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Volume 3, Issue 11, November – 2018 International Journal of Innovative Science and Research Technology

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
Dept of Biomedical Science, 2Dept of Pharmacology, 3Dept of Clinical Pathology, 4Dept of Internal Medicine
Faculty of Medicine – Universitas Brawijaya, Malang Indonesia


 Background Periodontal disease including gingivitis and periodontitis

Periodontitis was reported more often found in SLE is one of the most common chronic diseases. Worldwide,
patients than healthy controls, 54.3% higher than healthy periodontitis disease suggest approximately 22.9% of the adult
28.2%, and was estimated related to autoimmune population, and in Indonesia a prevalence of 38%1,2.
condition. Recently, SLE associated with the immune Recently, a prevalence of periodontitis is increasing due to age
aging, SLE patients had similarities with immune system and systemic disease. Periodontitis is characterized by chronic
of elderly. Expression of IL-2 and IL10 associated with inflammation and infection of periodontal tissues and causing
immune aging as T cell, were associated with cytotoxic bone resorption. Mostly, the further stage is tooth loss. Due to
activity, signaling and low number of naïve T cells were tooth loss condition can lead to decreasing intake and nutrients
known as biomarker of immune aging. to the body, resulting in higher mortality3.

 Objectives Main causes of periodontitis is gram-negative bacteria,

To analyze correlation between periodontitis severity mostly found on dental plaque. Bacteria could have potent
with disease activity, IL-2, IL-10expression in SLE mechanisms to attack and damage human defenses. It
patients. produces bacteria strain making PMN and macrophages
damaged. As example, collagenases could damage collagen
 Methods tissue directly4. Moreover, the abnormalities of human
Subjects were 61 patients with SLE ( age 18-55 years; immune response may also contribute tissue damaged and
SLEDAI score 0-42) collected from Dr. Saiful Anwar severity of the disease5.
General Hospital, Malang Indonesia. Periodontitis severity
was measured using Periodontal Index (PI) criteria. Recent studies reported an correlation between
Expression of IL-2 and IL-10 using ELISA . periodontitis with Systemic Lupus Erythematosus (SLE)
disease. In SLE patients, a prevalence of periodontitis was
 Result reported 54.3% higher than healthy patients with no systemic
Clinical manifestations of periodontitis were bleeding abnormality of 28.2%6. This condition affect stability of oral
gum 88.3%, high calculus index 44.9%, found periodontal cavity. But, the association between SLE and periodontitis
pocket 73.8% and loose teeth 13.2% among patients. PI never been explained clearly. The connection of SLE with
score patients was 2.45 ± 0.82. There were significantly periodontitis is assuming that in SLE patients had similarities
positive correlation between PI score and SLEDAI score of immune response with elderly, associated with immune
(r:0.930; p = 0.000), with IL-2 (r: -0927.; p = <0.0001), with aging7.
IL-10 (r: 0.886; p = <0.0001).
Immune response changing in SLE coming from
interaction between genetic and environmental factors. It
 Conclusion
Our study showed that periodontitis were associated results in hyperactivity of immune cells, including T and B
with SLE disease activity, and biomarker of immune lymphocytes, and production of autoantibodies such as anti-
aging. Furthermore, biomarker could be predictor for dsDNA antibodies. Correlation of autoantibodies with target
periodontal condition, prognosis of periodontitis and best antigens results in formation of immune complexes deposited
treatment for periodontitis on SLE patient. in various places and triggers tissue through organ damaged.
Impact of immune responses on SLE patients, triggered
Keywords :- SLE, Periodontitis, IL-2, IL-10. 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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ISSN No:-2456-2165
cross-reactions or autoantigens new reactivity lead to tissue  Biomarker of SLE Using ELISA
damage. It is believed that SLE immune response of Sample 10-15 mL subject vein blood was performed at
hyperactivity, triggering immune aging and causing secretion Poly Rheumatic / Internal Diseases RSSA. We used serum for
of inflammatory cytokines, mostly IL-2 and IL-10 which leads cytokine examination9. Measurement of Cytokine Levels of
to increased infection and destroy periodontal tissue8. IL-2, and IL-10. Samples in EDTA were centrifuged for 10
Furthermore, no study prove that if there is a correlation min at 1,000 x g. plasma at <-200C and then measured the
between the severity of periodontitis and SLE biomarkers. levels of IL-2 using enzyme-linked immunosorbent assay
This study was comparing the periodontal findings in SLE Human IL-2 ELISA (Human IL-2 ELISA MAXTM Biolegend
patients and systemically healthy controls, and to determine if Catalog No. 431803). Added 100 uLnologiHuman IL-2
there is a correlation between periodontal condition and SLE Capture Antibody that has been diluted, and incubated for 1
biomarkers. 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.
II. AIM OF THE STUDY Microplate received with calibrator and plasma. After as much
as 60 μl then added buffer 11.94 μl, incubation 2 hours while
 Determine the association of periodontitis in SLE patients in shaker at room temperature (18-25 º C). Washed 4 times
with immune aging. with a wash and add a 100 μl IL-2 human antibody detection
 Knowing correlation between SLEDAI, IL-2, and IL-10 solution each strip after it was incubated for 1 hour at room
with the severity of periodontitis. temperature (18-25ºC). 4 days ago added 100 ml of Avidin-
 Provide new biomarker both in blood serum for SLE and HRP solution, incubated at room temperature for 30 minutes.
Periodontitis diagnostic. washing 5 times with washing buffer. Added TM 100 μl
substrate, Incubation 15 min at room temperature outside dark
III. MATERIAL AND METHOD without dishaker and plus stop solution 100 μl,
The design of this study was an observational analytic spectrophotometric print result at 450 nm wave. Doing same
study with cross sectional approach. The research received an step but different using 100 uL Lemism IL-10 Capture
ethical approval from the UB Medical Ethics Committee from Antibody diluted using Elisa Max ™ Deluxe Set
Faculty of Medical, Brawijaya University Malang, East Java. (Biolegend Catalog no.430106) for IL-10 in Biomedical
All patients included in this study were required to sign an laboratory Faculty of Medicine Brawijaya University Malang.
informed consent.  Data Processing and Analysis
The study was conducted on 61 SLE patients and 61 The collected data will be analyzed using of SPSS
healthy subject. Study held from September 2017 until June version 20 program. The difference of Immune aging markers
2018 on Rheumatology Department Saiful Anwar Hospital on LES patients with and without periodontitis was analyzed
Malang, Indonesia. In all SLE patients clinical examination of by Kolmogorov Smirnof for normality test, Spearman/Pearson
the oral cavity to assess the presence of periodontal for correlation test and Mann Whitney for comparison test11.
abnormalities using periodontal index (PI), gingival index IV. RESULTS
(GI), plaque index, pocket depth and numbers of loose teeth.
Clinical examination and laboratory tests are conducted to  Characteristics of Research Subjects
assess the activity of the disease. Severity of SLE measured A total 122 subjects (61 with SLE and 61 control) were
using SLEDAI criteria and biomarker using elisa to measured included in this study. We found that 54/61 (88,53%) subjects
IL-2, and IL-10 expression. Inclusion criteria was female with SLE had periodontal disease, based on Periodontal Index
subjects with a confirmed diagnoses of SLE, willing to assessed. As shown in table 1, the mean age for SLE subject
become the subject of study, could read and write and had full was 29. The mean score of Periodontal index, gingival index,
consciousness. Exclusion criteria were smoking, pregnancy, plaque index, a large number of teeth periodontal pockets and
diabetes, and another systemic disease. For the healthy subject loose teeth was 22,66±1,2, 1,85±1,02, 0,75±0,59 mm, and
had similar inclusion, and exclusion criteria. 0,26±0,65, respectively. The mean SLEDAI score was 17.70 ±
 Severity of Periodontitis Assessment and SLE Patients
Periodontal assessments were collected from all subjects. We also performed laboratory test for the cytokines level
Periodontal assessments consisted of the following: from SLE subjects. Data shown in table 2 includes level of IL-
periodontal index (PI), gingival index (GI), plaque index, 2, and IL-10. The mean level of of IL-2, and IL-10 was pg
pocket depth and numbers of loose teeth. Severity of SLE 30,56±17,91 µg/ml, 1,13±0,99 µg/ml.
using SLEDAI index with clinical examination and laboratory

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Volume 3, Issue 11, November – 2018 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
 Differences in the Occurrence of Periodontitis in SLE The regulation of the expression of enzymes and proteins
Subjects and Control could affect on periodontal inflammatory response, such as
Dental status examination was performed in both groups, stimulating, migration and stoppaging of immune cells,
and it was obtained that in SLE group, periodontal disorders exacerbation and resolution. This response is functioning by
tend to shown more severe and advanced clinical complement, cytokines and other biomarker molecules.
manifestation compared to those in control group. The clinical Cytokine proteins may have important roles during different
manifestations assessed were shown in table 3. There was a human physiological and pathological processes. For example,
significant difference in periodontal index, gingival index, much Interleukin concentration changes in GCF, suggest these
plaque index and periodontal pocket between two groups. SLE cytokines as a predictable marker of gingival inflammation in
subject had higher periodontal index, gingival index, and chronic periodontitis patients. It results proven from studies
periodontal pocket but lower plaque index than control. There with periodontal disease is related to other general disease
is no significant different the number of loose teeth between such cardiovascolar and autoimmune. There are others fact
two groups. that an association between periodontitis and atherosclerotic
vascular disease, including stroke, myocardial infarction,
 Periodontitis Severity and SLE Characteristics peripheral vascular disease, abdominal aortic aneurysm,
When the periodontitis severity status divided into two coronary heart disease, cardiovascular death and in our case
groups based on Periodontal Index, SLE subject with severe systemic lupus erythematosus16.
periodontitis tend to had higher SLEDAI score, anti-dsDNA
level, and inflammatory cytokines level compared to mild There are many cytokine that playing role on systemic
periodontitis group (table 4 and table 5). There was a lupus erythematosus. TCD4+ cells were initially subdivided
significant difference in several SLE characteristics between into two subsets, designated Th1 and Th2, based on their
two groups. 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-
 Correlation between Periodontitis Status and SLE 13. Th1 is an important standard in the response against
Manifestations Severity intracellular microorganisms and is responsible for inducing
The correlation between periodontitis status (based on cell-mediated inflammation4,17. Cytockine that have an
Periodontal Index) with SLE manifestation severity were important role on periodontitis is IL-2, and IL-10 among
assessed using Pearson correlation test and the results were others.
shown in table 5. It can be seen that there was a significant Recent study, IL-2 was decreasing related to pocket,
and strong correlation between the periodontitis status and which is related to advanced periodontitis, resulting in a
severity of SLE manifestations in all five characteristics of greater severity of the disease. Interleukine-2 is a
SLE (figure 1). 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
Periodontitis is chronic inflammation disease on periodontal diseases. P. gingivalis can influence responses of
periodontal tissue. Periodontitis began from complex T cell lineages to evade or suppress their adaptive responses.
interactions between host and bacteria causing destruction of This is achieved by inhibiting the expression and
the gingival tissue, ligament periodontal, cementum and accumulation of IL-2, which attenuates T cell proliferation and
alveolar bone. Recently, periodontitis associated several communication. IL-2 is affected by P. gingivalis at the protein
systemic disease. There has been an increasing interest in the level and partially through suppression of activator protein 1
relationship between periodontitis and autoimmune disease, (AP-1). AP-1 is a transcription factor.T cells were not able to
Systemic Lupus Erythematosus (SLE). SLE patients have maintain a stable IL-2 accumulation. On other hand decreasing
abnormalities of immune response called immune aging. SLE of IL2 could be affecting P.gingivalis at the protein level and
patients have similarities systemic condition with elderly. It partially through suppression of AP-1 protein and inducing
caused increasing prevalence and severity of periodontitis12. bone resorption18.
Increasing occurring of periodontitis also proven in vivo study
with non-human primates and rodentsa13. The change in IL-2 levels is changing adaptive immune
response and might contribute to progression of the
These abnormalities have been described for adaptive inflammatory state in systemic condition such as osteoporosis
immune B and T cells. Immune aging effect on periodontal and systemic lupus erythematosus due to the role of IL-2 in
tissues have been suggested based on molecular changes the the clonal expansion of regulatory T cells19. This failure
cells array and inflammation condition of the periodontium. It causes calcium robus inlux, hyperphosphorylation and an
affected differentiation and bone process (osteoblasts, increase in Fc receptors. This situation disrupts immune
osteoclasts), changing microbial condition, environment and dysregulation, the terms CREM and CREB, resulting in severe
systemic condition related to host because of cytokines14,15. inflammation. It had same result with our study proven that
systemic IL-2 had negative correlation with severity of

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Volume 3, Issue 11, November – 2018 International Journal of Innovative Science and Research Technology
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periodontitis. Lower levels of IL-2 indicated higher incidence VII. CONFLICT OF INTERESTS
of periodontitis and bad prognosis.
The authors declare that we have no competing and
The result with our study proven that systemic IL-10 had conflict of interests.
positive correlation with severity of periodontitis. Higher REFERENCES
levels of IL-10 indicated increasing of periodontitis and poor
prognosis. Literature suggest that there is a positive correlation [1]. Slade, GD, Spencer, AJ, Roberts‐Thomson, KF. 2007.
with anti-inflammatory cytokines IL-10, discovered on Australia’s Dental Generations: The National Survey of
periodontal disease. Interleukin-10 is known controlling and Adult Oral Health 2004‐06, AIHW Dental Statistics and
production many mediators. Myeloid cells are key target cells Research Series No. 34, pp.82‐84.
of IL-10 in infection stimulated alveolar bone loss. Significant [2]. Tampubolon SN. 2016. Impact of dental caries and
of CD40L T cell responses in infection stimulated alveolar periodontal disease on quality of life. Medan : USU.
bone destruction. IL-10 is essential as a modulator of the Available from:
response to infection at the Janus Kinase-Signal Transducers [3]. Goncalves, TMSV ; Campos, CH ; Goncalves, GM ;
and Activators of Transcription (JAK-STAT) signaling axis of Moraes, dM ; Garcia, RCMR. 2013.Mastication
host responses. IL-10 was first identified by its ability to Improvement After Partial Implant-supported Prosthesis
incresing the immune response by inhibiting the production of Use. JDR Clinical Research Suplement. Sao Paulo :
a number of cytokines resulting mortality. IL-10 has been University of Campinas. 92: 189-194.
recognized to have potent and broad-spectrum inflammatory [4]. Newman, MG, Takei, HH, Klokkevoid, PR, & Carranza,
activity, which has been proven in various models of infection, FA. 2012. Carranza’s Clinical Periodontology, 9th.
inflammation, and even in cancer20. St.Louis Missouri: Saunders Elsevier. Pp. 160-164, 320-
IL10 had sometimes function to the pro-inflammatory [5]. Salama, R. et al., 2014. Cellular senescence and its
ones, as higher levels of these mediators were associated with effector programs Cellular senescence and its effector
a increase probability of having periodontitis. Among other programs. , pp.99–114.
cytokines, interleukin-10 (IL-10) is an important [6]. Wu, Chen et al. 2017. ‘Association between a history of
multifunctional cytokine. It inhibit the synthesis of pro- periodontitis and the risk of systemic lupus
inflammatory cytokines such as interleukin 1 (IL 1), erythematosus: A nationwide, population-based, case-
interleukin 2 (IL 2), interleukin 6 (IL 6), interleukin 8 (IL 8), control study’, Annals of the Rheumatic Diseases, 72(7),
tumor necrosis factor – α (TNF α) and interferon γ (IFNγ). IL- pp. 1–11.
10 increasing the production of metalloproteinases, and [7]. Al-Mutairi, K. D. et al. (2015) ‘Periodontal findings in
incduce synthesis of tissue metalloproteinases in macrophages. systemic lupus erythematosus patients and healthy
Moreover, it stimulates production of osteoprotegrin, which controls’, Saudi Medical Journal, 36(4), pp. 463–468.
consequently causing bone resorption by bond RANK- doi: 10.15537/smj.2015.4.10746.
RANKL engagement. IL 10 can be a protective cytokine in [8]. Rees, F., Doherty, M., Grainge, M. J., Lanyon, P., &
periodontal disease but in SLE parient seems as pro- Zhang, W. (2017). The worldwide incidence and
inflammatory cytokines, including those implicated in alveolar prevalence of systemic lupus erythematosus: a
bone loss. Individuals who are high producers of IL 10 might systematic review of epidemiological studies.
be more frequently got chronic periodontitis due to Rheumatology, (August), 1945–1961.
proinflammatory role of IL 1020,21,22. [9]. Pawelec, G. 2012. Hallmarks of human
“immunosenescence”: adaptation or dysregulation?
VI. CONCLUSION AND SUGGESTION Immunity & Ageing : I & A, 9(1), 15.
Chronic periodontitis has correlation with severity
[10]. Robinson, PG. 2017. Dental Epidemiology, International
clinical manifestation of SLE (using SLEDAI. SLE patients
Encyclopedia of Public Health, 10.1016/B978-0-12-
with periodontitis show that greater frequency immune aging
803678-5.00104-1, (258-263), Crossref.
biomarker than SLE patients without chronic periodontitis.
[11]. Mukaka, M. (2012). A guide to appropriate use of
Immune aging biomarker and chronic periodontitis could be
Correlation coefficient in medical research. Malawi
predictor for severity of SLE. This result could explain
Medical Journal : The Journal of Medical Association of
association SLE with cormobidities collateral to aging
Malawi, 24(3), 69–71.
process. Furthermore, the results could be used as information
[12]. Hajishengallis G. 2014. Aging and its Impact on Innate
by doctor to determine patient treatment and education plans.
Immunity and Inflammation: Implications for
Hopefully there will be further research with markers in the
Periodontitis. J Oral Biosci. February 1; 56(1): 30–37.
oral cavity.
[13]. Pandruvada SN, Gonzalez OA, Kirakodu S, Gudhimella
S, Stromberg AJ, Ebersole JL, Orraca L, Gonzalez-
Martinez J, Novak MJ, Huja SS. Bone biology-related

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Volume 3, Issue 11, November – 2018 International Journal of Innovative Science and Research Technology
ISSN No:-2456-2165
gingival transcriptome in ageing and periodontitis in Study in Chronic Periodontitis. PLoS ONE, 9(3):
non-human primates. J Clin Periodontol 2016; 43: 408– e91636.
417. doi: 10.1111/jcpe.12528. [18]. Nanakaly HT. 2016. Effect of Periodontal Therapy on
[14]. Wherry EJ and Kurachi M. 2009. Moleculer and celluler Serum and Salivary Interleukin-2 Levels in Chronic
insight into T cell. NIH Public Access. 49(18), pp. 1841– Periodontitis. Journal of Baghdad College of Dentistry,
1850. doi: 10.1016/j.jacc.2007.01.076.White. 28(2): 73-78.
[15]. Ebersole JL, Kirakodu SS, Novak MJ, Orraca L, [19]. Acharya AB, Thakur S, Muddapur MV. 2015.
Martinez JG, Cunningham LL, Thomas MV, Stromberg Evaluation of serum interleukin-10 levels as a predictor
A, Pandruvada SN and Gonzalez OA. 2016. of glycemic alteration in chronic periodontitis and type 2
Transcriptome Analysis of B Cell Immune Functions in diabetes mellitus.
Periodontitis: Mucosal Tissue Responses to the Oral [20]. Fenol A, Sasidharan RK, Krishnan S. 2014. Levels of
Microbiome in Aging. Front. Immunol. 7:272. doi: Interleukin-10 in Gingival Crevicular Fluid and its Role
10.3389/fimmu.2016.00272. in the Initiation and Progression of Gingivitis to
[16]. Morozumi T, Yashima A, Gomi K, Ujiie Y, Izumi Y, Periodontitis. Journal of Oral Hygiene & Health, 2:135.
Akizuki T, Mizutani K, Takamatsu H, Minabe M, [21]. Napimoga MH, Nunes LHAC, Maciel AAB, Demasi
Miyauchi S, Yoshino T, Tanaka M, Tanaka Y, Hokari T, APD, Benatti BB, Santos VR, Bastos MF, de Miranda
Yoshie H. 2018. Increased systemic levels of TS, Duarte PM. 2011. Possible involvement of IL-21
inflammatory mediators following one-stage full-mouth and IL-10 on salivary IgA levels in chronic periodontitis
scaling and root planning. Journal of Periodontal subjects. Scandinavian Journal of Immunology, 74(6):
Research, 53(4): 536-544. 596–602.
[17]. Souto GR, Queiroz-Junior CM, de Abreu MHNG, Costa [22]. Fu QY, Zhang L, Duan L, Qian SY, Pang HX. 2013.
FO, Mesquita RA. 2014. Pro-inflammatory, Th1, Th2, Correlation of chronic periodontitis in tropical area and
Th17 Cytokines and Dendritic Cells: A Cross-sectional IFN-γ, IL-10, IL-17 levels. Asian Pacific Journal of
Tropical Medicine, 6(6): 489–492.

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 =


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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