ICS2/2: Aggressive Periodontitis Flashcards
aggressive periodontitis: characterized by?
deep pockets, advanced bone loss typically in children, adolescents and young adults; without any associated systemic disease
AgP: affects which dentition rarely?
AgP can affect both primary and secondary dentitions, but rarely the primary teeth
what are 2 unusual traits of AgP?
- degree of periodontal destruction is inconsistent with levels of plaque/calculus
- aetiological agents cause disease within a short time, fast rate of progression
AgP: what are the 3 primary features?
- non-contributory medical history: no associated systemic disease resulting in perio destruction
- rapid LOA and bone loss
- strong family history: genetic influence
AgP: what are 5 secondary features?
- severity of perio destruction inconsistent with OH levels
- high levels of A.a, and occasionally P. gingivalis
- phagocyte abnormalities, ineffective killing of perio-pathogens
- hyper-responsive macrophage phenotype: production of excess levels of prostaglandins and interleukins
- disease may self-arrest/burnout
why is knowledge of primary and secondary features important?
helps differentiate AgP and chronic periodontitis when diagnosing a patient
from the old to new classification of periodontal disease, what did AgP replace and what were the 3 categories involved?
AgP replaced Early onset periodontitis, with the 3 categories:
pre-pubertal periodontitis
juvenile periodontitis
rapidly progressive periodontitis
AgP is subdivided into?
localized AgP
generalized AgP
localized AgP:
onset?
localized to where?
response to infecting bacteria results in?
- 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
clinical features of localized AgP: gingivae appearance? plaque/calculus level? pocketing and levels of LOA? other features?
- 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
when the patient with LAP complains of mobility, abscessing and formation of a maxillary diastema, what is this a sign of?
it is a sign that the disease has advanced, will continue to progress rapidly and it may be “too late” at this stage
what are the radiographic features of LAP?
- classically affects 6s, 1s, 2s
- angular/vertical bony defects (examine bitewing of 6s for evidence)
- lesions are often symmetrical; mirror images
describe the inflammatory response in localized AgP x3
- associated with high serum antibody response to A.a bacteria
- associated with defective phagocyte function, unable to response appropriately to bacteria
- hyper-responsive macrophages/neutrophil phenotypes: excessive production of prostaglandins and interleukins
generalized AgP: what is the 1999 international workshop definition?
- 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
clinical features of generalized AgP:
- 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
inflammatory response in generalized AgP? how is it different from the one in LAP?
- 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
epidemiology of LAP:
affects how many in the western population?
describe the racial prevalence?
are there any gender differences?
- 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)
explain how AgP might have multifactorial aetiology
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
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?
- 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
which other bacteria species are associated with AgP (especially GAP)?
T. forsythia
P. gingivalis
what is the issue with using perio-pathogens to diagnose disease? why? what does this suggest?
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
AgP: genetics.
what type of inheritance?
autosomal dominant
genetic changes in AgP cases - what do these genetic changes affect in those with AgP?
genetic changes affects the host response, with regard to (reduced) neutrophil function - a common finding in AgP
wilson & kalmar 1996: what were the two forms of neutrophil receptor reported and what do they bind?
- high affinity receptor allotype (high binding) and low affinity receptor allotype (low binding)
- they bind IgG2
wilson & kalmar 1996: what happens when there is increased tendency for low affinity receptor allotype?
decreased binding of IgG2 to neutrophils, thereby compromising the host response
why is it important to screen for evidence of AgP?
the disease can cause rapid permanent destruction of the periodontal tissues, therefore early detection is required
what are the difficulties of screening for AgP?
- low prevalence
- high occurrence of false pockets in mixed dentition of healthy cases
- low cooperation in children, may not tolerate periodontal probing
screening for AgP: what to look out for in clinical exam?
what to beware of?
significant periodontal pocket depths
LOA (true pocketing), particularly affecting the 6s and incisors
- false pocketing around erupting/newly erupted teeth
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?
- bitewing
- 2-3mm, distance should be 1mm in health
- angular/vertical bone loss, particularly affecting 6s + evidence of furcation lesions
AgP - options of treatment?
- 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
what is the current dose of antibiotics given to those with AgP?
previous regime? what was the problem with this?
- 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
AgP: reassessment
what to do when disease has stabilized?
go on maintenance/supportive periodontal therapy
frequent recalls - may have high rate of reoccurrence. disease reactivation will cause significant damage
AgP: reassessment
what to do when disease has not stabilized?
consider causes of failure
if pt has maintained good OH, consider periodontal surgery
what are some other causes of localized LOA?
- true recession of gums
- trauma
- removal/presence of impacted teeth
- tooth position
- orthodontic tooth movement
- advanced dental caries
- subgingival margins of restorations
chronic periodontitis - features?
- 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
chronic periodontitis - clinical features?
- BOP/inflammation
- tissue shrinkage
- increased mobility
- furcation involvement
- drifting of teeth
what are the variable types of subgingival plaque in CP?
- A.a
- P. gingivalis
- Prevotella intermedia
- T. forsythia
