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 Table of Contents  
Year : 2023  |  Volume : 15  |  Issue : 1  |  Page : 8-13

Comparison of pre- and postsurgical periodontal therapeutic effects on serum sclerostin in confirmed periodontitis cases

Department of Periodontics, Panineeya Institute of Dental Sciences, Hyderabad, Kaloji Naran Rao University of Health Sciences, Warangal, Telangana, India

Date of Submission04-Apr-2022
Date of Decision26-May-2022
Date of Acceptance03-Jun-2022
Date of Web Publication29-Dec-2022

Correspondence Address:
Jammula Surya Prasanna
Department of Periodontics, Panineeya Institute of Dental Sciences, Dilsuck Nagar, Hyderabad - 500 060, Telangana, India. Kaloji Naran Rao University of Health Sciences, Warangal, Telangana
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jorr.jorr_12_22

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Context: Connective tissue and alveolar bone loss in the region of the teeth is very frequent in inflammatory conditions like periodontitis (PD). As things go, apical movement of junctional epithelium deepens the periodontal pocket, ultimately tooth loss. Periodontal research advancements in biomarker assay prop up the risk by prior identification. Sclerostin, a skeletal marker, has been assessed to explore the intensity of PD and its effect after periodontal therapy.
Aims: This study aimed to estimate serum sclerostin in patients affected with PD at the reference point and after periodontal therapy.
Settings and Design: This was an interventional prospective study.
Materials and Methods: Age-matched 30 PD patients, both male and female, were chosen. Clinical considerations, probing pocket depth and clinical attachment level, were assessed. Serum sclerostin levels were estimated using ELISA at baseline, 4 weeks after nonsurgical periodontal therapy (NSPT), and after 6 weeks of Surgical Periodontal Therapy (SPT).
Statistical Analysis Used: Data were scrutinized by the SPSS version 23. A descriptive, paired t-test was done for values obtained at various intervals.
Results: A positive correlation of sclerostin was found with severity of PD and was declined from starting point to NSPT and further to SPT (P<0.001). Both clinical as well as biochemical parameters reduced to NSPT and more significant reduction to SPT (< 0.001).
Conclusions: Sclerostin severity was reduced in NSPT stage compared with baseline values, and furthermore reduced in SPT stage. Concluding that periodontal therapy is effective on biochemical marks, intensity and periodontal disease initiation can prior be detected by markers such as sclerostin.

Keywords: Biomarker, periodontal surgery, periodontitis, scaling, sclerostin

How to cite this article:
Madhavi B, Prasanna JS, Rani KR. Comparison of pre- and postsurgical periodontal therapeutic effects on serum sclerostin in confirmed periodontitis cases. J Oral Res Rev 2023;15:8-13

How to cite this URL:
Madhavi B, Prasanna JS, Rani KR. Comparison of pre- and postsurgical periodontal therapeutic effects on serum sclerostin in confirmed periodontitis cases. J Oral Res Rev [serial online] 2023 [cited 2023 May 30];15:8-13. Available from: https://www.jorr.org/text.asp?2023/15/1/8/365913

  Introduction Top

Bone reduction is the hallmark of periodontitis (PD), as caused by bacterial invasion contributes to the collapse of tooth-supporting structures that often consequences in tooth loss. Several body responses to periodontal infection have been described to illuminate the pathophysiology involved in PD.[1] Illuminating the dissimilar mechanisms of coupling between bone reduction and development is very important for understanding and managing periodontal disease.[2] Sclerostin, a repercussion of the SOST gene, is a secreted glycoprotein, production of osteocytes. It has an effect on bone turnover by slowing down osteoblast differentiation.

Sclerostin blocks the Wnt signaling pathway by binds with low-density lipoprotein receptor-related protein. Sclerostin hinders bone morphogenic protein signaling and hence has a negative influence on bone synthesis.[3],[4] Based on the abovementioned mechanisms, it is hypothesized that Wnt–β-catenin signaling pathway and its antagonists SOST are key players in the pathophysiology of several conditions such as ankylosing spondylitis, rheumatoid arthritis, bone metastatic cancer, osteoporosis, and multiple myeloma.[5],[6] Bone markers are valuable tools to assess bone morphology and have been slowly recognized in clinical practice. The continued progress of these new markers has increased the understanding related to PD.[7] Null hypothesis: H0 = no variation between pre- and posttreatment values (clinical and biochemical factors).

The purpose of this article was to estimate serum sclerostin concentrations in periodontally affected patients pre- and postintervention, which could validate the effectiveness of treatment as well as its role as a biomarker.

  Materials and Methods Top

This was an interventional prospective study. Initially, 60 subjects were chosen, and later, depending on criteria, only 30 were included [Figure 1], comprising both sexes and having chronic periodontitis (CP) which is conferred to the American Academy of Periodontology (AAP) classification.[8] Subjects were selected from the outpatient ward of the department of periodontics. Ethical consent from the ethical committee of institute (ref no. 0010) and written approval from the patients were taken, and the study was registered. The protocol was completed from December 2018 to May 2019. Patients aged between 30 and 50 years who were systemically healthy with 50% of the teeth remaining with PD as per the AAP classification were included.[8] After nonsurgical periodontal therapy (NSPT), patients with residual pocket depths and clinical attachment level (CAL) = 5 mm were involved in the surgery. Patients who were systemically compromised, on steroids, or with any other drug history; smokers; patients who had experienced periodontal treatment during the past 6 months; and expectant and breastfeeding women were omitted from the study. Clinical and biochemical changes were assessed at baseline, 4 weeks after NSPT, and 6 weeks after surgical therapy. The total evaluation period from baseline to SPT was 10 weeks. The serum was separated and preserved at −20°C until analysis. Before processing, testers and components were brought to room temperature. Clinical parameters assessed were probing pocket depth (PPD) and CAL.
Figure 1: Patients' selection criteria. N: No. of patients, NSPT: Nonsurgical periodontal therapy, SPT: Surgical therapy, PPD: Probing pocket depth, CAL: Clinical attachment level, ELISA: Enzyme-linked immunosorbent assay

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Clinical measurements

Clinical measurements were done using Williams calibrated periodontal probe (Hu-Friedy, USA). Biochemical parameters assessed were serum sclerostin in CP patients using ELISA (Catalog No: EH0599, Clementia Biotech).

Periodontal therapy

All the patients meeting the selection criteria were given comprehensive directions on self-performed plaque control procedures using a soft toothbrush and interdental cleaning devices. Full-mouth supra- and subgingival scaling and root planing were performed.

Subgingival debridement was done using ultrasonic devices (Woodpecker UDS-J Ultrasonic Scalar) and area-specific Gracey curettes (Hu-Friedy, USA) under local anesthesia. The full-thickness flap was raised and defects were thoroughly debrided. The flap was relocated and sutured. Patients were informed to rinse with 0.12% chlorhexidine gluconate oral rinse after 24 h two times per day for support in plaque control for 2 weeks.

Two weeks postsurgery, patients were requested to continue oral hygiene twice daily with a soft toothbrush.

Sample collection and storage

Two milliliters of peripheral venous blood was drawn from the antecubital vein through the vein puncture method. Whole blood was collected in serum clot activator vacutainer tubes (red-capped) (Greiner Bio-One International).

Blood was allowed to clot initially at room temperature by keeping the tubes in standing position for 30 minutes. Thereafter, serum was obtained by centrifuging for 10 min at 3000 rpm in a centrifuge (Remi Revolutionary General Purpose Centrifuge Machine) immediately liquid component, serum was transferred into sterile Eppendorf tubes (Greiner Bio-One International) using a pipette (Greiner Bio-One International).

These tubes were stored at −20°C until used for evaluation of sclerostin levels. Multiple freeze-thaw cycles are avoided.

Biochemical analysis

For sclerostin estimation, the normal room temperature was maintained before the use of samples and centrifuged at 10,600 rpm for 10 min at 4°C.

Principle of the assay

This kit was based on sandwich enzyme-linked immune-sorbent assay technology. A 96-well plate is precoated with anti-SOST antibody.

Moreover, the biotin-conjugated anti-SOST antibody was used as a detection antibody. The standards, test samples, and an anti-SOST antibody conjugated to biotin were used as a detection antibody. Standards, test samples, and biotin-conjugated detection antibodies were then added to the wells and washed with wash buffer. After adding horseradish peroxidase (HRP)-streptavidin conjugate, wash buffer was used to unbound compounds. HRP enzymatic reaction was visualized by adding tetramethylbenzidine (TMB). TMB was catalyzed by HRP to produce a blue-colored product that turned yellow after the addition of an acid-stopping solution. The density of the yolk is proportional to the amount of SOST sample captured in the plate.

Read the optical density at 450 nm in a microplate reader, and then the concentration of SOST was calculated. The primary outcome measured was the sclerostin concentration beforehand and subsequently NSPT and SPT. The secondary outcome was the correlation of sclerostin and clinical parameters such as PPD and CAL.

Statistical analysis

Data were analyzed using the SPSS version 23. (IBM SPSS Statistics version 23, IBM Corporation, Armonk, NY, USA). A descriptive, paired t-test was used to relate the mean scores at various intervals. The association/correlation between the variables was assessed using the two-tailed test.

  Results Top

Thirty patients were evaluated. PPD values at baseline, after NSPT, and after SPT were 7.22 ± 0.58, 6.90 ± 0.58, and 2.95 ± 0.46, respectively. A decrease in the PPD is statistically significant when compared between baseline and after NSPT (P < 0.001), between baseline and SPT (P < 0.001), and between NSPT and SPT (P < 0.001) [Table 1]. CAL values at baseline, after NSPT, and after SPT were 5.43 ± 0.45, 5.06 ± 0.52, and 1.25 ± 0.24, respectively. Improvement in CAL is statistically significant when compared between baseline and after NSPT (P < 0.001), between baseline and SPT (P < 0.001), and between NSPT and SPT (P < 0.001) [Table 2].
Table 1: Comparison of probing depth at various intervals

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Table 2: Comparison of mean clinical attachment level at various intervals

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Serum sclerostin (SOST) values at baseline, after NSPT, and after SPT are 762.91 ± 426.50, 246.19 ± 222.49, and 74.14 ± 123.11, respectively. A decrease in SOST levels was statistically significant when compared between baseline and after NSPT (P < 0.001), between baseline and SPT (P < 0.001), and between NSPT and SPT (P < 0.001) [Table 3]. When the correlation coefficient® was compared along with a two-tailed test between biochemical and clinical variables, there was a statistically significant positive correlation present between all the parameters (P < 0.01) [Table 4]. Statistical significance at baseline between PPD and CAL (r = 0.757), CAL and sclerostin (r = 0.794), PPD and sclerostin (r = 0.763) [Table 4]a. After NSPT, between PPD and CAL (r = 0.888), between CAL and sclerostin (r = 0.631), and in between PPD and sclerostin (r = 0.637) [Table 4]b. Moreover, after SPT also, a positive correlation is observed between PPD and CAL (r = 0.406) [Table 4c].
Table 3: Comparison of serum sclerostin values at various intervals

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Table 4: Correlation between clinical and biochemical parameters

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There was no correlation between clinical parameters PPD, CAL, and sclerostin after SPT (r = −0.258 and 0.93, respectively). Even though the sclerostin levels decreased significantly after SPT (P < 0.001), there is no correlation with the clinical signs because could be more time intervals required after SPT to show the correlation [Table 4].

  Discussion Top

PD is a chronic inflammatory disease if left untreated, continues to aggravate bone loss which eventually leads to mobility and tooth loss. Prior identification of course of disease serves as a source for successful outcome of treatment. Advantages of traditional basic examination and using basic tools are their effort less of use, cost-effectiveness, and that they are comparatively noninvasive but they have their limitations. With basic instrumentation and examination, will know of the disease history only but not the present disease status.

Advances in biomarkers research quantify the objective measures like initial inflammatory changes, which is an early sign of collagen degradation and bone turnover. Advances in biomarker research will be useful for prior identification of risk and limit the further progression of oral diseases of the periodontium.[9],[10] Bone remodeling is a constant phenomenon and therefore synthesis and degradation of bone happen together.

Biological markers of bone are a useful, noninvasive, and popular cost-effective tool for studying bone metabolism in population studies and are gradually gaining ground in clinical practice. Their main use, however, is to observe the response to treatment. The continued advancement of new markers of bone turnover will improve our knowledge of PD pathophysiology.[11] Sclerostin, a secreted glycoprotein product 1a of the SOST gene, that binds to proteins 5 and 6 linked to lipoprotein receptors. Density on the cell membrane of osteoblasts inhibits the Wnt signaling pathway. Its expression, which diminishes the osteoblast and osteocyte activity, leads to lopsided osteoblastogenesis. These results are more toward the bone resorption due to obstructing Wnt and also the bone morphogenetic protein signaling.[12] Wnt molecules connect to the receptors of the Frizzled family and low-density lipoprotein receptor-related protein 5 or 6 (LRP5/6) co-receptors. Because LRP5 is a key gene in functioning osteoblast, sclerostin emerged rapidly as an effective inhibitor of the Wnt signaling pathway in osteoblasts. Indeed, sclerostin inhibits osteoblasts' differentiation and diminishes bone formation.

The anti-anabolic action of sclerostin is accomplished by stimulating osteoclast differentiation in a Receptor activator of nuclear factor kappa-Β ligand (RANKL)-dependent mode and therefore has an unintentional action in bone resorption. Interestingly, osteocytes can directly generate a process of osteolysis because sclerostin controls the acidification of the extracellular matrix. Finally, sclerostin negatively regulates the mineralization process expressly or by implication by regulating Fibroblast growth factor-23 (FGF23), another molecule induced by osteocytes and associated with mineralization.[12] Through out life, bone remodeling and modeling are two significant events that influence the skeletal bones. The continuous renewal of the bone remodeling process is by virtue of osteoblasts, formative cells, and osteoclasts, resorptive which are strongly united within a basic multicellular unit. During osteocyte mineralization, sclerostin may negatively act on osteoblasts to compensate for resorption.

In addition, sclerostin keeps bone lining cells in an inactive state, thereby inhibiting osteoclast activation and formation of bone.[13] As far as we know, this is the first study to compare NSPT and SPT in individuals with CP. In this present study, there was a statically noteworthy diminution in clinical parameters such as PPD, CAL, and sclerostin after NSPT. Decreased PPD from 7.22 ± 0.58 mm to 6.90 ± 0.58 mm 4 weeks after NSPT. CAL gained from 5.43 ± 0.45 mm to 5.06 ± 0.52 mm.

Serum sclerostin levels were decreased from 762.91 ± 426.50 pg/ml to 246.91 ± 222.49 pg/ml (pg-picogram) after NSPT. The current study results were as per the work done by Napimoga et al.[3] utilized gingival crevicular fluid to estimate sclerostin in PD patients. Results exhibited that sclerostin was considerably greater in patients with PD than in healthy people (P < 0.025) and reduced after treatment (P < 0.05).

In their study clinical parameters, PPD was significantly (P ≤ 0.05) lessened after treatment from 4.91 mm to 2.46 mm. CAL also significantly (P ≤ 0.05) gained from 5.63 mm to 3.48 mm.[14] In this study, we similarly evaluated clinical parameters and sclerostin levels after 6 weeks of SPD, decreased PPD levels from 6.90 ± 0.58 mm (after NSPT) to 2.95 ± 0.46 mm 6 weeks after SPT. CAL gained from 5.06 ± 0.52 mm (after NSPT) to 1.25 ± 0.24 mm. Serum sclerostin was reduced from 246.91 ± 222.49 pg/ml (after NSPT) to 74.14 ± 123.11 pg/ml after SPT. Napimoga et al. evaluated sclerostin in PD and found higher circulating sclerostin in the PD than in without PD group.[3] In our current study, the results showed that sclerostin concentration was higher in PD at the beginning which is linked with disease severity during the study period. These results confirm the hypothesis that sclerostin concentration is related to the intensity of CP and decreases with the treatment. Additional research is required to validate this proposed hypothesis.

  Conclusion Top

This study revealed the fact that disease severity was positively related to intensified concentrations of serum sclerostin, which was authenticated by biochemical analysis and clinical correlations. Downregulated serum sclerostin levels showed a strong correlation with a decrease in clinical signs evaluated after the NSPT and SPT. Hence, quantitative assessment of the sclerostin levels can be contemplated as an early disease marker and strong diagnostic tool for assessing active PD. Further longitudinal studies in a larger population and follow-up are required to quantitatively assess the association between serum sclerostin and grimness of the PD.

Ethical clearance

PMVIDS&RC/IEC/PERI/DN/0112-16, REF NO: 0010.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Hienz SA, Paliwal S, Ivanovski S. Mechanisms of bone resorption in periodontitis. J Immunol Res 2015;2015:615486.  Back to cited text no. 1
Taubman MA, Valverde P, Han X, Kawai T. Immune response: The key to bone resorption in periodontal disease. J Periodontol 2005;76:2033-41.  Back to cited text no. 2
Napimoga MH, Nametala C, da Silva FL, Miranda TS, Bossonaro JP, Demasi AP, et al. Involvement of the Wnt-β-catenin signalling antagonists, sclerostin and dickkopf-related protein 1, in chronic periodontitis. J Clin Periodontol 2014;41:550-7.  Back to cited text no. 3
Chatzopoulos GS, Mansky KC, Lunos S, Costalonga M, Wolff LF. Sclerostin and WNT-5a gingival protein levels in chronic periodontitis and health. J Periodontal Res 2019;54:555-65.  Back to cited text no. 4
Samiei M, Janjić K, Cvikl B, Moritz A, Agis H. The role of sclerostin and dickkopf-1 in oral tissues-A review from the perspective of the dental disciplines. F1000Res 2019;8:128.  Back to cited text no. 5
Weivoda MM, Youssef SJ, Oursler MJ. Sclerostin expression and functions beyond the osteocyte. Bone 2017;96:45-50.  Back to cited text no. 6
Shazam H, Shaikh F, Hussain Z. Bone turnover markers in chronic periodontitis: A literature review. Cureus 2020;12:e6699.  Back to cited text no. 7
Caton JG, Armitage G, Berglundh T, Chapple ILC, Jepsen S, Kornman KS, et al. A new classification scheme for periodontal and peri-implant diseases and conditions-Introduction and key changes from the 1999 classification. J Clin Periodontol 2018;45 Suppl 20:S1-8.  Back to cited text no. 8
He W, You M, Wan W, Xu F, Li F, Li A. Point-of-care periodontitis testing: Biomarkers, current technologies, and perspectives. Trends Biotechnol 2018;36:1127-44.  Back to cited text no. 9
Rakic M, Pejcic N, Perunovic N, Vojvodic D. A Roadmap towards Precision Periodontics. Medicina (Kaunas) 2021;57:233.  Back to cited text no. 10
Ram VS, Parthiban, Sudhakar U, Mithradas N, Prabhakar R. Bonebiomarkers in periodontal disease: A review article. J Clin Diagn Res 2015;9:E07-10.  Back to cited text no. 11
Koide M, Yamashita T, Murakami K, Uehara S, Nakamura K, Nakamura M, et al. Sclerostin expression in trabecular bone is downregulated by osteoclasts. Sci Rep 2020;10:13751.  Back to cited text no. 12
Moester MJ, Papapoulos SE, Löwik CW, van Bezooijen RL. Sclerostin: Current knowledge and future perspectives. Calcif Tissue Int 2010;87:99-107.  Back to cited text no. 13
Balli U, Aydogdu A, Dede FO, Turer CC, Guven B. Gingival crevicular fluid levels of sclerostin, osteoprotegerin, and receptor activator of nuclear factor-κB ligand in periodontitis. J Periodontol 2015;86:1396-404.  Back to cited text no. 14


  [Figure 1]

  [Table 1], [Table 2], [Table 3], [Table 4]


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