CASE REPORT

Presentation of Localized Aggressive Periodontitis in Monozygous Twins:

Case Report
Sharon Phamduong∗ and Clara S. Kim†

Introduction: Localized aggressive periodontal disease is an uncommon finding observed in adolescents and
children. Studies have been conducted to elucidate the etiology, contributing factors, and genetic roles in the phenomena.
In particular, twin studies have shown genetic makeup to be a substantial risk factor for periodontitis. This case is, to
the best of the authors’ knowledge, the first to be presented in literature of a same dwelling, set of monozygotic twins,
displaying similar presentation of localized aggressive periodontitis, however with different microbial profiles.
Case Presentation: A set of 17-year-old black male monozygous twins were referred for a full-mouth periodontal
evaluation and any necessary periodontal treatment on July 7, 2007. a complete mouth radiographic series, periodontal
charting, and intraoral photographs were performed on each individual. A family history was obtained through the biological
mother, which yielded no known history of early tooth loss or treatment of severe periodontal disease. The father was not
involved in the rearing of the children and his periodontal history was unavailable. An initial and surgical treatment plan
was developed. Microbial analysis of subgingival plaque samples was collected on the affected sites. Initial treatment with
scaling and root planing, subgingival irrigation, with administration of systemic antibiotics, and oral hygiene instruction,
were rendered on both individuals.
Conclusion: Within limitations of this report, it is demonstrated that different microbial pattern exists on aggressive
periodontitis even in genetically identical individuals with the same environmental exposure. Clin Adv Periodontics
2018;0:1–6.
Key Words: Aggressive periodontitis; genetics; gingival crevicular fluid; microbiology; alveolar bone loss; twin studies.

Background multifactorial including bacterial and viral aspect, host

immune response, and genetic components.2 The role
Aggressive periodontitis is a rare form of periodon-
of specific bacterium such as Aggregatibacter actino-
tal disease, unlike the chronic form, where there is an
mycetemcomitans and Porphyromonas gingivalis is sug-
abnormal immune response, resulting in severe and rapid
gested as possible causative agents for periodontitis in
connective tissue loss and alveolar bone resorption.1
young individuals.2 The purpose of this case report is
The etiology of aggressive periodontitis is complex and
to demonstrate that different microbial patterns exist
∗ Private
on aggressive periodontitis even in genetically identical
practice, Sunnyvale, CA
individuals with the same environmental exposure.
† Department of Periodontics, Western University of Health Sciences,
College of Dental Medicine, Pomona, CA
Clinical Presentation
Received January 5, 2018; accepted April 2, 2018 A set of 17-year-old black male identical twins (TH and
SH) was referred to the University of Southern California,
doi: 10.1002/cap.10041 Herman Ostrow School of Dentistry, Advanced

Clinical Advances in Periodontics, Vol. 0, No. 0, xxx 2018 1

C A S E R E P O R T

Periodontics Clinic by their general dentist for a full-

mouth periodontal evaluation and necessary periodontal
treatment (Figs. 1 through 8). The patients gave oral and
written consent to participate.

Case Management and Clinical

Outcomes
Pooled microbial sampling using paper points were per-
formed on each patient. On each patient a single paper
point was used to obtain a sample from three sepa-
rate affected sites as per USC Oral Microbiology Testing
Laboratory instructions.3 These samples were placed in
a transport medium vial (VMGA III) provided by the
FIGURE 1 Patient TH, frontal photo.
laboratory.3 Specifically, for patient TH, samples were
taken at the mesial buccal of tooth #30, distal buccal of
#30, and mesial buccal of #3. For patient SH, samples
were taken at the mesial buccal of tooth #30, mesial
buccal of #19, and mesial buccal of #3. Scaling and
root planing with local anesthesia, subgingival irrigation
with 10% povidone iodine, and administration of sys-
temic antibiotics (8 days of 250 mg amoxicillin three
times a day and 250 mg metronidazole three times a
day) was rendered however follow-up and re-evaluation
could not be completed due to lack of patient’s interest
and motivation to complete further treatment. Attempts
to contact the patients were unsuccessful. The decision
to use 10% povidone iodine and systemic antibiotics
as adjunctive therapy was based on recommendations
from the American Academy of Periodontology position
FIGURE 2 Patient SH, frontal photo. paper on systemic antibiotics and adjunctive therapy.4,5
Furthermore, recommendations
on specific antibiotics were
provided in the laboratory
report.

Discussion
The benefit of doing a twin
study is that within the
same environment, they share
most relevant oral habits and
practices. “Thus the similarity
FIGURE 3 Posterior periapical radiographs of patient TH (3A through 3H). of such factors as personal
habits, lifestyles, and access to
health care should not be differ-
ent (on average) for members
of twin pairs whether they
are monozygous or dizygous.”6
Schenkein reported in mono-
zygous twins, the difference
in attachment loss is only due
to environment.6 However,
even in the same environment,
our study patients exhibited
different microbial make up yet
FIGURE 4 Posterior periapical radiographs of patient SH (4A through 4H). similar clinical presentations.

2 Clinical Advances in Periodontics, Vol. 0, No. 0, xxx 2018 Localized Aggressive Periodontitis in Twins
 C A S E R E P O R T

FIGURE 5 Initial periodontal charting for patient TH - maxilla.

FIGURE 6 Initial periodontal charting for patient TH - mandible.

Phamduong, Kim Clinical Advances in Periodontics, Vol. 0, No. 0, xxx 2018 3

C A S E R E P O R T

FIGURE 7 Initial periodontal charting for patient SH - maxilla.

FIGURE 8 Initial periodontal charting for patient SH - mandible.

4 Clinical Advances in Periodontics, Vol. 0, No. 0, xxx 2018 Localized Aggressive Periodontitis in Twins
 C A S E R E P O R T

TABLE 1 Laboratory Specimen Analysis for Patients TH and SH

TH SH
Putative Presumptive Periodontal % Cultivable Microbiota % Cultivable Microbiota
Pathogen Identification from culture from culture

A. actinomycetemcomitans 0 0
P. gingivalis 0 3.8
P. intermedia 6.2 0
T. forsythia 3.8 3.8
Campylobacter sp. 4.6 5.4
Eubacterium sp. 0 0
Fusobacterium sp. 5.4 4.6
P. micros 3.8 0
Enteric Gram-negative rods 0 0
Beta hemolytic streptococci 0 0
Yeast 0 0
Eikenella corrodens 0 0
Staphylococcus sp. 0 0
D. pneumosintes 3.8 0

TABLE 2 Tooth Site Affected Based on Observed Radiographic Bone Loss

Observed radiographic Observed radiographic bone

Tooth site affected bone loss on patient TH? loss on patient SH?

Maxilla
Second molar (#2) Yes Yes
First molar (#3) Yes - Mesial Yes - Distal and Mesial
Mandible
Second molar (#18) No No
First molar (#19) Yes - Distal Yes - Mesial
First molar (#30) Yes - Mesial Yes - Mesial
Second molar (#31) No No

To assist in gathering diagnostic information for treat- Health (NIH)-supported microbiome project to identify
ing active periodontal disease, microbiological sampling all major microorganisms in the oral cavity to estab-
of the gingival crevicular fluid found in the periodontal lish a database of microorganisms that can be used
pocket may be performed.7 This often can yield infor- to study specific oral disease processes and infections.9
mation on predominant microbiota and assist in proper An interesting finding in the present study was regard-
choice of antimicrobial therapy. Also, the information ing the presence of different bacterial species within
can be used as predictors of clinical outcome.7 Aggre- monozygotic twins with same environmental condi-
gatibacter actinomycetemcomitans (Aa) is very strongly tions. Both patients shared common periodontopathogens
associated with localized aggressive periodontitis in both such as Tannerella forsythia, Campylobacter species
prevalence and abundance.2 However, Aa was not found and Fusobacterium. However, one patient had Porphy-
in either of our patients in an environment like the romonas gingivalis and the other did not. P. gingi-
oral cavity, it is not one specific organism from a valis has been associated with aggressive periodontitis
pure culture that contributes to a disease or infection in other populations.10 One patient had Prevotella inter-
but that of the community of bacteria inhabiting a media, Peptostreptococcus micros, and Dialister pneu-
biofilm that populates any one surface of the body.8 mosintes whereas the other patient did not (Table 1).
It has been thus the goal of the National Institutes of Both patients had all four first molar involvement with

Phamduong, Kim Clinical Advances in Periodontics, Vol. 0, No. 0, xxx 2018 5

C A S E R E P O R T

severe attachment loss (Figs. 1 and 2; Table 2). Somatic is, epigenetic phenomena result in different expressions
mosaicism may explain for the differences in the sus- of identical genes between a pair of monozygous twins,
ceptibility of one individual for a certain profile of peri- even in genes having the same compositions and DNA
odontopathogens or possibly the effect of slightly vari- nucleotides.”15 Longitudinal evaluation of monozygous
able environmental factors.11,12 Differences in bacterial twin subjects could lead us to important understanding
composition did not seem to be associated with clinical of the role of these bacteria in the initiation and progres-
periodontal breakdown manifestation (Tables 1 and 2). sion oflocalized aggressive periodontitis and its treatment.
Bacterial causation alone cannot explain the symmetri-
cal and site-specific location of breakdown. Within this
concept of genetically and/or environmentally susceptible
Conclusions
individuals being affected, infectious agents such as vari-
With future advanced molecular techniques to elucidate
ous herpesviruses have been associated with severe types
of periodontal disease. 13 Further, herpesviruses in aggres- the relationship between specific microbiomes to differ-
ent presentations of periodontal disease, a clearer picture
sive periodontitis lesions have been shown to possibly play
of disease progression and behavior can be developed.
a role in disease development. The herpesviral–bacterial
role of periodontitis hypothesizes that herpesvirus initi- Also, techniques to perform in-depth viral analysis and to
evaluate epigenetic changes in host responses to periodon-
ates the disease and allows for opportunistic periodon-
topathogens may help to explain the complex etiology of
topathogen colonization.13 Another possible explanation
for the differences is by epigenetic modifications.14 “That aggressive periodontitis.

Summary

Why is this case new  To the best of the authors’ knowledge, this is the first report on the
information? nature of microbial analysis of genetically identical twins with localized
aggressive periodontitis

What are the keys to successful  Microbial sampling to differentiate bacterial challenges along with
management of this case? patient’s full compliance and motivation

What are the primary limitations  Long-term follow-up was not available due to patients’ non-compliance
to success in this case?  There are no studies on different microbes and the pattern of disease
progression in twin studies with aggressive periodontitis

7. Dahlén G. Role of suspected periodontopathogens in microbiological

Acknowledgment monitoring of periodontitis. Adv Dent Res 1993; Review.
The authors report no conflicts of interest related to this 8. Palmer RJ Jr. Composition and development of oral bacterial commu-
case report. nities. Periodontol 2000;2014:20-39.
9. Dewhirst FE, Chen T, Izard J, et al. The human oral microbiome.
CORRESPONDENCE J Bacteriol 2010;5002-5017.
Dr. Sharon Phamduong, Private practice, Sunnyvale, California 94087. 10. Gajardo M, Silva N, Gomez L, et al. Prevalence of periodontopathic
E-mail: drpham@bayareagums.com bacteria in aggressive periodontitis patients in a Chilean population.
J Periodontol 2005;289-294.
References 11. Tözüm TF, Berker, E., Akincibay, H. et al Tetraploid/diploid mosaicism
with generalized aggressive periodontitis. J Periodontol 2005;1567-
1. Lang N, Bartold M, Cullinan M, et al. Consensus report: aggressive 1571.
periodontitis. Anal Periodontol 1999.
12. Campbell IM, Shaw CA, Stankiewicz P, Lupski JR. Somatic mosaicism:
2. Armitage G, Cullinam M. Seymour, Comparative biology of chronic implications for disease and transmission genetics. Trends Genet
and aggressive periodontitis: introduction. Periodontology 2000; 2015;382-392.
2010:7-11.
13. Slots J. Periodontal herpesviruses: prevalence, pathogenicity, systemic
3. Retrieved from https://dentists.usc.edu/files/2015/02/Website-Kit-Inst risk. Periodontol 2000;2015:28-45.
ructions.pdf
14. Shaddox LM, Mullersman AF, Huang H, Wallet SM, Langaee T,
4. American Academy of Periodontology Report. Position paper: systemic Aukhil I. Epigenetic regulation of inflammation in localized aggressive
antibiotics in periodontics. Journal of Periodontology 2004. periodontitis. Clinical Epigenetics, The official journal of the Clinical
5. Hoang T, Jorgensen MG, Keim RG, Pattison AM, Slots J. Povidone- Epigenetics Society 2017.
iodine as a periodontal pocket disinfectant. J Periodontal Res. 15. Varela M, Trujillo-Tiebas MJ, Garcia-Camba P. Case report: iden-
2003;311-317. tical twins revealing discordant hypodontia. The rationale of dental
6. Schenkein HA. Finding genetic risk factors for periodontal diseases: is arch differences in monozygotic twins. Eur Arch Paediatr Dent 2011;
the climb worth the view? Periodontology 2000;2002:79-90. 318-2.

6 Clinical Advances in Periodontics, Vol. 0, No. 0, xxx 2018 Localized Aggressive Periodontitis in Twins