Transition from fibrous to bony ankylosis of the temporomandibular joint: A narrative literature review.

OBJECTIVE

To analyse the transition from fibrous to bony ankylosis of the temporomandibular joint (TMJ) by considering both etiological factors and underlying molecular mechanisms.

MATERIAL AND

METHODS

The search was conducted using the keywords "Temporomandibular Joint", "Ankylosis", "Fibrous", "Bony" or "Osseous", and "Pathogenesis" in the PubMed (MEDLINE) and Wiley Online Library databases. Relevant full-text articles in English published between 2000 and 2025 were included in this review.

RESULTS

The literature review revealed that the progression of fibrous TMJ ankylosis into the osseous form is mainly determined by prolonged inflammation, mechanical damage, inappropriate treatment, and ineffective postoperative rehabilitation. According to various studies, molecular mediators such as hypoxia-inducible factor 1-alpha (HIF-1α), bone morphogenetic proteins (BMP-2, BMP-7), vascular endothelial growth factor (VEGF), and transforming growth factor beta (TGF-β) act synergistically by promoting angiogenesis and endochondral ossification, thereby stimulating new bone formation within the joint. Moreover, the SMAD signaling pathway plays a central role in fibroblast-to-osteoblast differentiation, contributing to ossification in the ankylosed area.

CONCLUSIONS

The transition of fibrous TMJ ankylosis into its osseous form is complex and multifactorial process determined by inflammation, growth factors, mechanical stress, and hypoxia. To better understand the essence of this transformation, further studies are required to elucidate the molecular mechanisms underlying this process.