Therapeutic management of a case of generalised
aggressive periodontitis in an 8-year old child:
18-month results
K. Seremidi*, S. Gizani*, P. Madianos**
* Department of Paediatric Dentistry, ** Department of Periodontology,School of Dentistry, University of Athens, Greece
Key words: Generalised aggressive periodontitis,
children, Aggregatibacter actinomycetemcomitans,
periodontal treatment, tooth extraction.
Postal address: Dr. K. Seremidi, 8 Anaxagora Street, 16675 Glyfada,
Athens, Greece.
Email: kser51@otenet.gr
Abstract
BACKGROUND: Generalised aggressive periodontitis
(GAP) is a rare condition associated with rapid periodontal
destruction, in multiple teeth. The paper aims to present a
case of an 8-year old with GAP and discuss his response
to treatment. CASE REPORT: An 8-year old male was
referred to the postgraduate clinic of paediatric dentistry
of the University of Athens due to increased mobility in
his primary dentition. At initial clinical examination, plaque
accumulation, gingival inflammation and temporary
restorations were noted. Detailed periodontal examina-
tion revealed bleeding on probing, pocket depths of up
to 9 mm and second degree mobility in primary teeth.
Radiographic examination showed advanced bone loss
and carious lesions. Microbiological analysis revealed
increased percentages of peri-opathogens in pooled
subgingival samples. Final diagnosis of GAP was
made after ruling out any underlying systemic disorder.
TREATMENT: Periodontal therapy involved non-surgical
subgingival debridement, systemic administration of
antibiotics and retention of periodontally involved teeth.
FOLLOW-UP: This was based on a monthly recall pro-
gram for the first 6 months and a 3-monthly regime
thereafter. At 18-months after initial examination, a sub-
stantial improvement in clinical parameters was seen,
while levels of periodontal pathogens were sustained at
low levels. CONCLUSION: Non-surgical root debride-
ment along with systemic administration of antibiotics
and retention of the periodontally involved teeth, can be
successful in achieving improvement and maintenance of
periodontal health in the mixed dentition.
Introduction
Periodontal disease in children presents in various forms,
ranging from conditions limited to mild gingival inflammation
up to severe periodontal tissue destruction that can, in some
cases, cause early tooth exfoliation. Epidemiological studies
in children have indicated that the prevalence of gingivitis is
similar to that of the adults and ranges from 40-60%, while
periodontitis is relatively uncommon and ranges from 0.1-
5% [Califano, 2003]. In the past decades, a variety of terms
have been proposed to describe periodontal destruction in
young patients [Armitage and Cullinan, 2010]. Lately, the
term aggressive periodontitis was used to replace a group
266 European Archives of Paediatric Dentistry 13 (Issue 5). 2012
of dissimilar destructive periodontal diseases collectively
termed “Early-onset Periodontitis” [Armitage, 1999]. The
onset of the disease is often circumpubertal and its main
features include a history of rapid and severe bone loss as
well as familial aggregation in individuals who are systemi-
cally healthy [Clerehugh and Tugnait, 2001; Califano, 2003].
The main aetiological factors do not differ from those
associated with chronic periodontitis, such as virulent
periodontal pathogenic microbiota and/or impaired host
defence mechanisms [Clerehugh and Tugnait, 2001; Oh et
al., 2002; Portaro et al., 2008]. Aggressive periodontitis can
be either localised or generalised, depending on the percent-
age of sites affected (<30% localised and >30% generalised)
[Modeer and Wondimu, 2000; Wiebe and Putnins 2000].
Generalised aggressive periodontitis (GAP) may affect both
primary and permanent dentitions and causes rapid alveolar
bone destruction and attachment loss in multiple teeth, not
only limited to first molars and incisors. Controversy exists
concerning the presence of plaque and calculus. More
specifically older reports find very little if any supragingival
plaque, while recent ones demonstrate a positive correla-
tion between subgingival calculus, gingival inflammation and
periodontal destruction [Wara-aswapati et al., 1999; Clere-
hugh and Tugnait, 2001]. GAP has been associated with
recurrent infections, e.g upper respiratory tract and otitis
media as well as sinusitis, pneumonia and dermatitis [Wata-
nabe, 1991; Dibart et al., 1998; Aren et al., 2003].
In the literature there are few case reports published on GAP
in children [Watanabe, 1991; Firatli et al., 1996; Kamma et
al., 1998; Bodur et al., 2001; Aren et al., 2003; Vandana and
Venkata Ramesh Redy, 2003; Portaro et al., 2008] most of
which are associated with underlying systemic disease. The
aim of this paper is to a) describe the clinical, radiographic
and microbiological findings of a systemically healthy 8-year
old child with GAP and b) discuss the patient’s response to
treatment up to 18-months follow-up.
Case report
An 8-year old caucasian male was referred by a private
orthodontist to the post-graduate clinic of paediatric den-
tistry in the university of Athens, due to increased mobility of
the primary dentition. His medical history was non-contribu-
tory, although the mother reported episodes of recurrent ear
infections while the patient was younger (up to the age of 5
years). Both parents and his younger sister (6 years old) were
systemically healthy and reported no history of periodontitis.
The reported dental history revealed that the patient was a
sporadic attendee to the dentist and he had already received
restorative treatment of several primary teeth. He brushed
his teeth once a day and he did not use floss.
 Management of aggressive periodontitis in children

A A

B C B

Figure 1. Intra-oral pictures at initial examination: (a) frontal view, Figure 2. Dental panoramic radiographs (a) one year before visiting
(b) right and (c) left lateral views. Black arrows indicate areas with our clinic, (b) at initial examination. Circles indicate areas with bone
easily visible plaque accumulation. loss that progressed from the time the first radiograph was taken.

Table 1. Clinical results before treatment and during follow-up. Clinical examination. Clinical oral examination (Fig. 1)
revealed moderate oral hygiene with a PI (simplified plaque
Pocket
depth (mm)
index)[O’Leary et al., 1972] score of 35% and increased
gingival inflammation, with a GI (simplified gingival index)
MPD MP [Lindhe, 1981] score of 89%. Temporary restorations were
PI GI BOP
found in primary molars (teeth 54 and 55). Detailed periodon-
tal examination revealed bleeding on probing at 60% of the
Initial examination 35% 89% 60% 7.5 9
sites, as well as sites with probing pocket depths (PPD) up to
6 mm in all four permanent molars and up to 9 mm in primary
canines (Table 1). Second-degree mobility was noticed in
3-months recall 25% 65% 50% 6.2 8
the maxillary and mandibular primary canines. Orthodontic
assessment showed crowding in both maxillary and man-
6-months recall 20% 50% 40% 5.5 8 dibular arches and anterior cross-bite in central as well as
lateral permanent incisors.
Radiographic examination. Comparison of the two pano-
9-months recall 21% 40% 38% 4.8 7
ramic radiographs (Fig. 2) taken within a one year interval,
revealed rapid progression of vertical and horizontal bone
loss mainly around primary molars and canines (indicated
12-months recall 15% 30% 29% 4.3 6
with circles in the second panoramic radiograph). Periapical
radiographs (Fig. 3) showed advanced bone loss in primary
15-months recall 12% 25% 18% 4.0 5 molars and canines, with the alveolar bone covering at most
half of the root length. More specifically, the alveolar bone
was covering less than 1/3 of the length of the mesial root
18-months recall 10% 20% 12% 3.8 5 of 54 and 64, almost half of the length of the mesial and
less than 1/3 of the distal root of 74 and 84 respectively.
PI=plaque index, GI=gingival index, BOP=bleeding on probing, MPD=mean Similar findings were registered for the mesial roots of 75
pocket depth, MP=maximum pocket detected and 85. Regarding the primary canines, alveolar bone was

European Archives of Paediatric Dentistry 267

 K. Seremidi et al

covering 1/3 of both mesial and distal roots of 53 and 63

A
B samples were taken from primary canines and molars as
C determine the predominant cultivable microbiota [Syed et al.,
Figure 3. Full mouth periapical radiographs at initial examination: (a)
maxillary posterior teeth, (b) mandibular posterior teeth, (c) central
maxillary and mandibular teeth.
and 1/2 of the roots of 73 and 83, respectively. Maxillary and
mandibular permanent teeth were not severely affected, with
the bone loss being less than 1/3 of the root. Several carious
lesions (teeth 74, 75, 84 and 85) and periapical pathology in
primary molars (54 and 55) were also found.
Microbiological tests. Teeth were isolated and the suprag-
ingival plaque was removed. Pooled subgingival plaque
well as permanent molars, by inserting sterile paper points
into the deepest pockets of these teeth and allowing them
to remain for 10 sec. The samples were placed into RTF and
transferred to the laboratory. Aliquots of 0.1 ml of serial dilu-
tions were plated in duplicate onto a) enriched trypticase soy
agar (ETSA) supplemented with 4% defibrinated blood to
1980]; b) KVLB-2 agar (kanamycin 75µg/ml-vancomycin 2µg/
ml blood) for the isolation of pigmented and non-pigmented
Prevotella spp, Porphyromonas spp and Bacteroides spp;
c) TSBV (trypticase-soy-agar) supplemented with 5% serum
75 µg/ml bacitracin and 5 µg/ml vancomycin to quantify
Aggregatibacter actinomycetemcomitans [Slots, 1982]. After
incubation, the identification of the bacteria was performed
based on colony morphology, Gram staining and biochemi-
cal tests [Krieg and Holt, 1984]. The frequency of detection
for a given species was calculated on the basis of the total
isolated subgingival microbiota. The microbiological results
showed that in permanent molars, increased percentages of

Table 2. Frequency of detection of bacterial species in subgingival plaque samples at the initial examination (I.E) and recall visits.

Permanent Molars Primary Molars Primary Canines Premolars

Tooth
Microbes I.E 6 mth 12 mth 18 mth I.E 6 mth 12 mth 18 mth I.E 6 mth 12 mth 18 mth 12 mth 18 mth

P. g 24% / 12% 10% 21% / 9% 10% 25% / 16% 13% 12% 11%

A. a 18% 6% 2,5% 7% 24% / / 9% 19% / 4% 2% / 3%

P. i / / / / / / / 6% 11% / 5% 8% / 5%

E. c / / / 9% 3% / / / 3% / / / 9% /

F. n / 13% 9% / 9% 6% 6% 7% 5% 6% 6% / 12% /

P. g = Porphyromonas gingivalis. A. a = Aggregatibacter actinomycetemcomitans. P. i = Prevotella intermedia. E. c = Escherichia coli. F. n = Fusobacterium nucleatum

268 European Archives of Paediatric Dentistry 13 (Issue 5). 2012

 Management of aggressive periodontitis in children

Table 3. Laboratory results

B

Patient Normal range

HGB 12.5 10.3-14.9 g/dL

WBC 5600 4800-10800 /mm3

A

PLT 248000 140000-400000 /mm3

HCT 36.9 32-42 %

RBC 4800000 4000000-5200000 /mm3

A
MCV 76.9 73-87 m3=fL

Blood Glucose level 90% 70-110 mg (%)

ALP 227 130-560 U/L

IgG 1124 600-1300 mg/dL

IgM 82 40-160 mg/dL

Figure 4. Radiographic examination at 18-month recall appointment:

IgA 125 41-297 mg/dL (a) maxillary posterior teeth, (b) mandibular posterior teeth, (c) central
maxillary and mandibular teeth.
C3 129 90-180 mg/dL

C4 26 10-40 mg/dL
A. actinomycetemcomitans and Porphyromonas gingivalis
were isolated from the total subgingival microbiota. The
findings were similar in primary molars and canines with the
percentages of A. actinomycetemcomitans and P.gingivalis
varying from 19-25% (Table 2).
Differential and final diagnosis. Based on the medical his-
tory, as well as the clinical and radiographic findings reported
previously, differential diagnosis was made between GAP,
periodontal manifestations of systemic (e.g. eosinophilic
granuloma) and haematological disease (e.g. cyclic neu-
tropenia, leukaemia) or genetic disorder (e.g. leukocyte
adhesion deficiency syndrome, Papillon-Lefèvre syndrome).
The patient was referred for a more detailed medical exami-
nation for the exclusion of any underlying systemic disease.
The laboratory values of the blood counts and serum bio-
chemical tests were within normal limits for the patient’s age
(Table 3). A final diagnosis of GAP was made.
Treatment
The treatment plan consisted of an individualised oral
health preventive program followed by periodontal therapy
and restorative dental treatment. The oral health preventive
program included oral hygiene instructions and more specifi-
cally toothbrushing twice daily with a fluoridated toothpaste,
use of dental floss for interdental cleaning, and use of
disclosing tablets to increase the effectiveness of plaque
removal. Dietary instructions (decrease of sweets intake up
to once per day) were also given. In office fluoride appli-
cation was carried out every 3-4 mοnths. The periodontal
therapy included full mouth scaling and root planing under
local analgesia in two visits within a one week interval. Anti-
biotics were also administered at the end of the second visit
(amoxycillin 50mg/kg and metronidazole 30mg/kg tds) for
2 weeks [Lopez, 1992] along with the prescription of 0.2%
chlorohexidine mouthrinse for 10 days. Two weeks after the
completion of the initial phase of periodontal therapy, dental
treatment was carried out. Extraction of primary teeth with
periapical lesions was performed followed by restoration of
carious primary teeth with composite resin.

European Archives of Paediatric Dentistry 269

 K. Seremidi et al
Follow-up
A follow-up program was applied involving monthly recall
appointments for the first six months, and every three months
thereafter. At each follow-up visit, plaque accumulation and
gingival bleeding were assessed as well as oral hygiene and
dietary advice were reinforced. Supra- and sub-gingival
debridement was also performed where it was necessary.
Radiographic examination and plaque sampling for micro-
biological assessment was performed every 6 months.
Gradual improvement of oral hygiene (PI, initial examination:
35% vs 18 months: 10%), decrease of gingival inflam-
mation (GI, 89% vs 20%) and reduction in the number of
sites with bleeding on probing were found (60% vs 12%)
(Table 1). Radiographic findings revealed reduction of bone
loss, with alveolar bone covering more than 2/3 of the root
length of the previously affected teeth (Fig. 4). Permanent
incisors and premolars erupted with indications of a healthy
periodontium.
Microbiological findings indicated a significant decrease in the
detectable percentages of most periopathogenic microbes
especially in permanent teeth during the first six months when
the patient was kept in the monthly-recall program (Table 2).
At 12- and 18-month visits, P. gingivalis and A. actinomycet-
emcomitans were isolated from the affected sites, although at
lower levels than those detected at initial examination. Prevo-
tella intermedia, which was only detected in primary teeth at
initial examination, was isolated at recall visits, but at very
low levels, mainly from the canines (Table 2). Fusobacterium
nucleatum was isolated at low levels from almost all sites at
initial examination and remained so, at all visits.
Discussion
The current case report describes an 8-year-old boy that pre-
sented increased mobility in his primary dentition. Based on
the clinical and radiographic findings showing tooth mobility
and attachment loss at more than 30% of sites in the mouth
[Wiebe and Putnins, 2000], the patient was diagnosed as
having generalised aggressive periodontitis (GAP). Medical
history and further medical examination did not reveal a sys-
temic disease or other health problems while the family history
showed no immediate relatives with periodontal disease.
Despite having severe periodontitis, the child was apparently
healthy and showed no unusual infections. However, abnor-
malities in neutrophil function could not be ruled out, since
the required diagnostic methodology was not available.
Based on the literature, reports have shown that aggressive
periodontitis can occur in the absence of detectable neutro-
phil defects [Lopez, 1992; Bodur et al., 2001], while others
reported a decrease in neutrophil chemotaxis [Celenligil et
al., 1987; Firatli et al., 1996]. Hence, there is no consistent
association of functional defects with aggressive periodonti-
tis in the primary or permanent dentition.
270 European Archives of Paediatric Dentistry 13 (Issue 5). 2012
Destructive periodontal disease is associated with specific
bacterial pathogens, such as A. actinomycetemcomitans
and P. gingivalis, which are thought to play an important role
in the pathogenesis of the disease [Clerehugh and Tugnait,
2001; Portaro et al., 2008]. The microbiological examina-
tion of the subgingival plaque of the patient showed that P.
gingivalis was found in both primary and permanent teeth,
comprising the highest proportion of the periodontopathic
microbiota, followed by A. actinomycetemcomitans. Studies
have shown that highly virulent strains of A. actinomycet-
emcomitans in combination with Bacteroides-like species
such as P. gingivalis and P. intermedia have been implicated
in the aetiology of GAP [Haraszthy et al., 2000; Califano,
2003]. A. actinomycetemcomitans is suggested to be more
easily transmitted to humans with immature oral subgingival
biofilm, which is the case during eruption and exfoliation of
teeth. Consequently first molars and incisors are the first
teeth affected in GAP [Bodur et al., 2001].
Therapeutic strategies in the treatment of periodontal disease
are directed towards the reduction of supra- and subgingival
microorganisms. A combination of mechanical (non-surgical
or surgical) debridement with a systemic antibiotic regime
has been suggested in several studies for the treatment of
GAP [Bodur et al., 2001; Valenza et al., 2009; Aimetti et al.,
2012]. A similar approach was employed in the present case
using non-surgical debridement and administration of met-
ronidazole and amoxycillin.
Extraction of severely affected primary teeth has also been
suggested in the literature in order to reduce the risk of infec-
tion spread to the erupting permanent teeth [Modeer and
Wondimu, 2000; Bodur et al., 2001; Vandana and Venkata
Ramesh Redy, 2003; Portaro et al. 2008]. In our case, we
followed a more conservative approach, extracting only pri-
mary teeth with periapical lesions. Our treatment aim was
to maintain a functional and aesthetic dentition, based on
periodontal therapy and close monitoring. On the other
hand, the present approach has the drawback of relying on
patient compliance to achieve a positive treatment result,
which is a tough challenge for a patient at this age. Parental
involvement and tight periodontal maintenance is, therefore,
essential for a successful therapeutic outcome, when such
an approach is employed.
Clinical and radiographic parameters at the 18-month
follow-up showed that the improvement in periodontal con-
dition, attained immediately after active periodontal therapy,
was maintained. In addition, erupting permanent teeth were
not found to be periodontally affected microbiological find-
ings showed that the periopathogens were significantly
decreased at follow-up, however they reappeared at 12- and
18- months at low levels. A possible explanation is that,
despite thorough scaling and root planing, the bacteria
still remain in the tongue and other soft tissues and conse-
quently could recolonise the pockets [Quirynen et al., 2001;

Walker and Karpinia, 2002]. Although the reappearance of A.
actinomycetemcomitans and P. gingivalis was at low levels,
it reinforces the importance of close periodontal monitoring,
in order to maintain a periodontitis-free permanent dentition.
Conclusion
Management of GAP in children with non-surgical root
debridement along with systemic administration of anti-
biotics can be successful in achieving improvement and
maintenance of periodontal health in the mixed dentition,
despite retaining periodontally involved primary teeth. Long
term, close follow-up of such patients is essential, both dur-
ing the completion of the permanent dentition as well as
throughout life, since they are likely to remain highly suscep-
tible to periodontal disease.
References
Aimetti D, Romano F, Guzzi N, Carnevale G. Full-mouth disinfection and
systemic antimicrobial therapy in Generalised aggressive periodontitis: a
randomized, placebo-controlled trial. J Clin Periodontol. 2012; 39:284-294.
Aren G, Gurel N, Yalcin F, Firatli E. Clinical and immunological findings of two
siblings in a family with Generalised aggressive periodontitis. J Dent Child
2003; 70:266-271.
Armitage G. Development of a classification system for periodontal diseases
and conditions. Ann Periodontol 1999; 4:1-6.
Armitage GC, Cullinan MP. Comparison of the clinical features of chronic and
aggressive periodontitis. Periodontology 2000 2010; 53:12-27.
Bodur A, Bodur H, Bal B, Balos K. Generalised aggressive periodontitis in a
prepubertal patient: A case report. Quintessence Int 2001; 32:303-308.
Califano JV. Periodontal diseases of children and adolescents. J Periodontol
2003; 74:1696-1704.
Celenligil H, Kansu E, Eratalay K. Prepubertal periodontitis. A case report with
an analysis of lymphocyte populations. J Clin Periodontol 1987; 14:85-88.
Clerehugh V, Tugnait A. Periodontal diseases in children and adolescents: I.
Aetiology and diagnosis. Dent Update 2001; 28:222-232.
Dibart S, Chapple I, Skobe Z, Shusterman S, Nedleman HL. Microbiologi-
cal findings in prepubertal periodontitis: A case report. J Periodontol 1998;
69:1172-1175.
Firatli E, Gurel N, Efeoglu A, Cebeci I. Generalised prepubertal periodontitis.
A report of 4 cases with the immunological findings. J Clin Periodontol 1996;
23:1104-1111.
Management of aggressive periodontitis in children
Haraszthy V, Hariharan G, Tinoco E, et al. Evidence for the role of highly
leukotoxic Actinobacillus actinomycetem¬comitans in the pathogenesis of
localised and other forms of early-onset periodontitis. J Periodontol 2000;
71:912-922.
Kamma JJ, Lygidakis NA, Nakou M. Subgingival microflora and treatment in
prepubertal periodontitis associated with chronic idiopathic neutropenia. J
Clin Periodontol 1998; 25:759-765.
Krieg NR and Holt JG. Bergey’s manual for systemic bacteriology. Baltimore:
Williams & Wilkins, 1984.
Lindhe J. Treatment of localised juvenile periodontitis. In: Genco RJ, Mergen-
hagen SE, eds. Host-Parasite Interactions in Periodontal Disease. Washington,
DC: ASM;1981 pp382-394.
Lopez NJ. Clinical, laboratory and immunological studies of a family with a
high prevalence of Generalised prepubertal and juvenile periodontitis. J Peri-
odontol 1992; 63:457-468.
Modeer T, Wondimu B. Periodontal diseases in children and adolescents.
Pediatr Dent 2000; 44:633-654.
Oh TJ, Eber R, Wang HL. Periodontal diseases in the child and adolescent. J
Clin Periodontol 2002; 29:400-410.
Ο’Leary T, Drake RB, Nayer JE. The plaque control record. J Periodontol 1972;
43:38-40.
Portaro CP, Chopite YG, Cardenas AC. Generalised aggressive periodontitis
in preschoolers: Report of a case in a 3-1/2 year old. J Clin Pediatr Dent 2008;
33:69-74.
Quirynen M, De Soete M, Dierick k, Van Steenberghe D. The intra-oral trans-
location of periopathogens jeopardizes the outcome of periodontal therapy. A
review of the literature. J Clin Periodontol 2001; 28:499-507.
Slots J. Selective medium for isolation of Actinobacillus actinomycetemcomi-
tans. J Clin Microbiol 1982; 15:606-609.
Syed SA, Svanberg M, Svanberg G. The predominant cultivable dental plaque
flora of beagle dogs with gingivitis. J Periodont Res 1980; 15:123-136.
Valenza G, Veihelmann S, Peplies J et al. Microbial changes in periodontitis
successfully treated by mechanical plaque removal and systemic amoxicillin
and metronidazole. Int J Med Microb 2009; 299:427-438.
Vandana KL, Venkata Ramesh Redy B. Prepubertal periodontitis: A report of 2
cases. J Dent Child 2003; 70:82-85.
Walker C, Karpinia K. Rationale for use of antibiotics in periodontitis. J Peri-
odontol 2002; 73:1188-1196.
Wara-aswapati N, Howell TH, Needleman HL, Karimbux N. Periodontitis in the
child and adolescent. J Dent Child 1999; 66:167-173.
Watanabe K. Generalised juvenile periodontitis in a thirteen-year-old child. J
Dent Child 1991; 58:390-395.
Wiebe C, Putnins E. The periodontal disease classification system of the
American Academy of Periodontology--an update. J Can Dent Assoc. 2000;
66:594-7.
European Archives of Paediatric Dentistry 271
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