aggressive periodontitis

P MIKITHA
POSTGRADUATE
AECS MAARUTI COLLEGE OF DENTAL SCIENCES
AGGRESSIVE
PERIODONTITIS

CONTENTS
 Introduction
 History
 Classification
 Localized aggressive periodontitis
Prevalence
Clinical findings
Radiographic features
 Generalized aggressive periodontitis
Prevalence
Clinical findings
Radiographic findings
 Etiology and pathogenesis
 Diagnosis
 Treatment consideration
 Conclusion
 References

 Destructive periodontal diseases affecting the connective tissue attachment
& alveolar bone supporting the teeth have long been considered the
principal cause for tooth loss.
 At the 1999 International classification workshop, the different forms
of periodontitis were reclassified into three major forms (chronic,
aggressive, necrotizing forms of periodontitis and periodontal
manifestations of systemic diseases).
INTRODUCTION

HISTORY
Diffuse atrophy of
alveolar bone.
Gottlieb,1923
Early-onset
Periodontits.
Page & Boab 1989.
Juvenile
Periodontitis.
Deep cementopathia,
Gottlieb,1928
Chaput et
al,1967.
Butler 1969
1. Pre-pubertal Periodontitis.
2. Juvenile Periodontits.
3. RP Periodontiits
1999 AAP International
Workshop for
Classification
Aggressive
Periodontitis.
Lang LP and Carring T. Aggressive periodontitis In: Lindhe’s Clinical periodontology and implant dentistry. Elsevier 5:438-460.

In 1971, Paul Baer
Aggressive periodontitis
Disease of the periodontium occurring in an otherwise
healthy adolescent
Characterized by a rapid loss of alveolar bone about > 1
tooth of the permanent dentition.
The only teeth
affected are.
1. 1st Molars.
2. Incisors.
Amount of
destruction
manifestated is not
commensurate
with the amount of
local irritants.
Generalised form, it
may affect most of
the dentition.
Baer PN. The case for periodontosis as a clinical entity. J Periodontol 1971: 42: 516-520.

Baer proposed 7 criteria to define the disease
Early onset of the disease during the circumpubertal period. (11 & 13years)
Vertical alv bone loss at the 1st permanent molars & one or more incisor
teeth.
A rapid rate of disease progression
The disease affects only the permanent dentition.
The amount of local etiologic factors is not commensurate with the
severity of the pdl destruction.
Predominant in females (3:1)
It has a familial pattern.
Baer PN. The case for periodontosis as a clinical entity. J Periodontol 1971: 42: 516-520.

1999, International workshop for the classification of Pdl disease and
conditions defined the entity of AP as being characterised by “3 primary
features”-
Rapid loss of attachment and tooth-
supporting bone.
Subject is otherwise healthy.
Familial aggregation.

 Amount of microbial deposits inconsistent with the severity of
periodontal tissue destruction.
 Elevated proportions of Actinobacillus actinomycetemcomitans and
Porphyromonas gingivalis.
 Phagocytic abnormalities.
 Hyper-responsive macrophage phenotype, including production of
PGE2 and IL-1 in response to bacterial endotoxins.
 Progression of attachment loss and bone loss may be self-arresting.
Secondary features that are considered to be
generally but not universally present are:

American Academy of Periodontology workshop, 1999
Aggressive Periodontitis
Localized
Aggressive
Periodontitis
Generalized
Aggressive
Periodontitis

 Aggressive periodontitis is a specific type of periodontitis featuring
rapid attachment loss, bone destruction and familial aggregation
exhibiting inconsistent amounts of microbial deposits with severe
periodontal tissue destruction, phagocyte abnormalities and elevated
proportions of Aggregatibacter actinomycetemcomitans and, in some,
Porphyromonas gingivalis in otherwise healthy patients.
(Glossary of periodontal terms 2001, 4th ed)
DEFINITION
American Academy of Periodontology. Glossary of periodontal terms.4;2001.

 Localised Aggressive Periodontitis is characterised by
circumpubertal onset, localised first molar/incisor
presentation with interproximal attachment loss associated
with at least two permanent teeth and involving no more than
two teeth other than first molars and incisors having robust
serum antibody response to infecting agents.
(Glossary of periodontal terms 2001,4th ed)
LOCALISED AGGRESSIVE PERIODONTITIS

PREVALENCE AND DISTRIBUTION
 It is estimated to be below 1%.
 Blacks– mostly male blacks- 2.9 times more likely to have disease than black
females.
 (Baer 1971, Manson and Lehner 1974) concluded female to male ratio as 3:1
 Primary dentition: In 5 to 11 year olds it ranges from 0.9 - 4.5% of subjects
(Sweeney et al 1987)
 Permanent dentition: In the permanent dentition of 13-20 year old individuals
majority of studies have reported a prevalence of periodontitis of less than 1%
(usually 0.1-0.2% in caucasian population).

CLINICAL FINDINGS
 Localized first molar/incisor with interproximal attachment loss.
 The most striking feature
 Lack of clinical inflammation, despite the presence of deep
periodontal pockets

Disto-labial migration of
central incisor in LAP
Periodontal Abscess
Deep, dull radiating pain
may occur with mastication.
Regional lymph node
enlargement

 Clinically there is small amount of plaque ,which
forms a thin film on the tooth that rarely mineralizes
to become calculus.
 Most commonly there is migration and mobility of
first molars and incisors. Classically the maxillary
incisors move in distolabial direction.
 Concomitant to anterior tooth migration there is an
apparent increase in size of the clinical crown.

RADIOGRAPHIC FINDINGS
 Vertical loss of alveolar bone around first
molars and incisors.
 Rate of bone loss is 3-4times faster than in
chronic periodontitis.
 Arc-shaped bone loss from distal of 2nd
Premolar to Mesial of 2nd Molar and often
presents a mirror-image pattern on the
radiograph.
 Bone defects usually bilateral, affecting 1st
Molars & Incisors.

 Although the most important measurement is that of attachment loss
by probing in younger subjects a currently utilized approach is
measurement of distance between CEJ and alveolar crest on bitewing
radiographs.

DISTRIBUTION OF LESION
The classical distribution of lesions in first molar / incisor region may be
explained by following :
 After initial colonization of the first permanent teeth to erupt (first
molars and incisors) A.a evades the host defenses by different
mechanisms. After initial attack, adequate immune responses are
stimulated to produce opsonizing antibodies to enhance phagocytosis of
invading bacteria and neutralize destructive factors. In this manner
colonization of other sites may be prevented. (Zambon1983).
Armitage G C, Cullinan M. Comparison of the clinical features of chronic and aggressive periodontitis. Periodontol 2000; 2010,53:12–27.

 Bacteria antagonistic to A.a may develop, thereby decreasing the
destructiveness of the lesions and reducing the number of colonization
sites (Hillman 1982).
 A.a may lose its leukotoxin producing ability for unknown reasons.
When this happens the progress of the disease becomes arrested or
retarded and new colonization sites averted.
Armitage G C, Cullinan M. Comparison of the clinical features of chronic and aggressive periodontitis. Periodontol 2000; 2010,53:12–27.

 The possibility that a defect in cementum formation may be responsible
for localization of the lesion has been suggested (Page 1985). Root
surfaces of teeth extracted from patients with LAP have been found to
have hypoplastic or aplastic cementum (Lindskong 1983)

CLINICAL COURSE
 LAgP progresses rapidly.
 There is evidence that rate of progression is about three to four times
faster than found in typical periodontitis (Baer 1971,1974).
 In affected persons bone resorption progresses until the teeth are treated,
exfoliated or extracted.

BURN-OUT PHENOMENON
• Initially it was thought that LAP gradually becomes GAP over time. But
some cases of LAP don’t show any increased bone destruction, are
known to arrest spontaneously, leading to caessation of disease activity.
• Proposed by Ranney.
Novak K F and Novak J M:Aggressive Periodontitis in Carranza’s clinical periodontology,Elsevier,12,2010;506-512.

SEQUELAE OF LOCALIZED
AGGRESSIVE PERIODONTITIS
 Hormand and Frandsen (1979) in a study of 156 patients, presented
evidence for progression of the disease from a localized to generalized
form.
 Case report by Shapira, Van Dyke et al (1994) of periodontitis patients
who were followed up for many years and findings are:
 Idiopathic Prepubertal periodontitis at age 10.
 LJP at age 22, bone loss involving all the permanent first molars and
maxillary and mandibular incisors.
 Rapidly progressive periodontitis at age 29.

GENERALISEDAGGRESSIVE PERIODONTITIS
Encompasses the diseases that were previously
classified as generalised juvenile periodontitis and
rapidly progressive periodontitis.

 Generalised Aggressive Periodontitis usually affects person
under 30 years of age or may be older with generalised
interproximal attachment loss affecting at least three teeth other
than first molars and incisors and there is a pronounced episodic
nature of the destruction of attachment and alveolar bone having
poor serum antibody response to infecting agents.
(Glossary of periodontal terms 2001,4th ed)

PREVALENCE AND DISTRIBUTION
 Loe and colleagues (1986), in a study of Sri Lankan subjects aged 14 –
46 yrs showed that 8 % of the population had rapid progression of
periodontal disease characterized by yearly loss of attachment of 0.1 to
1mm.
 National survey of adolescents in U.S, aged 14-17 yrs old. ( Loe &
Brown, 1991) prevalence rate – 0.13 %
 Blacks were found to be at much higher risk than whites for all forms of
AgP .
 Males were more likely to have GAP than females.

CLINICAL FINDINGS
 As seen in LAP, patients with GAP often show small amount of bacterial plaque
associated with affected areas.
 Quantitatively the amount of plaque is inconsistent with the amount of destruction
seen. Qualitatively P.gingivalis, A.a and T.forsythus are frequently detected.
 Generalized interproximal attachment loss affecting atleast three permanent teeth
other than first molars and incisors.
 Pronounced episodic destruction of attachment and alveolar bone.
 Poor serum antibody response to infecting agents.
 < 30years of age, but patients may be older.

 Two gingival tissue responses can be found in cases of
GAgP .
Severe, acutely inflamed tissue
that is often proliferating,
ulcerated, and fiery red-
DESTRUCTIVE STAGE.
#Bleeding
#Suppuration
#Active loss of attachment & bone
Tissues appears pink, free of
inflammation and occasionally with
some degree of stippling– NON-
DESTRUCTIVE STAGE.
#Deep pockets
#Bone & attachment levels relatively
stable (Period of Quiscence)

 The destruction appears to occur episodically
followed by stages of quiescence of variable
time.
 Sometimes patients may also present with
systemic manifestations like weight loss,
mental depression, general malaise.
 Lesions may be arrested or spontaneous after
therapy, whereas others may continue to
progress inexorably to TOOTH LOSS
despite intervention with conventional
therapy.

RADIOGRAPHIC FINDINGS
No definite pattern of distributiom.
The radiographic picture in GAgP can range from severe bone loss associated
with number of teeth to advanced bone loss affecting majority of the teeth in
the dentition.

BONE LOSS IN GAgP
 Page and co-workers demonstrated osseous destruction ranging
from 25-60% during a 9-week period.
 Despite this extreme loss other sites in the same patient showed no
bone loss.

INCIDENTAL ATTACHMENT LOSS
Often subjects present with attachment loss that does not fit the specific
diagnostic criteria. (AP or CP)
It includes:
• Recessions associated with trauma or tooth position.
• Attachment loss associated with impacted 3rd molars, removal of
impacted 3rd molars, etc.
• These patients are a high-risk group for AP or CP.

ETIOLOGY AND PATHOGENESIS
Microbiologic factors
Genetic factors Immunologic factors
Current concepts
Environmental factors
AgP

MICROBIOLOGIC FACTORS
 Acceptance of bacterial etiology of aggressive forms of
periodontitis has been particularly difficult since clinical
presentation of cases frequently shows little visible plaque
accumulation.
 Of great importance is microscopic studies demonstrating
the layer of bacterial deposits on the root surface of
advanced AgP lesions (Listgarten 1976).
KononenE , Muller H. Microbiology of aggressive periodontitis. Periodontol 2000;2014,65: 46–78.

DOMINANT ORGANISMS
1. A.a (Approx. 90%)
2. Capnocytophaga sp
3. E.Corrodens
4. P.intermedia
5. Motile anaerobic
rods, such as
C.rectus
6. Gram-positive
isolates were mostly.
• Streptococci
• Actinomycetes
• Peptostreptococci
1. P.gingivalis
2. A.a
3. Bacteroides forsythus
LAP
GAP

A.a has been implicated as the primary pathogen associated with LAP. As summarized
by Tonetti and Mombelli, it is based on the following evidence.
1. It is found in high frequency (approx.90%) in lesions characteristic of LAP.
2. Sites with evidence of disease progression often show elevated levels of A.a.
3. Many pts with the clinical manifestations of LAP have significantly elevated serum
antibody titers to A.a.
4. Clinical studies show a correlation between reduction in the subgingival load of A.a
during treatment and a successful clinical response.
5. It produces a no. of virulence factors that may contribute to the disease process.

DETERMINANTS OF VIRULENCE AND
PATHOGENIC POTENTIAL OF A.
ACTINOMYCETEMCOMITANS
FACTOR SIGNIFICANCE
Leukotoxin Destroys human PMNs and
macrophages
Endotoxin Activates host cells to secrete
inflammatory mediators (PGs,IL-1β,
TNF-α)
Bacteriocin Inhibit growth of beneficial species
Immunosuppressive factors Inhibit IgG and Ig M production
Collagenase Cause degradation of collagen
Chemotactic inhibition factors Inhibit neutrophil chemotaxis

GENETIC FACTORS
 Segregation and Linkage analysis studies have shown an autosomal dominant
pattern of inheritance.
(Saxen & Nevanlinna 1984, Beaty et al 1987, Hart et al 1992)
 Marazita et al 1994 carried out the largest and most comprehensive
segregation analysis and concluded autosomal dominant model of inheritance.
 Antibody response to periodontal pathogens particularly A.a is under genetic
control, and that the ability to mount high titers of specific, protective antibody
(primarily IgG2) against A.a may be race dependent.
Vieira A , Albandar J. Role of genetic factors in the pathogenesis of aggressive periodontitis. Periodontol 2000; 2014,65:92–106.

 Boughman et al 1986 carried out a linkage study and concluded
linkage of Juvenile Periodontitis to a Vitamin D binding locus on
chromosome 4.
 Hart et al in 1993 suggested that a locus responsible for AgP was
located on chromosome 1q25.
 Lastly it supports a semigeneral transmission model which says that a
few loci with small effects contribute to AgP, with possibly the
influence of environmental factors.
Vieira A , Albandar J. Role of genetic factors in the pathogenesis of aggressive periodontitis. Periodontol 2000; 2014,65:92–106.

ENVIRONMENTAL FACTORS
 The amount and duration of smoking is important variable to influence
the extent of destruction seen in young adults.
 Patients with GAgP with smoking habit have more affected teeth and
more attachment loss than nonsmoking patients with GAgP.
 Smoking may not have the same influence on LAgP.

Schenkein et al. 1995: Cigarette smoking was
shown to be a risk factor for patients with generalized
forms of AgP.
Smokers with GAP had more affected teeth and
greater mean levels of attachment loss than patients
with GAP who did not smoke.
IgG2 serum levels as well as antibody levels against
A.a are significantly depressed in subjects with GAP
who smoked.

IMMUNOLOGIC OR HOST RELATED
FACTORS
 Human leukocyte antigens (HLA) - regulate immune response used as a marker for
Aggressive periodontitis mainly HLA-A9 and HLA-B15.
 Negative correlation between HLA-A2, HLA-A12 and localized aggressive
periodontitis (LAP) have been found.
 Risk of disease is found in subjects with HLA-A9 and B15 positive individuals
which is about 1.5 to 3.5 times greater than those lacking theses antigens.
Alpan AL. Aggressive Periodontitis In: Periodontology and Dental implantology. 2018;103-129.

 Functional defects of PMNs, monocytes, or both:-
 Impair the chemotactic attraction of PMNs to the site
of infection or their ability to phagocytose & kill
microorganisms.
 Hyperresponsiveness of monocytes from LAP
patients involving their production of PGE2 in
response to LPS.
Increased connective tissue or bone loss.

 There are characteristic functional defects of polymorphonuclear
leucocytes with hyperesponsive monocytes.
 Altered T helper or suppressor T-cell have also been studied.
 Polyclonal activation of B-cell is seen by microbial plaque.
 Schenkein et al have recently reported elevated Serum IL-17 levels in
GAgP. They Suggested “An altered systemic response to oral bacterial
antigens”.

DIAGNOSIS
 Clinical diagnosis is based on information derived from a specific medical
and dental history and from the clinical examination of the periodontium.
 The purpose of clinical diagnosis is the identification of patients suffering
from AgP and of factors that have an impact on how the case should be
treated and monitored.

 Clinical examination
 probing pocket depth and
 attachment loss
 Radiological examination
 Microbiological examination,
 Evaluation of host response
 Genetic susceptibility to diagnose AgP
 Site specific destruction around incisors and molars is an important criteria to
diagnose LAP
 Severe destruction around minimum no. of teeth or generalized moderate to severe
destruction in early age again indicates aggressive nature of disease.

 Rate of bone loss in between two or more consecutive visits should be
carefully observed which can indicate the rapid rate of progression of
disease or active stage of disease.
 Presence of any systemic disease like Neutropenia, Leucocyte adhesion
deficiency, Chidiak -Higashi disease should be ruled out.
 Differential white blood cell count is important to rule out neutropenic
condition, in relation to confirm AgP.

 Incidental attachment loss due to other causes like presence of impacted
tooth or tumor or orthodontic tooth movement or advance decay of tooth
should be ruled out.
 Establishing the trace of familial aggregation of cases, on the basis of
history and clinical examination of family members can be done.
 A common strategy employed to detect early disease is to closely
monitor high-risk patients such as the siblings.

MICROBIOLOGIC DIAGNOSIS
 The international classification workshop indicated that the presence of
specific microorganisms like A.a. in particular represents one of the
secondary features of AgP.
 As such, microbiological diagnosis may be a useful laboratory addition
to establish a differential diagnosis between aggressive and chronic
forms of periodontitis.

 Culture Methods
 Only current method capable of determining the in vitro
antimicrobial susceptibility of periodontal pathogens.
 Provide a quantitative measurement of all major
viable microorganisms in the specimen. Eg : Malachite
green bacitracin agar, TSBV agar
Saroch N. Periodontitis In: Periobasics A textbook of Periodontitis and implantology.2;2019:339-363.

Immunodiagnostic methods
It employs antibodies that recognize specific bacterial antigens to detect
target microorganism.
Advantages:
 Do not require viable bacteria
 Less susceptible to variations in sample processing
 Less time consuming
 Easier to perform than culture method

 Bonta et al (1985) described an indirect immunofluroscence identification
method of A.a. with a detection limit of 500 cells/ml, a sensitivity of 82 -
100% and a specificity of 88-92% compared with selective &
nonselective culture.
 Evalusite test
Antibody based sandwich enzyme linked immunosorbent assay.
 Bacterial concentration fluroscene immunoassay.
Monoclonal antibodies to whole cell antigens

GENETIC DIAGNOSIS
Nucleic acid probe
 DNA probes entails segments of single stranded nucleic acid, labeled
with an enzyme or radioisotope that can locate and bind to their
complementary nucleic acid sequences with low cross reactivity to non
target microorganism.
 DNA probe may target whole genomic DNA or individual genes.

MANAGEMENT OF AGGRESSIVE
PERIODONTITIS

PRINCIPLES OF THERAPEUTIC INTERVENTION
 Treatment of Aggressive Periodontitis should only be initiated after
completion of a careful diagnosis.
 Successful treatment of Aggressive Periodontitis is considered to be
dependent on
 Early diagnosis
 Therapy towards elimination or suppression of the infecting
microorganisms
 Providing an environment conducive to long term maintenance.

THERAPEUTIC MODALITIES
 Early detection is critically important in the treatment of aggressive
periodontitis (generalized or localized) because preventing further
destruction is often more predictable than attempting to regenerate
lost supporting tissues.
 Therefore, at the initial diagnosis, it is helpful to obtain any
previously taken radiographs to assess the rate of progression of
the disease.

• Systemic Phase
• Initial Phase
• Re-evaluation Phase
• Surgical Phase
• Restorative Phase
• Maintenance Phase
THE PHASES OF
TREATMENT
INCLUDE:

MANAGEMENTOF AGGRESSIVEPERIODONTITIS
NON-SURGICAL THERAPY
Antimicrobial Therapy; Local Delivery
Full-Mouth Disinfection
Host Modulaton
Conventional Periodontal Therapy
•Surgical Resective Therapy
•Regenerative Therapy

NON-SURGICAL THERAPY
 Its effect on aggressive periodontitis is much less clear.
 SRP reduced the total sub-gingival bacterial counts and the proportions of certain
gram negative bacteria, but no periodontal pocket became free of A.
Actinomycetemcomitans.
 GAP responds well to SRP in the short term (upto 6months). However, after
6months, relapse and disease progression is reported.
 Gunsolley et al
 Haas et al, 2008
 Sigusch et al, 1998

Nonsurgical therapy alone as a treatment of localized aggressive
periodontitis -
 Slots & Rosling 1983, evaluated nonsurgical treatment alone in AgP.
Upon re-evaluation the combination of oral hygiene instructions along
with subgingival scaling and root planing did not eliminate, the
number of spirochetes, Aggregatibacter actinomycetemcomitans and
Capnocytophaga species but resulted in a small improvement in post-
treatment probing depths.

Nonsurgical therapy alone as a treatment of
Generalized Aggressive Periodontitis
 Purucker et al 2001 provided scaling and root planing for 30 patients
with generalized aggressive periodontitis. Two months after scaling
they found that the deepest sites in each quadrant experienced an
approximate 1 mm reduction in probing depth and a 0.5 mm gain in
attachment levels.

Antimicrobial Therapy
 Systemic tetracycline (250 mg of tetracycline hydrochloride
4x/day for atleast 1 week) in conjunction with local mechanical
therapy.
Nutalapati R, Kasagani SK et al in 2014 , concluded that systemic
administration of doxycycline with full mouth SRP resulted in better
improvement of periodontal parameters and elimination of putative
periodontal pathogens such as A.a, P.g, T. forsythia, than amoxicillin plus
metronidazole alone in patients with LAP.
Nutalapati R et al. Comparative evaluation of amoxicillin plus metronidazole and doxycycline alone in the nonsurgical treatment of localized
aggressive periodontitis . Indian J Oral Sci 2014;5:112-8

 If surgery is indicated, systemic TTC 1000mg stat should be
prescribed approximately 1 hour before surgery.
 TTC resistant A.A - Amoxcillin-MTZ
Ciprofloxacin-MTZ
 Doxycline, 100 mg/day, may be used instead of TTC.
 Chlorhexidine rinses should be prescribed and continued for
several weeks to enhance plaque control and facilitate healing.
Nutalapati R et al. Comparative evaluation of amoxicillin plus metronidazole and doxycycline alone in the nonsurgical treatment of localized

 Genco et al treated LAP patients with-
SRP+Systemic administration of TTC
(250mg q.i.d x 14days every 8weeks).
18mths
Bone loss stopped, 1/3rd of defects demonstrated an increase in bone level
 Liljenberg and Lindhe treated LAP patients with
Systemic administration of TTC (250mg q.i.d for 2 weeks)
Modified Widman flap
Periodic recall visits (one visit every month for 6mnths, then one visit every 3 mnths)
The lesions healed more rapidly and more completely.

 In practice, antibiotics are often used empirically without
microbial testing.
 Empiric use of antibiotics, such as a combination of amoxicillin &
MTZ, may be more clinically sound and cost-effective than
bacterial identification & antibiotic-sensitivity testing.

GENERALISEDAGGRESSIVE PERIODONTITIS
 Sigusch et al (2001), Xajigeorgiou et al (2006), Guerrero at al
(2007) suggested use of Clindamycin + SRP showed increase in
clinical attachment gain and reduction in pocket depth.
 Kaner et al (2007) showed use of MTZ/amoxicillin given
immediately after SRP will be more effective in resolving deep
sited in GAP patients.

Local delivery agents including solutions, gels,
fibers, chips
 Smaller dosages of topical agents can be delivered inside the
pocket.
 Avoidance the side effects of systemic antibacterial agents.
 Increases the exposure of the target microorganisms to higher
concentrations, of the medication.

Local drug delivery as an adjunct
 Sakellari D et al 2003 reported that tetracycline fibers, in
conjunction with scaling and root planing, in patients with
generalized aggressive periodontitis was more effective than scaling
and root planing alone and can also be used in situations where
systemic antibiotics are contraindicated.

Full-Mouth Disinfection
 Another approach to antimicrobial therapy
 The concept, described by Quirynen et al, consists of ;-
 Full mouth debridement completed in 2 appointments within a 24
hour period.
 The tongue is brushed with a chlorhexidine gel (1%) for 1 minute.
 Mouth rinsed with a chlorhexidine solution (0.2%) for 2minutes.
 Periodontal pockets irrigated with a chlorhexidine solution. (!%)

Host Modulation
 A novel approach in the treatment of AP and difficult to control
forms of periodontal disease.
Modulates the host response to disease.
TTCs
Growth factors
EMPs
BMPs
Bisphosphonates
NSAIDs
Teughels W, Dhondt R, Dekeyser C & Quirynen M. Treatment of aggressive periodontitis Periodontology 2000; 2014, 65:107–133.

Access surgery
 Modified Widman flap procedure effective in reducing PPD.
Christersson et al, 1985
 SRP + TTC administration + MWF surgery.
Lindhe & Liljenberg, 1984

Lindhe & Liljenberg 1984, treated 16 cases of localized Aggressive
Periodontitis with a combination of tetracycline and modified Widman
flap surgery. After 5years of maintenance they found significant
improvements in probing depths and attachment levels and evidence
of radiographic bonefill.

Surgical Resective Therapy
 Effective to reduce or eliminate pocket depth
 Difficult to accomplish if adjacent teeth are unaffected, (in cases
of LAP)
 Careful evaluation of the risks versus the benefits of surgery must
be considered on a case-by-case basis.

Regenerative Surgery
 Bone grafting
• Guided tissue regeneration using membranes,
 The use of biologic modifiers &
 Combinations of the above
Designed for the regeneration of steep vertical defects & have very specific indications
:- defect morphology, tooth mobility & furcation involvement.

Bone grafting
 Yukna & Sepe, reported on average defect fill of 80% with FDBA in 12
patients with LAP at re-entry after 12months.
 Evans et al evaluated a 4:1 ratio combination of B-tricalcium phosphate/
TTC, hydroxyapatite/TTC or freeze-dried bone allograft/TTC in patients
with LAP which showed significant increase in defect depth & pocket
depth were detected for each graft material.
 Hydroxyapatite/TTC > B-tricalcium phosphate/ TTC.

 OTHERS
1. Autogenous bone chips (Oahrains and Kaslick-1981)
2. Osseous coagulum (Burnette and Steroark-1969)
3. Frozen autogenous hip marrow (De Marco and Scaletter-1970)

GUIDED TISSUE REGENERATION
 PD reduction & clinical attachment gain significantly greater in the PTFE
membrane-treated defects than in osseous surgery-treated defects.
Sirirat M, Kasetsuwan J, Jeffcoat MK. Comparison between 2 surgical techniques for the treatment of early-onset periodontitis. J
Periodontol1996:67: 603-607
ENAMEL MATRIX PROTEINS
Esposito et al (2003) reported that use of emdogain can improve clinical attachment level (1.3mm)
and reduction in probing depth (1.0mm) compared to flap debridement alone.

PHOTODYNAMIC THERAPY
 Study by Rafael R. de Oliveira et al (2009) concluded that PDT and SRP showed good
results in the treatment of aggressive periodontitis.

OZONIZED WATER IN TREATMENT
OF AP.
 Effect of ozonized water on oral microorganisms & dental plaque was studied by
Nagayoshi et al., (2002).
 Useful in reducing the infections caused by oral microorganisms in dental plaque.
 Ramzy et al assessed the clinical and antimicrobial effect of ozonized water in
management of aggressive periodontitis, found that ozone has a potent
antibacterial effect explained by the fact that it causes disruption of the envelope
integrity through peroxidation of phospholipids.

 Extraction when necessary with immediate replacement of anterior teeth with
a hopeless prognosis.
 Periodontal surgery / Regenerative therapy .
Pocket elimination procedure.
Isolated infrabony lesions - GTR / bone grafting techniques.
 The authors reported significant improvements in both probing depths and
attachment levels.

 Occlusal adjustment in case of tooth migration
In few cases after successful periodontal treatment and after the condition
has become fully stable, gentle orthodontic retraction of labially drifted
upper incisors might be considered if they can be stabilized behind the
lower lip or splinted in a stable position.
 Prosthetics - for missing teeth after extraction of teeth with poor prognosis.
 Maintenance - Patient should be recalled every 3 month for oral hygiene
reinforcement and scaling.

FUTURE DIRECTIONS
 Genetic tests in Diagnosis of Aggressive Periodontitis.
 Use of host modulation therapy.
 Periodontal vaccines.

PERIODONTAL MAINTENANCE
 The duration between recall visits should be usually short during the
period after completion of therapy, generally no longer than 3-month
intervals.
 Monitoring as frequently as every 3-4 weeks may be necessary when the
disease is thought to be active.
 If signs of disease activity and progression persist despite therapeutic
efforts, frequent visits and good patient compliance, microbial testing
may be indicated.

CONCLUSION
 AgP is definitely a different entity than commonly present chronic
periodontitis. Quality of plaque i.e. specific micro organisms seems to be
responsible for severe periodontal destruction. Susceptibility of individuals is
further determined by genetic, environmental and host immune factor.
 Phase I therapy is mandatory in controlling the infection and antibiotics act as
adjuvant to it. Periodontal surgical therapy has definitely given positive
results.
Thus a thorough examination leading to accurate diagnosis and subsequent
comprehensive treatment is the supreme responsibility.

REFERENCES
 Maurizio S, Tonetti and Mombelli A : Aggressive Periodontitis in Clinical
Periodontology and Implant Dentistry, Wiley 2010; 6: 428-458.
 Kulkarni C, Kinane D. Host response in aggressive periodontitis.
Periodontology 2000; 2008,14:79–91.
 American Academy of Periodontology. Glossary of periodontal terms.4;2001.
 Novak K F and Novak J M:Aggressive Periodontitis in Carranza’s clinical
periodontology,Elsevier,12,2010;506-512.
 Armitage G C, Cullinan M. Comparison of the clinical features of chronic and
aggressive periodontitis. Periodontol 2000; 2010,53:12–27.
 Armitage G C. Comparison of the microbiological features of chronic and

 Vieira A , Albandar J. Role of genetic factors in the pathogenesis of
 KononenE , Muller H. Microbiology of aggressive periodontitis.
Periodontol 2000;2014,65:46–78.
 Albandar J. Aggressive periodontitis:case deﬁnition and diagnostic
criteria. Periodontol 2000;2014,65:13–26.
 Baer PN. The case for periodontosis as a clinical entity. J Periodontol
1971: 42: 516-520.
 Nutalapati R, Kasagani SK, Jampani ND, Mutthineni RB, Chintala
S, Kode VS. Comparative evaluation of amoxicillin plus metronidazole
and doxycycline alone in the nonsurgical treatment of localized
 Lang LP and Carring T. Aggressive periodontitis In: Lindhe’s
Clinical periodontology and implant dentistry. Elsevier 5:438-460.

 Saroch N. Periodontitis In: Periobasics A textbook of Periodontitis and
implantology.2;2019:339-363.
 Alpan AL. Aggressive Periodontitis In: Periodontology and Dental
implantology. 2018;103-129.
 Teughels W, Dhondt R, Dekeyser C & Quirynen M. Treatment of
aggressive periodontitis Periodontology 2000; 2014, 65:107–133.
 Gottlieb B. The formation of the pocket: diffuse atrophy of alveolar bone. J
Am Dent Assoc;1998,15:462–476.

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