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Updated: Jan 3, 2026

Modeling Paracrine Noncanonical Wnt Signaling In Vitro
Published on: December 10, 2021
WNT signalling pathway in oral lesions
1Department of Oral Biology, University of Health Sciences, Lahore.
Abstract:
Wingless-Integrated/Beta-catenin (WNT/-catenin) signalling pathway is one of the principal intercellular signalling pathways in humans. It plays an intrinsic role in the cellular proliferation, differentiation and regeneration along with many other cellular functions. Epigenetic deoxyribonucleic acid methylations and silencing of WNT signalling pathway genes have a significant role in malignant transformation of oral lesions such as oral submucous fibrosis, oral leukoplakia, oral lichen planus and erythroplakia. The increase in WNT inhibitory proteins along with inflammatory factors cause bone loss in periapical lesions, such as chronic apical periodontitis. This review discusses the molecular genetics of potentially malignant oral lesions, sheds light on our understanding of WNT/-catenin signalling in bone loss pertaining to periapical lesions, and alteration of this pathway for therapeutic benefits.
Insights
The Wingless-Integrated/Beta-catenin (WNT/β-catenin) pathway is crucial for cell functions. Aberrations in this pathway contribute to oral cancers and bone loss in periapical lesions, suggesting therapeutic potential.
Area of Science:
- Molecular Biology
- Oral Pathology
- Regenerative Medicine
Background:
- The Wingless-Integrated/Beta-catenin (WNT/β-catenin) signalling pathway regulates fundamental cellular processes like proliferation and differentiation.
- Dysregulation of WNT/β-catenin signalling, through epigenetic DNA methylation and gene silencing, is implicated in oral potentially malignant disorders.
- Increased WNT inhibitory proteins and inflammation contribute to bone loss in periapical lesions, such as chronic apical periodontitis.
Purpose of the Study:
- To review the molecular genetics of potentially malignant oral lesions.
- To elucidate the role of WNT/β-catenin signalling in bone loss associated with periapical lesions.
- To explore therapeutic strategies targeting the WNT/β-catenin pathway.
Main Methods:
- Literature review focusing on molecular genetics and signalling pathways.
- Analysis of studies investigating WNT/β-catenin in oral lesions and bone metabolism.
- Synthesis of current understanding and potential therapeutic interventions.
Main Results:
- Epigenetic alterations in WNT pathway genes are linked to oral carcinogenesis.
- WNT signalling modulation by inhibitory proteins and inflammation drives bone resorption in periapical disease.
- The WNT/β-catenin pathway presents a potential target for treating oral lesions and bone loss.
Conclusions:
- WNT/β-catenin signalling is a key player in oral health and disease.
- Understanding pathway alterations offers insights into oral cancer development and periapical bone destruction.
- Targeting WNT/β-catenin signalling holds promise for novel therapeutic approaches in dentistry.
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