Aetiology & Pathogenesis of periodontal disease Flashcards
(87 cards)
1
Q
Which % of patients will have perio?
A
40%
2
Q
What two things need to be done before treating a perio patient in the PDH?
A
- Take radiographs
- Have good plaque scores
3
Q
What are the two things that cause perio?
A
Inherited (particularly more aggressive)
Behavioural (smoking)
4
Q
What are the two main stages of perio progression?
A
- Decreased host resistance (e.g. stress etc)
- Increased microbial activity (particularly virulent strains)
5
Q
What will happen if you treat a patient with a high plaque score?
A
Perio treatment will not succeed!!
6
Q
Why do we disclose?
A
To show plaque visually
7
Q
What is the probing pocket depth?
A
The distance from the gingival margin to the location of the tip of a periodontal prove inserted in the pocket with moderate probing force
8
Q
What does PAL stand for?
A
Probing attachment level
9
Q
What does CAL stand for?
A
Clinical Attachement level
10
Q
What is the PAL/CAL measurement?
A
The distance from the amelocemental junction to the botton if the pocket (recession + pocket depth)
11
Q
What is the recession measurement?
A
The distance from the amelodentinal junction to the gingival margin
12
Q
What does stippled mean?
A
icroscopic elevations and depressions of the surface of the gingival tissue due to the connective tissue projections within the tissue
13
Q
What are the 6 key features of healthy gingivae?
A
- Triangular interdental papilla
- Knife edged margin
- Stippled gingivae
- pink
- firm
- no bleeding
14
Q
What is the name of this junction?
A
Mucogingival junction
15
Q
What is free mucosa more prone to than attached?
A
Trauma
16
Q
What is the rate of turnover for epithelial cells in the mouth?
A
8-10 days
17
Q
Why is there permenantly a slight level of inflammation of the gingivae even in health?
A
The tissues are constantly being exposed to bacteria
18
Q
What is gingivitis?
A
Reversible inflammation of the gingivae (/the gingival crevice)
19
Q
What are the 7 clinical signs of gingivitis?
A
- Redness (starts at papillae and progresses along the gingival margin) = associated with plaque build up
- Loss of stippling
- Surface smooth and glossy
- Swelling (tissues become softer and depress on touch)
- Rolling of the gingival margin = bulbous areas between teeth
- Loss of triangular shape of the interdental papillae
- Bleeding on gentle probing
20
Q
In gingivitis is the junctional epithelium still attached?
A
Yes
21
Q
What is the histopathology of plaque induced gingivitis (4)?
A
- Increased gingival crevicular fluid
- Increased vasodilation and capillary permeability
- Collagen breakdown
- More inflammatoru cells (difficult to fight bacteria in plaque as most is not in tissue!)
22
Q
What is periodontitis?
A
Inflammation of tissues supporting the teeth (i.e. gingivae, periodontal ligament & alveolar bone)
= progressive destruction = loss of junctional epithelium, periodontal ligament, alveolar bone and eventually the teeth (irreversible)
23
Q
Following periodontitis what type of epithelium does the junctional epithelium become?
What are the properties of this?
A
‘long’ junctional epithelium
more friable and likely to break down
24
Q
What is the classification system for Periodontal disease?
A
Armitage
(no clear system on clinic)
25
What impact does smoking have on developing periodontistis?
Increases likelihood of having periodontal disease (it is also more likely to be severe)
26
What is another chronic inflammatory disease associated with periodontal disease?
Diabetes
27
What is the key difference between gingivitis and periodontitis?
Loss of attachement (junctional epithelium)
= bacteria ingress onto root surface
28
What are the different types of periodontitis?
General/local
Chronic (abscess)/Acute (necrotising)
Systemic disease assocated
Localised Agressive
29
What are the clinical signs of periodontitis (9)?
* Some/all signs of gingivitis
* True pocketing on probing (loss of attachement & periodontal pocket)
* Recession (root exposure)
* Suppuration (pus)
* Mobility above physiological levels
* Drifiting of teeth
* Exposure of furcations (root split = difficult to keep clean = faster progression)
* Bone loss (radiographic evidence)
* Loss of interdental papillae (black triangles)
30
What is the problem with supra-gingival calculus?
Bacteria cling to it more easily
(does not cause periodontal disease)
31
Why does subgingival calculus often look darker than supra-gingival calculus?
Picks up haemantic staining (from blood) = brown/green tinge
32
Is subgingival calculus often bigger or smaller than supragingival calculus?
Smaller
33
Why must you make sure a probe is at the right angle when measuring pocket depth?
Different angles give different readings
34
Why in disease is a probe more likely to pass through tissue?
It is more friable = more susceptible to break down
35
Is attachment loss the same as pocket depth?
No, it can be either bigger or smaller
36
Which do we measure...
Pocket depth or attachement loss?
Pocket depth
37
What is supuration?
Pus
38
Which % of the population with chronic periodontitis have mild perio?
8.5%
39
Which % of the population with chronic periodontitis have moderate perio?
30%
40
Which % of the population with chronic periodontitis have severe perio?
8.5%
41
Which % of the whole population have aggressive periodontitis?
1%
42
Which populations are more susceptible to aggressive periodontitis?
* North American and European caucasian (0.1%)
* African americans (2.5%)
* South Americans (3.7%)
* African (6%)
43
Is severe periodontal disease acute or chronic?
Chronic (slowly developing)
44
At which age does severe periodontal disease usually show itself?
Mid to early life
45
What is the relationship between severity of periodontal disease and progression?
More severe = more rapid progression
46
What is the relationship between severity of periodontal disease and number of missing teeth?
More rapid progression/severe = more teeth lost
47
What is the relationship between severity of periodontal disease and age?
Likely to get worse with age (and higher % have periodontal disease in the older populations)
48
What is aetiology?
What causes a disease
49
What is pathogenesis?
How do factors causes the disease
50
Can you get periodontal disease without bacteria?
No
Germ free mice have no periodontitis
51
Roughly how many bacterial species are known to colonise the periodontium?
400-500
52
What is the specific plaque hypothesis?
Specific micro-organsism are neccessary for the development of periodontal disease
e.g.
Localised aggressive periodonitis -\> Aggregibacter actinomycecomitans (Aa)
Generalised aggressive periodontitis -\> Porphomonas gingivalis (Pg)
n.b. also found in non disease sites
53
What is the non specific plaque hypothesis?
Disease results from sheer mass of pathogens
(not entirely true)
54
What is the environmental plaque hypothesis?
Pathogenic species are required in sufficient numbers in a biofilm (species are co-dependent)
55
What is the Hypothesis of the presenc of microbial complexes of varying virulence?
Clusters of bacteria in discrete micro-environments
n.b. this is the most accepted model
56
Name the 3 most pathogenic bacteria:
* P Gingivalis
* T forsynthia
* T denticola
57
Which two groups of factors must be in balance to avoid tissue damage?
Host (inflammatory & immunological response)
Bacterial virulence factors (bacterial load & composition)
58
In which two ways do host tissues protect themselves against damage from the host response?
host enzyme inhibitor
Anti-oxidant defence strategues
59
What is a neutrophil?
- multilobed nuclei
- can phagocytose
60
Which type of inheritied genetic disease is chronic periodontitis?
Complex
= inherited multiple gene defects which can sit silently and then do something with a change in other things i.e. smoking = makes even more susceptible
61
Approx which % of the populations varience if gingivitis, probing depth and clinical attachment loss is due to genetic variation?
38-82%
62
Which polymorphism has been linked to chronic periodontitis?
IL-1 polymorphosm
(n.b. there are likely to be a numver of different ones!)
63
Which type of periodontitis is beleived to have a familial pattern of inheritance?
Aggressive
(autosomal dominant, autosomal recessive & X- linked)
64
What genetic alterations occur in single gene conditions?
pathological mutations
present only in affected/carriers
Significantly alters the gene & protein
definitely going to get the disease
65
What genetic alterations occur in complex diseases?
Normal variant (present in everyone)
Subtly alters the gene and protein = turned on by certain environmental factors
66
Where abouts on the spectrum of predicitve power of genetic info do the following lie?
* Chronic periodonitits
* Aggressive periodontitits
* Periodontitis associated with systemic disease
Chronic periodontitis: Multifactorial
Aggressive periodontitis: Single gene
Periodontitis associated with systemic disease: varies depending on what the systemic disease is
67
What are the causal theories of periodontitis?
68
In which ways does smoking influence periodontal disease (6)?
* More pathogenic flora
* Poor systemic health
* Poor general health behaviour
* Periodonta symptoms and signs reduced
* Healing impaired
* Reduced biological defences
69
What happens to the rate of progression of periodontal disease when an individual stops smoking?
Decreases
70
What is the presentation of periodontal disease in a smoker (8)?
* More sites with deeper pockets
* Greater clinical attachment loss
* Greater bone loss
* Higher prevelance of furcation lesions
* More liely to suffer from necrotisisng ulcerative conditions of the periodontium
* Accumulate more calculus
* Less likely to respond favoourable to therapy
* Dose response (1 a day - increased attachment loss of 0.5%; 10 a day - 5%; 20 a day - 10%)
71
What is the action of nicotine on the periodontium?
Vasoconstriction of blood vessles
(also increases HR, CO & BP)
N.b. this masks bleeding on probing & decreases gingival crevicular flow - decreases amount of host defence factors provided in gingival crevicular gluid
72
The prolonged chemical and thermal iritation of oral mucosa causes which 3 conditions?
Smokers ketatosis
Speckled leukoplakia
Frank Carcinoma
73
What are the two principle carcinogens in cigarettes?
Polycylcic aromatic hydrogcarbons
Nitrosos compounds
74
Which two factors increase calculus is smokers?
Increased salivary flow rate (and precipitation of calcium phosphate)
Roughened surface encourages plaque accumulation
75
What is the effect of nicotine adsorbing on the root surface?
Causes fibroblast disorientation
76
Are e-cigarrettes still an issue with periodontal disease?
Yes
They still contain nicotine!
77
After which stage in life is incidence of periodontitis greater in diabetics?
Post puberty
78
What is the relationship between number of systemic complications of diabetes and the severity of periodontitis?
More systemic complications = more severe periodontitis
79
* Reduced collagen synthesis by fibroblasts
* Impaired PMNL function
* Impaired wound healing (decreased collagen solubility & increased collagenase)
* Advance glycation end products = increase collagen cross linkage (decreased solubility) & increased release of IL-1, TNF alpha & PGE2
80
What may be a presenting sign of Diabetes Mellitus?
Atypical or recurrent lateral periodontal abscesses that often do not respond to treatment
May contain pus
= gingival tissues not periapical
81
Name a risk factor for chronic peridontitis and necrotising ulcerative gingivitis and periodontitis:
Stress
82
How does stress alter your susceptibility for periodontitis?
Altered immune response
Altered lifestyle and behaviour (psychoses = indirect effect & self mutilation = rare unusual lesions)
83
Stress
= decreased saliva flow and increased viscocity, acidity & glycoproteins = favours accumulation of plaque
= increased NA & A = decreased gingival blood flow
= incresed salivary cortisol
= increased catecholamines in GCF = utilised by periodontal pathogens
84
What are the three different modes of calculus attachment?
Enamel:
* Attachement via pellicle = weak attachment strength
Root: difficult to remove
* microscopic irregularities = strong bond
* interlocking with organic crystals of tooth
85
What is burnished calculus?
When the edge has been smoothed = more difficult to detect & remove
86
What are the contraindications of polishing (9)?
* Lack of stain
* Sensitive teeth
* Exposed cementum or dentine
* Restored tooth surfaces
* Newly erupted teeth (not yet taken on fluoride)
* Implant abutments
* Areas of demineralisation
* Those requireing a strict low sodium diet (e.g. renal dialysis patients)
* Patient discomfort
NO INDICATION FOR IT AT EVERY APPOINTMENT
87
What does polishing remove?
Extrinsic stain
