Volume 3, Issue 11, November – 2018
ISSN No:-2456-2165
Immune Aging Marker Associated with Periodontitis in
Systemic Lupus Erythematosus Patients
Nanda Rachmad Putra Gofur 1, Nurdiana2, Kusworini Handono3, Handono Kalim4
1
Dept of Biomedical Science, 2Dept of Pharmacology, 3Dept of Clinical Pathology, 4Dept of Internal Medicine
Faculty of Medicine – Universitas Brawijaya, Malang Indonesia
Abstract:-
 Background
Periodontitis was reported more often found in SLE
patients than healthy controls, 54.3% higher than healthy
28.2%, and was estimated related to autoimmune
condition. Recently, SLE associated with the immune
aging, SLE patients had similarities with immune system
of elderly. Expression of IL-2 and IL10 associated with
immune aging as T cell, were associated with cytotoxic
activity, signaling and low number of naïve T cells were
known as biomarker of immune aging.
 Objectives
To analyze correlation between periodontitis severity
with disease activity, IL-2, IL-10expression in SLE
patients.
 Methods
Subjects were 61 patients with SLE ( age 18-55 years;
SLEDAI score 0-42) collected from Dr. Saiful Anwar
General Hospital, Malang Indonesia. Periodontitis severity
was measured using Periodontal Index (PI) criteria.
Expression of IL-2 and IL-10 using ELISA .
 Result
Clinical manifestations of periodontitis were bleeding
gum 88.3%, high calculus index 44.9%, found periodontal
pocket 73.8% and loose teeth 13.2% among patients. PI
score patients was 2.45 ± 0.82. There were significantly
positive correlation between PI score and SLEDAI score
(r:0.930; p = 0.000), with IL-2 (r: -0927.; p = <0.0001), with
IL-10 (r: 0.886; p = <0.0001).
 Conclusion
Our study showed that periodontitis were associated
with SLE disease activity, and biomarker of immune
aging. Furthermore, biomarker could be predictor for
periodontal condition, prognosis of periodontitis and best
treatment for periodontitis on SLE patient.
Keywords :- SLE, Periodontitis, IL-2, IL-10.
IJISRT18NV358
International Journal of Innovative Science and Research Technology
I. INTRODUCTION
Periodontal disease including gingivitis and periodontitis
is one of the most common chronic diseases. Worldwide,
periodontitis disease suggest approximately 22.9% of the adult
population, and in Indonesia a prevalence of 38%1,2.
Recently, a prevalence of periodontitis is increasing due to age
and systemic disease. Periodontitis is characterized by chronic
inflammation and infection of periodontal tissues and causing
bone resorption. Mostly, the further stage is tooth loss. Due to
tooth loss condition can lead to decreasing intake and nutrients
to the body, resulting in higher mortality3.
Main causes of periodontitis is gram-negative bacteria,
mostly found on dental plaque. Bacteria could have potent
mechanisms to attack and damage human defenses. It
produces bacteria strain making PMN and macrophages
damaged. As example, collagenases could damage collagen
tissue directly4. Moreover, the abnormalities of human
immune response may also contribute tissue damaged and
severity of the disease5.
Recent studies reported an correlation between
periodontitis with Systemic Lupus Erythematosus (SLE)
disease. In SLE patients, a prevalence of periodontitis was
reported 54.3% higher than healthy patients with no systemic
abnormality of 28.2%6. This condition affect stability of oral
cavity. But, the association between SLE and periodontitis
never been explained clearly. The connection of SLE with
periodontitis is assuming that in SLE patients had similarities
of immune response with elderly, associated with immune
aging7.
Immune response changing in SLE coming from
interaction between genetic and environmental factors. It
results in hyperactivity of immune cells, including T and B
lymphocytes, and production of autoantibodies such as anti-
dsDNA antibodies. Correlation of autoantibodies with target
antigens results in formation of immune complexes deposited
in various places and triggers tissue through organ damaged.
Impact of immune responses on SLE patients, triggered
immune activation and lead to various diseases, due to
immune aging8.
Immune aging in SLE lead to increased production of
various inflammatory cytokines such as IFNγ, TNFα, IL-2, IL-
10, IL-17, and IL-18, causing increase apoptosis, activate
effector cells, changes in signaling and complement systems,
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cross-reactions or autoantigens new reactivity lead to tissue
damage. It is believed that SLE immune response of
hyperactivity, triggering immune aging and causing secretion
of inflammatory cytokines, mostly IL-2 and IL-10 which leads
to increased infection and destroy periodontal tissue8.
Furthermore, no study prove that if there is a correlation
between the severity of periodontitis and SLE biomarkers.
This study was comparing the periodontal findings in SLE
patients and systemically healthy controls, and to determine if
there is a correlation between periodontal condition and SLE
biomarkers.
II. AIM OF THE STUDY
 Determine the association of periodontitis in SLE patients
with immune aging.
 Knowing correlation between SLEDAI, IL-2, and IL-10
with the severity of periodontitis.
 Provide new biomarker both in blood serum for SLE and
Periodontitis diagnostic.
III. MATERIAL AND METHOD
The design of this study was an observational analytic
study with cross sectional approach. The research received an
ethical approval from the UB Medical Ethics Committee from
Faculty of Medical, Brawijaya University Malang, East Java.
All patients included in this study were required to sign an
informed consent.
The study was conducted on 61 SLE patients and 61
healthy subject. Study held from September 2017 until June
2018 on Rheumatology Department Saiful Anwar Hospital
Malang, Indonesia. In all SLE patients clinical examination of
the oral cavity to assess the presence of periodontal
abnormalities using periodontal index (PI), gingival index
(GI), plaque index, pocket depth and numbers of loose teeth.
Clinical examination and laboratory tests are conducted to
assess the activity of the disease. Severity of SLE measured
using SLEDAI criteria and biomarker using elisa to measured
IL-2, and IL-10 expression. Inclusion criteria was female
subjects with a confirmed diagnoses of SLE, willing to
become the subject of study, could read and write and had full
consciousness. Exclusion criteria were smoking, pregnancy,
diabetes, and another systemic disease. For the healthy subject
had similar inclusion, and exclusion criteria.
 Severity of Periodontitis Assessment and SLE Patients
Periodontal assessments were collected from all subjects.
Periodontal assessments consisted of the following:
periodontal index (PI), gingival index (GI), plaque index,
pocket depth and numbers of loose teeth. Severity of SLE
using SLEDAI index with clinical examination and laboratory
test.
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International Journal of Innovative Science and Research Technology
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 Biomarker of SLE Using ELISA
Sample 10-15 mL subject vein blood was performed at
Poly Rheumatic / Internal Diseases RSSA. We used serum for
cytokine examination9. Measurement of Cytokine Levels of
IL-2, and IL-10. Samples in EDTA were centrifuged for 10
min at 1,000 x g. plasma at <-200C and then measured the
levels of IL-2 using enzyme-linked immunosorbent assay
Human IL-2 ELISA (Human IL-2 ELISA MAXTM Biolegend
Catalog No. 431803). Added 100 uLnologiHuman IL-2
Capture Antibody that has been diluted, and incubated for 1
day at a temperature of 2-8 ° C. Then add assay buffer at room
temperature (18-25 º C) for 1 hour, and washed 4 times.
Microplate received with calibrator and plasma. After as much
as 60 μl then added buffer 11.94 μl, incubation 2 hours while
in shaker at room temperature (18-25 º C). Washed 4 times
with a wash and add a 100 μl IL-2 human antibody detection
solution each strip after it was incubated for 1 hour at room
temperature (18-25ºC). 4 days ago added 100 ml of Avidin-
HRP solution, incubated at room temperature for 30 minutes.
washing 5 times with washing buffer. Added TM 100 μl
substrate, Incubation 15 min at room temperature outside dark
without dishaker and plus stop solution 100 μl,
spectrophotometric print result at 450 nm wave. Doing same
step but different using 100 uL Lemism IL-10 Capture
Antibody diluted using Elisa Max ™ Deluxe Set
(Biolegend Catalog no.430106) for IL-10 in Biomedical
laboratory Faculty of Medicine Brawijaya University Malang.
 Data Processing and Analysis
The collected data will be analyzed using of SPSS
version 20 program. The difference of Immune aging markers
on LES patients with and without periodontitis was analyzed
by Kolmogorov Smirnof for normality test, Spearman/Pearson
for correlation test and Mann Whitney for comparison test11.
IV. RESULTS
 Characteristics of Research Subjects
A total 122 subjects (61 with SLE and 61 control) were
included in this study. We found that 54/61 (88,53%) subjects
with SLE had periodontal disease, based on Periodontal Index
assessed. As shown in table 1, the mean age for SLE subject
was 29. The mean score of Periodontal index, gingival index,
plaque index, a large number of teeth periodontal pockets and
loose teeth was 22,66±1,2, 1,85±1,02, 0,75±0,59 mm, and
0,26±0,65, respectively. The mean SLEDAI score was 17.70 ±
12.70.
We also performed laboratory test for the cytokines level
from SLE subjects. Data shown in table 2 includes level of IL-
2, and IL-10. The mean level of of IL-2, and IL-10 was pg
30,56±17,91 µg/ml, 1,13±0,99 µg/ml.
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 Differences in the Occurrence of Periodontitis in SLE
Subjects and Control
Dental status examination was performed in both groups,
and it was obtained that in SLE group, periodontal disorders
tend to shown more severe and advanced clinical
manifestation compared to those in control group. The clinical
manifestations assessed were shown in table 3. There was a
significant difference in periodontal index, gingival index,
plaque index and periodontal pocket between two groups. SLE
subject had higher periodontal index, gingival index, and
periodontal pocket but lower plaque index than control. There
is no significant different the number of loose teeth between
two groups.
 Periodontitis Severity and SLE Characteristics
When the periodontitis severity status divided into two
groups based on Periodontal Index, SLE subject with severe
periodontitis tend to had higher SLEDAI score, anti-dsDNA
level, and inflammatory cytokines level compared to mild
periodontitis group (table 4 and table 5). There was a
significant difference in several SLE characteristics between
two groups.
 Correlation between Periodontitis Status and SLE
Manifestations Severity
The correlation between periodontitis status (based on
Periodontal Index) with SLE manifestation severity were
assessed using Pearson correlation test and the results were
shown in table 5. It can be seen that there was a significant
and strong correlation between the periodontitis status and
severity of SLE manifestations in all five characteristics of
SLE (figure 1).
V. DISCUSSION
Periodontitis is chronic inflammation disease on
periodontal tissue. Periodontitis began from complex
interactions between host and bacteria causing destruction of
the gingival tissue, ligament periodontal, cementum and
alveolar bone. Recently, periodontitis associated several
systemic disease. There has been an increasing interest in the
relationship between periodontitis and autoimmune disease,
Systemic Lupus Erythematosus (SLE). SLE patients have
abnormalities of immune response called immune aging. SLE
patients have similarities systemic condition with elderly. It
caused increasing prevalence and severity of periodontitis12.
Increasing occurring of periodontitis also proven in vivo study
with non-human primates and rodentsa13.
These abnormalities have been described for adaptive
immune B and T cells. Immune aging effect on periodontal
tissues have been suggested based on molecular changes the
cells array and inflammation condition of the periodontium. It
affected differentiation and bone process (osteoblasts,
osteoclasts), changing microbial condition, environment and
systemic condition related to host because of cytokines14,15.
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International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
The regulation of the expression of enzymes and proteins
could affect on periodontal inflammatory response, such as
stimulating, migration and stoppaging of immune cells,
exacerbation and resolution. This response is functioning by
complement, cytokines and other biomarker molecules.
Cytokine proteins may have important roles during different
human physiological and pathological processes. For example,
much Interleukin concentration changes in GCF, suggest these
cytokines as a predictable marker of gingival inflammation in
chronic periodontitis patients. It results proven from studies
with periodontal disease is related to other general disease
such cardiovascolar and autoimmune. There are others fact
that an association between periodontitis and atherosclerotic
vascular disease, including stroke, myocardial infarction,
peripheral vascular disease, abdominal aortic aneurysm,
coronary heart disease, cardiovascular death and in our case
systemic lupus erythematosus16.
There are many cytokine that playing role on systemic
lupus erythematosus. TCD4+ cells were initially subdivided
into two subsets, designated Th1 and Th2, based on their
cytokine production patterns. Th1 cells secrete IL-2 and IFN-
γ, whereas Th2 cells produce IL-5, IL-6, IL-4, IL-10 and IL-
13. Th1 is an important standard in the response against
intracellular microorganisms and is responsible for inducing
cell-mediated inflammation4,17. Cytockine that have an
important role on periodontitis is IL-2, and IL-10 among
others.
Recent study, IL-2 was decreasing related to pocket,
which is related to advanced periodontitis, resulting in a
greater severity of the disease. Interleukine-2 is a
multifunctional cytokine, considered a central regulator of
host resistance against a variety of pathogens and has been
recently demonstrated an active role in the pathogenesis of
periodontal diseases. P. gingivalis can influence responses of
T cell lineages to evade or suppress their adaptive responses.
This is achieved by inhibiting the expression and
accumulation of IL-2, which attenuates T cell proliferation and
communication. IL-2 is affected by P. gingivalis at the protein
level and partially through suppression of activator protein 1
(AP-1). AP-1 is a transcription factor.T cells were not able to
maintain a stable IL-2 accumulation. On other hand decreasing
of IL2 could be affecting P.gingivalis at the protein level and
partially through suppression of AP-1 protein and inducing
bone resorption18.
The change in IL-2 levels is changing adaptive immune
response and might contribute to progression of the
inflammatory state in systemic condition such as osteoporosis
and systemic lupus erythematosus due to the role of IL-2 in
the clonal expansion of regulatory T cells19. This failure
causes calcium robus inlux, hyperphosphorylation and an
increase in Fc receptors. This situation disrupts immune
dysregulation, the terms CREM and CREB, resulting in severe
inflammation. It had same result with our study proven that
systemic IL-2 had negative correlation with severity of
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periodontitis. Lower levels of IL-2 indicated higher incidence
of periodontitis and bad prognosis.
The result with our study proven that systemic IL-10 had
positive correlation with severity of periodontitis. Higher
levels of IL-10 indicated increasing of periodontitis and poor
prognosis. Literature suggest that there is a positive correlation
with anti-inflammatory cytokines IL-10, discovered on
periodontal disease. Interleukin-10 is known controlling and
production many mediators. Myeloid cells are key target cells
of IL-10 in infection stimulated alveolar bone loss. Significant
of CD40L T cell responses in infection stimulated alveolar
bone destruction. IL-10 is essential as a modulator of the
response to infection at the Janus Kinase-Signal Transducers
and Activators of Transcription (JAK-STAT) signaling axis of
host responses. IL-10 was first identified by its ability to
incresing the immune response by inhibiting the production of
a number of cytokines resulting mortality. IL-10 has been
recognized to have potent and broad-spectrum inflammatory
activity, which has been proven in various models of infection,
inflammation, and even in cancer20.
IL10 had sometimes function to the pro-inflammatory
ones, as higher levels of these mediators were associated with
a increase probability of having periodontitis. Among other
cytokines, interleukin-10 (IL-10) is an important
multifunctional cytokine. It inhibit the synthesis of pro-
inflammatory cytokines such as interleukin 1 (IL 1),
interleukin 2 (IL 2), interleukin 6 (IL 6), interleukin 8 (IL 8),
tumor necrosis factor – α (TNF α) and interferon γ (IFNγ). IL-
10 increasing the production of metalloproteinases, and
incduce synthesis of tissue metalloproteinases in macrophages.
Moreover, it stimulates production of osteoprotegrin, which
consequently causing bone resorption by bond RANK-
RANKL engagement. IL 10 can be a protective cytokine in
periodontal disease but in SLE parient seems as pro-
inflammatory cytokines, including those implicated in alveolar
bone loss. Individuals who are high producers of IL 10 might
be more frequently got chronic periodontitis due to
proinflammatory role of IL 1020,21,22.
VI. CONCLUSION AND SUGGESTION
Chronic periodontitis has correlation with severity
clinical manifestation of SLE (using SLEDAI. SLE patients
with periodontitis show that greater frequency immune aging
biomarker than SLE patients without chronic periodontitis.
Immune aging biomarker and chronic periodontitis could be
predictor for severity of SLE. This result could explain
association SLE with cormobidities collateral to aging
process. Furthermore, the results could be used as information
by doctor to determine patient treatment and education plans.
Hopefully there will be further research with markers in the
oral cavity.
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International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
VII. CONFLICT OF INTERESTS
The authors declare that we have no competing and
conflict of interests.
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Variables Mean (± SD) Range (Min-Max)

Age (yrs) 29.47±9.62 34 (17-51)

Periodontal Index 2,66±1.20 4.20 (0.1 to 4.9)

Gingival Index 1.95±1.02 3.00 (0 to 3.00)

Plaque Index 0.34±0.44 1,5 (0 to 2.5)

Periodontal pockets (mm) 0.72±0.62 2,5 (0 to 2.5)

Loose teeth 0.26±0.65 3 (0-3)

SLEDAI score 17.70±12.70 42 (0-42)

Table 1:- SLE patient characteristics

Variables Mean (± SD) Range (Min-Max)

IL-2 (pg / ml) 30,56±17,91 66,70 (10,3- 77,00)

IL-10 (pg / ml) 1,13±0,99 3,90(0,10 – 3,80)

Table 2:- Assessment of cytokines level

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Variables SLE (n = 61) Control (n = 61) p-value

Age (yrs) 29,50±9,57 28,57±9,33 0,540

Periodontal Index 2,66±1,02 0,51±0,81 <0,0001

Gingival index 1,95±1,02 0,83±0,65 <0,0001

Plaque Index 0,34±0,44 0,90±0,62 <0,0001

Periodontal pockets (mm) 0,75±0,59 0,34±0,55 <0,0001

Loose teeth 1,49±1,77 0,14±0,51 <0,0001

Table 3:- Comparisons of periodontitis clinical manifestations between SLE and control groups

Variables Mild (PI 0.7-1.9) Severe (PI 2.0-5.0) p-value

(n = 11) (n = 43)

SLEDAI score 5,09±1,86 23,48±10,42 <0,0001

IL-2 (pg / ml) 41,68±12,53 21,25±5,63 <0,0001

IL-10 (pg / ml) 0,25±0,52 1,52±0,92 <0,0001

Table 4:- Comparisons of SLE characteristics between periodontitis group

Variables Normal Mild (PI 0.7- Severe (PI 2.0- Terminal p-value

Periodontium (PI 1.9) 3.8) (PI 3.9-

0-0.6) n= 7 n = 11 n = 32 8.0) n =

14

SLEDAI 4.57 ± 4.11 6.36 ± 3.44 19.55 ± 12.33 29.35 ± <0.0001

score 6.67

Table 5:- Comparison between All Periodontitis Status and SLE Severity

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Variables p-value r
(Sig, 2 tailed)

SLEDAI score <0.0001 0,948

IL-2 (pg / ml) <0.0001 -0,930

IL-10 (pg / ml) <0.0001 0,886

Table 6:- Correlation between Periodontitis Status and SLE Manifestation Severity

Fig 1:- Correlation between periodontal index score and SLE characteristics. A) Periodontal index and SLEDAI score showed
significant (p<0.0001) and strong positive correlation (r=0.948); B) Periodontal index and IL-2 level showed significant (p<0.0001)
and strong positive correlation (r=-0,930); C) Periodontal index and IL-10 level showed significant (p<0.0001) and strong positive
correlation (r=0.886).

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