Die-punch fragments refer to articular cartilage and subchondral bone embedded in cancellous bone as part of an intra-articular fracture. Bartoní cek type IV posterior malleolar fractures with associated die-punch fragments are rare, and the appropriate surgical approach remains unclear. We determined outcomes, and the effect of diepunch fragment size on outcomes, for 32 patients with Bartoní cek type IV posterior malleolar fractures with diepunch fragments between January 2015 and December 2017. Mean follow-up for all patients was 23.8 (range 20.0-30.0) months. At the final follow-up visit, mean ankle dorsal extension was 24.6°and plantar flexion was 40.0°; American Orthopaedic Foot and Ankle Society ankle-hindfoot score was 88.6 § 4.3; visual analog scale weightbearing pain score was 1.5 § 0.6; and Bargon traumatic arthritis score was 0.8 § 0.4. There were no severe complications. We divided patients into a small-fragment (≤3 mm) group (n = 12) and large-fragment (>3 mm) group (n = 20). The Bargon scores at final follow-up were 0.5 and 1, respectively (P=.02). There were no statistically significant differences between the 2 groups for the other outcome scores at various time intervals. The posterolateral approach with distal locking plate internal fixation for Bartoní cek type IV posterior malleolar fractures with die-punch fragments can result in excellent anatomical reduction of the collapsed articular surface and the displaced fragment from the tibial plafond, recovery of articular surface congruity, and maintenance of joint stability. Die-punch fragment size may not impact clinical and functional outcomes but may contribute to post-traumatic arthritis.

Objectives: Human bone marrow mesenchymal stem cells (BMSCs) have multi-lineage differentiation potential and have been widely researched in regenerative medicine. The purpose of this research was to explore whether Krüppel-like factor 4 (KLF4) can regulate the osteogenic differentiation of BMSCs. Methods: We transfected human BMSCs with KLF4 overexpression plasmid and si-KLF4 to study the effects of KLF4. We performed cell proliferation assay, flow cytometry and Alizarin Red staining on BMSCs. Quantitative real-time PCR and western blot was performed to determined mRNA and protein expression of osteogenic differentiation markers, KLF4, SOX2 and IGF2. Bone defect animal model was created and the adenovirus containing KLF4 overexpression or knockdown plasmid was injected. Finally, HE staining was performed on tibia to assess the new bone formation. Results: Our results showed that KLF4 promotes not only the growth of BMSCs, but also their osteogenic differentiation. Also, it mediated these effects through SOX2/IGF2 signaling pathway. In addition, KLF4 overexpression could increase the bone regeneration in in-vivo model, whereas KLF4 knockdown decreased the bone regeneration. Conclusions: KLF4 regulates BMSC’s osteogenic differentiation via SOX2/IGF2 pathway.