PAP 6 - Pathogenesis of periodontal disease 1

Question 1

what is the primary cause of gingivitis and periodontitis?

Answer 1

plaque-induced inflammation

Question 2

what makes gingivitis different to periodontitis?

Answer 2

• There is no Loss of Attachment (LOA).
• The pockets are false pockets.
• This condition is reversible

Question 3

what makes periodontist different to gingivitis?

Answer 3

• There is Loss of Attachment (LOA)*.
• The pockets are true pockets.
• This condition is irreversible

Question 4

what can LOA also be called?

Answer 4

Clinical Attachment Loss (CAL)

Question 5

what are the 2 purposes of the host response to the plaque biofilm (inflammatory and immune) ?

Answer 5

1. Protection of the host against local microbial attack

2. Prevention of spread of micro-organisms beyond the immediate target attack site

Question 6

Is the host response beneficial?

Answer 6

The host response is not entirely beneficial

Question 7

why is the host response not entirely beneficial?

Answer 7

Majority of the LOA/bone loss in periodontitis is due to the host response (inflammatory/immune response) to the invading bacteria (by standard damage)

Question 8

what is the relationship of the host response?

Answer 8

There is a balance between the response being beneficial or destructive (if hyper responsive)

Question 9

what is the gradual breakdown theory?

Answer 9

periodontitis, once established, progressed continuously and inevitably with a simple straight line correlation
(not accurate)

Question 10

how was gradual breakdown theory supported?

Answer 10

supported by clinical studies which reduced measurements of probing depth or bone loss to average values for a given mouth

Question 11

what did the gradual breakdown theory eliminate?

Answer 11

intra-oral variation and obscured both sites with little/no disease and sites with more advanced disease

Question 12

what findings supported belief in a straightforward age-correlated linear progression (gradual breakdown theory)?

Answer 12

Epidemiological studies on various population groups also used average values for the different age groups

Question 13

what is the burst theory?

Answer 13

More recent longitudinal studies using detailed individual measurements of LOA at specific sites over 2-5 years contradicted the idea of continuous and inevitable disease progression

Question 14

what 3 things did the burst theory indicate?

Answer 14

• Gingivitis, even when persistent and untreated does not inevitably progress to periodontitis.
• Periodontal destruction is not continuous but progresses in a site-specific, episodic manner with ‘bursts’ of destructive activity alternating with periods of quiescence and possible repair. This is ‘BURST THEORY’ advocated by Socransky.
• There is great individual variation in the pattern of destruction, which also varies over time in the same individual

Question 15

when do these bursts occur (burst theory)?

Answer 15

• These bursts may occur randomly throughout an individual’s life (random burst)
• there may be periods when bursts of periodontal breakdown in many sites are more likely (asynchronous multiple burst)

Question 16

what does the burst theory concept suggest?

Answer 16

This concept suggests that periodontitis progression may be totally unpredictable

Question 17

In all the studies of burst theory, what was used?

Answer 17

manual periodontal probes

Question 18

what are the problems of manual periodontal probes?

Answer 18

• These are relatively inaccurate and have relatively poor reproducibility.
• They can only detect fairly large changes (2.5mm-3mm) in attachment level.
• Smaller changes cannot be reliably detected

Question 19

what could manual robes detect?

Answer 19

Could detect the site-specific, episodic disease progression where a small number of sites showed a relatively large LOA over a period of time (rapidly progressive attachment loss ie. RAL)

Question 20

what were manual oboes not accurate enough to pick up?

Answer 20

Other patterns such as slow regular progression (gradual attachment loss ie. GAL)

Question 21

why are electronic probes more accurate?

Answer 21

-reliably and accurately pick up changes of 0.3-0.8mm in attachment level
-remove the human actors which lead to inconsistencies :
>constant pressure set by the probe/computer
>measurements are automatic and not judged by human eye
-can detect both RAL and GAL

Question 22

what are the results from using electronic probes?

Answer 22

-results indicate that RAL, progressing by ‘bursts’ and GAL occur during the progression of Periodontitis

Question 23

what can GAL result from?

Answer 23

small ‘mini- bursts’ of activity (LOA of <0.5mm) or slow progressive LOA or both

Question 24

how will patients tend to progress who have high susceptibility?

Answer 24

Progress more by burst of RAL

Question 25

how will patients tend to progress who have low susceptibility?

Answer 25

progress more slowly & gradually with GAL

Question 26

what can modify/ increase the rate of progression of periodontitis?

Answer 26

• High genetic susceptibility
• smoking
• uncontrolled diabtetes
• immunodeficiency
• presence of virulent bacteria
• overhanging restorations / fillings
• alcohol
• stress

Question 27

What is the different between the look of ‘pristine’ and ‘clinically healthy’ gingiva?

Answer 27

• both look virtually the same

- more likely to see the free gingival groove clinical in pristine health

Question 28

what does ‘pristine’ gingiva look histologically?

Answer 28

Has little or no inflammatory infiltrate in the connective tissue. (Difficult to achieve)

Question 29

what does ‘clinically healthy’ gingiva look histologically?

Answer 29

-Gingiva does have an inflammatory infiltrate in the connective tissue. Seen in patients regularly practising good plaque control.
( Always plaque bacteria & their products in the gingival crevice)

Question 30

what are the actions of inflammatory cells in ‘clinical healthy’ gingiva?

Answer 30

• Has a definite infiltrate of inflammatory cells (mainly neutrophils) which occupy approximately 3-5% of the connective tissue in contact with the junctional epithelium (JE).
• These cells continuously migrate (chemotaxis) through the JE into the gingival sulcus to combat plaque micro-organisms
• Gingival Crevicular Fluid (GCF) flows into sulcus

Question 31

what does GCF contains?

Answer 31

Various components of blood and cells :
-various plasma proteins
-Defence cells/proteins:
>neurophils 
>antibodies 
>complement

Question 32

how much is the volume/ flow of GCF in gingival health?

Answer 32

very small

Question 33

Describe the defence in ‘clinically healthy’ gingiva during the outward flow of GCF.

Answer 33

• Killing of micro-organisms by inflammatory & immune cells.
• Shedding of organisms by desquamating epithelial cells.
• Destruction of micro-organisms by immunoglobulins &/or activation of the complement system.
• Normal flora restricts micro-organisms growth.

Question 34

what are the 4 changes of health to disease?

Answer 34

1. Increased GCF flow
2. Increase in inflammatory & immune cellular infiltrate in the connective tissue underlying Junctional Epithelium (JE).
3. Fewer fibroblasts in the gingival connective tissue underlying the JE.
4. Reduction in the collagen content of infiltrated connective tissue under the JE

Question 35

Describe the changes from healthy to disease : crevicular leukocytes and GCF production.

Answer 35

GCF volume/flow great increase in periodontal disease which is associated with a corresponding increase in the number of neutrophils (PMNs) in the gingival crevice/pocket

Question 36

what is periodontal disease associated with?

Answer 36

A significant increase in the inflammatory & immune cell infiltrate in the gingival connective tissue underlying the Junctional Epithelium (JE)