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Yr 2 - Competency in periodontology > Aetiology & Pathogenesis of periodontal disease > Flashcards

Aetiology & Pathogenesis of periodontal disease Flashcards

1
Q

Which % of patients will have perio?

A

40%

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2
Q

What two things need to be done before treating a perio patient in the PDH?

A
  1. Take radiographs
  2. Have good plaque scores
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3
Q

What are the two things that cause perio?

A

Inherited (particularly more aggressive)

Behavioural (smoking)

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4
Q

What are the two main stages of perio progression?

A
  1. Decreased host resistance (e.g. stress etc)
  2. Increased microbial activity (particularly virulent strains)
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5
Q

What will happen if you treat a patient with a high plaque score?

A

Perio treatment will not succeed!!

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6
Q

Why do we disclose?

A

To show plaque visually

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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

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8
Q

What does PAL stand for?

A

Probing attachment level

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9
Q

What does CAL stand for?

A

Clinical Attachement level

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10
Q

What is the PAL/CAL measurement?

A

The distance from the amelocemental junction to the botton if the pocket (recession + pocket depth)

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11
Q

What is the recession measurement?

A

The distance from the amelodentinal junction to the gingival margin

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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

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13
Q

What are the 6 key features of healthy gingivae?

A
  • Triangular interdental papilla
  • Knife edged margin
  • Stippled gingivae
  • pink
  • firm
  • no bleeding
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14
Q

What is the name of this junction?

A

Mucogingival junction

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15
Q

What is free mucosa more prone to than attached?

A

Trauma

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16
Q

What is the rate of turnover for epithelial cells in the mouth?

A

8-10 days

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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

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18
Q

What is gingivitis?

A

Reversible inflammation of the gingivae (/the gingival crevice)

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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
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20
Q

In gingivitis is the junctional epithelium still attached?

A

Yes

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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!)
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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)

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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

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24
Q

What is the classification system for Periodontal disease?

A

Armitage

(no clear system on clinic)

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25
Q

What impact does smoking have on developing periodontistis?

A

Increases likelihood of having periodontal disease (it is also more likely to be severe)

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26
Q

What is another chronic inflammatory disease associated with periodontal disease?

A

Diabetes

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27
Q

What is the key difference between gingivitis and periodontitis?

A

Loss of attachement (junctional epithelium)

= bacteria ingress onto root surface

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28
Q

What are the different types of periodontitis?

A

General/local

Chronic (abscess)/Acute (necrotising)

Systemic disease assocated

Localised Agressive

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29
Q

What are the clinical signs of periodontitis (9)?

A
  • 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)
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30
Q

What is the problem with supra-gingival calculus?

A

Bacteria cling to it more easily

(does not cause periodontal disease)

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31
Q

Why does subgingival calculus often look darker than supra-gingival calculus?

A

Picks up haemantic staining (from blood) = brown/green tinge

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32
Q

Is subgingival calculus often bigger or smaller than supragingival calculus?

A

Smaller

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33
Q

Why must you make sure a probe is at the right angle when measuring pocket depth?

A

Different angles give different readings

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34
Q

Why in disease is a probe more likely to pass through tissue?

A

It is more friable = more susceptible to break down

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35
Q

Is attachment loss the same as pocket depth?

A

No, it can be either bigger or smaller

36
Q

Which do we measure…

Pocket depth or attachement loss?

A

Pocket depth

37
Q

What is supuration?

A

Pus

38
Q

Which % of the population with chronic periodontitis have mild perio?

A

8.5%

39
Q

Which % of the population with chronic periodontitis have moderate perio?

A

30%

40
Q

Which % of the population with chronic periodontitis have severe perio?

A

8.5%

41
Q

Which % of the whole population have aggressive periodontitis?

A

1%

42
Q

Which populations are more susceptible to aggressive periodontitis?

A
  • North American and European caucasian (0.1%)
  • African americans (2.5%)
  • South Americans (3.7%)
  • African (6%)
43
Q

Is severe periodontal disease acute or chronic?

A

Chronic (slowly developing)

44
Q

At which age does severe periodontal disease usually show itself?

A

Mid to early life

45
Q

What is the relationship between severity of periodontal disease and progression?

A

More severe = more rapid progression

46
Q

What is the relationship between severity of periodontal disease and number of missing teeth?

A

More rapid progression/severe = more teeth lost

47
Q

What is the relationship between severity of periodontal disease and age?

A

Likely to get worse with age (and higher % have periodontal disease in the older populations)

48
Q

What is aetiology?

A

What causes a disease

49
Q

What is pathogenesis?

A

How do factors causes the disease

50
Q

Can you get periodontal disease without bacteria?

A

No

Germ free mice have no periodontitis

51
Q

Roughly how many bacterial species are known to colonise the periodontium?

A

400-500

52
Q

What is the specific plaque hypothesis?

A

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
Q

What is the non specific plaque hypothesis?

A

Disease results from sheer mass of pathogens

(not entirely true)

54
Q

What is the environmental plaque hypothesis?

A

Pathogenic species are required in sufficient numbers in a biofilm (species are co-dependent)

55
Q

What is the Hypothesis of the presenc of microbial complexes of varying virulence?

A

Clusters of bacteria in discrete micro-environments

n.b. this is the most accepted model

56
Q

Name the 3 most pathogenic bacteria:

A
  • P Gingivalis
  • T forsynthia
  • T denticola
57
Q

Which two groups of factors must be in balance to avoid tissue damage?

A

Host (inflammatory & immunological response)

Bacterial virulence factors (bacterial load & composition)

58
Q

In which two ways do host tissues protect themselves against damage from the host response?

A

host enzyme inhibitor

Anti-oxidant defence strategues

59
Q

What is a neutrophil?

A
  • multilobed nuclei
  • can phagocytose
60
Q

Which type of inheritied genetic disease is chronic periodontitis?

A

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
Q

Approx which % of the populations varience if gingivitis, probing depth and clinical attachment loss is due to genetic variation?

A

38-82%

62
Q

Which polymorphism has been linked to chronic periodontitis?

A

IL-1 polymorphosm

(n.b. there are likely to be a numver of different ones!)

63
Q

Which type of periodontitis is beleived to have a familial pattern of inheritance?

A

Aggressive

(autosomal dominant, autosomal recessive & X- linked)

64
Q

What genetic alterations occur in single gene conditions?

A

pathological mutations

present only in affected/carriers

Significantly alters the gene & protein

definitely going to get the disease

65
Q

What genetic alterations occur in complex diseases?

A

Normal variant (present in everyone)

Subtly alters the gene and protein = turned on by certain environmental factors

66
Q

Where abouts on the spectrum of predicitve power of genetic info do the following lie?

  • Chronic periodonitits
  • Aggressive periodontitits
  • Periodontitis associated with systemic disease
A

Chronic periodontitis: Multifactorial

Aggressive periodontitis: Single gene

Periodontitis associated with systemic disease: varies depending on what the systemic disease is

67
Q

What are the causal theories of periodontitis?

A
68
Q

In which ways does smoking influence periodontal disease (6)?

A
  • More pathogenic flora
  • Poor systemic health
  • Poor general health behaviour
  • Periodonta symptoms and signs reduced
  • Healing impaired
  • Reduced biological defences
69
Q

What happens to the rate of progression of periodontal disease when an individual stops smoking?

A

Decreases

70
Q

What is the presentation of periodontal disease in a smoker (8)?

A
  • 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
Q

What is the action of nicotine on the periodontium?

A

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
Q

The prolonged chemical and thermal iritation of oral mucosa causes which 3 conditions?

A

Smokers ketatosis

Speckled leukoplakia

Frank Carcinoma

73
Q

What are the two principle carcinogens in cigarettes?

A

Polycylcic aromatic hydrogcarbons

Nitrosos compounds

74
Q

Which two factors increase calculus is smokers?

A

Increased salivary flow rate (and precipitation of calcium phosphate)

Roughened surface encourages plaque accumulation

75
Q

What is the effect of nicotine adsorbing on the root surface?

A

Causes fibroblast disorientation

76
Q

Are e-cigarrettes still an issue with periodontal disease?

A

Yes

They still contain nicotine!

77
Q

After which stage in life is incidence of periodontitis greater in diabetics?

A

Post puberty

78
Q

What is the relationship between number of systemic complications of diabetes and the severity of periodontitis?

A

More systemic complications = more severe periodontitis

79
Q
A
  • 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
Q

What may be a presenting sign of Diabetes Mellitus?

A

Atypical or recurrent lateral periodontal abscesses that often do not respond to treatment

May contain pus

= gingival tissues not periapical

81
Q

Name a risk factor for chronic peridontitis and necrotising ulcerative gingivitis and periodontitis:

A

Stress

82
Q

How does stress alter your susceptibility for periodontitis?

A

Altered immune response

Altered lifestyle and behaviour (psychoses = indirect effect & self mutilation = rare unusual lesions)

83
Q
A

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
Q

What are the three different modes of calculus attachment?

A

Enamel:

  • Attachement via pellicle = weak attachment strength

Root: difficult to remove

  • microscopic irregularities = strong bond
  • interlocking with organic crystals of tooth
85
Q

What is burnished calculus?

A

When the edge has been smoothed = more difficult to detect & remove

86
Q

What are the contraindications of polishing (9)?

A
  • 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
Q

What does polishing remove?

A

Extrinsic stain

Yr 2 - Competency in periodontology (8 decks)

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