Cortical Button Fixation for Proximal Tibiofibular Instability: A Technical Report.

Instability of the proximal tibiofibular joint (PTFJ) is a rare injury pattern than can affect high-demand athletes involved in twisting or pivoting movements on a flexed knee. Instability may produce painful subluxations during provocative activity and occasional neuritic symptoms from tethering of the common peroneal nerve at the fibular neck. There are several reports of reconstruction for symptomatic PTFJ instability; however, no optimal treatment has been elucidated in the literature. Use of a cortical button suspensory device for fixation of the PTFJ offers the advantage of stabilizing the joint without need for free graft harvest or rigid screw fixation. The present technical report illustrates the operative technique and the advantages, disadvantages, pearls, and pitfalls associated with this operation.

A Staged Arthroscopic Approach to Fixation of Unstable Osteochondritis Dissecans in the Medial Femoral Condyle of the Knee Using Nonabsorbable Fixation Screws.

Osteochondritis dissecans is a focal lesion of articular cartilage that can result in fragment instability with progression of early osteoarthritis. Regarding the knee joint, salvage of an unstable lesion can be achieved using arthroscopic-assisted reduction and fixation via a 2-stage process. The first involves arthroscopic fixation of the fragment using nonbioabsorbable screws, whereas the second stage performed 12 weeks later involves removal of the screws and confirmation of successful healing of the lesion. Previous studies have demonstrated excellent outcomes in patients undergoing fixation for unstable chondral lesions not amenable to conservative treatment. A critical component of successful treatment is understanding the importance of hardware placement and technique. The purpose of the Technical Note is to describe a method performing this 2-stage arthroscopic repair of an unstable chondral lesion located on the medial femoral condyle of the knee.

Adipocyte hypoxia increases hepatocyte hepcidin expression.

Hepcidin plays a key role in regulating iron metabolism by blocking iron efflux from macrophages and enterocytes. Hepcidin is synthesized primarily in the liver, and its expression is increased by iron overload and inflammation. Obesity is associated with chronic inflammation as well as poor iron status. Central obesity causes adipocyte hypoxia resulting in chronic inflammation. Therefore, the objective of the present study was to determine if adipocyte hypoxia and associated inflammation signal hepatocyte hepcidin expression. The effect of adipocyte hypoxia on hepcidin expression was modeled using a 3T3-L1 adipocyte/Huh7 hepatocyte co-culture model. Adipocytes were cultured at either standard conditions (19% O2) or hypoxic conditions (1% O2). Compared to standard conditions, hypoxic 3T3-L1 cells had significantly higher IL-6 and leptin expression. Treatment of Huh7 cells with media from hypoxic or LPS-treated 3T3-L1 adipocytes significantly increased hepcidin promoter activity and mRNA compared to cells treated with normoxic 3T3-L1 media or control media. When the hepcidin STAT3 binding site was mutated, promoter activation by hypoxic media was abrogated. These data suggest that adipocyte hypoxia (a feature of central obesity) may increase hepcidin expression and plays a role in the association between obesity and poor iron status.