Periodontitis
Conditions
Keywords
periodontitis, sclerostin, periodontal surgery, scaling and root planing
Brief 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.
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.
Interventions
OTHERnon surgical and surgical periodontal therapy
scaling and root planing periodontal flap surgery
Sponsors
Panineeya Mahavidyalaya Institute of Dental Sciences & Research Centre
Study design
Intervention model
SEQUENTIAL
Primary purpose
SCREENING
Masking
NONE
Intervention model description
interventional prospective study
Eligibility
Sex/Gender
ALL
Age
30 Years to 50 Years
Healthy volunteers
No
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
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| sclerostin level response to only scaling and root planing | 4 weeks | measuring serum sclerostin levels in pg/ml(Pico grams per milli liter), |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| sclerostin level response to periodontal surgery | 6 weeks | measuring serum sclerostin levels after surgery in pg/ml(Pico grams per milli liter) |
Other
| Measure | Time frame | Description |
|---|---|---|
| periodontal parametors | 0-4-6 weeks | pocket probing depth,Clinical Attachment Level(CAL), both are in mm |
Countries
India
Outcome results
None listed