ICS2/2: Aggressive Periodontitis Flashcards
(37 cards)
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
