Prediction of fracture lines of the calcaneus using a three-dimensional finite element model.

The various lines of calcaneal fractures indicate their complex nature and make their treatment challenging. There is still much debate regarding the position and direction of these fracture lines, even for the primary fracture line. The computed tomography-based finite element model is known to provide accurate predictions of fracture loads and virtual fracture locations for the femur and distal radius. This study aimed to establish how to predict the calcaneus fracture lines using the computed tomography-based finite element model for patients with contralateral calcaneal fractures and to investigate whether the predicted lines were similar to those of the fractured calcaneus. The calcanei of five men and two women aged 44-77 years (average age, 60 years) with contralateral calcaneal fractures were analyzed. To assess the precision of the predicted fracture lines of the contralateral calcanei, they were compared with the fracture locations found by three-dimensional models of the calcanei. The fracture lines of the finite element model simulated the actual fracture lines and diagnosed joint depression types of fractures (five cases) and tongue types (two cases), but only under certain conditions for each case. This trial simulated calcaneal fractures using a patient-specific computed tomography-based nonlinear finite element model. Therefore, we suggest that it is possible to reproduce calcaneal fractures using the finite element model. It was possible to predict with precision the actual calcaneal fracture for each patient and to reproduce fracture conditions. Therefore, this method is valuable because it can provide an understanding of the pathomechanism of calcaneal fractures. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 37:483-489, 2019.

Plate presetting arthroscopic reduction technique for the distal radius fractures.

Wrist arthroscopy for the distal radius fractures is an effective adjunct to evaluate the reduction of intraarticular fragments and soft tissue injuries. In recent years, volar locking plate fixation has become popular, and arthroscopic procedures for distal radius fracture reduction have become problematic because vertical traction has to be both on and off during surgery. We developed a plate presetting arthroscopic reduction technique to simplify the combination of plating and arthroscopy. The fracture was reduced, and anatomic alignment was regained under an image intensifier, and then the volar locking plate was preset. Wrist arthroscopy was introduced under vertical traction, and the intraarticular condition was assessed. If dislocations of the intraarticular fragments were residual, they were reduced arthroscopically, and soft tissue injuries were treated subsequently. Finally, the traction was removed, and the plate was securely fixed. Since May 2005, the authors have used this technique in more than 50 patients. This article will review the history, indications, contraindications, technique, rehabilitation, and complications for the plate presetting arthroscopic reduction technique for distal radius fractures.

Age-dependent changes in the mechanical properties of tail tendons in TGF-beta inducible early gene-1 knockout mice.

The purpose of this study is to investigate age-dependent changes in the architecture and mechanical properties of tendon in TGF-beta inducible early gene-1 (TIEG) knockout mice. Wild-type and TIEG knockout mice, aged 1, 2, and 15 mo, were used. The mechanical properties of tail tendons isolated from these mice were determined using uniaxial tensile ramp (0.05 mm/s) and relaxation (5 mm/s) tests, with a strain of 10%. Mechanical parameters (Young's modulus from the ramp test; fast and static stresses from the relaxation test) were measured and recorded. The structure of the tail tendon fascicle was characterized by transmission electron microscopy. The results of the mechanical testing revealed no significant difference between the knockout and wild-type groups at 1 or 15 mo of age. However, the fascicles of the knockout mice at 3 mo of age exhibited decreased fast and static stresses compared with those of the wild-type mice. Electron microscopy revealed an increase in fibril size in the knockout mouse tendons relative to wild-type controls at 1 and 3 mo of age. These data indicate an important role for TIEG in tendon microarchitecture and strength in adult mice.

Effect of TGF-beta inducible early gene deficiency on flexor tendon healing.

The role of transforming growth factor beta (TGF-beta) in tendon healing is still not clearly established. TGF-beta affects gene expression primarily through the activation of the Smad signaling pathway. The first step in the Smad pathway is the expression of TGF-beta inducible early gene (TIEG). Recently, a TIEG knockout mouse has been developed. The purpose of this study was to examine the healing potential of flexor tendons in mice lacking the TIEG gene, and to further examine what role the TIEG pathway plays in flexor tendon repair. Twenty-two mice, consisting of 11 normal wild-type mice and 11 TIEG knockout mice, were euthanized at 8 to 12 weeks of age. The second through fifth FDL tendons of both hind feet were transected and repaired in zone 2. The repaired tendons were removed from the mice and placed into tissue culture. Tendons were then examined at days 3, 7, 14, 21, and 42 after surgery. Hematoxylin and eosin (HE) staining and immunohistochemical staining for TGF-beta, collagen type I, and collagen type III were performed. Reverse transcriptase polymerase chain reaction (RT-PCR) was performed to examine expression of TGF-beta1, beta2, beta3, and collagen type I and III. At 42 days after surgery, HE staining showed coaptation of lacerated tendon ends in both groups. Both groups showed healing of the lacerated tendon, but the chronologic expression pattern of TGF-beta was different between the knockout and normal tendons. TIEG deficient tendons had delayed expression of TGF-beta when compared with control tendons. The collagen mRNA expression pattern was similar with both groups, but the expression level was different, with TIEG knockout tendons having a lower expression of collagen type I mRNA (p < 0.001). TGF-beta is thought to play a major role in tendon healing. Healing of tendons in the TIEG knockout mouse suggests the possibility of tendon healing in the absence of the Smad pathway. The knockout mouse model described in the present study provides a novel means for further understanding of the tendon healing process through isolated deletion of specific growth factors.

Effect of gap size on gliding resistance after flexor tendon repair.

BACKGROUND: Gap formation is a common complication after flexor tendon repair and is associated with adhesion formation, tendon rupture, and decreased strength. The purpose of this study was to investigate the effect of gap formation on tendon gliding resistance after flexor tendon repair in a human cadaver model. METHODS: Twelve index, middle, and ring fingers from four adult human cadaveric hands were used. Gliding resistance versus excursion between the flexor digitorum profundus tendon and the A2 pulley was first measured in intact tendons. After full laceration, each tendon was repaired with the Pennington suture technique and the gliding resistance was measured again. Then, the repaired tendon (a 0-mm gap) was stretched to form a 1-mm gap, and gliding resistance was remeasured. A magnified video image was used to monitor gap size. This process was repeated to evaluate gap sizes of 2, 3, and 4 mm at the repair site. Peak gliding resistance was determined, and the peak gliding resistance was compared among the groups. RESULTS: No significant difference in peak gliding resistance was detected between repaired tendons without a gap and tendons with a 1-mm gap. Repaired tendons with a 2-mm gap could pass through the A2 pulley; however, peak gliding resistance was significantly higher than that for tendons with a 0 or a 1-mm gap (p < 0.05). When the gap reached > or =3 mm, all tendons caught at the A2 pulley edge, causing a dramatically increased peak gliding resistance. CONCLUSIONS: The presence of a 2-mm gap after flexor tendon repair significantly increased tendon peak gliding resistance (p < 0.05), while a gap of > or =3 mm further increased peak gliding resistance because of catching at the pulley edge.

Expression of growth factors in canine flexor tendon after laceration in vivo.

Growth factors, transforming growth factor beta (TGF-beta), epidermal growth factor (EGF), platelet-derived growth factor (PDGF), insulin-like growth factor (IGF), basic fibroblast growth factor (bFGF), and vascular endothelial growth factor (VEGF), are critical components of the cutaneous wound healing process. Little is known, however, about the expression of these growth factors in normal flexor tendon healing. In this study, we wished to examine which of these growth factors are present at 10 days following tendon injury in a canine flexor tendon repair model. Using immunohistochemical analysis, we found positive staining for all growth factors in both timing groups. TGF-beta was detected around the repair site and proximal to it. PDGF-AA, PDGF-BB and VEGF appeared in the whole tendon section following repair. EGF, IGF and bFGF were not seen in tenocytes but were present in inflammatory cells surrounding the repair site. These findings provide evidence that TGF-beta, EGF, PDGF-AA, PDGF-BB, IGF, bFGF and VEGF are all expressed at 10 days after tendon injury but by different cell types and in different locations. The time course of growth factor expression is an important element in wound healing, and a better understanding of where and when such factors are expressed may help in the development of methods to manipulate this expression, accelerate healing, and reduce adhesions.

Effects of cessation of immunosuppression on skeleton reconstructed by vascularized bone allograft in rats.

In the present study, we investigated the effects of cessation of immunosuppression on skeleton reconstructed by vascularized allogenic bone transplantation in a rat tibio-fibula graft model. Twelve-week-old male 25 Dark Agouti rats with the major histocompatibility antigen (MHC) RT1a were used as donors and age-matched male 25 Lewis rats with MHC RT1l were used as recipients. Among them, 20 rats were randomly allocated to 8-week cyclosporine A (CsA) followed by 8-week CsA vehicle group or continuous 16-week CsA group. The remaining 5 rats received CsA for 8 weeks followed by no further treatment for next 40 weeks (long-term observation group). In the CsA followed by vehicle group as well as the continuous CsA group, the structure of the reconstructed bones was maintained, though the transplanted bones in former group were found to be partly non-vital. The CsA followed by vehicle group had higher bone mineral density of the transplanted bones and stronger strength of the reconstructed bones than the continuous CsA group. In the long-term observation group, the structure of the reconstructed bones was still maintained and the transplanted bones were almost vital. These results suggest that long-term strong immunosuppression may not be necessary for successful reconstruction of large bone defect by vascularized bone allograft.