4. Introduction
Periodontitis is the pathological
manifestation of host response against
bacterial challenge.
Aggressive Periodontitis is the rapid loss
of periodontal attachment and tooth
supporting bone in otherwise healthy
individuals.
5. Definition :
Aggressive Periodontitis refers to a multi-factorial,
severe and rapidly progressive form of
periodontitis, which primarily but not exclusively
affects young patients.
-Intl’s workshop classification of
Periodontal Diseases and Conditions (1999)
6. Historical background
Diffuse atrophy of alveolar bone – Gottlieb, 1923
Deep Cementopathia – Gottlieb, 1928
Juvenile Periodontitis – Chaput, 1967 and Butler, 1969
Early onset Periodontitis- Page and Baab, 1989
1. Pre-pubertal Periodontitis
2. Juvenile Periodontitis
3. Rapidly Progressive Periodontitis
7. Historical background
The term juvenile periodontitis was introduced by
Chaput et al in 1967 and by Butler in 1969. Baer
defined it as “A disease of periodontium which is
charecterised by a rapid loss of alveolar bone
about more than one tooth of the permanent
dentition.”
It was categorised as localised and generalised
juvenile periodontitis.
In the new classification, several rapidly
progressing periodontitis forms were united under
the term Aggressive Periodontitis.
9. Clinical Features
o Early onset of disease during the circum-pubertal period
(11-13 years of age)
o A distinctive radiographic pattern of bone loss depicting
vertical loss of alveolar bone at permanent first molars
and at one or more incisors.
o Rapid rate of disease progression.
o Disease affects only permanent dentition.
o The amount of local etiological factors is not
commensurate with the severity of periodontal
destruction.
10. Classification and Clinical
Characteristics
Three primary features are essential for classification
of Aggressive Periodontitis. They are :
1. The rapid loss of attachment of tooth-supporting
bone.
2. The subject is otherwise healthy i.e not suffering
from any systemic disease or condition that could
be responsible for present periodontitis.
3. The presence of familiar aggregation.
11. Secondary features :
1. Inconsistency of presence of low amount of
etiological factor i.e plaque and tissue destruction.
2. Strong colonization by Aggregatibacter
actinomycetemcomitans and Porphyromonas
gingivalis.
3. Self limiting disease.
4. Immunological differences that do not entail the
diagnosis of periodontitis as a manifestation of
systemic disease :
a ) Hyper-responsive macrophages
b ) Abnormalities of neutrophil function.
12. Diagnostic criteria
Circumpubertal age of
onset.
Localised loss of
attachment at incisors and
1st molars.
Interproximal loss of
attachment at two or more
teeth one of which is a first
molar and involvement of
two or fewer teeth other
than incisor and 1st molar.
Robust serum antibody
response.
Most often <30 years of
age, but also seen in
older individuals.
Generalised attachment
loss at 3 or more than 3
teeth other than incisor
and 1st molars.
Episodic nature of
attachment loss.
Poor serum antibody
response.
13. GENERALISED AGGRESSIVE
PERIODONTITIS
It is characterised by highest severity, large extent of
disease and large heterogenity.
Clinically it is characterised by “ generalised interproximal
loss of attachment affecting atleast 3 permanent teeth
other than incisor and 1st molars.
Generalised aggressive periodontitis encompasses
diseases that were previously classified as generalised
juvenile periodontitis and rapidly progressive periodontitis.
• Two gingival responses can be seen in generalised
aggressive periodontitis. They are :
1. Severe, acutely inflammed tissue often proliferating, fiery
red, ulcerated with spontaneous bleeding.
2. Pink, free of inflammation with some degree of stippling
and with deep pockets.
15. LOCALISED AGGRESSIVE PERIODONTITIS
It is characterised as having localised 1st molar and incisor
presentation with interproximal loss of attachment on
atleast two permanent teeth and involving no more than
two teeth other than the incisors and 1st molars.
The reasons for its localised distribution are as follows:
1. Bacteria tend to invade first erupted teeth i.e. 1st molars
and incisors.
2. Bacteria antagonistic to actinomaycetemcomitans
colonise the remaining teeth and prevent invasion of
remaining teeth.
3. Aggregatibacter loses its leucotoxin producing capacity.
4. Defect in cementum formation maybe responsible for
localisation of the lesions.
17. Pathobiology and risk factors
specific bacteria in Localised aggressive periodontitis
include Aggregatibacter actinomycetemcomitans.
Host response to bacterial change : Recent studies show that
stronger activation of Natural killer and Natural killer T cells
is seen in Aggressive periodontitis.
• Earlier studies showed that defect of neutrophil function
resulted in aggressive periodontitis.
• Recent studies proved that neutrophils secrete lytic
enzymes which inturn cause tissue destruction.
• A familial aggregation is considered a secondary feature of
the disease entity.
18. Diagnosis
Diagnosis of Aggressive Periodontitis includes
assessment of clinical presentation.
Periodontal probing is the most reliable marker in
diagnosing Aggressive Periodontitis.
Diagnosis is made by assessing primary and
secondary features of Aggressive Periodontitis.
Often it is identified during routine periodontal
screening and the younger individuals who present
with the primary and secondary features should be
closely monitored.
19. Management of Aggressive Periodontitis
Early detection is critically important in the
treatment of Aggressive Periodontitis because
preventing further more destruction is more
predictable than attempting to regenerate the lost
supporting tissues.
At the initial diagnosis, it is helpful to obtain any
previously taken radiographs to assess the rate of
progression of the disease.
20. Management of Aggressive Periodontitis
1. Non surgical therapy
2. Antimicrobial therapy : Local delivery
3. Full mouth disinfection
4. Host modulation
5. Conventional periodontal therapy
21. Non Surgical Therapy
It is not much effective in the case of Aggressive
Periodontitis as relapse of the condition can be
seen.
22. Anti-microbial therapy
Systemic Tetracycline – 250 mg tetracycline
Hydrochloride – 4 times a day – atleast one week.
Tetracycline resistance – Amoxicillin +
Metronidazole, Ciprofloxacin + Metronidazole.
Chlorhexidine should be prescribed to prevent
plaque growth and facilitate healing.
26. Bone Grafting :
Bone grafts are the materials used for replacement or
augmentation of the bone.
Autogenous Bone Chips
Osseous Coagulum
Frozen Autogenous Hip marrow
FDBA + Tetracycline,
These grafts can be used to surgically treat Aggressive
Periodontitis.
28. Guided Tissue Regeneration
It is the method for prevention of epithelial migration along
the cemental wall of the pocket.
Two types of barriers can be used for guided tissue
regeneration :
Non Bio-reabsorbable membrane :
- PTFE i.e. Titanium reinforced Polytetraflouroethylene
membrane, Nucleopore and Millipore filters, silicon
barriers and sterilized rubber dam.
Bio Reabsorbable membrane :
- Collagen (Periogen, Biomend), Polylactic acid and
Polyglycolic acid polymer (Guidor, Vicryl, Epiguide) etc
29. Biomodifications of root surface :
Along with root planing, the root surface of the pocket can
be treated in order to improve the chances of accepting
new gingival attachments
Citric acid, EDTA, Tetracycline, Fibronectin are some of the
substances which can be used as biomodifiers.
Biological Mediators :
These are the substances used to enhance the bone
regeneration while using the bone grafts.
- Bone Morphogenic Protein (BMP)
- Platelet derived Growth Factor
- Insulin derived growth Factor
- Transforming Growth Factor
- Basic Fibroblast Growth Factor etc, are commonly used.
30. Conclusion
Aggressive periodontitis comprises of a group of rare,
severe, rapidly progressive forms of periodontitis
characterised by early age of onset and tendency
for cases to aggregate in families.
Diagnosis of one of these forms require absence of
systemic diseases that may severely impair the
host differences and lead to premature exfoliation
of teeth.
Optimal plaque control is of main importance in
obtaining favourable clinical prognosis.