Background The fixation method of syndesmotic injuries in ankle fractures remains controversial. The goal of the study was to compare radiographic and clinical outcomes between anterior inferior tibiofibular ligament (AITFL) anatomical repair with syndesmosis screw fixation in syndesmotic injuries. Methods We analyzed 62 patients who were treated with AITFL anatomical repair or syndesmosis screw fixation for syndesmotic injuries in an advanced teaching hospital between March 2016 and March 2019. Fixation was performed with AITFL anatomical repair in 30 patients (AAR group) and syndesmosis screw in 32 patients (SS group). Radiographic evaluations were the differences in mean anterior and posterior (A difference and P difference) tibiofibular distance between injured and uninjured ankle computed tomography (CT) scan at 6 months postoperatively. Clinical evaluation of patients was done using the American Orthopaedic Foot & Ankle Society (AOFAS) Ankle Hindfoot Score, the Olerud-Molander Ankle (OMA) score and visual analogue scale (VAS) score at 1, 3, 6 months and 1, 2 years postoperatively. Results The A difference and P difference on CT was no differences (1.6 ± 0.8 mm, 1.3 ± 0.7 mm vs. 1.5 ± 0.7 mm, 1.2 ± 0.7 mm) between the two groups (All of P > 0.05). The AAR group had higher mean AOFAS score (65.6 ± 5.9, 82.3 ± 4.2, 87.6 ± 5.6 vs. 61.8 ± 5.2, 79.1 ± 4.0, 83.8 ± 4.9; P = 0.008, 0.003, 0.007) and higher mean OMA score (45.7 ± 8.7, 79.2 ± 6.5, 84.1 ± 5.3 vs. 40.4 ± 7.3, 74.8 ± 6.3, 80.3 ± 5.8; P = 0.012, 0.009, 0.010)) at 1, 3 and 6 months postoperatively. The AAR group had lower mean VAS scores (2.6 ± 1.2, 1.7 ± 0.7 vs. 3.4 ± 1.2, 2.2 ± 1.1; P = 0.018, 0.038) at 1 and 3 months postoperatively. Conclusions The results of this study suggest that the AITFL anatomical repair technique could effectively improve ankle function during daily activity. Therefore, AITFL anatomical repair technique is expected to become a better fixation method for syndesmotic injuries.

Background. The microenvironment of bone defects displayed that M2 polarization of macrophagocyte could promote the osteoblast growth and benefit the wound healing. Bone scaffold transplantation is considered to be one of the most promising methods for repairing bone defects. The present research was aimed at constructing a kind of novel bone scaffold nanomaterial of MSN@IL-4 for treating bone defects responding to the wound microenvironment of bone defects and elucidating the mechanics of MSN@IL-4 treating bone defect via controlling release of IL-4, inducing M2 polarization and active factor release of macrophagocyte, and eventually relieving osteoblast injury. Methods. MSN@IL-4 was firstly fabricated and its release of IL-4 was assessed in vitro. Following, the effects of MSN@IL-4 nanocomplex on the release of active factors of macrophage were examined using Elisa assay and promoting M2 polarization of the macrophage by immunofluorescence staining. And then, the effects of active factors from macrophage supernatant induced by MSN@IL-4 on osteoblast growth were examined by CCK-8, flow cytometry, and western blot assay. Results. The release curve of IL-4 in vitro displayed that there was more than 80% release ratio for 30th day with a sustained manner in pH 5.5. Elisa assay data showed that MSN@IL-4 nanocomplex could constantly promote the release of proproliferative cytokine IL-10, SDF-1α, and BMP-2 in macrophagocyte compared to only IL-4 treatment, and immunofluorescent image showed that MSN@IL-4 could promote M2 polarization of macrophagocytes via inducing CD206 expression and suppressing CD86 expression. Osteoblast injury data showed that the supernatant from macrophagocyte treated by MSN@IL-4 could promote the osteoblast proliferation by MTT assay. Flow cytometry data showed that the supernatant from macrophagocyte treated by MSN@IL-4 could suppress the osteoblast apoptosis from 22.1% to 14.6%, and apoptosis-related protein expression data showed that the supernatant from macrophagocyte treated by MSN@IL-4 could suppress the expression of Bax, cleaved caspase 3, and cleaved caspase 8. Furthermore, the immunofluorescent image showed that the supernatant from macrophagocyte treated by MSN@IL-4 could inhibit nucleus location of p65, and western blot data showed that the supernatant from macrophagocyte treated by MSN@IL-4 could suppress the phosphorylation of IKK and induce the expression of IκB. Conclusion. MSN@IL-4 could control the sustaining release of IL-4, and it exerts the protective effect on osteoblast injury via inducing M2 polarization and proproliferative cytokine of macrophagocyte and following inhibiting the apoptosis and NF-κB pathway-associated inflammation of osteoblast.