Target in Smoking-Associated Periodontal Bone Loss: A Narrative Review

Abstract

Periodontitis is a chronic inflammatory disease that destroys the tooth supporting tissues. In advanced stages, it causes alveolar bone loss and tooth loss. Smoking is a major modifiable risk factor linked to faster progression, poorer response to periodontal therapy, yet how it affects the molecular control of bone loss is unclear. Sclerostin is an osteocyte derived glycoprotein, inhibits canonical Wnt/β-catenin signaling, limits bone formation. It has been proposed as an indicator of bone remodeling activity. This narrative review examines its role as a therapeutic target in smoking associated periodontal bone loss. Methods: A narrative literature review was conducted using PubMed/MEDLINE, Scopus, and Web of Science, till March 2026. Search terms are “sclerostin,” “periodontitis,” “smoking,” “Wnt/β-catenin,” and “periodontal regeneration,” used in relevant combinations. Eligible publications included: human clinical studies, preclinical investigations, reviews addressing sclerostin in periodontal tissues or biological fluids, smoking associated periodontal changes, and potential therapeutic applications. Publications unrelated to periodontal biology or lacking relevant sclerostin findings were excluded. Results: Human studies link higher sclerostin to periodontitis , but results differ by sample type (gingival tissue, GCF, saliva, and serum) and by study population. Few human studies compared sclerostin levels in smokers and non-smokers. The findings were inconsistent because of confounding by age. In animal models, sclerostin inhibition enhanced alveolar bone regeneration; this has not been tested in patients with periodontitis. In conclusion, Sclerostin is a promising candidate biomarker, potential therapeutic target in periodontal bone loss. Its specific role in smoking-associated periodontitis and the clinical effectiveness of sclerostin targeted therapy require further investigation.