One-stage revision anatomic anterior cruciate ligament reconstruction with rectangular tunnel technique

We developed the anatomic rectangular tunnel anterior cruciate ligament reconstruction (ART ACLR) with a bone–patellar tendon–bone graft to mimic fibre arrangement inside the native ACL via tunnels with smaller apertures. With a 10-mm-wide graft, the cross-sectional area of the tunnels of 50 mm2 in ART ACLR is less than that of 79 mm2 in a 10-mm round tunnel one. Because tunnel encroachment would be less of a problem, the ART ACLR technique could be most frequently applied to patients after a failed primary ACLR. In this instructional lecture, the indication and technical considerations for ART ACLR as one-stage revision ACLR are described

Excursion of bone-patella tendon-bone grafts during the flexion–extension movement in anterior cruciate ligament reconstruction: Comparison between isometric and anatomic reconstruction techniques

Background/objective: The purpose of this study was to elucidate the biomechanical differences between anterior cruciate ligament (ACL) grafts reconstructed by isometric and anatomic reconstruction techniques, based on their length changes. Methods: One hundred and thirty-three knees with primary ACL reconstruction using the bone-patellar tendon-bone (BTB) graft were retrospectively identified. Twenty-two knees and 111 knees underwent isometric round tunnel (IRT) ACL reconstruction and anatomic rectangular tunnel (ART) ACL reconstruction, respectively. Results: After femoral-side fixation of the graft in the surgery, the length change of the graft from 120° flexion to full extension was measured by using an isometric positioner at the tibial side. Both reconstructive techniques showed little length change from 120° to ∼20° of flexion, followed by elongation of the graft, until full extension. The amount of length change of the grafts was 1.0 ± 0.7 mm with the IRT technique, and 3.4 ± 0.9 mm with the ART technique. These findings were significantly different, based on the Mann–Whitney U test (p < 0.001). Conclusion: The native ACL has an intrinsic length change of 3–6 mm, and therefore the ART technique may more closely replicate the biomechanical function of the native ACL

Vibration acceleration promotes endochondral formation during fracture healing through cellular chondrogenic differentiation.

Vibration acceleration through whole body vibration has been reported to promote fracture healing. However, the mechanism responsible for this effect remains unclear. Purpose of this study was to determine whether vibration acceleration directly affects cells around the fracture site and promotes endochondral ossification. Four-week-old female Wistar Hannover rats were divided into two groups (vibration [V group] and control [C group]). The eighth ribs on both sides were cut vertically using scissors. From postoperative day 3 to 11, vibration acceleration using Power Plate® (30 Hz, low amplitude [30-Low], 10 min/day) was applied in the V group. Mature calluses appeared earlier in the V group than in the C group by histological analysis. The GAG content in the fracture callus on day 6 was significantly higher in the V group than in the C group. The mRNA expressions of SOX-9, aggrecan, and Col-II in the fracture callus on day 6 and Col-X on day 9 were significantly higher in the V group than in the C group. For in vitro analysis, four different conditions of vibration acceleration (30 or 50 Hz with low or high amplitude [30-Low, 30-High, 50-Low, and 50-High], 10 min/day) were applied to a prechondrogenic cell (ATDC5) and an undifferentiated cell (C3H10T1/2). There was no significant difference in cell proliferation between the control and any of the four vibration conditions for both cell lines. For both cell lines, alcian blue staining was greater under 30-Low and 50-Low conditions than under control as well as 30-High and 50-High conditions on days 7 and 14. Vibration acceleration under 30-L condition upregulated chondrogenic gene expressions of SOX-9, aggrecan, Col-II, and Col-X. Low-amplitude vibration acceleration can promote endochondral ossification in the fracture healing in vivo and chondrogenic differentiation in vitro

Vibration acceleration enhances proliferation, migration, and maturation of C2C12 cells and promotes regeneration of muscle injury in male rats

Abstract Vibration acceleration (VA) using a whole‐body vibration device is beneficial for skeletal muscles. However, its effect at the cellular level remains unclear. We aimed to investigate the effects of VA on muscles in vitro and in vivo using the C2C12 mouse myoblast cell line and cardiotoxin‐induced injury in male rat soleus muscles. Cell proliferation was evaluated using the WST/CCK‐8 assay and proportion of Ki‐67 positive cells. Cell migration was assessed using wound‐healing assay. Cell differentiation was examined by the maturation index in immunostained cultured myotubes and real‐time polymerase chain reaction. Regeneration of soleus muscle in rats was assessed by recruitment of satellite cells, cross‐sectional area of regenerated muscle fibers, number of centrally nucleated fibers, and conversion of regenerated muscle from fast‐ to slow‐twitch. VA at 30 Hz with low amplitude for 10 min promoted C2C12 cell proliferation, migration, and myotube maturation, without promoting expression of genes related to differentiation. VA significantly increased Pax7‐stained satellite cells and centrally nucleated fibers in injured soleus muscles on Day 7 and promoted conversion of fast‐ to slow‐twitch muscle fibers with an increase in the mean cross‐sectional area of regenerated muscle fibers on Day 14. VA enhanced the proliferation, migration, and maturation of C2C12 myoblasts and regeneration of injured rat muscles

Identification of MMP1 as a novel risk factor for intracranial aneurysms in ADPKD using iPSC models.

Cardiovascular complications are the leading cause of death in autosomal dominant polycystic kidney disease (ADPKD), and intracranial aneurysm (ICA) causing subarachnoid hemorrhage is among the most serious complications. The diagnostic and therapeutic strategies for ICAs in ADPKD have not been fully established. We here generated induced pluripotent stem cells (iPSCs) from seven ADPKD patients, including four with ICAs. The vascular cells differentiated from ADPKD-iPSCs showed altered Ca[2+] entry and gene expression profiles compared with those of iPSCs from non-ADPKD subjects. We found that the expression level of a metalloenzyme gene, matrix metalloproteinase (MMP) 1, was specifically elevated in iPSC-derived endothelia from ADPKD patients with ICAs. Furthermore, we confirmed the correlation between the serum MMP1 levels and the development of ICAs in 354 ADPKD patients, indicating that high serum MMP1 levels may be a novel risk factor. These results suggest that cellular disease models with ADPKD-specific iPSCs can be used to study the disease mechanisms and to identify novel disease-related molecules or risk factors