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CompletedNCT03639636itsmcpUpdated Aug 21, 2018

is the Sclerostin Marker of Chronic Periodontitis

An interventional study of non surgical and surgical periodontal therapy in Periodontitis, sponsored by Panineeya Mahavidyalaya Institute of Dental Sciences & Research Centre. Completed at 1 site in India. Open to participants aged 30 Years to 50 Years. Per ClinicalTrials.gov, last updated 2018-08-21.

Sponsored by Panineeya Mahavidyalaya Institute of Dental Sciences & Research Centre · Not applicable, Interventional, and Screening

From the registry’s dates

  • Registered 1 year 2 months after the study started (first participant enrolled Jun 2017, registered Aug 2018).
Phase
Not applicable
Study type
Interventional
Enrollment
30
Ages
30 Years to 50 Years
Sex
All
01

Study summary

Reviewed literature suggests that sclerostin will inhibit the bone formation and ultimately leads to chronic periodontitis. Estimation of Sclerostin levels in the serum of periodontitis patients before and after intervention could explore the effectiveness of therapy and also give a more detailed insight into its diagnostic and prognostic potential as a biomarker of periodontal disease.

Read the detailed description

Advances during the last decade provided relevant information on the regulation of Sost/sclerostin and its mechanism(s) of action. Several stimuli have been reported to regulate Sost/Sclerostin expression, however how these factors interplay to regulate the expression of this gene in a spatiotemporal manner is unknown. Animal studies demonstrate that sclerostin is key for skeletal homeostasis, and required for the bone anabolic response to mechanical loading although appears dispensable for PTH-induced bone gain. The knowledge provided by preclinical investigations resulted in clinical trials based on the neutralization of sclerostin activity as a novel osteoanabolic therapeutic approach. It is now clear that sclerostin is capable of uncoupling bone formation and bone resorption, by inhibiting osteoblast function while stimulating osteoclast function, as the bone gain achieved by pharmacologic inhibition of sclerostin results from stimulation of osteoblast activity and inhibition of bone resorption. Furthermore, the recent observations show that activation of βcatenin in osteocytes increases bone resorption and Rankl production in a sclerostin-dependent manner. Anti-sclerostin therapy has shown beneficial skeletal outcomes in osteoporotic patients, however more recent evidence shows that the anabolic effects of this therapy attenuate with time and that after discontinuation BMD returns to pretreatment levels over time. The new evidence showing increased levels of Sost/sclerostin (and Dkk1) after activation of Wnt-βcatenin signaling suggest that sclerostin (and Dkk1) act as a negative feedback limiting bone formation stimulated by this pathway.

In this study is there any alterations in sclerostin levels in serum response to periodontal therapy was checked. Periodontal therapy alters the inflammation pathway is a proven fact.

02

Conditions studied

  • Periodontitis

Keywords

  • periodontitis
  • sclerostin
  • periodontal surgery
  • scaling and root planing
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In context

Periodontitis

1,635 studies on the registry are indexed under Periodontitis; 327 are open to participants now.

This study's enrollment of 30 is below the median of 45 across 1,191 interventional studies indexed under Periodontitis.

Browse Periodontitis studies →

Lead sponsor

Panineeya Mahavidyalaya Institute of Dental Sciences & Research Centre is the lead sponsor of 25 studies on the registry; none are open to participants now.

Counted across the registry records on this site, refreshed daily.

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Who can participate

Ages eligible
30 Years to 50 Years
Sexes eligible
All
Accepts healthy volunteers
No

Eligibility criteria

Inclusion Criteria:• Systemically healthy individuals with more than 50% remaining natural teeth

  • All the patients who are diagnosed as having generalized chronic periodontitis based on the American Academy of Periodontology (AAP) classification.
  • Probing Pocket Depth (PPD)/ Clinical Attachment Loss(CAL) ≥ 5mm
  • Patients indicated for periodontal surgery

Exclusion Criteria:• The patients who have aggressive periodontitis/localized periodontitis

  • Patients having any other systemic diseases
  • Patients taking high-dose steroid therapy, radiation or immunosuppressive therapy and any other drug history.
  • Pregnant and lactating woman.
  • History of smoking within the past five years.
  • Patients who had undergone periodontal therapy in the last six months.
  • Intellectual disability
05

Study design

Phase
Not applicable
Primary purpose
Screening
Intervention model
Sequential assignment
Masking
None (open label)
Enrollment
30 participants (actual)

Study arms

  • Other
    interventional prospective study

    nonsurgical periodontal therapy(scaling and root planing) surgical therapy( flap surgery)

    Other: non surgical and surgical periodontal therapy

Interventions

  • Othernon surgical and surgical periodontal therapy

    scaling and root planing periodontal flap surgery

06

What researchers measure

Primary outcomes

  1. sclerostin level response to only scaling and root planing

    measuring serum sclerostin levels in pg/ml(Pico grams per milli liter),

    Time frame: 4 weeks

Secondary outcomes

  1. sclerostin level response to periodontal surgery

    measuring serum sclerostin levels after surgery in pg/ml(Pico grams per milli liter)

    Time frame: 6 weeks

Other outcomes

  1. periodontal parametors

    pocket probing depth,Clinical Attachment Level(CAL), both are in mm

    Time frame: 0-4-6 weeks

07

Study locations

1 site
  • Panineeya Institute of Dentalsciences and Research Center
    Hyderabad, Telangana 500060, India
08

References and documents

Publications

  • Liu M, Kurimoto P, Zhang J, Niu QT, Stolina M, Dechow PC, Feng JQ, Hesterman J, Silva MD, Ominsky MS, Richards WG, Ke H, Kostenuik PJ. Sclerostin and DKK1 Inhibition Preserves and Augments Alveolar Bone Volume and Architecture in Rats with Alveolar Bone Loss. J Dent Res. 2018 Aug;97(9):1031-1038. doi: 10.1177/0022034518766874. Epub 2018 Apr 4. PubMed 29617179 ↗
  • Chen H, Xu X, Liu M, Zhang W, Ke HZ, Qin A, Tang T, Lu E. Sclerostin antibody treatment causes greater alveolar crest height and bone mass in an ovariectomized rat model of localized periodontitis. Bone. 2015 Jul;76:141-8. doi: 10.1016/j.bone.2015.04.002. Epub 2015 Apr 11. PubMed 25868799 ↗
  • Taut AD, Jin Q, Chung JH, Galindo-Moreno P, Yi ES, Sugai JV, Ke HZ, Liu M, Giannobile WV. Sclerostin antibody stimulates bone regeneration after experimental periodontitis. J Bone Miner Res. 2013 Nov;28(11):2347-56. doi: 10.1002/jbmr.1984. PubMed 23712325 ↗
  • Balli U, Aydogdu A, Dede FO, Turer CC, Guven B. Gingival Crevicular Fluid Levels of Sclerostin, Osteoprotegerin, and Receptor Activator of Nuclear Factor-kappaB Ligand in Periodontitis. J Periodontol. 2015 Dec;86(12):1396-404. doi: 10.1902/jop.2015.150270. Epub 2015 Sep 14. PubMed 26367496 ↗

Individual participant data

Plan to share: No

09

Updates

Tracking since Sep 25, 2026
No changes since tracking began. The registry record was last updated on Aug 21, 2018, before this site started recording changes on Sep 25, 2026. Its history is on ClinicalTrials.gov ↗
10

Registry details

Key details

Study ID
NCT03639636
Lead sponsor
Panineeya Mahavidyalaya Institute of Dental Sciences & Research Centre
Responsible party
Banda Madhavi (Dr.banda madhavi, Panineeya Mahavidyalaya Institute of Dental Sciences & Research Centre) — Principal investigator
First posted
Aug 21, 2018
Start date
Jun 1, 2017
Primary completion
Dec 20, 2017
Completion
May 15, 2018
Last update
Aug 21, 2018

Study contacts

Jammula surya prasanna, mds
study director · panineeya institute of dental sciences and research center

Oversight

Data monitoring committee
Yes
FDA-regulated drug
No
FDA-regulated device
No
View the source record on ClinicalTrials.gov ↗

Not currently enrolling

This study is completed, as verified in Aug 2018. You cannot join it, but the record below documents what was studied.

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