Comparative clinical outcomes and radiological images of clavicle hook plate versus Scorpion Plate® for unstable distal clavicle fractures.

BACKGROUND: Although various surgical methods are available for unstable distal clavicle fractures, consensus remains lacking on the optimal technique. Therefore, the present retrospective study aimed to compare the clavicle hook plate and Scorpion Plate® in terms of clinical outcomes and radiological findings for unstable distal clavicle fractures. METHODS: Fifty-seven patients with unstable distal clavicle fractures who underwent treatment using a clavicle hook plate (Group H; 28 patients) or Scorpion Plate® (Group S; 29 patients) were included in the present study. No patients received additional augmentation and all were followed-up for >1 year (mean follow-up, 28 months). Clinical outcomes were operation time, bleeding volume, complications, range of motion (ROM) at 6 months after surgery and final follow-up, and clinical scores (Constant-Murley score and University of California, Los Angeles (UCLA) shoulder score). Radiological outcomes assessed were coracoclavicular distance (CCD), difference in CCD between affected and non-affected sides (ΔCCD), and acromioclavicular subluxation ratio (%ACS) from plain X-rays. The χ2 test and Mann-Whitney U test were used to compare each outcome. RESULTS: Complications were seen in 3 shoulders (10.7%) in Group H. ROM was significantly worse in Group H at 6 months postoperatively, but no significant differences between groups were evident at final follow-up. Moreover, no significant differences in clinical outcomes were seen between groups. In terms of radiological results, Group H showed greater improvement in CCD and ΔCCD than Group S. Further, %ACS was significantly worse in Group S. CONCLUSIONS: The clavicle hook plate allows reconstruction of a more anatomical position than the Scorpion Plate®, but carries a greater risk of complications. Conversely, the Scorpion Plate® has a low risk of complications, but acromioclavicular subluxation remains. However, no significant differences in ROM or clinical outcomes were apparent at final follow-up.

Automated neuronal reconstruction with super-multicolour Tetbow labelling and threshold-based clustering of colour hues.

Fluorescence imaging is widely used for the mesoscopic mapping of neuronal connectivity. However, neurite reconstruction is challenging, especially when neurons are densely labelled. Here, we report a strategy for the fully automated reconstruction of densely labelled neuronal circuits. Firstly, we establish stochastic super-multicolour labelling with up to seven different fluorescent proteins using the Tetbow method. With this method, each neuron is labelled with a unique combination of fluorescent proteins, which are then imaged and separated by linear unmixing. We also establish an automated neurite reconstruction pipeline based on the quantitative analysis of multiple dyes (QDyeFinder), which identifies neurite fragments with similar colour combinations. To classify colour combinations, we develop unsupervised clustering algorithm, dCrawler, in which data points in multi-dimensional space are clustered based on a given threshold distance. Our strategy allows the reconstruction of neurites for up to hundreds of neurons at the millimetre scale without using their physical continuity.

One-shot screening: Utilization of a two-dimensional convolutional neural network for automatic detection of left ventricular hypertrophy using electrocardiograms.

BACKGROUND AND OBJECTIVE: Left ventricular hypertrophy (LVH) can impair ejection function and elevate the risk of heart failure. Therefore, early detection through screening is crucial. This study aimed to propose a novel method to enhance LVH detection using 12-lead electrocardiogram (ECG) waveforms with a two-dimensional (2D) convolutional neural network (CNN). METHODS: Utilizing 42,127 pairs of ECG-transthoracic echocardiogram data, we pre-processed raw data into single-shot images derived from each ECG lead and conducted lead selection to optimize LVH diagnosis. Our proposed one-shot screening method, implemented during pre-processing, enables the superimposition of waveform source data of any length onto a single-frame image, thereby addressing the limitations of the one-dimensional (1D) approach. We developed a deep learning model with a 2D-CNN structure and machine learning models for LVH detection. To assess our method, we also compared our results with conventional ECG criteria and those of a prior study that used a 1D-CNN approach, utilizing the same dataset from the University of Tokyo Hospital for LVH diagnosis. RESULTS: For LVH detection, the average area under the receiver operating characteristic curve (AUROC) was 0.916 for the 2D-CNN model, which was significantly higher than that obtained using logistic regression and random forest methods, as well as the two conventional ECG criteria (AUROC of 0.766, 0.790, 0.599, and 0.622, respectively). Incorporating additional metadata, such as ECG measurement data, further improved the average AUROC to 0.921. The model's performance remained stable across two different annotation criteria and demonstrated significant superiority over the performance of the 1D-CNN model used in a previous study (AUROC of 0.807). CONCLUSIONS: This study introduces a robust and computationally efficient method that outperforms 1D-CNN models utilized in previous studies for LVH detection. Our method can transform waveforms of any length into fixed-size images and leverage the selected lead of the ECG, ensuring adaptability in environments with limited computational resources. The proposed method holds promise for integration into clinical practice as a tool for early diagnosis, potentially enhancing patient outcomes by facilitating earlier treatment and management.

Cost-Effective Cas9-Mediated Targeted Sequencing of Spinocerebellar Ataxia Repeat Expansions.

Hereditary repeat diseases are caused by an abnormal expansion of short tandem repeats in the genome. Among them, spinocerebellar ataxia (SCA) is a heterogeneous disease, and currently, 16 responsible repeats are known. Genetic diagnosis is obtained by analyzing the number of repeats through separate testing of each repeat. Although simultaneous detection of candidate repeats using current massively parallel sequencing technologies has been developed to avoid complicated multiple experiments, these methods are generally expensive. This study developed a cost-effective SCA repeat panel [Flongle SCA repeat panel sequencing (FLO-SCAp)] using Cas9-mediated targeted long-read sequencing and the smallest long-read sequencing apparatus, Flongle. This panel enabled the detection of repeat copy number changes, internal repeat sequences, and DNA methylation in seven patients with different repeat expansion diseases. The median (interquartile range) values of coverage and on-target rate were 39.5 (12 to 72) and 11.6% (7.5% to 16.5%), respectively. This approach was validated by comparing repeat copy number changes measured by FLO-SCAp and short-read whole-genome sequencing. A high correlation was observed between FLO-SCAp and short-read whole-genome sequencing when the repeat length was ≤250 bp (r = 0.98; P < 0.001). Thus, FLO-SCAp represents the most cost-effective method for conducting multiplex testing of repeats and can serve as the first-line diagnostic tool for SCA.

Glucokinase Variant Proteins Are Resistant to Fasting-Induced Uridine Diphosphate Glucose-Dependent Degradation in Maturity-Onset Diabetes of the Young Type 2 Patients.

We previously reported that glucokinase undergoes ubiquitination and subsequent degradation, a process mediated by cereblon, particularly in the presence of uridine diphosphate glucose (UDP-glucose). In this context, we hereby present evidence showcasing the resilience of variant glucokinase proteins of maturity-onset diabetes of the young type 2 (MODY2) against degradation and, concomitantly, their influence on insulin secretion, both in cell lines and in the afflicted MODY2 patient. Hence, glucose-1-phodphate promotes UDP-glucose production by UDP-glucose pyrophosphorylase 2; consequently, UDP-glucose-dependent glucokinase degradation may occur during fasting. Next, we analyzed glucokinase variant proteins from MODY2 or persistent hyperinsulinemic hypoglycemia in infancy (PHHI). Among the eleven MODY2 glucokinase-mutated proteins tested, those with a lower glucose-binding affinity exhibited resistance to UDP-glucose-dependent degradation. Conversely, the glucokinaseA456V-mutated protein from PHHI had a higher glucose affinity and was sensitive to UDP-glucose-dependent degradation. Furthermore, in vitro studies involving UDP-glucose-dependent glucokinase variant proteins and insulin secretion during fasting in Japanese MODY2 patients revealed a strong correlation and a higher coefficient of determination. This suggests that UDP-glucose-dependent glucokinase degradation plays a significant role in the pathogenesis of glucose-homeostasis-related hereditary diseases, such as MODY2 and PHHI.

Microglia Are Dispensable for Developmental Dendrite Pruning of Mitral Cells in Mice.

During early development, neurons in the brain often form excess synaptic connections. Later, they strengthen some connections while eliminating others to build functional neuronal circuits. In the olfactory bulb, a mitral cell initially extends multiple dendrites to multiple glomeruli but eventually forms a single primary dendrite through the activity-dependent dendrite pruning process. Recent studies have reported that microglia facilitate synapse pruning during the circuit remodeling in some systems. It has remained unclear whether microglia are involved in the activity-dependent dendrite pruning in the developing brains. Here, we examined whether microglia are required for the developmental dendrite pruning of mitral cells in mice. To deplete microglia in the fetal brain, we treated mice with a colony-stimulating factor 1 receptor (CSF1R) inhibitor, PLX5622, from pregnancy. Microglia were reduced by >90% in mice treated with PLX5622. However, dendrite pruning of mitral cells was not significantly affected. Moreover, we found no significant differences in the number, density, and size of excitatory synapses formed in mitral cell dendrites. We also found no evidence for the role of microglia in the activity-dependent dendrite remodeling of layer 4 (L4) neurons in the barrel cortex. In contrast, the density of excitatory synapses (dendritic spines) in granule cells in the olfactory bulb was significantly increased in mice treated with PLX5622 at postnatal day (P) 6, suggesting a role for the regulation of dendritic spines. Our results indicate that microglia do not play a critical role in activity-dependent dendrite pruning at the neurite level during early postnatal development in mice.

Open reduction and Kirschner wire fixation method using a cylindrical block of unidirectional porous ß-tricalcium phosphate for tongue-shaped calcaneal fracture: Report of three cases.

Background: The artificial bone grafts are performed on the defect after reduction of the calcaneal fracture. Generally, it is an artificial bone graft with an implant, and there are a few reports of an artificial bone graft without an implant. Cases: We report three cases (42-year-old male, 67-year-old male, 21-year-old female) of a tongue-shaped calcaneal fracture treated using a cylindrical unidirectional porous ß-tricalcium phosphate artificial bone (Affinos®, Kurare co Ltd., Hyougo, Japan) to surgically repair bone defects after reduction. The bone defect is often observed when fracture is reduced in calcaneal fracture. There were significant bone defects, which were then fixed using Affinos® (forming a cylindrical shape block; diameter 10 mm x height 20 mm) to support the bone fragment, an artificial ß-tricalcium phosphate bone with a porosity of 57 % (pore size 25-300 µm), characterized by a novel unidirectional porous structure. Postoperative early rehabilitation started with partial load from 5 weeks after surgery and was full weight bearing at 9 weeks after surgery. There was no correction loss and good bone fusion was obtained. By 12 months postoperatively, patients were able to be walking without pain and absorption and bone fusion around the artificial bone were observed maintaining the morphology immediately after reduction. The result was a good clinical result of one excellent (92 points) and two good (81 and 84 points) 1 year after surgery in the postoperative AOFAS Ankle-Hindfoot Scale. Conclusion: Affinos® has a frost-like structure, which endows it with good tissue invasive properties because of the capillary effect. Moreover, it has excellent osteoconduction capability. In these 3 cases, Affinos® showed good strength, affinity, absorption, and bone substitution in a tongue-shaped calcaneal fracture. Further prospective studies are required to confirm our findings.

Effective Hand Rearing of Neonatal Mice for Developmental Studies.

Chronic manipulation in neonatal mice is a technical challenge, but it can achieve greater insights into how mice develop immediately after birth. However, these manipulations can often result in maternal rejection and consequently serious malnourishment and occasional death. Here, we describe a method to effectively hand rear mice to develop normally during the first post-natal week. In our experiments, we were able to negate the feeding deficiencies of anosmic mutant mice when compared to littermate controls. As a result, the delayed neuronal remodeling seen in maternally reared mutant mice was not seen in the hand-reared mutant mice. This methodology is user intensive but can be useful for a broad range of studies either requiring many interventions or one intervention that can result in maternal rejection or being outcompeted by healthy littermates.

Activity-dependent local protection and lateral inhibition control synaptic competition in developing mitral cells in mice.

In developing brains, activity-dependent remodeling facilitates the formation of precise neuronal connectivity. Synaptic competition is known to facilitate synapse elimination; however, it has remained unknown how different synapses compete with one another within a post-synaptic cell. Here, we investigate how a mitral cell in the mouse olfactory bulb prunes all but one primary dendrite during the developmental remodeling process. We find that spontaneous activity generated within the olfactory bulb is essential. We show that strong glutamatergic inputs to one dendrite trigger branch-specific changes in RhoA activity to facilitate the pruning of the remaining dendrites: NMDAR-dependent local signals suppress RhoA to protect it from pruning; however, the subsequent neuronal depolarization induces neuron-wide activation of RhoA to prune non-protected dendrites. NMDAR-RhoA signals are also essential for the synaptic competition in the mouse barrel cortex. Our results demonstrate a general principle whereby activity-dependent lateral inhibition across synapses establishes a discrete receptive field of a neuron.

Differentiation Capacity of Porcine Skeletal Muscle-Derived Stem Cells as Intermediate Species between Mice and Humans.

Large animal experiments are important for preclinical studies of regenerative stem cell transplantation therapy. Therefore, we investigated the differentiation capacity of pig skeletal muscle-derived stem cells (Sk-MSCs) as an intermediate model between mice and humans for nerve muscle regenerative therapy. Enzymatically extracted cells were obtained from green-fluorescence transgenic micro-mini pigs (GFP-Tg MMP) and sorted as CD34+/45- (Sk-34) and CD34-/45-/29+ (Sk-DN) fractions. The ability to differentiate into skeletal muscle, peripheral nerve, and vascular cell lineages was examined via in vitro cell culture and in vivo cell transplantation into the damaged tibialis anterior muscle and sciatic nerves of nude mice and rats. Protein and mRNA levels were analyzed using RT-PCR, immunohistochemistry, and immunoelectron microscopy. The myogenic potential, which was tested by Pax7 and MyoD expression and the formation of muscle fibers, was higher in Sk-DN cells than in Sk-34 cells but remained weak in the latter. In contrast, the capacity to differentiate into peripheral nerve and vascular cell lineages was significantly stronger in Sk-34 cells. In particular, Sk-DN cells did not engraft to the damaged nerve, whereas Sk-34 cells showed active engraftment and differentiation into perineurial/endoneurial cells, endothelial cells, and vascular smooth muscle cells, similar to the human case, as previously reported. Therefore, we concluded that Sk-34 and Sk-DN cells in pigs are closer to those in humans than to those in mice.

Anti-myelin Oligodendrocyte Glycoprotein Antibody-positive Myelitis after Coronavirus Disease 2019.

We herein report a case of anti-myelin oligodendrocyte glycoprotein (MOG) antibody-related myelitis caused by coronavirus disease (COVID-19) infection in 2021. A 22-year-old man with no history of any related illness contracted COVID-19. Eight days later, he developed bladder problems, paraplegia and sensory disturbances. Cervical spinal cord magnetic resonance imaging revealed extensive hyperintensity at T2 and spinal cord lesions extending from C4 to Th1. The patient was diagnosed with transverse myelitis and started on intravenous methylprednisolone, plasma exchange and intravenous immunoglobulin therapy. The symptoms improved only after intravenous methylprednisolone therapy. Anti-MOG antibodies were found in his serum and cerebrospinal fluid during routine screening. As this observation is unusual and could cause serious health problems, we wonder if COVID-19 triggered this autoimmune response.

Group II truncated haemoglobin YjbI prevents reactive oxygen species-induced protein aggregation in Bacillus subtilis.

Oxidative stress-mediated formation of protein hydroperoxides can induce irreversible fragmentation of the peptide backbone and accumulation of cross-linked protein aggregates, leading to cellular toxicity, dysfunction, and death. However, how bacteria protect themselves from damages caused by protein hydroperoxidation is unknown. Here, we show that YjbI, a group II truncated haemoglobin from Bacillus subtilis, prevents oxidative aggregation of cell-surface proteins by its protein hydroperoxide peroxidase-like activity, which removes hydroperoxide groups from oxidised proteins. Disruption of the yjbI gene in B. subtilis lowered biofilm water repellence, which associated with the cross-linked aggregation of the biofilm matrix protein TasA. YjbI was localised to the cell surface or the biofilm matrix, and the sensitivity of planktonically grown cells to generators of reactive oxygen species was significantly increased upon yjbI disruption, suggesting that YjbI pleiotropically protects labile cell-surface proteins from oxidative damage. YjbI removed hydroperoxide residues from the model oxidised protein substrate bovine serum albumin and biofilm component TasA, preventing oxidative aggregation in vitro. Furthermore, the replacement of Tyr63 near the haem of YjbI with phenylalanine resulted in the loss of its protein peroxidase-like activity, and the mutant gene failed to rescue biofilm water repellency and resistance to oxidative stress induced by hypochlorous acid in the yjbI-deficient strain. These findings provide new insights into the role of truncated haemoglobin and the importance of hydroperoxide removal from proteins in the survival of aerobic bacteria.

UDP-glucose, cereblon-dependent proinsulin degrader.

Insulin secretion is regulated in multiple steps, and one of the main steps is in the endoplasmic reticulum (ER). Here, we show that UDP-glucose induces proinsulin ubiquitination by cereblon, and uridine binds and competes for proinsulin degradation and behaves as sustainable insulin secretagogue. Using insulin mutagenesis of neonatal diabetes variant-C43G and maturity-onset diabetes of the young 10 (MODY10) variant-R46Q, UDP-glucose:glycoprotein glucosyltransferase 1 (UGGT1) protects cereblon-dependent proinsulin ubiquitination in the ER. Cereblon is a ligand-inducible E3 ubiquitin ligase, and we found that UDP-glucose is the first identified endogenous proinsulin protein degrader. Uridine-containing compounds, such as uridine, UMP, UTP, and UDP-galactose, inhibit cereblon-dependent proinsulin degradation and stimulate insulin secretion from 3 to 24 h after administration in ß-cell lines as well as mice. This late and long-term insulin secretion stimulation is designated a day sustainable insulin secretion stimulation. Uridine-containing compounds are designated as proinsulin degradation regulators.

Medical Image Sharing in Japan.

This paper reports the history, background including politics, current status of Japan's health imaging study and other information sharing. Its realization was slow until the Ministry of Health, Labour and Welfare (MHLW) started paying digital image storage at the same rate as films in 2008. Information sharing was initiated in early 2010s, which was before vendors became ready for Integrating the Healthcare Enterprise (IHE) cross-enterprise document sharing (XDS), with the result that most of 34 large regional sharing systems are in non-standardized protocol. One standardized example is the Hamamatsu area where inexpensive online PDI (portable data for imaging) was introduced.

UDP-Glucose: A Cereblon-Dependent Glucokinase Protein Degrader.

We previously reported that glucokinase is ubiquitinated and degraded by cereblon with an unknown endogenous glucokinase protein degrader. Here, we show that UDP-glucose is a glucokinase protein degrader. We identified that both glucose and UDP-glucose bind to glucokinase and that both uridine and UDP-glucose bind to cereblon in a similar way to thalidomide. From these results, UDP-glucose was identified as a molecular glue between cereblon and glucokinase. Glucokinase produces glucose-6-phosphate in the pancreas and liver. Especially in ß-cells, glucokinase is the main target of glucose for glucose-induced insulin secretion. UDP-glucose administration ubiquitinated and degraded glucokinase, lowered glucose-6-phosphate production, and then reduced insulin secretion in ß-cell lines and mice. Maturity-onset diabetes of the young type 2 (MODY2) glucokinaseE256K mutant protein was resistant to UDP-glucose induced ubiquitination and degradation. Taken together, glucokinase ubiquitination and degradation signaling might be impaired in MODY2 patients.

Quantitative Evaluation of the Reduced Capacity of Skeletal Muscle Hypertrophy after Total Body Irradiation in Relation to Stem/Progenitor Cells.

The effects of total body irradiation (TBI) to the capacity of skeletal muscle hypertrophy were quantified using the compensatory muscle hypertrophy model. We additionally assessed the responses of stem and/or progenitor cells in the muscles. A single TBI of 9.0, 5.0 and 2.5 Gy was delivered to C57BL/6 mice. Bone marrow stromal cells were obtained from GFP-Tg mice, and were injected into the tail vein of the recipient mice (1 × 106 cells/mouse), for bone marrow transplantation (BMT). Five weeks after TBI, the mean GFP-chimerism in the blood was 96 ± 0.8% in the 9 Gy, 83 ± 3.9% in the 5 Gy, and 8.4 ± 3.4% in the 2.5 Gy groups. This implied that the impact of 2.5 Gy is quite low and unavailable as the BMT treatment. Six weeks after the TBI/BMT procedure, muscle hypertrophy was induced in the right plantaris muscle by surgical ablation (SA) of the synergist muscles (gastrocnemius and soleus), and the contralateral left side was preserved as a control. The muscle hypertrophy capacity significantly decreased by 95% in the 9 Gy, 48% in the 5 Gy, and 36% in the 2.5 Gy groups. Furthermore, stem/progenitor cells in the muscle were enzymatically isolated and fractionated into non-sorted bulk cells, CD45-/34-/29+ (Sk-DN), and CD45-/34+ (Sk-34) cells, and myogenic capacity was confirmed by the presence of Pax7+ and MyoD+ cells in culture. Myogenic capacity also declined significantly in the Bulk and Sk-DN cell groups in all three TBI conditions, possibly implying that skeletal muscles are more susceptible to TBI than bone marrow. However, interstitial Sk-34 cells were insusceptible to TBI, retaining their myogenic/proliferative capacity.

Paraneoplastic cerebellar degeneration with anti-Yo antibodies and an associated submandibular gland tumor: a case report.

BACKGROUND: As a debilitating syndrome, paraneoplastic cerebellar degeneration (PCD) remains challenging to treat. Further, anti-Yo antibody (directed against human cerebellar degeneration-related protein 2) detection in patients with PCD is associated with unsatisfactory responses to existing therapies. Here, we present the case of a 60-year-old woman who developed PCD with anti-Yo antibodies and a submandibular gland tumor. CASE PRESENTATION: A 60-year-old woman presented with a 5-day history of unsteadiness of gait and inadequate coordination of her extremities, along with truncal instability. Although walking without aid was possible, dysmetria of all four limbs, trunk, and gait ataxia was observed. While routine biochemical and hematological examinations were normal, the patient's blood was positive for anti-Yo antibodies. When the neurological symptoms deteriorated despite administration of intravenous methylprednisolone, fluorodeoxyglucose-positron emission tomography (FDG-PET) and computed tomography (CT) images with contrast enhancement were performed, which showed a tumor in the left submaxillary gland. She underwent total left submandibular gland resection, including the tumor; histological and immunohistochemical results revealed a salivary duct carcinoma. She was administered intravenous methylprednisolone, followed by 10 plasma exchange sessions, intravenous immunoglobulins, and cyclophosphamide therapy. Following treatment, her symptoms were not alleviated, even after the reduction of anti-Yo titers. CONCLUSIONS: Although tumor detection was delayed, early tumor detection, diagnosis, and PCD treatment are essential because any delay can result in the progression of the disorder and irreversible neurological damage. Therefore, we recommend that the possibility of a salivary gland tumor should be considered, and whole-body dual-modality CT, including the head and neck, and FDG-PET should be performed at the earliest for patients with well-characterized paraneoplastic antibodies when conventional imaging fails to identify a tumor.

R1526 residue in arginine/proinsulin binding domain of UGGT1 is involved in proinsulin binding.

Arginine releases proinsulin from binding to UGGT1 in the endoplasmic reticulum (ER). PSIPRED analysis showed that the arginine/proinsulin binding domain (A/PBD) in the C-terminal region of UGGT1 forms a disordered region, which is flexible and outside of the main protein structure. Both arginine and proinsulin may easily access the disordered region of A/PBD. Using the SNP library, two variants, Q1518∗ and R1526C, were identified in this region. UGGT1Q1518∗ protein is a deficient form of A/PBD and ER-retention signal (ERRS). UGGT1Q1518∗ protein in cell analysis reveals that mutated protein is mainly secreted from the cells because it lacks ERRS. We found another UGGT1 variant, UGGT1R1526C. At the molecular level, less interaction of proinsulin with UGGT1 was observed in both human UGGT1R1526C and mouse UGGT1L1518C with/without arginine. However, UGGT1R1526C and UGGT1WT interact with arginine similarly. We identified several amino acid residues for the arginine and proinsulin interaction. Here, the R1526 residue of UGGT1 is involved in proinsulin-interaction and is not involved in arginine-interaction.

Relationship Between Subacromial Bone Erosion and Hook Position of Clavicular Plate in Distal Clavicle Fractures.

OBJECTIVES: To evaluate the influence of posterior hook position on subacromial bone erosion during surgical treatment of distal clavicle fractures with locking compression plate clavicle hook plate (CHP). DESIGN: Single-center retrospective study. SETTING: Level V trauma center (university hospital). PATIENTS: Twenty-one patients (mean age, 45.8 years) treated with CHP were included. One, 3, 15, and 2 patients had Neer type I, IIa, IIb, and V fractures, respectively. INTERVENTION: Open reduction and internal fixation were performed with locking compression plate CHP. All implants were removed after a mean of 6.1 months postoperatively. MAIN OUTCOME MEASUREMENTS: Japanese Orthopaedic Association shoulder scores were used to assess recovery. Radiographically, the coracoclavicular distance was measured as the distance between the tip of the coracoid process and the undersurface of the clavicle. Three-dimensional computed tomography was performed to identify bone erosion at the hook tips after implant removal. The distance from the acromioclavicular joint center to the bone erosion was divided into 5 areas at 5-mm intervals, and the position and depth of bone erosion were measured in each area. RESULTS: The mean follow-up period was 17.4 months; mean ± SD Japanese Orthopaedic Association score was 75.9 ± 4.7 at the final follow-up, whereas the mean duration of bony union was 4.4 ± 1.0 (SD) months. Delayed bony union was observed in one patient, whereas a second surgery was required in another due to acromion cut-out. Radiography showed overreduction in 95% of cases. The correlation coefficient showed a difference between coracoclavicular distance and the position of bone erosion measured by CT (Rs = 0.32, P = 0.006). Erosion under the acromion surface was found in all patients. The depth of erosion correlated with the posterior hook position (Rs = 0.29, P = 0.023). CONCLUSIONS: Posterior hook tip placement increased the likelihood of bone erosion and complications due to overreduction. CHP should be set more anteriorly beneath the acromion to prevent complications. LEVEL OF EVIDENCE: Therapeutic Level IV. See Instructions for Authors for a complete description of levels of evidence.

Long-term outcomes of open modified inferior capsular shift for traumatic anterior shoulder instability: over 20 years of follow-up.

BACKGROUND: This study aimed to assess the long-term outcomes of the open modified inferior capsular shift procedure across more than 20 years in patients with traumatic anterior shoulder instability. METHODS: Participants in this study comprised 84 patients (86 shoulders; 67 men, 17 women). Mean follow-up was 28.0 years. We compared the recurrent instability rate after surgery, apprehension, revision rate, satisfaction, return to preinjury sporting activity, and patient background characteristics between recurrent and nonrecurrent groups. Twenty-seven patients who were examined directly were evaluated for differences in range of motion and muscle strength between affected and nonaffected sides. Clinical outcome scores used for this study were the Western Ontario Shoulder Instability Index and the Rowe score. RESULTS: Nine shoulders (10.5%) showed recurrent instability, as dislocation in 3 shoulders and subluxation in 6 shoulders, but no revisions were required. All patients with recurrent instability were males with new trauma. Three shoulders developed recurrent instability ≤5 years after surgery, and the remaining 6 shoulders showed recurrent instability >5 years after surgery. No significant differences in any patient characteristic were identified between the recurrent and nonrecurrent groups. Significant differences between affected and nonaffected sides were seen in the mean active range of motion or muscle strength for external rotation in the anatomic position or in 90° of abduction. Western Ontario Shoulder Instability Index and Rowe score were significantly worse in the recurrent group than in the nonrecurrent group. Patients reported that 84 shoulders (97.7%) were "much better." Most athletes (88.4%) had returned to sports activity at a level >70%. CONCLUSION: We investigated long-term outcomes of the open modified inferior capsular shift procedure for traumatic anterior shoulder instability. Our data suggest that recurrent instability might result from new trauma even if a long time has passed since the open modified inferior capsular shift procedure, so follow-up should be continued as long as possible after surgery. As in other reports, satisfaction was high and clinical scores were good. We thus believe this surgical method offers good results even after more than 20 years.