RESUMEN
Posterior sternoclavicular joint (SCJ) dislocations are rare but serious injuries. We report our experience with a patient with hemophilia who experienced posterior dislocation of the SCJ and was treated with an open repair technique. A 17-year-old man with hemophilia had a posterior dislocation of the SCJ and the proximal clavicle was an approximation to the brachiocephalic artery. Cardiovascular surgeons and pediatricians were consulted on the day of injury. The patient underwent open reduction of the SCJ and the SCJ was stabilized with strong sutures using a tension-band technique. The patient returned to playing rugby three months after surgery. Posterior dislocation of the SCJ has a risk of vascular injury. Although our patient required more attention because of his hemophilia, the surgery was successful through collaboration with other departments. Reconstruction of the SCJ using a tension-band technique with strong sutures was useful and allowed early return to sports.
RESUMEN
Aging is one of the major pathologic factors associated with osteoarthritis (OA). Recently, numerous reports have demonstrated the impact of sirtuin-1 (Sirt1), which is the NAD-dependent deacetylase, on human aging. It has been demonstrated that Sirt1 induces osteogenic and chondrogenic differentiation of mesenchymal stem cells. However, the role of Sirt1 in the OA chondrocytes still remains unknown. We postulated that Sirt1 regulates a hypertrophic chondrocyte lineage and degeneration of articular cartilage through the activation of osteogenic transcriptional activator Runx2 and matrix metalloproteinase (MMP)-13 in OA chondrocytes. To verify whether sirtuin-1 (Sirt1) regulates chondrocyte activity in OA, we studied expressions of Sirt1, Runx2 and production of MMP-13, and their associations in human OA chondrocytes. The expression of Sirt1 was ubiquitously observed in osteoarthritic chondrocytes; in contrast, Runx2 expressed in the osteophyte region in patients with OA and OA model mice. OA relating catabolic factor IL-1ßincreased the expression of Runx2 in OA chondrocytes. OA chondrocytes, which were pretreated with Sirt1 inhibitor, inhibited the IL-1ß-induced expression of Runx2 compared to the control. Since the Runx2 is a promotor of MMP-13 expression, Sirt1 inactivation may inhibit the Runx2 expression and the resultant down-regulation of MMP-13 production in chondrocytes. Our findings suggest thatSirt1 may regulate the expression of Runx2, which is the osteogenic transcription factor, and the production of MMP-13 from chondrocytes in OA. Since Sirt1 activity is known to be affected by several stresses, including inflammation and oxidative stress, as well as aging, SIRT may be involved in the development of OA.