Available online 4 May 2024, 105987

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Clinical parameters were positively correlated with IL-1β, NLRP3, and caspase-1.

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IL-1β, IL-18, NLRP3, ASC and caspase-1 were increased in serum of periodontitis.

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IL-1β, NLRP3 levels were reduced in periodontitis following NSPT.

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Salivary IL-1β and NLRP3 may act as biomarkers for periodontitis.

ABSTRACTObjective

The purpose of this study was to investigate interleukin (IL)-1β, IL-18, nod-like receptor pyrin domain-containing protein 3 (NLRP3), apoptosis-related speck-like protein containing a caspase activation and recruitment domain (ASC), and caspase-1 levels in saliva and serum in different periodontal diseases and to evaluate the changes after non-surgical periodontal treatment (NSPT).

Design

A total of 45 participants, 15 healthy, 15 gingivitis, and 15 stage III grade C (SIIIGC) periodontitis patients, were included in the study. Periodontal parameters were assessed, and salivary and serum samples were collected at baseline in all groups and one and three months after NSPT in gingivitis and periodontitis groups. An enzyme-linked immunosorbent assay was used to analyse IL-1β, IL-18, NLRP3, ASC, and caspase-1 levels.

Results

After NSPT, improvement was observed in all clinical parameters, along with periodontal inflamed surface area (PISA) in gingivitis and periodontitis groups. PISA scores were positively correlated with IL-1β, NLRP3, and caspase-1 at baseline (p<0.05). Salivary and serum IL-1β, NLRP3 levels were higher in periodontitis compared to healthy controls at baseline and reduced after treatment (p<0.05). Receiver operating characteristic analysis revealed that salivary IL-1β, NLRP3, and caspase-1 had the ability to discriminate SIIIGC periodontitis patients from healthy subjects (p<0.05).

Conclusion

In conclusion, salivary IL-1β, NLRP3, and caspase-1 are at aberrantly high levels in SIIIGC periodontitis and are remarkably decreased following NSPT; these inflammasome biomarkers may show potential utility in diagnosing and monitoring periodontitis.

Section snippetsINTRODUCTION

Periodontal diseases are multifactorial inflammatory conditions characterized by periodontal tissue damage which may cause tooth loss if left untreated (Papapanou et al., 2018). One of the main factors in the onset of disease is the individual's immune-inflammatory response to microbial dysbiosis (Kinane, 2000). Several activated pro-inflammatory cytokines, such as interleukin (IL)-1ß, produced by lymphocytes, neutrophils, monocytes/macrophages, fibroblasts, keratinocytes, periodontal ligament

Study Design and Sample Size Calculation

The Clinical Research Ethics Committee of Marmara University's School of Medicine approved the study (Protocol No: 09.2022.384). Additionally, the study was registered on clinicaltrials.gov (NCT06075680). Before the trial commenced, every participant provided their consent by signing a form aligned with the principles of the Helsinki Declaration of 1975, updated in 2013. A software package (G*Power Version 3.1.7 Software, Kiel, Germany) was used to calculate the minimum sample size based on a

Characteristics and clinical findings of the population

The initial study comprised 45 participants; however, the ultimate study sample was reduced to 42 participants due to the withdrawal of three individuals. Periodontitis group had higher median age than healthy and gingivitis groups (p<0.05) (Table 1). The gender distribution was similar among the groups (p>0.05) (Table 1). At baseline, the periodontitis group had significantly higher clinical parameters, including PI, BOP, PD, CAL, PESA, and PISA, compared to healthy controls and gingivitis

DISCUSSION

Complex mechanisms are involved in the immunopathogenesis of periodontal diseases. Inflammasomes are one of these protein complexes that detect various inflammation-triggering stimuli. They regulate the production of significant inflammatory cytokines such as IL-1β and IL-18. In our study, we evaluated the serum and salivary levels of NLRP3 inflammasome markers in gingivitis, SIIIGC periodontitis, and healthy patients and the changes in the levels of these markers responding to the NSPT,

CONCLUSIONS

In conclusion, salivary and serum IL-1β, NLRP3, and caspase-1 levels were increased in non-smoking, systemically healthy SIIIGC periodontitis patients, and NSPT exerted a notable influence on the salivary concentrations of these inflammasome biomarkers. PISA can also provide potential benefits in both the diagnosis and follow-up of periodontal diseases. Our study highlights the intricate relationship between inflammasome biomarkers and SIIIGC periodontitis and gingivitis. Additional

CRediT authorship contribution statement

Hafize Öztürk Özener: Writing – review & editing, Supervision, Methodology, Formal analysis, Conceptualization. Bilge Kabacaoğlu: Writing – original draft, Investigation, Formal analysis, Data curation.

Declaration of Competing Interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

ACKNOWLEDGMENTS

This study was supported by grants from the Marmara University Scientific Research Projects Coordination Unit with TDK-2022-10763 protocol ID.

CONFLICT OF INTEREST

The authors declare no potential conflicts of interest with respect to the authorship and/or publication of this article.

REFERENCES (56)P.V. Bawankar et al.Evaluation of stress, serum and salivary cortisol, and interleukin-1beta levels in smokers and non-smokers with chronic periodontitis.

J Periodontol

(2018)

N. Bostanci et al.Expression and regulation of the NALP3 inflammasome complex in periodontal diseases

Clin Exp Immunol

(2009)

F.Q. Bui et al.Fusobacterium nucleatum infection of gingival epithelial cells leads to NLRP3 inflammasome-dependent secretion of IL-1beta and the danger signals ASC and HMGB1

Cell Microbiol

(2016)

R. Cheng et al.Interleukin-1beta is a potential therapeutic target for periodontitis: a narrative review.

Int J Oral Sci

(2020)

C.M. CobbClinical significance of non-surgical periodontal therapy: an evidence-based perspective of scaling and root planing

J Clin Periodontol

(2002)

R.C. Coll et al.Questions and controversies in innate immune research: what is the physiological role of NLRP3?

Cell Death Discov

(2016)

A.S. Ertugrul et al.Comparison of CCL28, interleukin-8, interleukin-1beta and tumor necrosis factor-alpha in subjects with gingivitis, chronic periodontitis and generalized aggressive periodontitis.

J Periodontal Res

(2013)

C.M.S. Figueredo et al.Increased Interleukin-1beta Concentration in Gingival Crevicular Fluid as a Characteristic of Periodontitis.

J Periodontol

(1999)

A.L. Garcia-Hernandez et al.Upregulation of proteins of the NLRP3 inflammasome in patients with periodontitis and uncontrolled type 2 diabetes

Oral Dis

(2019)

N.G. Gorgulu et al.Effect of non-surgical periodontal treatment on salivary and serum biomarkers in Stage III Grade B and C periodontitis

J Periodontol

(2022)

R.W. Grant et al.Mechanisms of disease: inflammasome activation and the development of type 2 diabetes

Front Immunol

(2013)

X. Huang et al.Hyperglucose contributes to periodontitis: involvement of the NLRP3 pathway by engaging the innate immunity of oral gingival epithelium

J Periodontol

(2015)

D.M. Isaza-Guzman et al.Salivary Levels of NLRP3 Inflammasome-Related Proteins as Potential Biomarkers of Periodontal Clinical Status

J Periodontol

(2017)

G. Isola et al.Periodontitis activates the NLRP3 inflammasome in serum and saliva

J Periodontol

(2022)

T. Karasawa et al.Role of NLRP3 Inflammasomes in Atherosclerosis

J Atheroscler Thromb

(2017)

J.Y. Kim et al.Changes in Inflammatory Cytokines in Saliva after Non-Surgical Periodontal Therapy: A Systematic Review and Meta-Analysis

Int J Environ Res Public Health

(2020)

J.Y. Kim et al.The Potential Impact of Salivary IL-1 on the Diagnosis of Periodontal Disease: A Pilot Study

Healthcare (Basel)

(2021)

D.F. KinaneRegulators of tissue destruction and homeostasis as diagnostic aids in periodontology

Periodontol 2000

(2000)

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