is the Sclerostin Marker of Chronic Periodontitis (itsmcp)

Panineeya Mahavidyalaya Institute of Dental Sciences & Research Centre

Status: Completed

Conditions: Periodontitis

Treatments: Other: non surgical and surgical periodontal therapy

Study type: Interventional

Funder types: Other

Identifiers

NCT03639636

madhavisclerostin

Details and patient eligibility

About

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.

Full 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.

Enrollment: 30 patients

Sex: All

Ages: 30 to 50 years old

Volunteers: No Healthy Volunteers

Inclusion and exclusion 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

Trial design

30 participants in 1 patient group

interventional prospective study

Other group

Description:

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

Treatment:

Other: non surgical and surgical periodontal therapy