effect of nonsurgical periodontal therapy on salivary ... · proceeding book of international...

( ICASEE 2018 )International Conference on Applied Science, Energy and Environment Proceeding book of 2018 th9 - thApril , 7 Ishik UniversityEducation Faculty /

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Effect of Nonsurgical Periodontal Therapy on Salivary Interleukin-8 Levels in

Patients with Chronic Periodontitis

Haween T. Nanakaly 1 , Hozan Wrya Azeez 2 and Solav M. Abdul-Qadir 2

1Department of Basic Sciences, College of Dentistry, Hawler Medical University 2Department of Periodontology, College of Dentistry, Hawler Medical University

doi:10.23918/ICASEE2018.20

Correspondence: Haween T. Nanakaly

Email: [email protected]

Abstract: Cytokines play an important role in the pathogenesis of inflammatory disease,

including chronic periodontitis (CP). Because of pro-inflammatory and neutrophil

chemotactic properties of Interleukin-8 (IL-8), the IL-8 may play a significant role in the

pathogenesis of periodontitis.

Aim: This study was done to estimate and compare salivary levels of IL-8 in periodontal

health and disease, and also to assess the effect of non-surgical periodontal therapy on

its levels in chronic periodontitis patients, in relation to clinical parameters.

Materials and Methods: Thirty chronic periodontitis patients and 30 healthy controls

were recruited for the study. The periodontal status was assessed by gingival index(GI),

Probing pocket depth (PPD), Bleeding on probing (BOP) and Clinical attachment level

(CAL). The level of IL-8 in salivary fluid was measured by enzyme-linked

immunosorbent assay kit. Non-surgical periodontal therapy (Scaling and root planning;

SRP) was performed on chronic periodontitis patients and a follow-up was done after 4

weeks.

Results: The level of IL-8 in saliva of periodontitis patients was significantly higher (p<

0.001) compared to healthy controls at baseline. SRP therapy improved all clinical

parameters and salivary IL-8 levels in periodontitis patients. A significant correlation

was observed between CAL and IL-8(r=0.312, p= 0.052), BOP and IL-8 (r=0.332, p=

0.050) before therapy, and BOP and IL-8 (r=0.373,p=0.04) after therapy

Conclusion: These data suggest that levels of salivary IL-8 generally decrease after non-

surgical periodontal therapy. Correlation between some clinical periodontal parameters

and level of salivary IL-8 was found.

Keywords: Cytokines, Interleukin-8, Saliva, Nonsurgical periodontal therapy

mailto:[email protected]


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1. Introduction

Chronic periodontitis is an inflammatory disorder of periodontium resulting in

destruction of periodontal ligament and loss of the adjacent bone (Wei et al., 2010). The

initiation and progression of periodontitis are dependent on the presence of numerous virulent

microorganisms in the subgingival biofilm. There is strong evidence that points to

Porphyromonas gingivalis, as the major etiological agent in the development of periodontitis.

P. gingivalis is a Gram-negative anaerobic bacterium that has a number of virulence factors,

including lipopolysaccharides (LPS) (Oʼ Brein-Simpson et al., 2004). LPS acts as a potent

stimulus to a range of host cells, which consequently results in the expression of inflammatory

cytokines leading to the development and progression of the related host immune response in

periodontal diseases (Ren et al., 2005).

Saliva is a main growth environment for flora of the oral cavity. Salivary secretions

are protective in nature because they play an important role in preservation and maintenance

of oral health. The protective effect of saliva may be accomplished by means of secretion rate,

buffering capacity, phosphate and calcium concentration and antibacterial system (Ahmadi et

al., 2010). Saliva being non-invasive, easy to collect, hence has a great potential for use in

scientific researches on diagnosis of periodontal disease and monitor response to treatment

(Miller et al., 2010). Various compounds, such as cytokines, were detected in saliva and may

be especially beneficial for diagnosis current periodontal status and addressing the effects of

periodontal treatment (Sexton et al., 2011).

Interleukin-8 (IL-8) is a member of the IL-8 supergene family that includes small

peptides with chemotactic activity for specific types of leukocyte populations (Birkedal-

Hansen, 1993). This cytokine is induced and secreted by many cells including

monocyte/macrophages, fibroblasts lymphocytes, endothelial cells and epithelial cells

(Erdemir et al., 2010). IL-8 is a potent chemoattractant and activator polymorphonuclear

leukocytes (PMN) in inflammatory regions (Matsushima et al., 1992). IL-8 also induces the

adhesion of PMN to endothelial cells and facilitating transendothelial migration (Maurizio et

al., 1998). IL-8 also implicated in the stimulation of PMN to release granule enzymes such as

Myeloperodixase,α-mannosidase, arachidonate-5-lipoxygenase, β-glucoronidase, and

elastase, as well as induce the formation of superoxide and hydrogen peroxide (H2O2) as a

part of the respiratory burst emphasizes its role as a proinflammatory mediator(Chung et al.,

1997).

However, continuous and excessive IL-8 mediated chemotactic and activation effects

on neutrophils in the inflamed gingiva could contribute to the periodontal tissue destruction

(Bastos et al., 2009) , and it is suggested that IL-8 may play a significant role in the

pathogenesis of periodontitis (Chung et al., 1997).

In periodontal patients, IL-8 was reported in both gingival crevicular fluid GCF and

periodontal tissues. The expression of IL-8 mRNA and protein were significantly higher in

chronically inflamed periodontal tissues, as well as in GCF of patients with periodontitis (Tsai

et al., 1995; Dongari-Bagtzoglou and Ebersole 1998).

Studies in the literatures reported the beneficial effects of scaling and root planning

(SRP) therapy on some key local inflammatory markers particularly IL-8 in GCF (Goutoudi

et al., 2012). However, few studies addressed the effect of periodontal therapy on local


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clinical, salivary inflammatory markers in conjunction with salivary chemokine

markers. Therefore, the present study assesses the effect of SRP therapy on clinical and

salivary IL-8 levels in patients with chronic periodontitis.

2. Materials and Methods

2.1 Study population

The participants were recruited between November 2016 and May 2017 from persons

seeking treatment at the Hawler Medical University, College of Dentistry. The present

interventional study was approved by the Ethical committee of the college of

Dentistry/Hawler Medical University. Written informed consent was obtained from all

participants. A total of 60 participants (n=60; women=27 and 33 men; age range: 30-55) were

divided into two groups: Group-I=30 periodontally healthy individuals as controls, and

Group-II =30 patients chronic periodontitis.

Clinical history was recorded for all participants (personal data and medical history).

Study inclusion criteria were as follows: individuals in the chosen age range with at least 20

standing teeth, with more than 30% of the teeth with probing pocket depth (PPD) ≥ 4 mm

and clinical attachment loss (CAL) ≥ 3 mm with radiographic evidence of alveolar bone loss.

No antibiotic taken prior to 6 months of initial examination, no periodontal treatment, no

periodontal surgery performed in the preceding six months, and had no periapical lesions, or

restoration. The control group enclosed individuals without any history of periodontal disease

and attachment loss, as well as with probing pocket depth (PD) ≤ 3 mm and with bleeding

index (PBI) simplified < 20% to exclude the presence of gingivitis. The patients in the study

group were clinically evaluated for chronic periodontitis according to the criteria accepted by

the American Academy of Periodontology (Armitage, 1999) and periodontal status was

evaluated as described by (Armitage, 2004)

Subjects who had past illness and undergoing any treatment; diabetics, Malignant

tumour, liver diseases ; smoker and tobacco consumers, alcoholics; pregnant and lactating

women were excluded from the study.

2.2 Saliva collection and analysis:

The saliva sample was collected twice once at baseline and the other 30 days after a

completion of periodontal therapy for patients in group II, and only once for subjects in group

I. Participants were instructed to refrain from eating, drinking, and practicing oral hygiene

procedures at least 2 hours prior to saliva collection. Whole un-stimulated saliva was collected

from all subjects between 8:00-11:00 A.M. The subjects were asked to rinse their mouth with

distilled water, after that they expectorated at least 2 mL of un-stimulated whole saliva into a


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5mL sterile plastic tubes before periodontal examination according to the method

described by (Navazesh, 1993). Collected samples were placed immediately on ice pack and

transported to the laboratory, where they centrifuged at 3500 rpm for 10 minutes, and the

clear supernatant were stored in aliquots at -40 º C. The samples were thawed, and analysed

were performed within 6 months of collection. Salivary IL-8 levels were measured with an

ELISA kit using Human Interleukine-8(IL-8) provided by Expert chem SERV (Catalog #

DRE10290) according to manufacturerʼs instructions. The standard range was 50ng/L- 1000

ng/L.

2.3 Clinical Parameters:

Clinical data included: Gingival index (GI), Probing pocket depth (PPD), Clinical

attachment level (CAL) and Bleeding on probing (BOP), were measured on six sites of teeth.

Full –mouth periapical radiographs were taken to determine the level of periodontal bone loss

of the patients. These data were recorded and the treatment performed by a single experienced

periodontist after saliva collection. All these periodontal parameters were recorded again after

completion of periodontal therapy to constitute group II (post-treatment group).

2.4 Non-surgical periodontal therapy:

Following collection of saliva, patients with chronic periodontitis (group II) received

non-surgical periodontal treatment which included oral hygiene instructions (teaching

brushing, flossing and usage of interdental bruch), full mouth scaling and rootplaning (using

ultrasonic scaler and Gracey curettes). Treatment was performed by the same periodontist

under local anesthesia. No antibiotic were prescribed after the treatment. The patients were

monitored periodically, were followed up after 4 weeks and their clinical parameters evaluated

and saliva samples were collected for re-examination of the levels of IL-8. Subjects in the

control group (group I) received no periodontal treatment during the course of the study and

were evaluated only once.

2.5 Statistical analysis:

Statistical analysis were performed by commercially available software (Statistical

Package for Social Sciences, version 22 for windows, SPSS Inc., Chicago, IL, USA). All data

were expressed as mean and standard deviation. Comparison of clinical periodontal

parameters and salivary IL-8 levels between CP and control groups were done using

independent sample "t" test. In group II the effect of SRP (after 4 weeks post-treatment with

the corresponding baseline parameters) on clinical periodontal parameters and salivary IL-8

levels was assessed using paired "t" test. The Spearman’s rank correlation test was used to

detect relationship between salivary IL-8 levels and clinical parameters. A differences was

considered statistically significant if p was < 0.05.


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3. Results

In this study comparison of mean values of clinical periodontal parameters: GI, PD,

CAL, and BOP evaluated between groups are given in Table 1. The patients with chronic

periodontitis at baseline (group II) had significantly higher mean values of GI (p< 0.001),

PPD (p< 0.001), CAL (p< 0.001), and BOP (p< 0.001) compared to healthy controls (group

I), there was no attachment loss in controls. Thirty days after non-surgical periodontal therapy

(SRP) all clinical parameters reduced significantly (p< 0.001) compared to their

corresponding baseline values in group II.

The statistically comparison of mean values of salivary IL-8 analyzed between groups are

shown in Table 1 and Figure 1. The baseline mean salivary IL-8 level was found to be

significantly higher (p< 0.001) in group II as compared to group I. Following SRP therapy,

salivary IL-8 levels decreased significantly (p< 0.001) compared to their corresponding

baseline values in group II.

In this study correlations between clinical parameters and salivary IL-8 level were analysed.

The correlation between the clinical parameters and salivary IL-8 in the control group was not

significant (p>0.0.5). A significant positive correlation was observed between CAL and IL-

8(r=0.312, p= 0.052), BOP and IL-8 (r=0.332, p= 0.050) before therapy, as well as a positive

correlation BOP and IL-8 (r=0.373,p=0.04) after therapy (Table 2).

4. Discussion

This study was performed to assess the relationship between periodontitis and IL-8

levels in saliva, and effect of SRP therapy on salivary level of IL-8 in monitoring the

progression of periodontal disease.

Periodontitis is a chronic inflammatory disease of microbial origin, that results in the

breakdown of tooth-supporting tissues, including alveolar bone, and ultimately leads to tooth

loss (March and Devine, 2011). Numerous of pathogens are known to play a role in the

initiation and progression of periodontitis, however the gram-negative, anaerobic bacterium

Porphyromonas gingivalis is considered as the keystone pathogen in periodontitis (Grenier et

al., 2015). It is suggested that major tissue destruction in established periodontitis lesions

results from recruitment of host cells via activation of monocytes/macrophages, dendritic

cells, lymphocytes, fibroblasts, and other cell types. There was a significant effort to study the

cytokines released by different host cells when exposed to components of periodontopathic

bacteria. Certain cytokines were suggested as potentially useful diagnostic or prognostic

markers of periodontal destruction (Giannopoulou et al., 2003).

Previous studies (George and Janam 2013; Zekeridou et al., 2017) associated altered

clinical parameters in chronic periodontitis when compared to healthy controls. Our result

showed that GI, PD, and BOP were significantly higher in group II at baseline compared to

group I. There was an improvement in all the clinical parameters after one month of SRP

treatment in group II compared to their respective baseline values. Our study coincidence with

(Aziz et al., 2013; Sharma et al., 2014;) who observed that SRP was effective at improving

all clinical parameters.


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IL-8 is an important chemokine of interest in periodontal diseases. It has a

significant role in the initiation and development of inflammatory response and periodontal

tissue destruction through its critical role in recruitment and functional activation of

neutrophilic granulocytes (Paul et al., 2012). Our finding indicates that in group II salivary

IL-8 was higher level at baseline compared to group I (p< 0.01). This was also documented

by previous studies in chronic periodontitis. Michiels et al., (2009) who showed that the

concentration of IL-8 in saliva was significantly higher in chronic periodontitis (CP) than in

periodontally healthy subjects. These authors suggested that the level of IL-8 could be related

to the pathogenesis of inflammatory periodontal disease. Another study by (Teles et al., 2009)

noticed that the level of IL-8 had a tendency to be higher in periodontitis patients saliva

compared to healthy control group but there were not significant different (p> 0.05).

Ertugrul et al., (2013) reported that IL-8 levels in GCF was significantly higher in

periodontitis patients compared to healthy subjects. In a study performed by (Andia et al.,

2011) who showed the increase of IL-8 mRNA expression in gingival fibroblasts of

individuals with CP compared to healthy individuals. Park et al., (2013) demonstrated that IL-

8 mRNA expression was higher in the gingival tissues of all the patients with periodontitis.

These results coincidence with those reported by (Tonetti et al., 1994) who founded that

increased IL-8 levels in gingival tissues could result in an increased accumulation of

neutrophils-indicating an active host immune response, also founded positive association

between IL-8 levels with the progressive periodontitis in animals. Andrukhov et al., (2014),

observed that Lipopolysaccharide (LPS) of Porphyromonas gingivalis induces the expression

of proinflammatory cytokines including: IL-1β, IL-6 and TNF-α and chemokines IL-8 in

human gingival fibroblasts, which induce periodontal tissue destruction. Moreover, Dongari-

Bagtzoglou and Ebersole, (1998) also observed that after bacterial challenge, expression of

IL-8 in gingival fibroblast is significantly higher compared to healthy controls. They reported

that IL-8 could play a role in amplifying the local immune response and promoting

inflammation in periodontium. The investigation of the above studies indicated that IL-8 may

play a significant role in periodontal pathogenesis because of its pro-inflammatory and

neutrophil chemotactic properties. These findings, together with our results, confirm that IL-

8 cytokine/chemokine highly related to the inflammatory conditions of the periodontium.

Conversely, in a study done by (Khalaf et al., 2014) who reported that IL-8 levels had

significantly higher in saliva from periodontally healthy individuals compared to those

affected by CP. The diversity of the results coincidence with (Zhang et al., 1999) who

confirmed that both gingival and oral epithelial cells infected with Porphyromonas gingivalis

produced IL-8, and after infection these cells continued to express IL-8 mRNA, although the

accumulation of the secreted protein could not be detected. The authors also suggested that

IL-8 could be degraded locally by P. gingivalis proteinases.

The results of the present study also observed that SRP therapy resulted in a significant

decrease in salivary IL-8 levels in subjects with chronic periodontitis (p< o.o1). These results

are similar to those reported by (Tsai et al., 1995) who observed that GCF mean IL-8 level

of the subjects with chronic periodontitis was significantly higher than the control group.

They also observed that nonsurgical periodontal therapy was effective at improving clinical

parameters and significantly decreasing GCF IL-8 levels in adult periodontitis patients.


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Another study by (Mathure et al., 1996) reported that total amount of IL-8 (TAIL-

8) was higher in diseased sites compared to healthy sites, also observed that periodontal

treatment resulted in a significant decrease of mean TAIL-8 in diseased and non-diseased sites

at 6 week. The results of the present study indicates improved IL-8 levels after SRP therapy.

This could be attributed to the beneficial effects of SRP therapy, which lowers the

inflammatory burden on the periodontium. The results of our study explain the hypothesis that

large amounts of inflammatory cells in the connective tissues of gingival cervices can lead to

release IL-8, by stimulation with bacterial products and interaction with host cells. Neutrophils

form a defence curtain between the dental plaque and junctional epithelium. These neutrophils

may provide protection for the periodontium. IL-8 is a chemoattractant and activator of

neutrophils, it can be released during the process of phagocytosis to attract more neutrophils

into the site of bacterial infection (Tsai et al., 1995). The aim of SRP therapy was to reduce

the microbial disease associated with oral plaque. This may lead in decreasing the

inflammatory manifestations. The decreased pathogen load and local inflammation may help

in lowering proinflammatory cytokines secretion and reducing the IL-8 as observed in our

study.

The present study shows the correlation of clinical parameters with salivary IL-8 level,

of control group, and CP patients before and after SRP therapy. There was no significant

correlation within the control group , when salivary IL-8 level was correlated with the clinical

parameters like GI,PPD,CAL, and BOP. However, in the diseased group, before SRP therapy,

when salivary IL-8 level correlated with clinical parameters, there was a positive significant

correlation with CAL and BOP(p< 0.05). This indicates that there is a correlation between

the increase of CAL and BOP values and the increase of salivary IL-8 level . After SRP

therapy, it was found a positive significant correlation between the decrease of salivary IL-8

level with decrease of BOP (p< 0.05). This finding suggests that IL-8 is highly related to the

inflammatory condition of periodontium. Thus the presence of elevated levels of IL-8 in saliva

of CP, along with the significant correlation with clinical assessments of periodontal tissue

destruction, strongly suggests an important role of IL-8 in the pathogenesis of periodontal

disease. However, in study by, (Goutoudi et al., 2012) who examined the correlations of

IL-6,IL-8 levels in GCF of CP patients before and after therapy and clinical periodontal

parameters (PII,GI,PD,CAL ), reported that the sites with increased GCF levels of IL-8 after

periodontal therapy were not characterized by significant loss of attachment or inflammation.

Weak correlation between TAIL-8 and clinical parameters were observed, positive with GI

and negative with PD. Although the expression pattern is variable, these findings, together

with our results, indicate that there is an association between IL-8 and periodontal disease.

Results of this study demonstrated that salivary IL-8 level decreased from CP patients after

SRP, the clinical parameters before and after periodontal therapy were statistically different,

suggesting that IL-8 level might be a precise marker of clinical status. This effect is probably

due to the reduction of the inflammatory condition, which was proved after the therapy most

probably due to the reduction of microorganisms involved in periodontal disease.

It was suggested that IL-8 may have both inflammation-retarding effects in the stages

of gingival inflammation and inflammation-enhancing effects in the stages of periodontal

destruction, Under the latter condition, disturbance of IL-8-driven neutrophil recruitment to


200

the periodontal pocket may not only damage the potential of the host to provoke the

microbiological challenge, but also result in neutrophil-associated tissue destruction due to

amplified release of lysosomal enzymes and matrix metalloproteinases. Moreover, IL-8 might

thus act on migrating neutrophils in a dose-dependent mode, controlling neutrophil motility

at low concentrations and contributing to the activation of neutrophil degranulation and

respiratory burst at high concentrations (Jin et al., 2000). Furthermore, IL-8 up-regulates the

transmigration of neutrophils and their accumulation at the surface of the subgingival plaque

biofilm. Neutrophils thus play a key role as the primary effector cells to detect

periodontopathogens. IL-8 plays an essential role in the maintenance of local host-parasite

equilibrium and in the limitation of neutrophil-associated tissue damage. Normally, IL-8

expression relates well to the pattern of neutrophil infiltration and appropriate release of IL-8

contributes to eliminating the infecting bacteria by neutrophils. Conversely, an uncontrolled,

excessive release of IL-8 contributes to eliminating the excessive release of IL-8 and the

resultant hyperactivity of neutrophils may result in tissue destruction (Jin et al., 2000) .

5. Conclusion

Patients with chronic periodontitis show higher clinical periodontal damage and

inflammation when compared to healthy control individuals. Obviously, the study

demonstrates the efficacy of SRP in effectively removing the etiological agent, thus helping

in decreasing the inflammatory effect on the periodontal tissues by improving clinical

parameters and salivary IL-8 levels. Therefore, we suggest that salivary IL-8 level could be

additional inflammatory marker to connect salivary markers with periodontal status. More

research is being directed to explore this possibility. The findings also suggest that significant

relations are present between salivary IL-8 levels and periodontal status, and that IL-8 may

play a significant role in the pathogenesis of periodontitis.

Acknowledgments

The authors are thankful to Dr. Ziwar Ahmed Qasib, Assistant Professor, Department of

Periodontology for his valuable help and guidance; Dr.Baxtiar M, Department of Basic

Sciences , for the timely help, and Mr. Dara Al-Banna, for helping in the statistical analysis

of the study.

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Table 1: Comparison of mean values of clinical parameters and salivary IL-8

levels between groups I and II

Parameters Group I

(n=30)

Group II (n=30)

Baseline Post-

treatment

avalues-p

group Ivs

group II

(baseline)

bvalues-p

group II baseline

vs Post-treatment

GI 0.52±

0.43

2.30 ±

0.67

1.24 ±

0.55

0.001 0.001

PPD (mm) 1.53 ±

0.72

5.50 ±

0.55

2. 45 ±

0.88

0.001 0.001

CAL (mm) 0.00 ±

0.00

5.12 ±

0.53

2.21 ±

0.55

0.001 0.001

BOP(% sites

with BOP)

0.00 ±

0.00

79.03±

22.11

23.52 ±

9.53

0.001 0.001

Salivary IL-8

(ng/L)

92.30 ±

16.66

289.67±

49.84

133.68 ±

23.84

0.001 0.001

GI; Gingival Index, PPD; Probing pocket depth, CAL; Clinical attachment loss, BOP;

Bleeding on probing, Values are mean± SD; Standard deviation; ap-values for mean ± SD

by independent sample 't' test; bp-values for mean± SD obtained by paired 't' test; p-values ≤

0.05 is considered to be statistically significant

Table 2: Correlation coefficient of IL-8 with clinical parameter

Group

Clinical

Parameter

Interleukin-8

r P-value

Control

N=30

GI 0.27 0.32

PPD 0.06 0.79

CAL ---- ----

BOP ---- ----

Baseline

N=30

GI 0.007 0.97

PPD 0.108 0.57

CAL 0.312 0.052*

BOP 0.332 0.050*

Post-treatment

N=30

GI -0.067 0.72

PPD -0.133 0.48

CAL 0.360 0.061

BOP 0.373 0.04*

r= Spearman rank correlation coefficient


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