Abstract
The contributing factors and the origins of precursor cells in traumatic heterotopic ossification around the temporomandibular joint (THO-TMJ), which causes obvious restriction of mouth opening and maxillofacial malformation, remain unclear. In this study, our findings demonstrated that injured chondrocytes in the condylar cartilage, but not osteoblasts in the injured subchondral bone, played definite roles in the development of THO-TMJ in mice. Injured condylar chondrocytes without articular disc reserves might secrete growth factors, such as IGF1 and TGFβ2, that stimulate precursor cells, such as endothelial cells and muscle-derived cells, to differentiate into chondrocytes or osteoblasts and induce THO-TMJ. Preserved articular discs can alleviate the pressure on the injured cartilage and inhibit the development of THO-TMJ by inhibiting the secretion of these growth factors from injured chondrocytes. However, the exact molecular relationships among trauma, the injured condylar cartilage, growth factors such as TGFβ2, and pressure need to be explored in detail in the future.
Highlights
Heterotopic ossification (HO) is a kind of pathological osteogenesis that often develops in the soft tissue around large joints, such as the hip, shoulder, and temporomandibular joint (TMJ; Ranganathan et al, 2015)
The results further showed that there was obvious HO around the injured TMJ when the articular disc and half of the condylar cartilage were both removed, and the development process was proven through various imaging methods
There was no obvious HO around the injured TMJ when all of the condylar cartilage and the articular disc were removed, which further indicated that injured cartilage but not subchondral bone is an important contributing factor related to the THO-TMJ pathological process
Summary
Heterotopic ossification (HO) is a kind of pathological osteogenesis that often develops in the soft tissue around large joints, such as the hip, shoulder, and temporomandibular joint (TMJ; Ranganathan et al, 2015). Many kinds of injury around the joint, such as burns around the elbow or shoulder and even spinal cord injury, can induce the development of HO (Barfield et al, 2017). Some previous studies showed that trauma induced responses and changes in the local microenvironment, which may stimulate some precursor cells to participate in the induction of ectopic chondrogenesis or osteogenesis (Dey et al, 2017); in addition, local oxygen concentrations decrease after trauma, which could promote the expression of Hif-1α and Vegf-α, followed by induction of angiogenesis.
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