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ICS - PERIODONTOLOGY > ICS2/2: Aggressive Periodontitis > Flashcards

ICS2/2: Aggressive Periodontitis Flashcards

1
Q

aggressive periodontitis: characterized by?

A

deep pockets, advanced bone loss typically in children, adolescents and young adults; without any associated systemic disease

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2
Q

AgP: affects which dentition rarely?

A

AgP can affect both primary and secondary dentitions, but rarely the primary teeth

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3
Q

what are 2 unusual traits of AgP?

A
  • degree of periodontal destruction is inconsistent with levels of plaque/calculus
  • aetiological agents cause disease within a short time, fast rate of progression
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4
Q

AgP: what are the 3 primary features?

A
  1. non-contributory medical history: no associated systemic disease resulting in perio destruction
  2. rapid LOA and bone loss
  3. strong family history: genetic influence
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5
Q

AgP: what are 5 secondary features?

A
  1. severity of perio destruction inconsistent with OH levels
  2. high levels of A.a, and occasionally P. gingivalis
  3. phagocyte abnormalities, ineffective killing of perio-pathogens
  4. hyper-responsive macrophage phenotype: production of excess levels of prostaglandins and interleukins
  5. disease may self-arrest/burnout
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6
Q

why is knowledge of primary and secondary features important?

A

helps differentiate AgP and chronic periodontitis when diagnosing a patient

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7
Q

from the old to new classification of periodontal disease, what did AgP replace and what were the 3 categories involved?

A

AgP replaced Early onset periodontitis, with the 3 categories:
pre-pubertal periodontitis
juvenile periodontitis
rapidly progressive periodontitis

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8
Q

AgP is subdivided into?

A

localized AgP

generalized AgP

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9
Q

localized AgP:
onset?
localized to where?
response to infecting bacteria results in?

A
  • typically around puberty
  • first molars & incisors,
    interproximal LOA on at least 2 permanent teeth (can only be first molar/incisors)
  • results in high serum antibody response to bacteria
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10
Q 
clinical features of localized AgP: 
gingivae appearance? 
plaque/calculus level?
pocketing and levels of LOA?
other features?
A
  • may appear healthy, little inflammation present
  • low levels of plaque/calculus
  • deep pocketing, LOA >3mm around affected teeth (1/2s & 6s)
  • BOP
  • patient may complain of mobility, abscessing, formation of maxillary diastema
  • some cases may self-arrest and be self limiting
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11
Q

when the patient with LAP complains of mobility, abscessing and formation of a maxillary diastema, what is this a sign of?

A

it is a sign that the disease has advanced, will continue to progress rapidly and it may be “too late” at this stage

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12
Q

what are the radiographic features of LAP?

A
  • classically affects 6s, 1s, 2s
  • angular/vertical bony defects (examine bitewing of 6s for evidence)
  • lesions are often symmetrical; mirror images
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13
Q

describe the inflammatory response in localized AgP x3

A
  1. associated with high serum antibody response to A.a bacteria
  2. associated with defective phagocyte function, unable to response appropriately to bacteria
  3. hyper-responsive macrophages/neutrophil phenotypes: excessive production of prostaglandins and interleukins
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14
Q

generalized AgP: what is the 1999 international workshop definition?

A
  • typically affects those under 30
  • interproximal LOA (>3mm) in 3 other teeth other than 6s and incisors
  • episodic nature of destruction
  • poor serum antibody response to infecting bacteria
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15
Q

clinical features of generalized AgP:

A
  • more heterogenous than LAP
  • affects those under 30
  • LOA >3mm in 3 other teeth other than 6s and incisors
  • episodic nature of destruction
  • vertical & horizontal bony defects on radiographs
  • amount of periodontal destruction out of proportion to plaque/calculus levels
  • clinical features similar to chronic periodontitis, diagnosis difficult if risk factors e.g. smoking & poor OH present
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16
Q

inflammatory response in generalized AgP? how is it different from the one in LAP?

A
  • poor association with serum antibody response with A.a and P. gingivalis
  • occasionally associated with defective phagocytes
  • associated with hyper-responsive macrophages/neutrophil phenotypes, increased production of prostaglandins/interleukins
17
Q

epidemiology of LAP:
affects how many in the western population?
describe the racial prevalence?
are there any gender differences?

A
  • 1:1000, ~1-2%
  • 0.8% afro-carribean (highest)
    0. 2% asian
    0. 02% caucasian
  • according to current studies it is F=M (no difference)
18
Q

explain how AgP might have multifactorial aetiology

A

AgP encompasses several disease entities, which result in the same disease outcome (rapid periodontal destruction)
- the underlying genetic tendency requires the transmission/presence of virulent bacteria, and may be enhanced by the presence of environmental factors such as smoking to initiate the disease

19
Q

bacteria in AgP: which is the most common?
treatment failure of AgP is due to?
how many serotypes does this bacteria have and which is the most virulent?

A
  • Aggregatibacter actinomycetemcomitans is present in 90% of cases, and there is association of high serum antibody response to it in those affected by AgP.
  • treatment failure is due to continued high subgingival levels of A.a
  • 5 serotypes, serotype b is the most virulent
20
Q

which other bacteria species are associated with AgP (especially GAP)?

A

T. forsythia

P. gingivalis

21
Q

what is the issue with using perio-pathogens to diagnose disease? why? what does this suggest?

A

presence/absence of Aa cannot be used to discriminate AgP & CP
- A.a etc are present at low levels in health sites
not always isolated from disease
they are also commonly isolated from CP cases
- suggests that there are other factors required for AgP

22
Q

AgP: genetics.

what type of inheritance?

A

autosomal dominant

23
Q

genetic changes in AgP cases - what do these genetic changes affect in those with AgP?

A

genetic changes affects the host response, with regard to (reduced) neutrophil function - a common finding in AgP

24
Q

wilson & kalmar 1996: what were the two forms of neutrophil receptor reported and what do they bind?

A
  • high affinity receptor allotype (high binding) and low affinity receptor allotype (low binding)
  • they bind IgG2
25
Q

wilson & kalmar 1996: what happens when there is increased tendency for low affinity receptor allotype?

A

decreased binding of IgG2 to neutrophils, thereby compromising the host response

26
Q

why is it important to screen for evidence of AgP?

A

the disease can cause rapid permanent destruction of the periodontal tissues, therefore early detection is required

27
Q

what are the difficulties of screening for AgP?

A
  • low prevalence
  • high occurrence of false pockets in mixed dentition of healthy cases
  • low cooperation in children, may not tolerate periodontal probing
28
Q

screening for AgP: what to look out for in clinical exam?

what to beware of?

A

significant periodontal pocket depths
LOA (true pocketing), particularly affecting the 6s and incisors
- false pocketing around erupting/newly erupted teeth

29
Q

screening for AgP: what type of radiographs should be taken for caries screening in young people?
distance between ACJ & alveolar bone crest is ____mm in possible cases of AgP?
what are other kinds of further evidence of AgP in radiographs?

A
  • bitewing
  • 2-3mm, distance should be 1mm in health
  • angular/vertical bone loss, particularly affecting 6s + evidence of furcation lesions
30
Q

AgP - options of treatment?

A
  • referral
  • non-surgical therapy:
    1. OHI (high susceptibility to plaque)
    2. stop smoking
    3. remove plaque retentive factors
    i. defective restorations
    ii. poorly designed dentures
    iii. orthodontic appliances
    4. scale & polish/RSD
    5. antibiotics
31
Q

what is the current dose of antibiotics given to those with AgP?
previous regime? what was the problem with this?

A
  • metronidazole 400mg
    amoxicillin 250mg
    3 times a day for 7 days
  • tetracycline 250mg four times a day for 2-3 weeks. had problems with bacterial resistance
32
Q

AgP: reassessment

what to do when disease has stabilized?

A

go on maintenance/supportive periodontal therapy

frequent recalls - may have high rate of reoccurrence. disease reactivation will cause significant damage

33
Q

AgP: reassessment

what to do when disease has not stabilized?

A

consider causes of failure

if pt has maintained good OH, consider periodontal surgery

34
Q

what are some other causes of localized LOA?

A
  • true recession of gums
  • trauma
  • removal/presence of impacted teeth
  • tooth position
  • orthodontic tooth movement
  • advanced dental caries
  • subgingival margins of restorations
35
Q

chronic periodontitis - features?

A
  • LOA
  • bone loss (radiographs): typically horizontal bone loss, sometimes vertical
  • slow to moderate progression
  • no significant family history involved
  • destruction consistent with patient’s age and presence of risk factors: OH, calculus levels, smoking, diabetes, heavily restored dentition
36
Q

chronic periodontitis - clinical features?

A
  • BOP/inflammation
  • tissue shrinkage
  • increased mobility
  • furcation involvement
  • drifting of teeth
37
Q

what are the variable types of subgingival plaque in CP?

A
  • A.a
  • P. gingivalis
  • Prevotella intermedia
  • T. forsythia

ICS - PERIODONTOLOGY (10 decks)

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