Fibroblast growth factor-21 may be a potential novel drug for preventing the development of traumatic TMJ bony ankylosis

Trauma is the leading cause of temporomandibular joint (TMJ) bony ankylosis. The treatment of the condition poses a significant challenge because of the high incidence of recurrence. We previously proposed a new view that the development of traumatic TMJ bony ankylosis may be a course similar to hypertrophic nonunion, and the ensuing animal experiments preliminarily verified this view through histological analysis and molecular biology examination. In view of the similarity between bone healing and bony ankylosis, and the importance of recruitment and differentiation of mesenchymal stem cells (MSCs) during the course of bone healing, it is reasonable to select MSCs as the breakthrough point for prevention of bony ankylosis. Recent studies reveal that fibroblast growth factor 21 (FGF21), a key mediator of peroxisome proliferator-activated receptor-γ (PPARγ), can promote adipocyte differentiation, inhibit osteoblast differentiation of MSCs and stimulate osteoclast activity by activation of PPARγ. Therefore, we hypothesize that local FGF21 injection may prohibit the onset of traumatic TMJ bony ankylosis through formation of a fat pad separating the condyle from the glenoid fossa, inhibition of new bone formation and promotion of bone resorption in the joint space, which thus may be a potential novel treatment for TMJ bony ankylosis.