Background Articular fractures of the distal radius may include a small fragment from the volar margin of the lunate fossa: volar marginal fragments (VMFs); these fragments are prone to loss of fixation and avascular necrosis, and often result in wrist subluxation. We present our experience managing acute and delayed VMFs. The first is treated using a hook plate extension to a volar locking plate and the latter using a volar opening wedge osteotomy to redistribute loads on the remaining articular surface. Materials and Methods We retrospectively reviewed the records of all patients treated at our facility with a hook plate extension for a VMF and for patients treated with a volar opening wedge osteotomy. Medical charts were examined for complications and functional results. Technique A hook plate extension was used to fix the VMF when plate buttressing was insufficient. For patients who presented a collapsed and reabsorbed VMF, a volar opening wedge osteotomy was used to reorient the articular surface, restoring joint stability. Results The hook plate extension was successful in managing 19 of the 21 acute VMFs. The volar opening wedge osteotomy provided concentric reduction and improved pain and motion in all treated patients. Conclusion We demonstrated that hook plate fixation of the VMF is an effective means of fixing the acute VMF and that a volar opening wedge osteotomy can be used to salvage a distal radius fracture with a collapsed VMF.

Locked volar plating is the most common surgical procedure to address distal radius fractures. The extended flexor carpi radialis approach continues to be an excellent method for visualizing distal radius fractures and applying a volar plate. A new understanding of the anatomy allows for better visualization and reduction of the many different distal radius fracture patterns surgeons commonly see. Within the extended flexor carpi radialis approach, we describe the radial septum in further detail including the anatomy which comprises the radial septum triangle. Knowledge of this area allows for better visualization, more anatomic reductions, and fewer complications.

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Background:Acute cartilage injuries induce cell death and are associated with an increased incidence of osteoarthritis development later in life. The objective of this study was to investigate the effect of posttraumatic cyclic compressive loading on chondrocyte viability and apoptosis in porcine articular cartilage plugs.Hypothesis:Compressive loading of acutely injured cartilage can maintain chondrocyte viability by reducing apoptosis after a traumatic impact injury.Study Design:In vitro controlled laboratory study.Level of Evidence:Level 5.Methods:Each experiment compared 4 test groups: control, impact, impact with compressive loading (either 0.5 or 0.8 MPa), and no impact but compressive loading (n = 15 per group). Flat, full-thickness articular cartilage plugs were harvested from the trochlear region of porcine knees. A drop tower was utilized to introduce an impact injury. The articular plugs were subjected to two 30-minute cycles of either 0.5 or 0.8 MPa of dynamic loading. Cell viability, apoptosis, and gene expression of samples were evaluated 24 hours postimpaction.Results:Cell viability staining showed that 0.5 MPa of dynamic compressive loading increased cell viability compared with the impact group. Apoptotic analysis revealed a decrease in apoptotic expression in the group with 0.5 MPa of dynamic compressive loading compared with the impact group. Significantly higher caspase 3 and lower collagen II expressions were observed in impacted samples without compressive loading, compared with those with. Compressive loading of nonimpacted samples significantly increased collagen II and decreased caspase 3 expressions.Conclusion:In this porcine in vitro model, dynamic compressive loading at subphysiological levels immediately following impact injury decreases apoptotic expression, thereby maintaining chondrocyte viability.Clinical Relevance:Therapeutic exercises could be designed to deliver subphysiological loading to the injured cartilage, thereby minimizing injury.

Deficiency in the ligamentous restraints of the central band leads to positive ulnar variance, which could be a factor (among others) that contributes to idiopathic ulnar impaction syndrome.