Aggressive periodontitis

AGGRESSIVE PERIODONTITIS
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 Introduction
 Key diagnostic criteria of aggressive periodontitis
 Localized aggressive periodontitis
 Generalized aggressive periodontitis
 Histopathology of aggressive periodontitis
 Risk factors for aggressive periodontitis
 Epidemiology
 Diagnostics
 Prognosis of aggressive periodontitis
 Considerations when redefining aggressive periodontitis
 References
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1) Aggressive periodontitis generally affects:-
 systemically healthy individuals
 less than 30 years of age,
 although patients may be older.

2) Aggressive periodontitis may be universally distinguished from chronic
periodontitis by:-
i) the age of onset,
ii) the rapid rate of disease progression,
iii) associated subgingival microflora – nature and composition,
iv) host's immune response alterations, and
v) a familial aggregation of diseased individuals.
vi) In addition, a strong racial influence is observed in the United States (US); the
disease is more prevalent among African Americans.

3) Aggressive periodontitis describes three of the diseases
formerly classified as “early-onset periodontitis.” They
are :-
i) localized aggressive periodontitis (LAP), which was
formerly termed localized juvenile periodontitis (LJP),
and
ii) generalized aggressive periodontitis (GAP), which
encompasses the diseases previously classified as
generalized juvenile periodontitis (GJP) and rapidly
progressive periodontitis (RPP).

With regard to its clinical and para-clinical aspects, Agp can be
distinguished from Chronic periodontitis.
Agp is defined by the following characteristics:-
 Except of the presence of periodontitis, patients are otherwise
clinically healthy.
 Rapid attachment loss and bone destruction.
 Familial aggregation.

Non-constant characteristics of the disease:
 Amounts of microbial deposits are inconsistent with the
severity of periodontal tissue destruction,
 Elevated proportion of Actinobacillus
actinomycetemcomitans, and in some populations
Porphyromonas gingivalis may be elevated,
 Phagocyte abnormalities,
 Hyper-responsive macrophage phenotype including elevated
levels of PGE2 and IL-1β,
 Progression of attachment loss and bone loss may be self-
arresting.

 Presented a contemporary case definition of aggressive periodontitis.
 Key diagnostic criteria of this disease include an:
Early age of onset,
Involvement of multiple teeth with a distinctive pattern
of clinical attachment loss and radiographic bone loss
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Relatively high rate of disease progression and the absence of systemic
diseases that compromise the host's response to infection. Although in some
patients the disease may start before puberty, in most patients the age of
onset is during, or somewhat after, the circumpubertal period. A typical
patient shows disease onset at an early age (i.e., before 25 years of age),
although identification of the affected patient usually occurs after disease
commencement.
9

Initially, the periodontal lesions show a distinctive pattern, depicted
radiographically as vertical bone loss at the proximal surfaces of posterior
teeth, and the bone loss usually occurs bilaterally. In advanced cases of
aggressive periodontitis the periodontal lesions may be depicted
radiographically as a horizontal loss of bone.
The primary teeth may also be affected, although early exfoliation of these
teeth is not common.
10

Aggressive periodontitis may be localized or generalized, in localized
aggressive periodontitis (LAP), tissue loss usually starts at the permanent first
molars and incisors, and with increasing patient age the disease may progress to
involve the adjacent teeth. The generalized form of aggressive periodontitis
involves most or all of the permanent teeth.
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II) LOCALIZED
AGGRESSIVE
PERIODONTITIS (LAP)
III) GENERALIZED
AGGRESSIVE
PERIODONTITIS (GAP)
Consensus Report of the Workshop for the Classification of Periodontal
Diseases (Lang et al, 1999) identified certain clinical and paraclinical
features, which allow a subclassification of AgP into:

A) Historical background
1) 1923 (Gottlieb) :-
i) reported a patient with a fatal case of epidemic
influenza and a disease that Gottlieb called
“diffuse atrophy of the alveolar bone.”
II) LOCALIZED AGGRESSIVE PERIODONTITIS (LAP)

1) 1923 (Gottlieb) :-
ii) “diffuse atrophy of the alveolar bone” characteristics –
- Periodontal ligament : loss of collagen fibers and their replacement by
loose connective tissue.
- bone : extensive resorption resulting in widened periodontal space.

2) 1928 (Gottlieb) :-
i) termed the disease “deep cementopathia” because -
he attributed this condition to the inhibition of continuous cementum
formation,
(which he considered essential for maintenance of the periodontal fibers).

2) 1928 (Gottlieb) :-
ii) “deep cementopathia” , Gottlieb hypothesized that –
this was a “disease of eruption” and that cementum initiated a foreign body
response.
As a result, it was postulated that the host attempted to exfoliate the tooth,
resulting in the observed bone resorption and pocket formation.

3) 1938 (Wannenmacher) :-
described incisor–first molar involvement and
called the disease “parodontitis marginalis progressiva.”

4) Many authors considered this to be a degenerative, noninflammatory disease
process and
therefore gave it the name “periodontosis.”

5) Other investigators –
denied the existence of a degenerative type of
periodontal disease and
attributed the changes observed to trauma of occlusion.

6) 1966 (World Workshop in Periodontics) :-
i) concluded that the concept of periodontosis as a
degenerative entity was unsubstantiated and that the
term should be eliminated from periodontal
nomenclature.
ii) The committee did recognize that a clinical entity
different from adult periodontitis might occur among
adolescents and young adults.

7) 1967 (Chaput and colleagues) and
1969 (by Butler) :-
- Introduced the term Juvenile periodontitis.

8) 1971 (Baer) :-
defined it as "a disease of the periodontium occurring in
an otherwise healthy adolescent which is characterized
by a rapid loss of alveolar bone about more than one
tooth of the permanent dentition. The amount of
destruction manifested is not commensurate with the
amount of local irritants."

9) 1989 (World Workshop in Clinical Periodontics) :-
categorized this disease as localized juvenile periodontitis
(LJP), a subset of the broad classification of early onset
periodontitis (EOP).
Under this classification system, age of onset and
distribution of lesions were of primary importance
when making a diagnosis of LJP.

10) Most recently,
disease with the characteristics of LJP has
been renamed localized aggressive
periodontitis.

B) Clinical characteristics:-
1) usually has an age of onset around puberty.
2) Clinically, it is characterized as having "localized first
molar/incisor presentation with interproximal
attachment loss on at least two permanent teeth, one of
which is a first molar, and involving no more than two
teeth other than first molars and incisors"

3) Possible reasons for the limitation of periodontal
destruction to certain teeth have been suggested:
Reason 1- A strong antibody response to infecting agents.
Reason 2- Bacteria antagonistic to A. actinomycetemcomitans.
Reason 3 - A. actinomycetemcomitans may lose its leukotoxin
producing ability for unknown reasons.
Reason 4 - A defect in cementum formation.

- After initial colonization of the first permanent teeth to erupt (the first molars
and incisors),
- Aa evades the host defenses by:-
production of polymorphonuclear leukocyte chemotaxis-inhibiting factors,
endotoxin,
collagenases,
leukotoxin, and other factors
- thus, allowing the bacteria to colonize the pocket and initiate the destruction of
the periodontal tissues.

- After this initial attack, adequate immune defenses are
stimulated to produce opsonic antibodies:-
* to enhance the clearance,
* phagocytosis of invading bacteria and
* neutralize leukotoxic activity.
- In this manner, colonization of other sites may be
prevented.

Reason 2- Bacteria antagonistic to A. actinomycetemcomitans.
- colonize the periodontal tissues and inhibit
A. Actinomycetemcomitans from further colonization of
periodontal sites in the mouth.
- This would localize A. Actinomycetemcomitans infection and
tissue destruction.

Reason 3 - A. actinomycetemcomitans may lose its leukotoxin
producing ability for unknown reasons.
- If this happens,
the progression of the disease may become arrested
or retarded and colonization of new periodontal
sites averted.

Reason 4 - A defect in cementum formation.
- Root surfaces of teeth extracted from patients with localized
aggressive periodontitis have been found to have hypoplastic or
aplastic cementum.
- This was true not only of root surfaces exposed to periodontal
pockets but also of roots still surrounded by their periodontium.

4) A striking feature of localized aggressive periodontitis
is the lack of clinical inflammation despite the presence
of deep periodontal pockets.
5) In many cases the amount of plaque on the affected teeth is
minimal, which seems inconsistent with the amount of
periodontal destruction present.

6) As the name suggests, localized aggressive periodontitis
progresses rapidly.
7) Evidence suggests that the rate of bone loss is about three to four
times faster than in chronic periodontitis.

Other clinical features may include:-
8) distolabial migration of the maxillary incisors with
concomitant diastema formation,
9) increasing mobility of the first molars,
10) sensitivity of denuded root surfaces to thermal and
tactile stimuli,

Other clinical features may include:-
11)deep, dull, radiating pain during mastication,
(probably because of irritation of the supporting structures by
mobile teeth and impacted food).
12)Periodontal abscesses may form at this stage,
13)regional lymph node enlargement may occur.

C) Clinical characteristics:-
 It should be noted that not all cases of localized aggressive
periodontitis progress to the degree described
previously.
 In some patients, the progression of attachment
loss and bone loss may be self-arresting.

D) Radiographic findings:-
1)Vertical loss of alveolar bone around
the first molars and incisors, beginning
around puberty in otherwise healthy
teenagers, is a classic diagnostic sign.

D) Radiographic findings:-
2)may include an "arc-shaped loss of
alveolar bone extending from the distal
surface of the second premolar to the
mesial surface of the second molar”.

E) Prevalence and Distribution by age and
gender:-
1) The prevalence in geographically diverse
adolescent populations is estimated
to be below 1%.
2) Most reports suggest a low prevalence,
about 0.2%.

gender:-
3)
STUDY AGE PREVALENC
E
Radiographic study – performed
individually in :-
Finland
Switzerland
16year old
adolescents
0.1%
Clinical and radiographic study
of 7266 English adolescents
15 t0 19 years 0.1%
U.S. National survey 14 to 17 years 0.53%

gender:-
4) black males were 2.9 times more likely to have
the disease than black females.
5) In contrast, white females were more likely to
have localized aggressive periodontitis
than white males.

gender:-
6) highest prevalence of localized aggressive
periodontitis among black males, followed in
descending order by black females, white
females, and white males.

E) Prevalence and Distribution by age and gender:-
7) Localized aggressive periodontitis affects both males and females and
8) Seen most frequently in the period between puberty and 20 years of age.
9) Some studies have suggested a predilection for female patients, particularly in
the youngest age groups, whereas others report no male-female differences
incidence when studies are designed to correct for ascertainment bias.

E) Prevalence and Distribution by age and gender:-
9) Some studies have suggested a predilection for female
patients, particularly in the youngest age groups.
10)Whereas others report no male-female differences in
incidence when studies are designed to correct for
ascertainment bias.

 Ascertainment bias seems to be defined to two different, but
related ways.
 Ascertainment bias generally refers to situations in which the way
data is collected is more likely to include some members of a
population than others. This can happen when there is more
intense surveillance or screening for the outcome of interest in
certain populations. For example, one might find a higher rate of
breast cancer in a richer population with easy access to
mammography when compare to a poorer population with limited
healthcare access.
 Ascertainment bias is also used to refer to the situation when the
results of a clinical trial are distorted by knowledge about which
intervention each participants is receiving, either because of lack
of blinding or improper allocation concealment.

Daniel H. Fine, Amey G. Patil, Bruno G. Loos (2018)
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III) GENERALIZED AGGRESSIVE PERIODONTITIS
(GAP)

(GAP)
A) Clinical characteristics:-
1) affects individuals under the age of 30, but older patients also may be affected.
2) produce a poor antibody response to the pathogens present.
3) "generalized interproximal attachment loss affecting at least three permanent
teeth other than first molars and incisors"

(GAP)
4) The destruction appears to occur episodically with
periods of advanced destruction followed by stages
of quiescence of variable length (weeks to months or
years).

(GAP)
5) Quantitatively, the amount of plaque seems
inconsistent with the amount of periodontal
destruction.
6) Qualitatively,
P. gingivalis, A. actinomycetemcomitans and
Bacteriodes forsythus frequently are detected in the
plaque that is present.

(GAP)
7) Gingival tissue response 1 :-
- severe, acutely inflamed tissue, often proliferating,
ulcerated and fiery red.
- Bleeding may occur spontaneously or with slight
stimulation.
- Suppuration may be an important feature.
This tissue response is considered to occur in the
destructive stage, in which attachment and bone are
actively lost. Copyright ©2021 Periowiki.com 53

(GAP)
8) Gingival tissue response 2 :-
 the gingival tissues may appear pink, free of inflammation,
 occasionally with some degree of stippling, although stippling
may be absent.
 However, deep pockets can be demonstrated by probing.
 This tissue response has been considered by Page and Schroeder"
to coincide with periods of quiescence in which the bone level
remains stationary.

(GAP)
9) Some patients with GAP may have systemic manifestations such as :-
weight loss,
mental depression and
general malaise.
These patients should receive medical evaluations to rule out possible
systemic involvement.

(GAP)
10) As seen with localized aggressive periodontitis,
cases of generalized aggressive periodontitis may be
arrested spontaneously or after therapy,
 Whereas,
others may continue to progress inexorably to tooth loss
despite intervention with conventional treatment.

(GAP)
B) Radiographic findings:-
1) range from severe bone loss associated
with the minimal number of teeth, as described
previously,
to advanced bone loss affecting the majority of
teeth in the dentition

(GAP)
B) Radiographic findings:-
2) A comparison of radiographs taken at different times illustrates
the aggressive nature of this disease.
 Page and co-workers described sites in GAP (formerly RPP)
patients that demonstrated osseous destruction of 25% to 60%
during a 9-week period.
 Despite this extreme loss, other sites in the same patient showed
no bone loss.

(GAP)
C) Prevalence and Distribution by age and
gender:-
 In a study of untreated periodontal disease conducted
in Sri Lanka by Loe and colleagues,
36.8% of the population had rapid progression of
periodontal disease characterized by a yearly loss of
attachment of 0.1 to 1.0 mm

(GAP)
gender:-
 In the U.S., a national survey of adolescents aged
14 to 17 reported that,
 0.13% had generalized aggressive periodontitis.

(GAP)
gender:-
 blacks were at much higher risk than whites for
all forms of aggressive periodontitis and
 males were more likely to have generalized
aggressive periodontitis than females.

(GAP)
Generalized Aggressive Periodontitis in Preschoolers: Report of a
case in a 3-1/2 year old boy:
Camila Palma Portaro, Yndira Gonzalez Chópite , Abel Cahuana Cárdenas (2008):
 The clinical oral examination revealed a full primary dentition, heavy plaque
accumulation, absence of lower incisors (71, 81), severe gingival inflammation,
generalized gingival recession and abscesses at the level of the maxillary second
primary molars (55 and 65).

(GAP)
 No evidence of caries. The panoramic X-ray revealed severe generalized vertical
and horizontal bone loss.

(GAP)
 Complete medical evaluation :
 complete blood count was within normal limits, including basal glucose and
creatinine levels, coagulation factors, alkaline phosphatase levels, absolute T4
lymphocyte count, immunoglobulins G, A, M and IgG subclasses.
 Absolute monocyte and neutrophil counts were slightly elevated.
Subgingival plaque samples revealed:
 Aerobic and anaerobic flora, especially Streptococcus Viridans and
Peptostreptococcus spp.
 Microbiological tests on selective media Aggregatibacter (actinobacillus
actinomycetemcomitans) or Prevotella intermedia were not available.

(GAP)
 Due to the age of the patient, the severity of bone loss, following teeth were
extracted: 54, 52, 51, 61, 62, 64, 74, 72, 82 and 84. Canines and second primary
molars were maintained. Due to uncooperative behavior, dental extractions were
done under general anesthesia.

(GAP)
 Extracted teeth had an irregular external resorptive pattern.
 Camila Palma Portaro, Yndira Gonzalez Chópite , Abel Cahuana Cárdenas (2008):
hypothesized that,
 the presence of extensive eroded areas devoid of cementum in the extracted primary teeth of
this patient could have facilitated the progress of periodontal disease.
 Alternatively, the external root resorption may have been a pulp reaction to
periodontopathic bacteria.

(GAP)
Treatment:
 The remaining teeth underwent root planing and scaling every month during the first year.
Moreover, parents were advised to brush the boy’s teeth with a 0.12% chlorhexidine rinse
three times a day during 3 months.
 Once the patient’s periodontal condition was stabilized 12 months post-treatment, at parent
and patient’s request, and in view of his good compliance, rehabilitation was done partial
acrylic appliances (“pedi-partials”) to restore function and esthetics.
 At this point the patient was referred for another complete blood count;all the results were
normal, including the absolute monocyte and neutrophil counts.

(GAP)
 More than 3-1/2 years post-treatment and with monthly recall appointments, the
gingival and periodontal health of the patient remains good.
 Clinical and radiographic examinations reveal that permanent incisors and first
molars have erupted without signs of periodontal disease.

(GAP)
 Camila Palma Portaro, Yndira Gonzalez Chópite , Abel Cahuana Cárdenas (2008):

70

Authors have observed that extracted teeth in patients with aggressive
periodontitis exhibit thin cementum areas and have suggested that this
alteration may be a major determinant of disease progression due to
the increased risk of pathogen invasion.
 Bodur A, Bodur H, Bal B, Balo? K. Generalized aggressive periodontitis in a
prepubertal patient: a case report Quintessence Int, 32: 303–8, 2001.
 Page RC, Baab DA. A new look at the etiology and pathogenesis of early-onset
periodontitis. Cementopathia revisited. J Periodontol, 56: 748–51, 1985.
 Bimstein E, Wignall W, Cohen D, Katz J. Root surface characteristics of children
teeth with periodontal diseases. J Clin Pediatr Dent, 32: 101–4, 2008.

 Stambolieva and Bourkova (1970) found increase in the numbers of acid
phosphatase positive macrophages (phagocytic macrophages) in
aggressive periodontitis patients.
 In the pretreatment biopsies of LAP, there was predominant plasma cell
inflammatory infiltration, (Liljenberg B, Lindhe J. 1980) and the root
surfaces of individuals with aggressive periodontitis were observed to be
heavily covered by neutrophils (Fine DH, Greene LS 1984).
 The abundant plasma cells in the connective tissue and a significant
increase in numbers of plasma cells as the severity of the lesion increased
can be noted in both aggressive and chronic periodontitis (Syed Wali
Peeran , Karthikeyan Ramalingam 2021).

 A fully developed lesion consists of plasma cell dominated infiltration in the
connective tissue with neutrophils migrating through the pocket lining epithelium
and creating a layer between the plaque and tissues (Joshipura V, Yadalam U,
Brahmavar B. (2015)
 IgM and IgA levels are comparable with that of chronic periodontitis
(Syed Wali Peeran , Karthikeyan Ramalingam 2021).

A)
Microbiologic
factors
B)
Immunologic
factors
C) Genetic
factors
D)
Environmental
factors

MICROBIOLOGIC FACTORS:-
A. actinomycetemcomitans has been implicated
as the primary pathogen associated with LAP.

MICROBIOLOGIC FACTORS:- As evidence provided by
Tonetti and Mombelli –
1) Aa is found in high frequency (approximately 90%) in lesions
characteristic of LAP,
2) sites with evidence of disease progression often show elevated levels of Aa,
3) many patients with the clinical manifestations of LAP have significantly
elevated serum antibody titers to Aa,
4) clinical studies show a correlation between reduction in the subgingival
load of Aa during treatment and a successful clinical response,
5) Aa produces a number of virulence factors that may contribute to the
disease process. Copyright ©2021 Periowiki.com 76

MICROBIOLOGIC FACTORS:-
Electron microscopic studies of LAP have revealed bacterial invasion
of connective tissue that reaches the bone surface.
The invading flora has been described as morphologically mixed but
composed mainly of gram-negative bacteria, including cocci, rods,
filaments, and spirochetes.
Using different methods, including immunocytochemistry and
electromicroscopy, several tissue-invading microorganisms have been
identified as Aa, Capnocytophaga sputigena, Mycoplasma spp. and
spirochetes.

B) IMMUNOLOGIC FACTORS:-
The human leukocyte antigens (HLA), which regulate
immune responses, are candidate markers for
aggressive periodontitis.
Although the findings with many HLA antigens have
been inconsistent, HLA-A9 and B15 antigens are
consistently associated with aggressive periodontitis

Functional defects of polymorphonuclear leukocytes
(PMNs) :-
impair either the chemotactic attraction of PMN to the
site of infection or
impair their ability to phagocytose and kill
microorganisms.

hyperresponsiveness of monocytes from LAP
patients with respect to their production of PGE2 in
response to lipopolysaccharide (LPS).
This hyperresponsive phenotype could lead to
increased connective tissue or bone loss due to
excessive production of these catabolic factors.

poorly functional inherited forms of monocyte
FcyRII, the receptor for human IgG2 antibodies, have
been shown to be disproportionately present in patients
with localized aggressive periodontitis.

Autoimmunity has been considered to have a role in GAP
according to Anusaksathien and Dolby,' who found host
antibodies to collagen, DNA, and immunoglobulin G (IgG).
Possible immune mechanisms include:-
-an increase in the expression of type II major histocompatibility
complex (MHC) molecules, HLA DR4 ,
- altered helper or suppressor T-cell function,
- polyclonal activation of B cells by microbial plaque,
- genetic predisposition.

C) GENETIC FACTORS:-
Currently, specific genes have not been identified that
are responsible for these diseases.
However, segregational analyses and linkage analyses of families
with a genetic predisposition for localized aggressive periodontitis
suggest that,
a major gene plays a role in this disease, which is transmitted
through an autosomal dominant mode of inheritance in U.S.
populations.

Some immunologic defects associated with aggressive
periodontitis may be inherited.
For example, Van Dyke et al reported a familial
clustering of the neutrophil abnormalities seen in LAP.
This clustering suggests that the defect(s) may be
inherited. Copyright ©2021 Periowiki.com 84

It is unlikely that all patients affected with aggressive periodontitis have the
same genetic defect.
As summarized by Tonetti and Mombelli,
"It seems that specific genes may be different in various populations and/or
ethnic groups and therefore true heterogeneity in disease susceptibility may be
present. The role of specific genes remains to be elucidated."

Interleukin-1 (IL-1) is a potent pro-inflammatory mediator that is mainly released
by monocytes, macrophages and dendritic cells and genetic polymorphisms of IL1
have been studied in association with AgP.
Three studies have reported no association between the carriage rates of the IL1A −
889 (+4845) C → T gene and AgP (Walker SJ et al 2000; Brett PM et al 2005;
Fiebig A 2008).
But one study have found an association with this gene and AgP in Chinese
Population. (Li QY et al 2004).
IL1B + 3954 (+3953) C → T gene polymorphisms and carriage rate of the rare (R)
allele in Caucasians found associated with AgP (Walker SJ et al 2000).

In a meta-analysis that conducted the evaluating IL-6 polymorphisms, there was
concluded an associated with AgP and IL-6 polymorphisms (Shao MY et al 2009).
IL-23 is a pro-inflammatory cytokine and found positively correlated with CP but
existing studies how that there is no significant association of IL-23 polymorphisms
with AgP (Maney P, Owens JL 2015).

A Japanese study reported an association for a composite genotype of the Fc cRIIIa
N allele and the Fc cRIIIb +141 R allele in AgP (Kobayashi T et al 2000).
in contrast in a study performed with Caucasian population there is no association
found in term of this gene (Nibali L et al 2006).
Vitamin D receptor was included various biological processes such as bone
metabolism and the immune response to microbial infections. Nibali et al. 2008 and
Park et al. 2006 found an association with AgP but Bret et al. 2005 could not find
any association.

Most studies performed about polymorphisms were limited by sample size and had
variations in case inclusion criteria.
Genetic studies can also be limited by geographic and ethnical differences.
To understand the pathogenesis of this complex disease multicenter studies and
large sample sizes are required.
Aysan Lektemur Alpan (2018)

HLA-DR4, HLA-A9, B-15 are found in high frequency in rapidly progressive
periodontitis patients (Katz J et al 1987; Shapira L et al 1994) and HLA-DQB1
plays a crucial role in pathogenesis of AP (Ohayama H et al 1996).
Miscellaneous genes associated with aggressive periodontitis are AGT-
angiotensinogen CTSC-cathepsin C, E-selectin in Iranian population, FPR-formyl
peptide receptor in Asian population, NADPH-NADPH oxidase, PAII-plasminogen
activator inhibitor 1, and S100A8-calprotectin in Asians, TIMP2-tissue inhibitor of
matrix metalloproteinase 2 in Asians, and t-PA-tissue plasminogen activator in
Caucasian (Joshipura V, Yadalam U, Brahmavar B 2015).

D) ENVIROMENTAL FACTORS:-
The amount and duration of smoking are important variables that can
influence the extent of destruction seen in young adults .
Patients with GAP who smoke have more affected teeth and more
loss of clinical attachment than non smoking patients with GAP.
However, smoking may not have the same impact on attachment
levels in younger patients with LAP.

D) ENVIROMENTAL FACTORS:-
o According to the 1999 workshop, the main feature in diagnosing of AgP is that
the individual should be medically healthy.
oHowever symptoms of the gum in some systemic diseases/conditions may
resemble AgP..
oThis group of diseases includes; neutropenia, hypophosphatasia, leukemias,
Cheidak-Higashi syndrome, leukocyte adhesion deficiency, Papillon-Lefevre
syndrome, trisomy 21, histiocytosis and agranulocytosis.
Armitage GC (1999)

 Topographical, possibly also racial factors should be considered.
 For Europe, low rates of 0.1% to 0.2% have been reported (Hansen
et al, 1984; Kronauer et al, 1986; Saxby, 1984).
 The values for the US fluctuate between less than 1% and 10%
depending on race(Albandar, Löe).
 Relatively high prevalence rates have been observed for some
South American (Albandar 1991), African (Albandar 2002), and
Asian (Timmerman) countries.
Barbara Noack, Thomas Hoffmann (2004)

 On the basis of the data mentioned in slide 66, it was generally concluded
that, only a small number of children and young adults are affected by any
form of periodontitis, and that most of these, however, have AgP.

95

Aggressive periodontitis in Indian population
 In a cross-sectional survey done to know the prevalence of aggressive
periodontitis in Moradabad population with their systemic manifestations,
 It was concluded that the frequency of systemic manifestations such as
fatigue, weight loss, and loss of appetite was significantly greater in
aggressive periodontitis and a significant correlation between
anxiety/depression and aggressive periodontitis was observed.
Sharma K, Rai R. (2014)

 In a study done by Rahul et al (2013), neutrophil functions like
chemotaxis, phagocytosis, and microbicidal activity, are deficient in LAP
patients. These abnormal neutrophil functions may predispose to increased
susceptibility for LAP.
 Bhansali Rahul Suresh et al (2017) through his study concluded:
 that defects in neutrophil function such as chemotaxis associated with AP
and may serve as predisposing factors for AP, specifically for LAP in
individuals of Indian origin.
 findings also support the hypothesis that suggests that defects in
neutrophil chemotaxis may also be inherited along with the clinical
occurrence of AP.

 Bhansali Rahul Suresh et al (2017) through his study concluded:
 that defects in neutrophil function such as chemotaxis associated with AP and
may serve as predisposing factors for AP, specifically for LAP in individuals
of Indian origin.
 findings also support the hypothesis that suggests that defects in neutrophil
chemotaxis may also be inherited along with the clinical occurrence of AP.
 The results of their study suggest high incidence of AP (LAP and GAP)
within families was associated with depressed neutrophil chemotaxis. High
prevalence of depressed neutrophil chemotaxis in the family members (61%)
of LAP probands exhibiting depressed chemotaxis suggests that the observed
abnormalities in neutrophil functions may also be inherited by the family
members.

 The incidence of A.a along with P.g and T. forsythia was high in
aggressive periodontitis patients in subgingival plaque in south
Indian population (Mahalakshmi K et al 2012).
 Viruses like herpes simplex virus (HSV)-1 and EBV were found to
be significantly associated with destructive periodontal disease,
including chronic and aggressive periodontitis. Further, HSV-1 was
found to be associated with severity and progression of destructive
periodontal disease (Das S, Krithiga GS, Gopalakrishnan S. 2012).

 FcγRIIIa V/V genotype and/or V allele, as well as the FcγRIIIb
NA2/NA2 and/or NA2 allele, along with the FcγRIIa-R allele, may be risk
factors for generalized aggressive periodontitits (GAgP) in the population
of South India (Hans VM, Mehta DS. 2011).
 In a study done by Shete et al., there was no gene polymorphism found in
patients with aggressive periodontitis (Shete AR, Joseph R, Vijayan NN,
Srinivas L, Banerjee M.2010).

 In Malayalam speaking Dravidian population, IL-4 + 33C/T loci appears to be
an important risk factor for periodontal disease with a leaning towards
aggressive periodontitis (Jain N, Joseph R, Balan S, Arun R, Banerjee M).
 The association between IL-17F at 7383A/G and 7488A/G loci with either
chronic or an aggressive periodontitis could not be ascertained (Jain N, Joseph
R, Balan S, Arun R, Banerjee M).
 In a study to know the clinical and genetic aspects of GAP in families of
Tumkur district in Karnataka, it was concluded that the disorder may not be
segregating as an autosomal recessive trait and could have been misled by
consanguinity in the family and it could be a multifactorial trait, or still
segregating as an autosomal recessive trait, but the region of homozygosity
could be small (Joshipura V et al 2013).

 In order to recognize an AgP case as early as possible, probing of the
entire periodontal region of children and young adults, if possible at six
different locations, is indispensable;
 the Periodontal Screening Index (PSI) is an efficient diagnostic tool for
this purpose.

 The differential diagnosis of AgP is made on the basis of its distinction
from other forms of periodontitis by further parameters.
 Necrotizing periodontitis is relatively simple to identify on account of its
characteristic clinical appearance.
 A comprehensive medical history is necessary for identifying the presence
of systematic conditions that impair host defense, and are thus
accompanied by periodontitis.

 Finally, after excluding these forms of periodontitis, a differential
diagnostic distinction from chronic periodontitis is necessary.
 The criteria of the international workshop for the classification of
periodontal diseases (1999) are decisive. The main characteristic of AgP
is, according to this, an extremely progressive form of tissue destruction.

 Although the 1999
classification system is no
longer principally based
on the age of the patient,
the evaluation of the loss
of periodontal support
tissue which has already
occurred in relation to age
can be helpful in the
evaluation of the
progression of the
disease.
Barbara Noack, Thomas
Hoffmann (2004)

 The specific distribution of the periodontal lesions (molars/incisors or
generalized occurrence) permits the identification of localized or
generalized AgP.
 The further diagnostic criteria for AgP include the presence of specific
microorganisms, mainly of A. a.; microbiological diagnostics also provide
insights relevant for differential therapy.
 Periodontal pathogens are normally identified using the methods of modern
molecular biology [Polymerase Chain reaction (PCR), DNA probes].

Nath SG, Raveendran R. 2011 in their literature concluded that:
Overall, while most clinicians would agree that aggressive forms of periodontitis exist
as clinical entities, the clinical distinction between chronic and aggressive
periodontitis (especially generalized) is not clear cut.
However, from a research perspective, it is essential that these diseases be clearly
distinguished in order to gain a complete understanding of their etiology and
pathogenesis.
The relative lack of clinical inflammation and the localized molar-and-incisor form is
typical for localized aggressive periodontitis. In contrast, the presence of clinical
inflammation in generalized aggressive periodontitis appears to be similar to that
observed in chronic periodontitis, and in this situation, age of onset and family
history are important additional criteria for either diagnosis or classification.
Moreover, chronic periodontitis could subsequently be superimposed on both
localized and generalized forms of aggressive periodontitis. This may have little
bearing on the treatment of such cases, but it could have an enormous impact on
both the design and interpretation of research studies, whether basic science or
clinical.

Assessment of host defence
In a suspect case of rapidly progressing AgP, one may consider the use of one of
the commercially available tests for markers of ongoing periodontal
inflammation and tissue breakdown in either gingival crevicular fluid or
saliva (e.g. matrix metalloproteinase-8) or other areas.
Dip test: Test used for the detection of matrix metalloproteinase-8 (MMP8) in
gingival crevicular fluid and integrated microfluidic platform for oral
diagnostics test used for the detection of MMP8 in saliva.
Still, none of the available tests to date can reliably discriminate AgP from other
conditions, and thus, the utility of these tests to assess ongoing tissue
breakdown is disputed (Newman MG, Takei H, Klokkevold PR, Carranza
FA).

Host response
Aggressive periodontitis should be present in a healthy individual; multiple
systemic conditions may be associated with attachment loss which needs to
be ruled out before giving the diagnosis as aggressive periodontitis because
in conditions like leukocyte adhesion deficiency syndrome and Papillon-
Lefevre syndrome the oral picture resembles aggressive periodontitis.
Polymorphonuclear neutrophils (PMNs) play an important role in host immune
response, qualitative and quantitative deficiency in PMNs can lead to
increased periodontal destruction, and this does not mean aggressive
periodontitis is caused by dysfunctional PMNs.
Although host factors can also play an enormous role in the progression of
disease, PMN dysfunction does not appear to be a cause for aggressive
periodontitis in nonsyndromic individuals (Kulkarni C, Kinane DF 2014).

 Prognosis of AgP depends on if it is localized or generalized, localized
has a better prognosis then generalized because less number of teeth
involved and also due to the presence of antibodies (robust) in the serum
of patients.
 Destruction at the time of diagnosis and ability to control progression are
also important factors for prognosis.
(Newman MG, Takei H, Klokkevold PR, Carranza FA).

 Any new definition should be based on the;
a) age of the subject,
b) location of lesions,
c) extent of disease (stages).

 The first diagnosis could be in;
1) childhood (prepubertal),
2) adolescence (puberty), and
3) early adulthood (postadolescence).

 Staged approach:
 Definition of disease in addition to age could include; a) the location of
the lesion and the stage or extent of disease (one, two or three or more
teeth).
 Would signify the severity of disease (i.e., one tooth is less severe than
two teeth, etc.).
 Would also enable the practitioner and researcher to identify the “burned
out” or contained disease (i.e., a disease confined to one tooth or two teeth
etc.).

 Staged approach:
 In its simplest form the staged definition could be categorized as:
 Stage 1, a disease limited to one tooth,
 Stage 2 limited to two teeth,
 Stage 3 limited to three teeth (molars and incisors), and
 Stage 4 the classic Löe and Brown definition of disease (Loe H, Brown
LJ. 1991).

Staged approach:
 To prevent confusion with trauma or other non-infectious disease initiators, a
diseased tooth would be defined as having proximal attachment loss but would
not be based on buccal or lingual recession.
 This staged definition would be helpful to examine microbial initiators,
host‐response elements, and pathophysiologic changes.
 It would also be helpful in genetic distinctions between the classic Löe and
Brown disease and early stage disease that is contained. It should be especially
helpful in establishing the multi‐causal nature of this localized form of
periodontal disease in young individuals.

 Richard J. Nagy and Karen F. Novak. Chapter 28 Aggressive Periodontitis. In:
Carranza’s clinical periodontology 9th edition.
 Barbara Noack, Thomas Hoffmann. Aggressive Periodontitis. Perio 2004; Vol 1, Issue 4:
335–344.
 Camila Palma Portaro, Yndira Gonzalez Chópite , Abel Cahuana Cárdenas . Generalized
Aggressive Periodontitis in Preschoolers: Report of a case in a 3-1/2 year old . J Clin
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 Albandar JM. Aggressive periodontitis: Case definition and diagnostic criteria.
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 Joshipura V, Yadalam U, Brahmavar B. Aggressive periodontitis: A review. J Int Clin
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 Hans VM, Mehta DS. Genetic polymorphism of Fcγ-receptors IIa, IIIa and IIIb in South
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 Shete AR, Joseph R, Vijayan NN, Srinivas L, Banerjee M. Association of single
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 Bhansali, Rahul Suresh et al. “Evaluation of peripheral neutrophil functions in
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 Mahalakshmi K, Krishnan P, Chandrasekaran SC, Panishankar KH, Subashini N.
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 Das S, Krithiga GS, Gopalakrishnan S. Detection of human herpes viruses in
patients with chronic and aggressive periodontitis and relationship between viruses
and clinical parameters. J Oral Maxillofac Pathol 2012;16:203-9.
 Jain N, Joseph R, Balan S, Arun R, Banerjee M. Association of interleukin-4 and
interleukin-17F polymorphisms in periodontitis in Dravidian ethnicity Indian. J
Hum Genet 2013;19:58-64.

 Joshipura V, Subbaiah SK, Saiprakash RP, Dasakariyappa NT, Smitha BV.
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Periodontology.12th ed. Elsevier; 2014. p. 700-890.
 Syed Wali Peeran,Karthikeyan Ramalingam. Chapter 25:Aggressive periodontitis.
In: Essentials of periodontics & Oral implantology 2021.

 For Slide nos. 25 & 49 :- Aysan Lektemur Alpan (November 5th 2018).
Aggressive Periodontitis, Periodontology and Dental Implantology, Jane Manakil,
IntechOpen, DOI: 10.5772/intechopen.76878. Available from:
https://www.intechopen.com/books/periodontology-and-dental
implantology/aggressive-periodontitis.
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 Nibali L, Parkar M, D'Aiuto F, Suvan JE, Brett PM, Griffiths GS, et al. Vitamin D
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 Park KS, Nam JH, Choi J. The short vitamin D receptor is associated with increased
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 Kulkarni C, Kinane DF. Host response in aggressive periodontitis. Periodontol 2000
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