Periodontology 2000, Vol. 65, 2014, 13–26  2014 John Wiley & Sons A/S.
iley & Sons A/S. Published by John Wiley & Sons Ltd
Printed in Singapore. All rights reserved
Aggressive periodontitis: case
definition and diagnostic criteria
J A S I M M. A L B A N D A R
HISTORICAL BACKGROUND
Terminology and classification
Before addressing the case definition and diagnostic
criteria of aggressive periodontitis it is useful to pro-
vide a brief review of the historical events pertaining to
the terminology of this disease. The classification and
terminology of periodontal diseases have evolved in
tandem with the advancement in the understanding
of the pathogenesis of these diseases. During the 19th
century and the first half of the 20th century the
prevailing view of what we now classify as chronic
periodontitis was that it was a noninflammatory dis-
ease (57). The pathogenesis of periodontitis in adults
was viewed as principally the development of a
pathological pocket and alveolar bone atrophy
attributed mainly to trauma from occlusion, while
local inflammation and bacterial infection were
viewed as playing only a secondary role (30, 31). Fur-
thermore, it has long been recognized that destructive
periodontal disease may also develop in children and
young adults, and although the phenotype of this
early-onset form is clinically different from that of the
adult form, both forms were considered manifesta-
tions of a degenerative, noninflammatory disease (45).
Based on histologic observations, Gottlieb (29, 31)
used the term Ôdiffuse atrophy of the alveolar boneÕ to
describe the disease, and he hypothesized that it was
caused by a Ôlack of an effective cementum barrierÕ,
which he called ÔcementopathiaÕ, that may lead to
gingival recession, alveolar bone loss and pathological
pocket formation (32).
In 1942, Orban & Weinmann (50) introduced the
term ÔperiodontosisÕ to describe severe periodontal
disease in young individuals. A 1950 report by the
American Academy of Periodontology defined peri-
odontosis as a Ôdegenerative non-inflammatory
destruction of the periodontium originating in one or
more of the periodontal structures, characterized by
migration and loosening of the teeth in the presence or
PERIODONTOLOGY 2000
absence of secondary epithelial proliferation and
pocket formation or secondary gingival diseaseÕ (45).
The terms Ôjuvenile periodontitisÕ and Ôearly-onset
periodontitisÕ were introduced in 1969 (19) and 1989
(11), respectively, and were widely used during the
last three decades of the 20th century. The latter
terms were readily adopted because they portray the
early-onset development of the disease and its
occurrence in younger age groups. Other terms were
proposed to describe the disease, such as Ôprecocious
advanced alveolar atrophyÕ(48) and Ôprecocious peri-
odontitisÕ (64), but were not widely adopted.
In the 1999 Classification Workshop of the Ameri-
can Academy of Periodontology (12), a consensus
report adopted the term Ôaggressive periodontitisÕ as a
new name for this unique disease classification,
replacing the term Ôearly-onset periodontitisÕ (43). For
consistency, in this article, the term Ôaggressive peri-
odontitisÕ is used when citing classic literature that
previously used synonymous terms of this disease.
Case definition by Baer, in 1971
Baer (15) defined aggressive periodontitis as Ôa disease
of the periodontium occurring in an otherwise healthy
adolescent, which is characterized by a rapid loss of
alveolar bone around more than one tooth of the
permanent dentitionÕ. He proposed the following
seven criteria to define the disease.
• Early onset of the disease during the circumpu-
bertal period (between 11 and 13 years of age).
• A distinctive radiographic pattern depicting vertical
alveolar bone loss at the first permanent molars and
at one or more incisor teeth. Notably, Baer described
criteria for a ÔclassicalÕ case of aggressive periodon-
titis and variant criteria for atypical cases of
aggressive periodontitis. Accordingly, a ÔclassicalÕ or
typical case of aggressive periodontitis would show
an arc-shaped loss of alveolar bone, extending from
the distal surface of the second bicuspid to the
mesial surface of the second molar. Furthermore,
13
Albandar
the bone loss at the posterior teeth occurs bilaterally,
and the left and right sides of the jaw may be de-
picted as mirror images of each other. On the other
hand, atypical cases of aggressive periodontitis also
occur, and the pattern of bone loss in these cases
differs from that found in the classical case. For in-
stance, atypical cases of aggressive periodontitis
may show bone loss at only one proximal surface of a
first molar, or that only the molars are affected and
not the incisors. Baer believed that the variations in
the clinical features of aggressive periodontitis are
caused by the variability in the phase of disease
development and whether the disease is diagnosed
at an early phase or an advanced phase. Baer
deemed the occurrence of a pattern of bone loss
localized to one proximal surface of the first molar in
multiple arches as an initial stage in the develop-
ment of the disease, or an ÔincipientÕ localized case.
Subjects with advanced disease may show a gener-
alized, severe, horizontal bone loss.
• A rapid rate of disease progression. Baer estimated
that, typically, an affected tooth can lose 75% of the
alveolar bone support at one or more root surfaces
within 5 years of disease initiation. In some atypical
cases of aggressive periodontitis, however, alveolar
bone loss progresses only to a certain point and then
may remain quiescent for many years.
• The disease affects only the permanent dentition.
The primary teeth are not affected and are not
prematurely exfoliated because of destructive
periodontal disease.
• The amount of local etiologic factors is not com-
mensurate with the severity of periodontal
destruction. Gross deposits of dental calculus are
uncommon in most cases of aggressive periodon-
titis, and in the early stages of the disease the
gingiva has a normal clinical appearance with no
clinical signs of gingival inflammation. However,
dental plaque is present on the root surfaces of the
affected teeth. Some patients do have poor oral
hygiene and detectable plaque and calculus. Clin-
ical signs of gingival inflammation are seen in
subjects with advanced disease.
• Predominance in female subjects. Baer reported
that cases of aggressive periodontitis have a female
to male ratio of approximately 3:1.
• The disease has a familial pattern.
Case definition in the 1999 American
Academy of Periodontology workshop
In 1999 the American Academy of Periodontology
organized a workshop to propose a new classification
14
of periodontal diseases and conditions (12). In this
workshop a subcommittee recommended that the
term Ôaggressive periodontitisÕ should be used, and
classified the disease into localized and generalized
forms (43). According to this report, the following
features are common to the localized and generalized
forms of aggressive periodontitis.
• Patients are clinically healthy, except for the pres-
ence of periodontitis.
• Rapid attachment loss and bone destruction.
• Familial aggregation.
Secondary features that are often, but not always,
present include the following.
• The amounts of microbial deposits are inconsistent
with the severity of periodontal tissue destruction.
• Elevated proportions of Actinobacillus actino-
mycetemcomitans (now termed Aggregatibacter
actinomycetemcomitans).
• Elevated proportions of Porphyromonas gingivalis
in some populations.
• Phagocyte abnormalities.
• A hyper-responsive macrophage phenotype,
including elevated levels of prostaglandin E2 and
interleukin-1b.
The following additional specific features were pro-
posed for defining the localized and generalized forms.
Localized aggressive periodontitis.
• Circumpubertal onset.
• 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.
• Robust serum antibody response to infecting
agents.
Generalized aggressive periodontitis.
• Usually affecting persons under 30 years of age,
but patients may be older.
• Generalized interproximal attachment loss affect-
ing at least three permanent teeth other than first
molars and incisors.
• Pronounced episodic nature of the destruction of
attachment and alveolar bone.
• Poor serum antibody response to infecting agents.
A perspective on previous and current
case definitions
Early reports published before 1970 did not present
detailed diagnostic criteria of aggressive periodonti-
tis, except for severe loss of periodontal tissue at a
young age. On the other hand, the criteria proposed

by Baer (15) constituted the first well-defined case
definition of aggressive periodontitis as a distinct
clinical entity, and these criteria were invaluable to
clinicians and scientists in the diagnosis of patients.
However, some of the parameters used in BaerÕs case
definition of aggressive periodontitis were not based
on sound evidence. More details on this subject are
presented later in this article.
The case definition of Ôearly-onset periodontitisÕ
was recommended in the 1989 World Workshop by
the American Academy of Periodontology (11) be-
cause one of the hallmarks of this disease is its
commencement at an early age. However, this case
definition had a key shortcoming, in that the term
Ôearly-onsetÕ is broad, and as such, was inclusive.
Hence, this new term conveyed that the classification
may also include other destructive forms of peri-
odontal disease that may develop in children. For
instance, young individuals showing localized,
incipient lesions with attachment loss, although not
fully matching BaerÕs criteria of typical lesions, were
also classified in the early-onset periodontitis classi-
fication, albeit subclassified as Ôincidental attachment
lossÕ (44) or Ôincidental early-onset periodontitisÕ (5,
6). There is evidence that some subjects showing
incidental attachment loss may progress to aggres-
sive periodontitis, whereas other subjects may not
(17). Furthermore, some studies have also included in
the disease category of Ôearly-onset periodontitisÕ
destructive forms of periodontitis that are merely oral
manifestations of systemic diseases (66) because
these forms are usually manifested in children.
Hence, the term Ôearly onsetÕ may have caused some
confusion leading to misclassification issues.
The 1999 American Academy of Periodontology
consensus report on aggressive periodontitis (43)
recommended that age at the time of disease pre-
sentation should not be used as a criterion for the case
definition of this disease. Nonetheless, the consensus
report used age as a descriptor in the subclassification
of cases of aggressive periodontitis. For instance, the
subclassification Ôlocalized aggressive periodontitisÕ
was defined as having a circumpubertal onset; and
Ôgeneralized aggressive periodontitisÕ was described as
affecting persons under 30 years of age, but that pa-
tients may be older. Hence, the 1999 consensus report
was ambivalent regarding the relevance of age for the
case definition of aggressive periodontitis. The report
also proposed certain other criteria based on immu-
nological profiles. Accordingly, localized aggressive
periodontitis was defined as having the specific fea-
ture of a ÔrobustÕ serum antibody response to infecting
agents, whereas generalized aggressive periodontitis
Aggressive periodontitis case definition
was defined as having a poor serum antibody response
to the pathogens. It is interesting to note, however,
that the literature contains inconclusive evidence of
the relationship between the serum antibody re-
sponse to infecting agents and the classification of
aggressive periodontitis (7, 20, 72). Therefore, it may
be concluded that, at the present time, the use of the
criterion of associations of certain immunological
profiles in the case definition of aggressive periodon-
titis is not warranted.
PARAMETERS FOR THE CASE
DEFINITION OF AGGRESSIVE
PERIODONTITIS
Age of onset of disease
Among early reports, Seidler et al. (58) described 35
subjects, 14–30 years of age, with advanced peri-
odontal disease and noted that the clinical peri-
odontal features and other demographics of these
subjects were different from the destructive peri-
odontal disease that is diagnosed in older adults.
These investigators wrote: ÔThis discovery was star-
tling, the more so when it was compared with statistics
comprising older patients with comparable peri-
odontal diseaseÕ (58). Seidler and colleagues (58)
called this disease Ôprecocious advanced alveolar
bone destructionÕ and concluded that its onset is
around puberty, or slightly later. Baer (15) also be-
lieved that aggressive periodontitis commences at the
circumpubertal period, between 11 and 13 years of
age. Several other studies support the hypothesis that
the onset of aggressive periodontitis is around the
circumpubertal period. Large population surveys
found cases of aggressive periodontitis with age of
onset as young as 12–14 years (9, 25, 26, 65), and
clinical studies in periodontal patients report cases of
aggressive periodontitis with an age of onset as young
as 10–14 years (18, 27, 35, 54, 60).
Notably, in all these studies – epidemiologic or
clinical – the reported age is the age at disease pre-
sentation (i.e. when the person is diagnosed as having
aggressive periodontitis). However, judging from the
amount of periodontal tissue loss that is often present,
in virtually all of these subjects the periodontal
destruction may have commenced earlier, sometimes
several years before diagnosis of the disease. Hence, in
these studies there is always a discrepancy between
the age of onset of aggressive periodontitis and the
age at disease presentation, with the actual age of
onset substantially preceding that at diagnosis. This
15
Albandar
discrepancy may be partly attributed to validity and
precision issues of the methods of disease detection
currently available (1, 22). More about this parameter
is discussed later in this article.
Permanent vs. primary teeth
The issue of the age of onset of aggressive peri-
odontitis also hinges on whether or not the primary
teeth are affected in this disease, and this issue has
often been overlooked. Baer (15) contemplated that
aggressive periodontitis is a disease of the permanent
dentition and it does not cause premature exfoliation
of the primary teeth. It should be noted, however,
that Baer did acknowledge that this disease may also
have an onset during the period of mixed dentition,
and therefore some of the primary teeth, particularly
the primary second molars, may develop alveolar
bone loss as a result of periodontitis.
During the early 1960s, Jamison (36) surveyed 5-
to 14-year-old children in the city of Tecumseh,
Michigan, and reported that approximately one-
quarter of the children had destructive periodontal
disease around the deciduous teeth. It has been
estimated that approximately 71% of all cases of
aggressive periodontitis show alveolar bone loss
affecting the primary dentition, and bone loss
affecting the mixed dentition is present in 86% of
the subjects (24).
Very often, young children with destructive peri-
odontal disease are not diagnosed at an early phase
of disease development and therefore, in these sub-
jects, the actual age of onset is unknown. There are
reports of children as young as 7 and 8 years of age
who showed clinical and radiographic signs of peri-
odontal destruction at some or all of their primary
teeth and who subsequently developed aggressive
periodontitis at their permanent teeth (23, 46, 49). A
study of a large group of 13- to 19-year-old individ-
uals with aggressive periodontitis retrospectively
assessed radiographs taken when the subjects were
5–12 years of age. The results showed that approxi-
mately half of the children had alveolar bone loss at
their primary teeth (61). These studies suggest that in
a large percentage of cases of aggressive periodontitis
the age of onset of the disease may be during the
mixed dentition (7–12 years of age), and in these
individuals the disease may affect both the primary
and the permanent teeth. However, it may be worth
remarking that the latter studies did not report that
the alveolar bone loss had caused an early exfoliation
of the involved primary teeth, and, as such, BaerÕs
contemplation, that aggressive periodontitis does not
16
typically cause premature exfoliation of the primary
teeth, may be valid.
There have been case reports of prepubertal chil-
dren with severe periodontal disease leading to ex-
foliation of the primary teeth (13, 16, 63), and based
on these reports Ôprepubertal periodontitisÕ was pro-
posed as a distinct clinical entity in the early 1980s
(51). However, the clinical criteria of aggressive
periodontitis are, to a large extent, distinguishable
from those of prepubertal periodontitis. Hence,
compared with aggressive periodontitis, prepubertal
periodontitis has an earlier disease onset (i.e. during
or immediately after the eruption of the primary
teeth), is characterized by early exfoliation of the
primary teeth and is usually associated with some
systemic defects, such as a functional defect in neu-
trophils or monocytes (51). There is evidence sug-
gesting that prepubertal periodontitis is a genetically
heterogeneous disease, and that in some families it
just represents a partially penetrant Papillon–Lefèvre
syndrome (34). For these reasons, the term Ôprepu-
bertal periodontitisÕ is no longer recognized as a
distinct clinical classification, and prepubertal chil-
dren with severe periodontitis who are diagnosed
with systemic disorders are currently classified in the
disease category ÔPeriodontitis as a Manifestation of
Systemic DiseaseÕ (12).
On the other hand, there are indications (71) that
the disease category classified previously as localized
prepubertal periodontitis (51) may indeed be a severe
form of aggressive periodontitis. A case report de-
scribed a medically healthy patient diagnosed with
prepubertal periodontitis at age 10 years; the patient
then developed localized aggressive periodontitis at
13 years of age, and the disease subsequently pro-
gressed to generalized aggressive periodontitis (59).
Hence, there is evidence that in certain individuals
with severe aggressive periodontitis, periodontal tis-
sue loss may commence at a prepubescent age, and
that an early age of onset may suggest a more severe
form, and possibly a larger component of systemic
etiology.
Pattern of attachment loss and alveolar
bone loss
Another key feature of aggressive periodontitis is that
the patients exhibit periodontal attachment loss at
multiple teeth and the tissue loss occurs bilaterally
(14, 15, 58). In the permanent dentition the disease
usually starts at the proximal surfaces of the perma-
nent first molars and ⁄ or incisors, and therefore the
loss of periodontal support around these teeth is

often more pronounced than around other teeth. At
the initial stage of the disease the tissue loss may be
too small to be detected using current examination
methods (1, 22). Early lesions may be identified as
loss of periodontal tissue localized to only one or a
few teeth (Fig. 1). The diagnosis of the disease during
the period of the mixed dentition poses particular
challenges (15) because of the biological processes
that take place locally during the normal exfoliation
of the primary teeth. Furthermore, during this period
eruption of the permanent teeth also occurs, and the
associated bone remodeling may mask the diagnosis
of pathologic bone loss that is associated with peri-
odontitis. For these reasons, incipient disease often
remains undetected in children during the mixed-
dentition age.
Radiographically, at the early stage of development
of aggressive periodontitis, the periodontal lesions
often show a vertical pattern of alveolar bone loss at
the proximal surfaces of the permanent first molars
(28, 35) (Fig. 1). Also, the incisors are often affected,
although the bone loss here is usually horizontal
because the alveolar bone is thinner than at the
Fig. 1. Radiographs of a 15-year-old
subject illustrating vertical bone loss
at the distal surfaces of the
mandibular first molars (arrows).
Vertical bone loss at multiple teeth
is an early sign of aggressive
periodontitis.
Fig. 2. Radiographs of a 17-year-patient diagnosed with localized aggressive periodontitis.
Aggressive periodontitis case definition
proximal surfaces of molars. In typical cases the bone
defects around the first molars are arc-shaped and
affect all first molars (Fig. 2), and may extend from
the distal surface of the second premolar to the me-
sial surface of the second molar (Figs 3 and 4). The
alveolar bone defects are usually similar on the right
and left sides of the mouth, and this has been referred
to as a Ômirror-imageÕ pattern (15). However, there are
variances from this typical pattern. For instance,
some subjects with aggressive periodontitis may
show significant bone loss around the incisors, and
only moderate bone loss around the molars; whereas
other subjects with aggressive periodontitis may
show involvement of only the molars with little or no
involvement of the incisors. In advanced cases of
aggressive periodontitis the bone loss may be gen-
eralized and show a horizontal pattern (Fig. 5).
The distinction between aggressive periodontitis
and chronic periodontitis is straightforward, partic-
ularly when adequate radiographic images of the case
are available for assessment. Consider the patient
depicted in Fig. 6. A radiographic examination of a
20-year-old person revealed a vertical bone lesion at
17
Albandar

the mesial surface of the mandibular right first molar
(Fig. 6), and a clinical examination found attachment
loss of 6 mm at the same site. However, local etio-
logic factors were present at the site of the bone
lesion. In addition, no other sites had clinical
attachment loss or radiographic bone lesions in this
person. Hence, one may infer that in this individual
the bone lesion is probably incidental to the presence
of local factors, and that these radiographic (Fig. 6)
and clinical criteria do not match the case definition
of aggressive periodontitis.
Rate of disease progression
When diagnosed with aggressive periodontitis, pa-
tients typically show a pronounced loss of periodontal
attachment on multiple teeth (58). Moreover,
although the precise age when the tissue loss

Fig. 3. Radiographs of the 16-year-old patient with aggressive periodontitis shown in Fig. 9. There is vertical bone loss at
the first molars and a Ômirror imageÕ pattern of bone loss.

Fig. 4. Radiographs of the 18-year-old patient with aggressive periodontitis shown in Fig. 7. Most of the teeth show bone
loss, and the most profound bone loss affects the incisors and the first molars.

Fig. 5. Radiographs of a 20-year-old patient with aggressive periodontitis showing generalized alveolar bone loss.

18

Fig. 6. Radiographs of a 20-year-old subject showing a vertical bone lesion and deposits at the mesial surface of the
mandibular right first molar. No other sites with significant bone loss can be identified on these radiographs. In this
subject the radiographic and clinical features do not match the case definition of aggressive periodontitis.
commenced is often unknown, judging from the
amount of tissue lost and the number of years since
the affected teeth erupted in the mouth, it can be
inferred that the rate of attachment loss and alveolar
bone loss is high. Based on this, it has been estimated
that in a typical case of aggressive periodontitis the
rate of bone loss is three to four times higher than the
rate of progression of chronic periodontitis (15).
Albandar (3) conducted a longitudinal follow-up
study, using clinical and radiographic measurements,
in a large group of 14-year-old schoolchildren. He
found that all children who were diagnosed with
aggressive periodontitis at 14 years of age showed
disease progression when they were re-examined at
15 years of age; and approximately half the proximal
surfaces of the permanent first molars in these chil-
dren had experienced 1–2 mm of alveolar bone loss
during the 1-year follow-up period. In the 1986 ⁄ 1987
National Survey of the Oral Health of US Children,
Brown and co-workers (17) identified 13- to 20-year-
old subjects with aggressive periodontitis, and these
subjects were later re-examined clinically when
19–26 years of age. During the 6-year follow-up per-
iod the periodontal status of these subjects had
continued to deteriorate and the severity of the dis-
ease had increased. The mean attachment loss over
6 years was 0.45 mm (0.08 mm ⁄ year) in the group of
subjects with localized aggressive periodontitis, and
was 1.12 mm (0.19 mm ⁄ year) in the group of sub-
Aggressive periodontitis case definition
jects with generalized aggressive periodontitis. In
contrast, the rate of attachment loss in male subjects
with chronic periodontitis has been estimated to be
0.05 mm ⁄ year (55). This shows that the rate of
attachment loss in aggressive periodontitis is higher
than that in chronic periodontitis.
On the other hand, Gunsolley et al. (33) performed
a 3- to 4-year follow-up study in a group of patients
with aggressive periodontitis and reported that the
mean attachment loss during the study was 0.24 mm
(or 0.08 mm ⁄ year) for ÔuntreatedÕ subjects with
localized aggressive periodontitis and 0.27 mm (or
0.07 mm ⁄ year) for subjects with generalized
aggressive periodontitis (total for treated and
untreated). The group studied by Gunsolley et al. (33)
were patients attending a dental clinic and their
mean age was 25 years (localized aggressive peri-
odontitis) and 30 years (generalized aggressive peri-
odontitis), whereas the group studied by Brown et al.
(17) were 13–20 years of age and were identified in a
population survey. This, and other differences in
measurement methods, may partly explain the
difference in the rates of attachment loss observed
between the two study groups.
Notably, in aggressive periodontitis not all peri-
odontal sites show continuous, quantifiable disease
progression. The study by Brown et al. (17) showed
that approximately 30% of mesial sites and 15% of
buccal sites showed attachment loss of ‡2 mm over a
19
Albandar
duration of 6 years. Albandar et al. (2) examined a
group of patients with aggressive periodontitis,
annually, over a 3-year period, and detected a con-
tinuous progression of alveolar bone loss at some,
but not all, sites. Mros & Berglundh (49) re-examined
a group of 14- to 19-year-old patients with localized
aggressive periodontitis following a baseline exami-
nation and periodontal treatment, and found that
half of the group showed extensive or limited recur-
rence of the disease, whereas the rest of the subjects
did not show further loss of periodontal attachment.
Hence, in aggressive periodontitis the rate of disease
progression varies between subjects, and between
different sites within the same subjects.
Presence of local etiologic factors
Typically, patients with aggressive periodontitis show
smaller amounts of local factors, such as dental pla-
que and supragingival calculus, than do patients with
chronic periodontitis with comparable periodontal
destruction (Figs 7 and 8). Baer (15) stated that in
aggressive periodontitis there is a lack of a relation-
ship between local etiologic factors and the amount
of periodontal destruction. Seidler et al. (58) did not
Fig. 7. Clinical photographs of a 18-year-old patient with aggressive periodontitis. The radiographs of this patient are
shown in Fig. 4.
Fig. 8. Clinical photographs of a 17-year-old patient with aggressive periodontitis. The radiographs of this patient are
shown in Fig. 10.
20
describe the status of the local factors in their pa-
tients, but judging from the radiographs depicted in
their paper there were no gross calculus deposits on
the involved teeth in the subjects illustrated. Fig-
ures 7 and 8 depict cases of aggressive periodontitis
in which the patients show an insignificant amount
of supragingival dental plaque or calculus on their
teeth.
The periodontal destruction in aggressive peri-
odontitis is initiated by the interaction between
pathogenic microorganisms and the host immune
system (41, 56), and this interaction is influenced by
many local and systemic factors (10). Although the
pathogenesis and mechanism of tissue loss are sim-
ilar in chronic and aggressive periodontitis (62), the
effect of host factors is markedly more pronounced in
the latter disease. For instance, there is strong evi-
dence for a familial aggregation of aggressive peri-
odontitis (47), and several genetic factors that may
increase the risk for developing the disease have been
identified (68). In contrast, in chronic periodontitis
local factors play a major role, with a less significant
role for host factors (8). Indeed, the significance of
factors other than dental plaque and calculus in
the pathogenesis of aggressive periodontitis is

manifested by the early onset of periodontal tissue
loss, even though many affected subjects show min-
imal amounts of local etiologic factors (15, 58).
The deposition of dental plaque is a prerequisite to
the initiation of the local inflammation and the
ensuing host response leading to periodontal tissue
loss (40). Among the pioneers who investigated the
role of dental plaque in the pathogenesis of peri-
odontitis, Waerhaug (69) studied autopsy specimens
from subjects with aggressive periodontitis and
showed that subgingival plaque is always associated
with attachment loss in these subjects, and also no-
ticed the presence of a severe chronic inflammation
in the soft tissue bordering upon the plaque. In
addition, Waerhaug (70) examined extracted teeth
from patients with aggressive periodontitis and found
no accumulation of subgingival plaque and no loss of
periodontal attachment at tooth sites where there
had been adequate supragingival plaque control. In
both studies Waerhaug remarked that the subgingival
plaque was very thin and had only occasionally cal-
cified to form dental calculus. These findings suggest
that the presence of a microbial insult is a pre-
requisite to the occurrence of attachment loss in
aggressive periodontitis, although alone it does not
fully explain the amount and rate of tissue loss in the
affected subjects.
It is also noteworthy that the criteria proposed by
Baer did not suggest that local factors were totally
absent in aggressive periodontitis. Rather, he con-
templated that the amount of periodontal destruc-
tion usually is not commensurate with the amount of
local factors observed (15). The amount and the rate
of formation of dental plaque and calculus vary be-
tween individuals (37). The lack of a correlation be-
tween the amount and the rate of tissue loss, and the
amount of local factors, is an observation suggesting
that other etiologic factors probably play a more
significant role in the development of the disease.
However, this observation should not be used as an
exclusion criterion in the diagnosis of the disease
because, for various reasons, the amounts of dental
plaque, calculus and other local etiologic factors vary
between patients. Indeed, large population studies
suggest that local factors are prevalent in some pa-
tients with aggressive periodontitis and that these
factors increase the risk of aggressive periodontitis
development in these populations (4, 65). Cappelli
et al. (21) surveyed schools in San Antonio (Texas,
USA) and showed a high prevalence of poor oral
hygiene and dental calculus in the study population,
including subjects diagnosed with aggressive peri-
odontitis.
Aggressive periodontitis case definition
Systemic diseases
An important feature of aggressive periodontitis is
that the subjects are healthy and not inflicted with a
debilitating systemic disease that affects their gen-
eral health and predisposes to periodontal destruc-
tion. There is ample evidence suggesting that host
factors play a key role in the predisposition of indi-
viduals to aggressive periodontitis (41), and not-
withstanding the advancement in the understanding
of the disease pathogenesis, these factors are yet to
be clearly defined. Patients who have periodontal
breakdown associated with a systemic disease that
enfeebles their health and well-being and contrib-
utes to periodontal destruction are not classified in
the aggressive periodontitis category. In the 1999
American Academy of Periodontology classification
this group is termed Periodontitis as a Manifestation
of Systemic Diseases (12) and includes several dis-
orders (see Khocht & Albandar (38) for a detailed
description).
Sex ratio
Baer (15) postulated that the female to male ratio of
cases of aggressive periodontitis was 3:1, and he
proposed this feature among the other criteria for
defining aggressive periodontitis as a distinct clinical
entity. However, the literature reveals inconsistent
findings, with some studies showing comparable
prevalence rates in male subjects and female sub-
jects, whereas other studies show higher rates in
either male subjects or female subjects (6, 65).
Undoubtedly, the prevalence ratio among the two
sexes is a descriptive variable, and if proven relevant
it may be useful in the assessment of the risk pre-
disposition to the disease. However, this descriptor is
not useful as a diagnostic criterion of aggressive
periodontitis because it is not exclusive.
Familial pattern
Baer (15) described a pattern where aggressive peri-
odontitis tends to cluster within families. Findings in
other studies corroborate the familial pattern of this
disease (47, 52). Several mechanisms of increased
predisposition to the disease by genetic factors have
been proposed (39, 42, 68). While the familial pattern
of the disease is an important feature that suggests a
genetic predisposition, it is a generic factor that is too
broad to be used in a case definition at present.
Future advancement in the understanding of the
genetic predisposition to aggressive periodontitis
21
Albandar
may allow for the inclusion of specific genetic profiles
in future case definitions.
Subclassification of aggressive
periodontitis
Aggressive periodontitis occurs in two forms: a
localized form that mainly affects the permanent first
molars and incisors; and a generalized form that
involves most or all of the permanent teeth (15).
Opinions vary as to whether these are two forms of
the same disease, or whether they represent two
distinct diseases. There is evidence that, at least in
some cases, the localized form progresses to a gen-
eralized form when the affected individuals become
older (17, 59), and in other cases the two forms
overlap. On the other hand, a clinical study by
Gunsolley et al. (33) found that patients with differ-
ent forms of the disease responded differently to
periodontal treatment, in that patients with the
localized form were stable after treatment, whereas
patients with the generalized form continued to lose
periodontal attachment and teeth.
It has been suggested that localized aggressive
periodontitis has a younger age of onset and shows a
strong serum antibody response to infecting agents,
whereas patients with the generalized form are older
Fig. 9. Clinical photographs of a 16-year-old patient with aggressive periodontitis showing pronounced gingival
inflammation. The radiographs of this patient are shown in Fig. 3.
Fig. 10. Radiographs of the 17-year-old patient with aggressive periodontitis shown in Fig. 8.
22
and have a poor serum antibody response to infect-
ing agents (43). However, the evidence supporting
these recommendations is scanty and inconclusive
(7, 20, 72). Furthermore, the data showing a pro-
gression, in certain subjects, from localized to gen-
eralized aggressive periodontitis at older age (17, 59)
do not support this postulate. More research is nee-
ded to demonstrate whether these two forms are
different diseases or are different forms of the same
disease.
Figure 2 illustrates a subject with localized aggres-
sive periodontitis, and Fig. 5 illustrates a subject with
generalized aggressive periodontitis. However, often
the distinction between the localized and generalized
forms of aggressive periodontitis is clinically unfea-
sible, particularly at the advanced stage of the disease
when more teeth are involved with periodontal
destruction. Three such cases are illustrated in Figs 3,
4, 7–10. In all of these three subjects with aggressive
periodontitis the early phase of the disease was
characterized by clinical attachment loss and alveolar
bone loss confined to the incisors and first molars,
and as the disease progressed most of the teeth
became involved with periodontal tissue loss. This
lack of distinctive clinical features of the two forms of
the disease, particularly as the disease progresses, is a
source of ambiguity for the classification of subjects

into localized or generalized disease groups, and this
has a profound bearing on the validity of studies that
use these subclassifications. On the other hand, there
is little evidence that the localized and generalized
disease groups are mutually exclusive clinical entities.
CASE DEFINITION OF
AGGRESSIVE PERIODONTITIS
If at all possible, the case definition of aggressive
periodontitis should be based on the presence of
distinctive clinical signs of the disease and the diag-
nosis of its causal factors. However, given the present
status of our understanding of the etiology of this
disease, specific etiologic factors that have high
validity and that can be reliably measured have not
yet been identified. Hence, the current case definition
relies to a large extent on the case history and on
clinical and radiographic findings.
Key diagnostic criteria of aggressive periodontitis
include an early age of onset, involvement of multiple
teeth with a distinctive pattern of periodontal
attachment and bone loss, a relatively high rate of
disease progression and absence of systemic diseases
that compromise the hostÕs response to infection.
The following distinctive criteria are recommended
for the case definition.
• An early age of onset, usually before 25 years of age.
The age of onset may be a predictor of the severity of
this disease, so the younger the age of onset, the
more severe the disease that may develop.
• Loss of periodontal tissue occurs at multiple per-
manent teeth. The tissue loss occurs because of a
microbial infection.
• The periodontal destruction is detectable clinically
and radiographically. Typically, the lesions are
depicted radiographically as vertical bone loss at
the proximal surfaces of posterior teeth because
the alveolar bone is thicker at the posterior region
than anteriorly. The pattern of bone loss is usually
similar bilaterally. In advanced cases the lesions
may be depicted radiographically as a horizontal
loss of the alveolar bone.
• There is a relatively high progression rate of peri-
odontal tissue loss.
• The primary teeth may also be affected, although
early exfoliation of these teeth due to periodontal
tissue loss is not common.
• The patients are systemically healthy.
Aggressive periodontitis may occur in different forms.
In the localized form, tissue loss usually starts at the
permanent first molars and ⁄ or incisors (Fig. 2), and
Aggressive periodontitis case definition
with increasing age tissue loss may affect the teeth
adjacent to the first molars and incisors. Localized
aggressive periodontitis may remain localized, but
more often it progresses by involving other teeth, and
at the advanced stage it presents a clinical picture
similar to that of generalized aggressive periodontitis
(Figs 4, 9 and 10). In generalized aggressive peri-
odontitis, tissue loss may also commence at the
permanent first molars and incisors because these
are the first teeth to erupt, and the disease progresses
rapidly so that most or all of the permanent teeth
become involved with severe attachment and bone
loss (Fig. 5). The rate of disease progression in the
generalized form of aggressive periodontitis may be
higher than in the localized form.
Multiple etiologic factors are often involved in the
pathogenesis of aggressive periodontitis. Insofar the
young age of onset is an indication of a significant
contribution of host factors and perhaps of other
nonplaque-related etiology. Younger age of onset
may suggest a higher contribution of nonplaque
etiologic factors. Similarly, higher rates of disease
progression and early exfoliation of the primary teeth
may suggest a higher contribution of host factors
and, at present, a poor prognosis of disease treatment
and control. Future advancements in understanding
the disease pathogenesis may help define case defi-
nitions of this disease that take into consideration
specific etiologic factors.
Use of the case definition in population
surveys
The use of the case definition of aggressive periodon-
titis for the diagnosis of patients in the dental office is
straightforward because clinical and radiographic
assessments are readily available. On the other hand,
population studies present a special challenge for the
diagnosis of aggressive periodontitis. Surveys typically
examine a large study sample in order to evaluate the
health status of the population. The examinations and
data collection are usually conducted under field
conditions, and this may lead to partial examinations
and/or less than optimal standardization of examina-
tion methods. Prospective surveys aimed at assessing
the periodontal health of populations, particularly
population studies in developing countries, often
do not have access to radiographic diagnostic
methods owing to limited resources. In addition,
Institutional Review Board regulations may object to
the use of radiographs or other diagnostic examina-
tions for health-safety concerns or other motives. For
these reasons, investigators often resort to clinical
23
Albandar
measurements of attachment loss for monitoring the
prevalence and severity of chronic and aggressive
periodontitis. Clinical measurement of periodontal
attachment is more invasive than measurements
made on radiographs, and this may result in higher
measurement errors. This is particularly true in chil-
dren because of poor cooperation during the clinical
examination. Moreover, the remodeling of alveolar
bone during tooth eruption may also contribute to
measurement errors in children.
Hence, the criteria of the case definition of
aggressive periodontitis outlined above, although
straightforward when used in the dental office, may
not be well suited for large surveys, particularly those
that do not gather adequate radiographic informa-
tion. In those situations where only clinical mea-
surements are available, the diagnosis of aggressive
periodontitis may be less accurate than when both
clinical measurements and adequate radiographs are
available. Given the inherent limitations in the
assessment of disease in surveys, it may be necessary
to modify the diagnostic criteria when used in these
surveys. However, the adjustment of the diagnostic
criteria should be based on a thorough analysis of the
measurement errors in the survey so that stringent
clinical criteria may be used if the measurement er-
rors are relatively high or if the age of the target
population is considerably older than the circumpu-
bertal age (65). However, one should bear in mind
that although such a modification may potentially
reduce the false-positive rate, it would also decrease
the sensitivity of diagnosing true cases of disease (i.e.
would increase the false-negative rate).
Concluding remarks and future
considerations
Early age of onset, high rate of disease progression,
involvement of multiple teeth with a distinctive pat-
tern of periodontal tissue loss and absence of
systemic diseases are key diagnostic criteria of
aggressive periodontitis. In some patients, tissue loss
may commence before puberty, whereas in most
patients the age of onset is during, or somewhat after,
the circumpubertal period. The literature lacks evi-
dence of patients showing commencement of the
disease during their late twenties or older. Cases of
aggressive periodontitis are often diagnosed years
after the onset of the disease, partly because current
assessment methods detect established disease more
readily and reliably than they detect incipient or
initial lesions where the tissue loss is minimal and
24
usually below the detection threshold of these
methods. Hence, individuals in their late twenties or
early thirties may also be diagnosed as having
aggressive periodontitis if, at presentation, the
severity and the pattern of periodontal tissue loss are
consistent with an aggressive disease, suggesting that
the loss had commenced at an earlier age.
The variability in the age of onset of aggressive
periodontitis may be associated with the type and
severity of etiologic factors. Hence, early age of onset
may suggest a higher potency or high level of etio-
logical factors than late-onset disease. However, the
presence of an etiologic factor is not sufficient to
define a case if other clinical signs of disease are not
present. Still, the presence of etiological factors is a
valuable determinant of increased risk of disease
development.
At present, the diagnosis of aggressive periodontitis
is achieved using case history, clinical examination
and radiographic evaluation. Some of these methods
are prone to relatively high measurement errors. In
addition, these methods measure past disease his-
tory. Assessment methods that generate smaller
measurement errors may contribute to an earlier
detection of cases of aggressive periodontitis before
significant tissue loss occurs. Also, clinical surveys in
populations present a special challenge for the
accurate diagnosis of cases of aggressive periodontitis
(53).
Genetic predisposition plays a key role in the
development of aggressive periodontitis and con-
tributes to the early onset of tissue destruction, which
is the hallmark of this disease. In susceptible indi-
viduals the presence and the intensity of other etio-
logic factors may determine the clinical features and
the severity of the disease. For instance, the presence
of specific periodontal pathogens subgingivally, to-
gether with one or more other risk factors, such as
smoking and poor oral hygiene, will contribute to the
onset of the disease at an early age, and may also lead
to a more severe and ⁄ or generalized disease. On the
other hand, individuals who are genetically predis-
posed but either do not harbor virulent periodontal
pathogens or have only low levels of these microor-
ganisms, and in addition lack other risk factors, may
develop a localized form of aggressive periodontitis
and the onset of the periodontal tissue loss may oc-
cur at an older age.
Future diagnostic methods of aggressive peri-
odontitis should diagnose the disease early (67).
These methods may entail the identification of key
etiologic and risk factors, combined with a higher
precision and early detection of initial lesions. Such

methods may significantly enhance the predictive
value of these tests and detect cases of aggressive
periodontitis before significant tissue loss develops.
References
1. Albandar JM. Validity and reliability of alveolar bone level
measurements made on dry skulls. J Clin Periodontol 1989:
16: 575–579.
2. Albandar JM, Buischi YA, Barbosa MF. Destructive forms of
periodontal disease in adolescents. A 3-year longitudinal
study. J Periodontol 1991: 62: 370–376.
3. Albandar JM. Juvenile periodontitis – pattern of progres-
sion and relationship to clinical periodontal parameters.
Community Dent Oral Epidemiol 1993: 21: 185–189.
4. Albandar JM, Brown LJ, Brunelle JA, Loe H. Gingival state
and dental calculus in early-onset periodontitis. J Period-
ontol 1996: 67: 953–959.
5. Albandar JM, Brown LJ, Genco RJ, Loe H. Clinical classifi-
cation of periodontitis in adolescents and young adults.
J Periodontol 1997: 68: 545–555.
6. Albandar JM, Brown LJ, Loe H. Clinical features of early-
onset periodontitis. J Am Dent Assoc 1997: 128: 1393–1399.
7. Albandar JM, DeNardin AM, Adesanya MR, Diehl SR, Winn
DM. Associations between serum antibody levels to peri-
odontal pathogens and early-onset periodontitis. J Period-
ontol 2001: 72: 1463–1469.
8. Albandar JM. Global risk factors and risk indicators for
periodontal diseases. Periodontol 2000 2002: 29: 177–206.
9. Albandar JM, Muranga MB, Rams TE. Prevalence of
aggressive periodontitis in school attendees in Uganda.
J Clin Periodontol 2002: 29: 823–831.
10. Albandar JM, Rams TE. Risk factors for periodontitis in
children and young persons. Periodontol 2000 2002: 29:
207–222.
11. American Academy of Periodontology. Proceedings of the
World Workshop in Clinical Periodontics. Chicago: Ameri-
can Academy of Periodontology, 1989.
12. Armitage GC. Development of a classification system for
periodontal diseases and conditions. Ann Periodontol 1999:
4: 1–6.
13. Baab DA, Page RC, Morton T. Studies of a family mani-
festing premature exfoliation of deciduous teeth. J Period-
ontol 1985: 56: 403–409.
14. Baer PN, Stanley HR, Brown K, Smith L, Gamble J,
Swerdlow H. Advanced periodontal disease in an adoles-
cent (periodontosis). J Periodontol 1963: 34: 533–539.
15. Baer PN. The case for periodontosis as a clinical entity.
J Periodontol 1971: 42: 516–520.
16. Boraz RA. Prepubertal periodontitis: report of a generalized
case involving the primary dentition. J Pedod 1985: 9: 165–168.
17. Brown LJ, Albandar JM, Brunelle JA, Loe H. Early-onset
periodontitis: progression of attachment loss during
6 years. J Periodontol 1996: 67: 968–975.
18. Burmeister JA, Best AM, Palcanis KG, Caine FA, Ranney RR.
Localized juvenile periodontitis and generalized severe
periodontitis: clinical findings. J Clin Periodontol 1984: 11:
181–192.
19. Butler JH. A familial pattern of juvenile periodontitis
(periodontosis). J Periodontol 1969: 40: 115–118.
Aggressive periodontitis case definition
20. Califano JV, Pace BE, Gunsolley JC, Schenkein HA, Lally ET,
Tew JG. Antibody reactive with Actinobacillus actinomyce-
temcomitans leukotoxin in early-onset periodontitis pa-
tients. Oral Microbiol Immunol 1997: 12: 20–26.
21. Cappelli DP, Ebersole JL, Kornman KS. Early-onset peri-
odontitis in Hispanic-American adolescents associated
with A. actinomycetemcomitans. Community Dent Oral
Epidemiol 1994: 22: 116–121.
22. Chapple IL. Periodontal disease diagnosis: current status
and future developments. J Dent 1997: 25: 3–15.
23. Cogen RB, Al-Joburi W, Caufield PW, Stanley HP, Donald-
son K. Periodontal disease in healthy children: two clinical
reports. Pediatr Dent 1984: 6: 41–45.
24. Cogen RB, Wright JT, Tate AL. Destructive periodontal
disease in healthy children. J Periodontol 1992: 63: 761–765.
25. Elamin AM, Skaug N, Ali RW, Bakken V, Albandar JM. Ethnic
disparities in the prevalence of periodontitis among
high school students in Sudan. J Periodontol 2010: 81: 891–
896.
26. Eres G, Saribay A, Akkaya M. Periodontal treatment needs
and prevalence of localized aggressive periodontitis in
a young Turkish population. J Periodontol 2009: 80: 940–
944.
27. Faveri M, Figueiredo LC, Duarte PM, Mestnik MJ, Mayer
MP, Feres M. Microbiological profile of untreated subjects
with localized aggressive periodontitis. J Clin Periodontol
2009: 36: 739–749.
28. Gjermo P, Bellini HT, Pereira Santos V, Martins JG, Ferra-
cyoli JR. Prevalence of bone loss in a group of Brazilian
teenagers assessed on bite-wing radiographs. J Clin Peri-
odontol 1984: 11: 104–113.
29. Gottlieb B. Die diffuse Atrophie des Alveolarknochens.
Weitere Beiträge zur Kenntnis des Alveolarschwundes und
dessen Wiedergutmachung durch Zementwachstum. Zeit-
schrift für Stomatologie 1923: 21: 195–262.
30. Gottlieb B. Tissue changes in pyorrhea. J Am Dent Assoc
1927: 14: 2178–2207.
31. Gottlieb B. The formation of the pocket: diffuse atrophy of
alveolar bone. J Am Dent Assoc 1928: 15: 462–476.
32. Gottlieb B. The new concept of periodontoclasia. J Peri-
odontol 1946: 17: 7–23.
33. Gunsolley JC, Califano JV, Koertge TE, Burmeister JA,
Cooper LC, Schenkein HA. Longitudinal assessment of
early onset periodontitis. J Periodontol 1995: 66: 321–328.
34. Hewitt C, McCormick D, Linden G, Turk D, Stern I, Wallace
I, Southern L, Zhang L, Howard R, Bullon P, Wong M,
Widmer R, Gaffar KA, Awawdeh L, Briggs J, Yaghmai R, Jabs
EW, Hoeger P, Bleck O, Rüdiger SG, Petersilka G, Battino M,
Brett P, Hattab F, Al-Hamed M, Sloan P, Toomes C, Dixon
M, James J, Read AP, Thakker N. The role of cathepsin C in
Papillon-Lefèvre syndrome, prepubertal periodontitis, and
aggressive periodontitis. Hum Mutat 2004: 23: 222–228.
35. Hørmand J, Frandsen A. Juvenile periodontitis. Localiza-
tion of bone loss in relation to age, sex, and teeth. J Clin
Periodontol 1979: 6: 407–416.
36. Jamison HC. Prevalence of periodontal disease of the
deciduous teeth. J Am Dent Assoc 1963: 66: 207–215.
37. Jin Y, Yip HK. Supragingival calculus: formation and con-
trol. Crit Rev Oral Biol Med 2002: 13: 426–441.
38. Khocht A, Albandar JM. Aggressive forms of periodontitis
secondary to systemic disorders. Periodontol 2000 2014: 65:
134–148.
25
Albandar
39. Kinane DF, Hart TC. Genes and gene polymorphisms
associated with periodontal disease. Crit Rev Oral Biol Med
2003: 14: 430–449.
40. Kornman KS. Mapping the pathogenesis of periodontitis: a
new look. J Periodontol 2008: 79: 1560–1568.
41. Kulkarni C, Kinane DF. Host response in aggressive peri-
odontitis. Periodontol 2000 2014: 65: 79–91.
42. Laine ML, Crielaard W, Loos BG. Genetic susceptibility to
periodontitis. Periodontol 2000 2012: 58: 37–68.
43. Lang N, Bartold PM, Cullinan M, Jeffcoat M, Mombelli A,
Murakami S, Page R, Papapanou P, Tonetti M, Van Dyke T.
Consensus report – aggressive periodontitis. Ann Period-
ontol 1999: 4: 53.
44. Loe H, Brown LJ. Early onset periodontitis in the United
States of America. J Periodontol 1991: 62: 608–616.
45. Lyons H, Kerr DM, Hine MK. Report from the 1949
Nomenclature Committee of the American Academy of
Periodontology. J Periodontol 1950: 21: 40–43.
46. Mandell RL, Siegal MD, Umland E. Localized juvenile
periodontitis of the primary dentition. ASDC J Dent Child
1986: 53: 193–196.
47. Meng H, Ren X, Tian Y, Feng X, Xu L, Zhang L, Lu R, Shi D,
Chen Z. Genetic study of families affected with aggressive
periodontitis. Periodontol 2000 2011: 56: 87–101.
48. Miller SC. Precocious advanced alveolar atrophy. J Peri-
odontol 1948: 19: 1946.
49. Mros ST, Berglundh T. Aggressive periodontitis in children: a
14-19-year follow-up. J Clin Periodontol 2010: 37: 283–287.
50. Orban B, Weinmann JP. Diffuse atrophy of the alveolar
bone (periodontosis). J Periodontol 1942: 13: 31–45.
51. Page RC, Bowen T, Altman L, Vandesteen E, Ochs H,
Mackenzie P, Osterberg S, Engel LD, Williams BL. Prepu-
bertal periodontitis. I. Definition of a clinical disease entity.
J Periodontol 1983: 54: 257–271.
52. Rapp GE, Pineda-Trujillo N, McQuillin A, Tonetti M. Ge-
netic power of a Brazilian three-generation family with
generalized aggressive periodontitis. Braz Dent J 2010: 21:
137–141.
53. Saxby M. Prevalence of juvenile periodontitis in a British
school population. Community Dent Oral Epidemiol 1984:
12: 185–187.
54. Saxén L, Murtomaa H. Age-related expression of juvenile
periodontitis. J Clin Periodontol 1985: 12: 21–26.
55. Schätzle M, Löe H, Lang NP, Heitz-Mayfield LJ, Bürgin W,
Anerud A, Boysen H. Clinical course of chronic periodon-
titis. III. Patterns, variations and risks of attachment loss.
J Clin Periodontol 2003: 30: 909–918.
56. Schenkein HA, Van Dyke TE. Early-onset periodontitis:
systemic aspects of etiology and pathogenesis. Periodontol
2000 1994: 6: 7–25.
26
57. Schluger S, Yuodelis RA, Page RC. Periodontal Disease.
Philadelphia: Lea & Febiger, 1977.
58. Seidler B, Miller SC, Wolf W. Systemic aspects of preco-
cious advanced alveolar bone destruction; preliminary re-
port. J Am Dent Assoc 1950: 40: 49–58, illust.
59. Shapira L, Smidt A, Van Dyke TE, Barak V, Soskolne AW,
Brautbar C, Sela MN, Bimstein E. Sequential manifestation
of different forms of early-onset periodontitis. A case re-
port. J Periodontol 1994: 65: 631–635.
60. Sims TJ, Moncla BJ, Darveau RP, Page RC. Antigens of
Actinobacillus actinomycetemcomitans recognized by pa-
tients with juvenile periodontitis and periodontally normal
subjects. Infect Immun 1991: 59: 913–924.
61. Sjodin B, Matsson L, Unell L, Egelberg J. Marginal bone loss
in the primary dentition of patients with juvenile peri-
odontitis. J Clin Periodontol 1993: 20: 32–36.
62. Smith M, Seymour GJ, Cullinan MP. Histopathological
features of chronic and aggressive periodontitis. Period-
ontol 2000 2010: 53: 45–54.
63. Spektor MD, Vandesteen GE, Page RC. Clinical studies of
one family manifesting rapidly progressive, juvenile and
prepubertal periodontitis. J Periodontol 1985: 56: 93–101.
64. Sugarman MM, Sugarman EF. Precocious periodontitis: a
clinical entity and a treatment responsibility. J Periodontol
1977: 48: 397–409.
65. Susin C, Albandar JM. Aggressive periodontitis in an urban
population in southern Brazil. J Periodontol 2005: 76: 468–475.
66. Tonetti MS, Mombelli A. Early-onset periodontitis. Ann
Periodontol 1999: 4: 39–53.
67. Van Dyke TE, Tohme ZN. Periodontal diagnosis: evaluation
of current concepts and future needs. J Int Acad Period-
ontol 2000: 2: 71–78.
68. Vieira AR, Albandar JM. The role of genetic factors in the
pathogenesis of aggressive periodontitis. Periodontol 2000
2014: 65: 92–106.
69. Waerhaug J. Subgingival plaque and loss of attachment in
periodontosis as observed in autopsy material. J Period-
ontol 1976: 47: 636–642.
70. Waerhaug J. Subgingival plaque and loss of attachment in
periodontosis as evaluated on extracted teeth. J Periodontol
1977: 48: 125–130.
71. Watanabe K. Prepubertal periodontitis: a review of diag-
nostic criteria, pathogenesis, and differential diagnosis.
J Periodontal Res 1990: 25: 31–48.
72. Xynogala I, Volgina A, DiRienzo JM, Korostoff J. Evaluation
of the humoral immune response to the cytolethal dis-
tending toxin of Aggregatibacter actinomycetemcomitans Y4
in subjects with localized aggressive periodontitis. Oral
Microbiol Immunol 2009: 24: 116–123.
Copyright of Periodontology 2000 is the property of Wiley-Blackwell and its content may not
be copied or emailed to multiple sites or posted to a listserv without the copyright holder's
express written permission. However, users may print, download, or email articles for
individual use.