Aggressive periodontitis

Prof(Dr) Vivek Kr. Sharma: Aggressive Periodontitis, BDS3rd yr 2019-2020
Aggressive Periodontitis(AgP)
DEFINITION:
1. Aggressive periodontitisis a destructive disease characterized by the following:
The involvementofmultiple teeth with a distinctive pattern of periodontaltissue loss;
Ahigh rate of disease progression; an earlyage ofonset; and the absence of systemic diseases
2. Aggressive periodontitiscomprisesa group ofrare, often severe, rapidly progressiveformsof periodontitis, often characterized by an early
age of clinical manifestation and a distinctive tendency for cases to aggregate in families.(Maurizio S. Tonettiand Andrea Mombelli, Clinical
Periodontologyand Implant Dentistry, Sixth Edition)
3. Aggressive periodontitis, a clinically challenging subform of periodontitis featuring rapid loss of periodontalattachment and tooth supporting
bone in otherwise healthy patients. (MoritzKebschull, HenrikDommisch, Newman and Carranza'sClinicalPeriodontology, 13 th edition).

ETIOLOGY
Aggressive periodontitisis a multifactorial and genetically complex disease. An increase in host susceptibility may be caused by the
combined effect of genetic predisposition, environmentalfactors(virulentpathogens, tobacco smoking, personaland professionalhygiene)and
local contributing factors. Furthermore, herpesviruscould be an additionalfactor of susceptibility and severity in aggressive periodontitis(5) .
The generalized formof aggressive periodontitis hasbeen strongly associated with bacteria such as Porphyromonasgingivalis,
Agregatibacter actinomycetemcomitans (Aa) and Tannerella forsythia; In generalized aggressive periodontitisthere is an inadequate response
to the action of the periodontalpathogenicbacteria caused by a variety of genetic and immunological risk factors.
Recentfindings suggest that the pathogenesisof localized aggressive periodontitis is associated with severe abnormalitiesin the
neutrophilfunction, producing neutrophil-mediated tissue injury. In addition, the neutrophilsof patients with localized aggressive periodontitis
show reduced calciumentry, defective calcium influx factor, and abnormalactivity of protein kinase C, among other abnormalities.
Epidemiology
The prevalence ofaggressive periodontitis is variable. Itis estimated that there is a low prevalence (lessthan 1%)in Caucasian subjects
living in developed countriescompared to those living in developing countries(-0.5 to 5%). One aspectthat complicates the interpretation of
aggressive periodontitis regarding epidemiologicalinformation is the parametersused to evaluate the identification of cases, which vary from
one study to the other. Africans and African-Americansseemto have the highest prevalence ofaggressive periodontitis: 1.0-3.0%.Theyare
followed by Asians, with 0.4-1.0%, and Hispanicsand South Americans, with 0.5-1.0%, compared to Caucasian young populations, with 0.1-
0.2%
Risk factors
One of the main riskfactors of aggressive periodontitisis family history associated with inherited genetic traits. There isstrong
evidence that showsfamily history in young patients with early onsetof aggressive periodontaldisease.
Regarding oralhygiene, studieshave suggested thatthere would be no correlation between plaque levelsand the presence of
disease. Risk factors identified for periodontaldiseasesare similar to the onesfor chronicperiodontitis and aggressive periodontitis. These
factors include: immunological host factors, ethnicity, microbiological factors, oralhygiene habits, age, gender, frequency ofdental visits,
demographicfactors, smoking habits and psychologicalfactors.
Histopathologyand immunopathology
No major differences between aggressive and chronicperiodontitisin terms of its histopathology and immunopathology are reported.
Both appear asplasma-celldominated lesions and mediated by Th2 cells. The localized form of aggressive periodontitismay representa
different entity with a genetic or epigeneticcomponent. Thiscould explain the association with the family history. On the other hand, aggressive
generalized periodontitiscould representan advanced chronicperiodontitisin young people with extreme susceptibility, which would explain the
common histopathological and immunopathological characteristics.
Localized aggressive periodontitis is frequently associated with deficiencies in the neutrophilicfunction and with high serum antibody
response againstperiodontopathogens; while generalized aggressive periodontitis is also associated with deficiencies in neutrophilfunction, but
with low serum antibody response againstperiodontopathogens. Furthermore,the colonization of the periodontalpocket by periodontal
pathogenicbacteria could lead to an overlap ofchronicperiodontitis, which may complicate the histological and immunohistological condition
Microbiology
Some reportssupportthe existence of subgingivalmicrobiota resistant to antibiotics of choice, which could explain eventualfailures
in the therapeutic modality. Localized aggressive periodontitisis mainly associated with the bacteria Aggregatibacter actinomycetemcomitans,
while generalized aggressive periodontitis is strongly associated with specific bacteria such as Porphyromonasgingivalis, Tannerella forsythia
and Aggregatibacter actinomycetemcomitans, Gram-negative coccobacillus, capnophile, microaerophilic. Microorganismsproduce several
virulence factorsthat could be involved in the destruction of periodontaltissues. The most important one seems to be leukotoxicactivity. The
highly leukotoxicbacterial strains of Aa (strain JP2) can produce 10 to 20 times more toxins than other strains, giving them the potential to
interfere with innate immune host defenses. Some studies have shown that highly leukotoxicstrains appear exclusivelyin individualsor families
with a history of aggressive periodontitis
Clinical forms
1) Localized aggressive periodontitis It beginsat peripubertalage. Itis mainly located in the first molars/incisors, with interproximal
attachment loss in at least two permanentteeth, one of which is a first molar, and which affects no more than two other teeth, apart from the first
molars and incisors. It can also presentatypicalpatterns, such as affecting other teeth instead of those mentioned.

2) Generalized aggressive periodontitis It usually affects people under 30, butthey may be older. There isan interproximalattachment
loss which affects at least three permanentteeth additional to the first molars and incisors. Attached gingiva tissue loss is episodic.
DIAGNOSIS
* Evaluation of the systemic condition
* The patient's medical history should be thoroughly evaluated.
* We must determine if there are risk factors such as smoking and psychosocialstress.
Since one of the characteristics of aggressive periodontitisis the absence of systemic diseases complementary tests can be run, if
necessary, to rule out background pathologies. Recordifthe patient is taking any medication. Inquire aboutfamily history regarding periodontal
condition .
Periodontalclinical examination The following should be evaluated:
Clinical attachment levels, periodontalpocket depth, bleeding on probing, furcationscompromised,
dental mobility, suppuration and oralhygiene.
Radiologicalexamination It is extremely important. The following are recommended:
 Periapicalradiographicseries: Itshould be done using the paralleltechnique and, preferably, a millimeter grid. There are
the following options: seven radiographsfor the upper arch and seven for the lower arch, two interproximalradiographsfor molarsand two for
premolars.
 Radiovisiography: Thisismainly indicated for cases of diagnostic doubt, regenerative therapyevaluation, periodontal
status monitoring, among others. It is especially recommended for young patients with mixed dentition, where probing can be confusing. A
distance greater than 2 mm between the cementoenamel junction and the alveolar crestin subjects with mixed dentition may suggest
aggressive periodontitis.
MANAGEMENTACCORDINGTOCOMPLEXITYLEVELAND RESOLUTIONABILITY
Studies agree that treatment should be supplemented with antibiotics. The objectivesof the treatment are the same as for chronic
periodontitis: reducing or eliminating the bacterial load and the contributory riskfactors, in addition to regenerating the attachment apparatusas
soon as possible.
TREATMENT PLANSEQUENCEFORPATIENTSWITH AGGRESSIVEPERIODONTITIS
1) Systemic Phase
Medicalreferral, if indicated
Medical interconsultation for the modulation of risk factors (tobacco, psychosocialstress)
2) Initial Phase
 Emergency treatment, if necessary
 Educating the patient aboutthe disease process, contributing factors, perpetuating factors and triggers
 Teaching the patient about oralhygiene, evaluation and reinforcementofplaque controlmeasures
 Study, diagnosisand treatment of occlusal disharmony and temporomandibular disorders
 Taking bacterialsamples from selected pockets, cultures and antibiotic sensitivity testing can also be
considered
 Prior dentaltreatments, if necessary
 Supragingivaland subgingivalscaling and rootplaning. Mechanicaltherapy iskey in the treatment of
aggressive periodontitis. Even currentconsensusisthat antimicrobial therapy should be preceded by
mechanical debridementto break the structure of the biofilm.
 Atraumatic extraction of non-viable teeth preserving the ridge.
 Localand systemic antibiotic treatment. The application of antibiotics via both pathways has
advantagesand limitations

LocalisedAggressivePeriodontitis(LAgP)
LAgPpatient; (a)-clinicalview of the LAgPpatient, (b) 7 mm probing depth at distal of the incisor tooth, (c) radiographicview ofthe LAgPpatient

Generalised Aggressive Periodontitis(GAgP)
GAgPpatient; (a) clinical view ofthe GAgPpatient, (b, c) increased probing depth around the teeth, (d) radiographicview ofthe GAgPpatient.
CONCLUSION
AgPis a complex disease and has multifactorial etiology. While bacterial plaque is essential for initiation of disease, it is generally
accepted that genetic factors and host immune response play a large role in the disease susceptibility. Also environmentaland behavioral
factors determine the final clinical outcome. The outcome of rapid and severe alveolar boneloss; gingivalrecession, pathologicalmigration of
teeth, mobility and eventualloss of teeth occur. Because of the clinical results, AgP patients suffer social problemsdue to esthetic, phonetic and
nutritional problemsand their quality of life diminishes. The treatment of these patients is quite challenging, due to the absence of a standard
treatment protocolfor this disease which its etiology is not fully understood, butalso because of the rapid progression, severe periodontaltissue
loss and recurrence ofthe disease. Non-surgicaland surgicalperiodontaltreatments combined with systemic antibiotics are recommended for
the complete eradication of deep periodontalpockets. In long term, active periodontaltreatment must followed by maintenance periodontal
treatment for preventing attachment and tooth loss.

Aggressive periodontitis

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