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Localized Aggressive Periodontitis in a Patient With Type 1 Diabetes Mellitus:

A Case Report

Article  in  Journal of Periodontology · October 2001

DOI: 10.1902/jop.2000.72.9.1265 · Source: PubMed

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0312_IPC_AAP_553331 9/7/01 10:27 AM Page 1265
Localized Aggressive Periodontitis in a Patient With Type 1
Diabetes Mellitus: A Case Report
Gülnur Emingil,* Sükran Darcan,† Ahmet Keskinoğlu,‡ Necil Kütükçüler,§ and Gül Atilla*
3
Background: Poor metabolic control of diabetes
mellitus (DM) has often been associated with the
severity of periodontal disease. The aim of this report
is to present a 9-year-old female with localized aggres-
sive periodontitis who had a history of type 1 DM
and the outcome of her treatment.
Methods: The patient had received medical, clini-
cal, and radiographic periodontal examinations.
Peripheral blood analysis was done as well. She had
non-surgical periodontal treatment, and medical man-
agement of her diabetes was performed at the same
time. She was followed longitudinally for 5 years.
Results: Medical examination revealed no patho-
logical findings except for growth retardation. Labo-
ratory tests showed that she had poor metabolic con-
trol, with 497 mg/dl fasting blood glucose and 15.6%
HbA1c. The random migration and neutrophil chemo-
taxis were significantly reduced. Periodontal treat-
ment and metabolic control of her diabetes resulted
in significant improvement in her periodontal condi-
tion. No incipient periodontal breakdown was
observed around the teeth after 5 years from base-
line.
Conclusions: This report proves the efficiency of
periodontal therapy in the prevention of future peri-
odontal breakdown in a systemically compromised
patient. It seems that in certain individuals who are
predisposed to the aggressive forms of periodontitis,
clinical and medical examinations and intervention to
the systemic condition, in combination with peri-
odontal treatment, are important in the management
of these individuals. J Periodontol 2001;72:1265-
1270.
KEY WORDS
Diabetes mellitus, insulin-dependent; periodontitis/
prevention and control; periodontitis/therapy;
neutrophils; chemotaxis; outcome assessment.
* Ege University, School of Dentistry, Department of Periodontology, Izmir,
Turkey.
† School of Medicine, Department of Pediatric Endocrinology and
Metabolism.
‡ Faculty of Medicine, Department of Pediatric Nephrology.
§ Department of Pediatric Immunology.
J Periodontol • September 2001
Case Report
Epidemiological studies have shown that periodontal
disease can occur in otherwise healthy children and
that it might be associated with many systemic dis-
eases.1-3 Most cases of aggressive periodontitis were
also diagnosed with systemic diseases, such as con-
genital neutropenia, Chédiak-Higashi syndrome, or
diabetes mellitus.4-7 Diabetes mellitus (DM) comprises
a group of chronic metabolic disorders, which shows
itself as altered glucose tolerance or impaired lipid and
carbohydrate metabolism.8
Several studies have shown that there is a higher
tendency towards gingivitis in diabetic children with
poor metabolic control compared to non-diabetic chil-
dren.9-11 The risk for developing periodontal disease
has also been demonstrated to be higher in diabetic
patients.12,13 It has also been reported that the inci-
dence of periodontitis among diabetic subjects
increases after puberty and by the duration of dia-
betes.3,12,13 Variations in periodontitis among dia-
betic subjects are related to metabolic control of their
diabetes.14 Uncontrolled or poorly controlled DM
patients were reported to have increased suscepti-
bility to periodontal disease.15-17 It has been demon-
strated in both uncontrolled and controlled studies
that periodontal treatment had beneficial effects on
the metabolic control of DM.14,18 Despite the find-
ings indicating that diabetes is associated with peri-
odontal disease, others have failed to demonstrate
significant association between DM and increased
severity of periodontal disease.19-21 Both periodon-
tal disease and DM share common risk factors.8
Although the exact mechanism is not known, vas-
cular changes, microbial factors, alterations in the
host response and collagen metabolism, and genetic
factors were suggested to be important in the patho-
genesis of periodontitis associated with DM.8,22
In the present case report, we examined a patient
with localized aggressive periodontitis who has type
1 DM. She was originally seen at the age of 9. Peri-
odontal treatment was performed and periodontal
conditions followed for 5 years.
CASE REPORT
A 9-year-old Turkish girl presented to Ege University,
School of Dentistry, Department of Periodontology
because of severe mobility and pain on the right lower
1265
0312_IPC_AAP_553331 9/7/01 10:27 AM Page 1266

Case Report
first permanent incisor in May 1995. She had a his- detailed instructions on proper tooth brushing and
tory of type 1 DM diagnosed when she was 3 and had referred to the Pediatric Endocrinology Department
been receiving 2 daily injections of insulin (0.8 at Ege University for medical evaluation.
U/kg/day). Her father reported that no other members
Medical Examination
of her family had diabetes; no consanguinity existed
The physical examination revealed no outstanding
between her parents, and there were no outstanding
findings except for growth retardation. Her weight
findings in the family medical histories.
was 22.5 kg (<10th percentile) and height 116.8 cm
Dental History
Dental history revealed that the patient had not sought
dental treatment previously and that she was not per-
forming any personal oral hygiene. The eruption of
her primary teeth had been normal according to her
father. Upon questioning, we learned that the patient’s
parents did not lose their teeth at an early age. The
patient’s younger sibling also had no history of early
tooth loss.

Clinical Examination
Clinical examination revealed poor oral hygiene and
heavy plaque accumulation; however, calculus deposit
was minimal. She had no caries. The gingiva was
intensely inflamed and edematous, and profuse sul-
cular bleeding occurred upon gentle probing. The
lower right first permanent incisor was loose and
extremely mobile. Periodontal probing depths ranging Figure 1.
from 10 to 12 mm were recorded around the affected Clinical appearance at baseline.The degree of inflammation of the
maxillary and mandibular anterior gingiva ranged from moderate to
tooth. The left lower incisor also exhibited slight mobil- intense. Migration of the lower right incisor was noticeable.
ity and a probing depth of 5 mm. There were no
abnormal findings in the other
primary and permanent teeth.
The patient had a normal denti-
tion for her age (Fig. 1).

Radiographic Examination
A full series of intraoral radio-
graphs showed localized severe
alveolar bone loss around the
lower right incisor with a float-
ing appearance and an enlarge-
ment of the periodontal spaces
around the incisor teeth. The
radiographic appearance of the
alveolar bone crest in the other
areas appeared to be within nor-
mal limits (Fig. 2).
At the initial exam, the
patient complained of pain and
discomfort from the lower right
first permanent incisor, which
had a hopeless prognosis and Figure 2.
Dental radiographs at baseline. Extreme bone loss was prominent at the lower right incisor with a
was extracted immediately. floating appearance. Advance bone loss was also noticeable at the lower left incisor at baseline.
Thereafter, she was given

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Case Report
(<3rd percentile). Initial blood analysis revealed that
the patient’s diabetes was poorly controlled (fasting
blood glucose 497 mg/dl, HbA1c 15.6%, urine analy-
sis >1,000 mg glucose/dl, but negative for ketones).
There were no long-term complications of diabetes.
Optic fundi, urinary microalbumin excretion, and elec-
tromyography were normal. After the first visit, she
and her parents were educated about self-manage-
ment of diabetes to achieve optimal glucose control.
After 5 years, her height was 147 cm (3rd percentile),
weight 43.7 kg (10th percentile), and puberty was
completed (Tanner grade 5). The remainder of the
physical examination was completely normal. She
did not have retinopathy, nephropathy, or neuropa-
thy. Blood analysis revealed that the patient’s dia-
betes was better controlled compared to her first visit Figure 3.
(fasting blood glucose 120 mg/dl, HbA1c 8.2%). Clinical appearance 6 months after completion of non-surgical
periodontal treatment.
Treatment
At the first visit, the lower right first permanent incisor,
which had a hopeless prognosis, was extracted. Non-
surgical periodontal treatment consisting of oral
hygiene instruction and scaling and root planing were
initiated and carried out once a week for 4 weeks. At
each visit, the patient was motivated to maintain daily
plaque control. After resolution of the periodontal
infection, the patient was placed on a maintenance
care program including evaluation and risk of dis-
ease progression. Although the patient attended recall
appointments frequently at the beginning, she became
less compliant. A marked improvement was noted in
the periodontal condition 6 months after completion
of her active periodontal treatment (Fig. 3). After 5
years from baseline, no periodontal attachment loss
was observed and the probing depths were approxi-
mately 3 mm, but proliferation and thickening of the Figure 4.
marginal gingiva were noted around upper anterior Clinical appearance 5 years after baseline. Proliferation and
thickening of the upper anterior gingiva were prominent.
teeth due to mouth breathing. Also, supragingival
plaque accumulation was very heavy around upper
anterior teeth. Accumulation of plaque and gingival and serum C3 and C4 complement components were
inflammation were not as intense on the other side analyzed by nephelometry.L
of the mouth (Fig. 4). Radiographic examination Phenotype analysis of peripheral blood lymphocyte
showed no incipient bone loss around the teeth com- subpopulations. The relative counts of CD3+, CD4+,
pared to baseline. The possibility of vertical bone loss CD8+, T cells, T cells exhibiting HLA DR antigen and
on the mesial aspect of both mandibular first molars interleukin-2 receptor, CD19+ B cells, and natural
may be related to the discrepancy in the cemento- killer (NK) cells were determined by 2-color flow
enamel junction position between the first molars and cytometry using monoclonal antibodies.¶
the adjacent second premolars (Fig. 5). Neutrophil function studies. Zymosan-activated
serum and a modification of Boyden’s technique23
Peripheral Blood Studies
Blood chemistry was measured with an autoanalyzer.
Serum immunoglobulin G (IgG), immunoglobulin A L Dade Behring, Marburg, Germany.
(IgA), and immunoglobulin M (IgM) concentrations ¶ Becton & Dickinson, Mountain View, CA.

J Periodontol • September 2001 Emingil, Darcan, Keskinoğlu, Kütükçüler, Atilla 1267

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Case Report
DISCUSSION
This report presents a case of a
patient with localized aggressive
periodontitis with type I DM and
poor metabolic control. We
observed localized aggressive
periodontitis and intensely in-
flamed and edematous gingiva
that bled upon gentle probing at
baseline. After non-surgical
treatment, significant improve-
ment of her periodontal condi-
tion was observed. The patient
was enrolled in a regular recall
program. Whereas proliferation
and thickening of the marginal
gingiva were noted around upper
anterior teeth due to mouth
breathing, no incipient peri-
odontal breakdown was ob-
served around the teeth after 5
Figure 5. years. Her diabetes was also well
Dental radiographs 5 years after baseline. No incipient bone loss was detectable. controlled by her physician. This
demonstates the efficiency of
periodontal therapy in prevent-
were used to evaluate neutrophil chemotaxis. Neu- ing future periodontal breakdown in a systemically
trophil leukocytes were obtained from peripheral compromised patient.
heparinized blood by the 2-step technique.24 Neu- Several studies of periodontal disease in children
trophil chemotaxis and random migration were with type 1 DM show that periodontal disease is more
assessed by the leading-front method described by severe in diabetic children than control subjects.3,11,13
Zigmond and Hirsch. 25 Increased gingivitis and periodontitis were shown in
Human leukocyte antigen (HLA) typing. HLA class patients with poor metabolic control compared to
I (ABC) and class II (DR, DQ) serological typing was well-controlled patients.9,15,16 Although DM has been
performed using the Terasaki microlymphocytotoxi- associated with periodontal breakdown, the exact role
city test.26 of this disease in the pathogenesis of periodontitis is
not completely understood. Susceptibility to peri-
Peripheral Blood Findings odontitis has often been associated with defects in
The results of blood analyses are shown in Table 1. the host defense system.27 Neutrophils play an impor-
The differential leukocyte counts revealed a slightly tant role in protection against bacterial infection.28,29
decreased percentage of peripheral blood neu- Altered neutrophil function may be significant in both
trophils and increased percentage of peripheral aggressive forms of periodontitis and responsible for
blood lymphocytes. The serum alkaline phosphatase accelerated periodontal breakdown in poorly con-
(ALP), IgG, and IgA levels were higher than normal trolled diabetics.30-34 It seems, therefore, possible
(Table 1). Neutrophil chemotaxis and random that the rapid progression of periodontitis in some
migration were found to be significantly reduced cases of diabetes, especially type 1, might be related
compared to the normal value (Table 2). The per- to impaired neutrophil chemotaxis. In accordance
centage of natural killer cells was lower than nor- with these findings,30,32-34 decreased neutrophil
mal ranges. There were no abnormalities in the lym- chemotaxis was observed in this patient with local-
phocyte subpopulations (Table 3). The HLA ized aggressive periodontitis. Moreover, the immuno-
phenotype of the patient was A24(9), A28, B51(5), logical data, including the slight increase in IgG, IgA,
B8, Cw7, Bw4, Bw6, DR17(3), DR4, DR52, DR53, and the percentages of lymphocytes, could demon-
DQ2, and DQ8(3). strate an existing immunological defect.

1268 Periodontitis in Type 1 Diabetes Mellitus Volume 72 • Number 9

0312_IPC_AAP_553331 9/7/01 10:27 AM Page 1269

Case Report
Table 1. Table 3.
Clinical Blood Examination Results Peripheral Blood Lymphocyte Populations
(%)
Patient Normal Range

Blood Counts Mononuclear Cells Patient Normal Range

WBC (x103 cells/mm3) 9.6 4.5-13.5 CD3+ (T cell) 87 60-85
RBC (x103 cells/mm3) 4.55 4-5.2
Hb g/dl 14.3 13-16 CD19+ (B cell) 7 7-14
Plt (x103 cells/mm3) 184 150-400
CD4+ (T-helper/inducer) 47 35-47
Neutrophils (%) 47 54-62
Lymphocytes (%) 46 25-33 CD8+ (T-suppressor/cytotoxic) 40 26-36
Monocytes (%) 7 3-7
CD4/CD8 1.2 0.7-2
Blood Chemistry
Fasting glucose level (mg/dl) 497 60-100 CD3-/CD16+56(+) NK 6 14-22
HbA1c (%) 15.6 3-6.2
CD3/HLA-DR+ (active T cell) 3 2-12
Calcium (mg/dl) 10.4 8.1-10.4
Phosphorus (mg/dl) 4.1 2.6-4.7 CD25+ (IL-2R) 11 3-14
Mg (mg/dl) 1.8 1.6-2.6
Urea (mg/dl) 23 10-50
Creatine (mg/dl) 0.56 0.5-1 patient were analyzed to determine if these markers
ALP (U/l) 763 130-525 might serve as an indicator for disease susceptibil-
Total cholesterol (mg/dl) 158 126-191
ity. The occurrence of HLA-A9, -DR4, and -DR53
Triglyceride (mg/dl) 85 36-138
Total protein (g/dl) 7.7 6.4-8.1
antigens in our patient might support the association
Albumin (g/dl) 4.7 4.0-5.3 of both periodontal disease and type 1 DM with these
CRP (ng/ml) 180 67-1800 genetic markers.
IgG (mg/dl) 1857 608-1572 Several investigators have shown that poor meta-
IgA (mg/dl) 329 33-236 bolic control of diabetes influences the severity of
IgM (mg/dl) 168 52-242 periodontal disease.13,15,16 The present case report
C3 (mg/dl) 84 77-195 suggests that intervention therapy for localized
C4 (mg/dL) 38 7-40 aggressive periodontitis and management of poorly
controlled diabetes may prevent future periodontal
breakdown in a systemically compromised patient.
Table 2.
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Send reprint requests to: Dr. Gülnur Emingil, Ege Üniver-
sitesi, Dişhekimliği Fakültesi, Periodontoloji Anabilim Dali,
Bornova-35100, Izmir-Türkiye. Fax: 232/3880325; e-mail:
emingil@usa.net
Accepted for publication March 2, 2001.
Volume 72 • Number 9