Osteochondral Cell Fate in the Mandibular Condyle: A Shared Fate Decision Across Development, Degeneration, and Regeneration
- 1Shanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Fudan University, Shanghai 200001, China.
Abstract
The mandibular condyle is highly responsive to mechanical loading, which shapes its development and maintains osteochondral homeostasis. Understanding how loading regulates osteochondral cell fate may connect developmental mechanisms with strategies to limit mechanically driven degeneration and promote repair. In this narrative review, we integrate evidence across development, degeneration, and regeneration into a framework centred on a shared cell-fate decision: coordination between progenitor renewal, chondrocyte maturation, and endochondral bone formation. We examine the reported dual modes of parathyroid hormone-related protein (PTHrP) signalling and their interactions with Indian hedgehog (IHH) and canonical Wnt/β-catenin signalling within the broader network governing this balance. Physiological loading supports the spatial and temporal coordination of these pathways, whereas persistent abnormal loading may accelerate hypertrophic differentiation and impair progenitor replenishment, contributing to cartilage damage and aberrant osteochondral remodelling. Effective regeneration may therefore depend on restoring both a favourable mechanical environment and coordinated cell-fate regulation. Accordingly, where pathological occlusal loading contributes to degeneration, correcting the mechanical environment may merit consideration alongside biological interventions tailored to the joint’s residual repair capacity. Potential approaches include pathway modulation to support responsive endogenous cells and cell supplementation when progenitor reserves are insufficient.
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BibTeX
@article{xu2026osteochondral,
title = {{Osteochondral Cell Fate in the Mandibular Condyle: A Shared Fate Decision Across Development, Degeneration, and Regeneration}},
author = {Lingfeng Xu and Meiqing Wang},
journal = {Cells},
year = {2026},
month = oct,
doi = {10.3390/cells15201913},
url = {https://www.mdpi.com/2073-4409/15/20/1913},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Osteochondral Cell Fate in the Mandibular Condyle: A Shared Fate Decision Across Development, Degeneration, and Regeneration
AU - Lingfeng Xu
AU - Meiqing Wang
PY - 2026
DA - 2026/10/21
JO - Cells
DO - 10.3390/cells15201913
UR - https://www.mdpi.com/2073-4409/15/20/1913
AB - The mandibular condyle is highly responsive to mechanical loading, which shapes its development and maintains osteochondral homeostasis. Understanding how loading regulates osteochondral cell fate may connect developmental mechanisms with strategies to limit mechanically driven degeneration and promote repair. In this narrative review, we integrate evidence across development, degeneration, and regeneration into a framework centred on a shared cell-fate decision: coordination between progenitor renewal, chondrocyte maturation, and endochondral bone formation. We examine the reported dual modes of parathyroid hormone-related protein (PTHrP) signalling and their interactions with Indian hedgehog (IHH) and canonical Wnt/β-catenin signalling within the broader network governing this balance. Physiological loading supports the spatial and temporal coordination of these pathways, whereas persistent abnormal loading may accelerate hypertrophic differentiation and impair progenitor replenishment, contributing to cartilage damage and aberrant osteochondral remodelling. Effective regeneration may therefore depend on restoring both a favourable mechanical environment and coordinated cell-fate regulation. Accordingly, where pathological occlusal loading contributes to degeneration, correcting the mechanical environment may merit consideration alongside biological interventions tailored to the joint’s residual repair capacity. Potential approaches include pathway modulation to support responsive endogenous cells and cell supplementation when progenitor reserves are insufficient.
SN - 2073-4409
ER -