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Plaque Related Disease > Pathogenesis Of Periodontal Disease > Flashcards

Pathogenesis Of Periodontal Disease Flashcards

1
Q

What is the muco gingival complex made up of?

A

Gingival sulcus
Gingival epithelium
Junctional epithelium
Collagen fibres

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2
Q

How can gingivitis be classified?

A

No LOA
pockets are false- JE remains at ACJ
Condition is reversible

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3
Q

How can periodontitis be classified?

A

LOA
true pocketing
Condition is reversible

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4
Q

What is the role of the host response

A

Protects the host against local attack
Prevent spread of micro organisms beyond immediate target site

Can cause a lot of the damage seen in gingivitis and periodontitis

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5
Q

Describe the 3 main points re. The new approach

A

Gingivitis, even when persistent and untreated does no inevitably progress to periodontitis

Perio destruction is not continuous but progresses in site specific manner with bursts of destruction

There is great individual variation in pattern of destruction

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6
Q

According to the burst theory, what do patients with high susceptibility suffer from re. Attachment loss?

A

Rapid attachment loss

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7
Q

According to the burst theory, what do patients with low susceptibility suffer from re. Attachment loss?

A

Gradual attachment loss

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8
Q

What are the main risk factors re. Perio disease?

A 
High genetic susceptibility 
Smoking
Uncontrolled diabetes
Immunodeficiency 
Presence of virulent bacteria
Overhanging restorations
Acohol
Stress
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9
Q

What can be seen in clinically healthy gingivae

A

PMNs and GCF present in small volumes

These flow into sulcus to combat plaque organisms

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10
Q

Describe features of gingival crevicular fluid

A

Contain neutrophils, antibodies and complement
Produced from post capillary venules of dentine gingival plexus
In health, volume very small

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11
Q

Describe what happens in defence in clinically healthy gingivae

A

Outward flow of GCF
microorganisms killed by PMNs and antibodies
Shedding of pathogenic organisms by des quarantine epithelial cells
Destruction of pathogens by activation of complement
Normal flora restricts micro organism growth

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12
Q

What changes occur re. Health to disease?

A

Increased GCF flow
Increased inflammatory and immune cell infiltrate in connective tissue under JE
fewer fibroblasts in connective tissue under JE
Reduction in collagen content of connective tissue under JE

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13
Q

Who classified progression of gingival and periodontal inflammation

A

Page and Schroeder 1976

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14
Q

What were the 4 classifications of progression

A

Initial
Early
Establish
Advance - lesion

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15
Q

Describe the initial lesion

A 
Associated with early gingivitis
24-48 hours of plaque accumulation 
Gram +be aerobic and saccharolytic 
Increased GCF
Vasodilation minimal tissue damage
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16
Q

Describe the early lesion

A 
After 1 week
ig production
Increased size of PMNs and lymphocytes 
Retreat peg formation in JE 
Gingival swelling
Favours growth of gram -eV
17
Q

Describe the established lesion

A 
Associated with chronic gingivitis
JE replaced with pocket epithelium 
Although not attached to tooth- no LOA 
increased PMNs and complement. 
Loss of collagen
18
Q

Describe the advanced lesion

A

Associated with periodontitis
Ulceration and apical migration of JE
breakdown of PDL fibres
Growth of GNABs

19
Q

Describe how apical migration of JE is possible

A

Damage to the PDL fibres bellwether the JE allows epithelium to migrate into the space
Damage to underlying connective tissue results in inability to regulate apical migration of tissues

20
Q

Describe how breakdown of PDL occurs

A

Loss of collagen fibres inserting into bone and cementum
Damage to fibroblasts
Increased host factor in PDL causes damage to connective tissues
Increased bacterial penetration into PDL causes tissue damage

21
Q

Describe how resorption of alveolar bone occurs

A

Osteoclastic activity
Host derived resorption factors present in gingival tissues in periodontitis
Potent bone resourcing factors produced are
Prostaglandin E2
Interleukin 1

Plaque Related Disease (18 decks)

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