Relationship between asporin expression and the pathological progression of murine temporomandibular joint osteoarthritis after partial discectomy.

OBJECTIVES

Temporomandibular joint osteoarthritis (TMJ-OA) involves cartilage degeneration and bone changes; however, the mechanisms of onset and progression are unclear. Recently, it has been shown that asporin, an extracellular matrix protein, increases as knee osteoarthritis progresses and suppresses the TGF-β pathway. However, the asporin levels in later stages of TMJ-OA, when cartilage destruction occurs, are not known. In this study, we examined the relationship between asporin and the pathological progression of TMJ-OA.

METHODS

We constructed TMJ-OA models in 12-week-old male C57BL/6J mice by partial discectomy and evaluated these at 3 days and 2, 4, 8, 12, and 16 weeks postoperatively. Cartilage degeneration was evaluated using a modified Mankin scoring system after safranin O staining. The mRNA and protein expression of asporin, Tgfb1, and Smad2/3 were compared between experimental and sham-operated control mice using reverse-transcription polymerase chain reaction and immunohistochemical staining, respectively.

RESULTS

Safranin O staining intensity increased at 8 weeks postoperatively, and partial cartilage loss was observed at 16 weeks postoperatively. The modified Mankin score was higher in the experimental group than in the control group, and peaked at 16 weeks postoperatively. Asporin mRNA and protein expression was higher in the experimental group at all time points. Smad2/3 mRNA expression was higher, whereas p-SMAD2/3 levels were lower in the experimental group. TGF-β levels were higher in the experimental group.

CONCLUSION

Asporin mRNA and protein levels are high in the early and late stages of TMJ-OA. Asporin may be a potential biomarker of TMJ-OA and a potential therapeutic target.