

Answer 22

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

Mostly plasma cells in pocket

Question 23

What mediates the majority fo tissue destruction in periodontitis?

Answer 23

Host immune response

Question 24

How does the innate immunity contribute to periodontitis?

Answer 24

Saliva
Epithelium
Inflammatory response

Question 25

How does the innate response present in saliva?

Answer 25

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

Question 26

How does the innate response present in epithelium?

Answer 26

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

Question 27

How does innate response present in inflammatory response?

Answer 27

Fluid component - GCF | Cellular = neutrophils and macrophages

Question 28

What does GCF contain?

Answer 28

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

Question 29

List 4 inflammatory mediators

Answer 29

Cytokines Prostaglandins Matrix metalloproteinases Growth factors

Question 30

Role of prostaglandins

Answer 30

Bone resorption, neutrophil chemotaxis, vascular permeability and vasodilation

Question 31

Role of matrix metalloproteinases

Answer 31

Pro-inflammatory, degrade connective tissues

Question 32

Role of growth factors

Answer 32

Growth factors from osteoblasts which regular osteoclast recruitment

Question 33

How can adaptive immune response be divided?

Answer 33

``` Humoral = antibody Cellular = lymphocytes ```

Question 34

Role of adaptive immune response

Answer 34

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

Question 35

How can tissue destruction be caused indirectly by host response?

Answer 35

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