W4 Biofilm

Question 1

What are the characteristics of bacteria?

Answer 1

Fimbriae: hair like structures

Capsule: protection against phagocytosis

Peptides: Induce inflamation.

Exotoxins: damage host immune cells

Enzymes: damage host protein acquisition of nutrients

Question 2

How do you classify bacteria?

Answer 2

Gram staining: Positive and negative Positive, purple, thick peptidoglycan Negative, red, thin layer of peptidoglycan on the

Cell morphology: cocci, bacilli, spirilla

Motile vs non-motile

Relationship with Oxygen to sustain life, will affect sub/supra

Question 3

What are the stages of biofilm formation?

Answer 3

Acquired pellicle Associated/Adhesion: Coaggregation/Multiplycation Microcolony Formation Maturation & Dispersal

Question 4

Describe Association

Answer 4

Within a few hours after pellicle formation, bacterial associate loosely with the acquired pellicle , fibriae.

Question 5

Describe Adhesion

Answer 5

Some bacteria have surface molecules called adhesions that bind to pellicle receptors that aid in stronger attachment. Early colonisers

Question 6

What is the acquire pellicle?

Answer 6

Made from saliva that consists of glycoproteins & antibodies. It can facilitate adhesion of platonic bacteria

Question 7

Describe Coaggregation

Answer 7

Secondary colonizers: not random, bacteria have specific coaggregation partners, important in biofilm development

Question 8

Describe multiplication

Answer 8

Multiplication of attached micro-organisms

Question 9

Describe Microcolony Formation

Answer 9

Attachment of Fusobacterium Nucleatum coaggregates with initial, early and late colonizers, acts at the bridge. → Coaggregation of Late Colonizers Gram negative species (rods, cocci, spirochetes) pathogenic species

Question 10

Describe Maturation and Dispersal

Answer 10

Bacteria proliferate and begin to grow away from the tooth surface in mushroom-shaped microcolonies. Allows coaggregation of Periodontal pathogens

Question 11

What bacteria cause caries?

Answer 11

Streptococci Mutans: S.mutans and S. sobrinus - which are faculative anaerobe and gram positive

Lactobacilli - facultative anaerobe, gram positive. Both are acidogenic and produce lactic acid. Thrive in low pH

Question 12

What causes periodontal pathogens?

Answer 12

Porphyromonas gingivalis: obligate anaerobes promotes inflammatory response in phagocytic cells.

Fusbacterium Nucleatum: Anaerobe, activates inflammatory pathway in epithelial cells,

Tannerella Forsythia: most significant risk factor

Spirochetes Aggregatibacter: strongly associated with aggressive tissue destruction characteristic of disease

• Prevotella Intermedia*
• Treponema denticola*

Question 13

What Socranskys colours are related to health?

Answer 13

Yellow and green

Question 14

What Socranskys colours are associated with periodontal disease?

Answer 14

Orange and red

Question 15

What are the benefits for bacteria living in a plaque biofilm?

Answer 15

Protection and resistance from the host defence mechanism Protection and resistance from anti microbial agents

Question 16

What are the benefits of the Supragingival Environment?

Answer 16

Avaliable nutrients (dietry carbs) Salivary glycoproteins pH (aerobic initially)

Question 17

What are the benefits of Subgingival environment?

Answer 17

Available nutrients comes from gingival crevicular fluid Little to no saliva Periopocket depth

Question 18

What is the enamel caries zone?

Answer 18

4 zones,

1. Translucent zone (porosity 1%)
2. Dark zone (porosity 2-4%)
3. Body of lesion (porosity 25%)
4. Surface zone (relatively unaffected)

Question 19

What is the first zone to be affected by enamel caries?

Answer 19

Surface Zone - not always present the superficial, relatively unaffected

Question 20

What is reactionary/reparative dentine?

Answer 20

Bacterial by products reaching tubules triggers its synthesis

Question 21

What is sclerotic dentine?

Answer 21

Sclerotic dentine shows occluded tubules wih a thich peritubular layer and a calcified tubular lumen that contains minerals

Question 22

What are dead tracts?

Answer 22

Due to tubular occlusion within the sckerotic zone and retraction of the odontoblastic cellular processes, the dentinal tubules in the dead-tract zone appear empty and cut off from the living odontoblast

Question 23

Define the zone of demineralization

Answer 23

AFFECTED:Clinically referred to as affected dentine. It is caused by the diffusion of bacterial acids into dentine, contains less mineral that sclerotic dentine, becomes stained and progressively more stained (darkbron) leather and hard in texture

Question 24

Define the zone of demineralization

Answer 24

AFFECTED:Clinically referred to as affected dentine. It is caused by the diffusion of bacterial acids into dentine, becomes stained and progressively more stained (darkbrown) leather and hard in texture

Question 25

Define the Zone of penetration

Answer 25

INFECTED:Referred to clinically as infected dentine. Occurs after cavitation permits direct bacterial invasion; appears clinically soft, yellow-brown mass of cheesy texture.

Question 26

What is pulpal inflammation?

Answer 26

The progressing carious lesion triggers an inflammatory pulpal reaction due to the permeability of dentine ti soluble products of bacteria. Lymphocytes, macrophages and plasma cell early response. It may be reversible. Odontoblasts stimulated to synthesis tertiary dentine.

Question 27

What happens once caries lesion has progressed to secondary dentine or pulp cavity’?

Answer 27

Large inflammatory response will take place and production of acute inflammatory cells mostly neutrophils in the tissue beneath the lesion. Lysosomal enzymes discharged by the neutrophils result in wide spread tissue damage and suppuration

Question 28

What are the stages of disease pathogenesis?

Answer 28

Kiane and Lindhe.

1. Clinical healthy
2. Normal healthy gingiva
3. Early gingivitis
4. Established gingivitis
5. Periodontitis

Question 29

What should normal healthy gingiva look like?

Answer 29

Histological inflammation signs appear within 4 days of plaque accumulation, it is not clinically visible.

Sucular and Junctional are immunologically active sensors of plaque biofilm, epithelium has receptors that recognise pathogens and release chemical mediators to initiate immune response.

Tight epithelial cell junctions act as a physical barrier to bacterial invasion.

Question 30

What are the signs of early gingivitis?

Answer 30

Approx after 7 days of plaque accumulation an inflammatory infiltrate of leukocytes develops at sight of initial lesion.

Cytokines result in destruction of collagen. Biochemical mediators are released - clinical signs of redness and swelling

Question 31

What are the signs of established gingivitis?

Answer 31

After 2-3 weeks of plaque accumulation the early lesion evolves into an established lesion.

↑ size of affected area lots of plasma cells and lymphocytes. Macrophages and lymphocytes are most numerous in CT, Neutrophil infiltration into the sulcus. Gingival sulcus deepens, ↑ probing depth redness and swelling

Question 32

What are the signs of periodontitis?

Answer 32

Plaque biofilm grows along the root surfac, changes marked by T-cell to B-cell predominance, accompanied by destruction of CT, apical migration of epithelial attachment.

Clinical sings include periodontal pocket formation, surface ulceration suppuration, destruction of alveolar bone, tooth mobility, drifting and tooth loss

Question 33

On a cellular level what is periodontitis?

Answer 33

Chronic inflammation results in sustained overproduction of pro-inflammatory biochemical mediators

Cytokines: recruit cells to the infection site

Matrix metalloproteinases: over production break down CT and collagen

Prostoglandins: trigger osteoclasts to destroy crest of alveolar bone