is the Sclerostin Marker of Chronic Periodontitis

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Clinical Phase

NA

Total Enrollment

30 participants

Study Classification

INTERVENTIONAL

Study Start Date

2017-06-01

Study Completion Date

2018-05-15

Brief Summary

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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.

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Detailed Description

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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.

Conditions

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Periodontitis

Study Design

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Intervention Model

SEQUENTIAL

interventional prospective study

Primary Study Purpose

SCREENING

Blinding Strategy

NONE

Study Groups

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interventional prospective study

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

Group Type OTHER

non surgical and surgical periodontal therapy

Intervention Type OTHER

scaling and root planing periodontal flap surgery

Interventions

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non surgical and surgical periodontal therapy

scaling and root planing periodontal flap surgery

Intervention Type OTHER

Eligibility Criteria

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Inclusion Criteria

* 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

* 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

Minimum Eligible Age

30 Years

Maximum Eligible Age

50 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

No