Shingo Komura

Lower incidence of adjacent segment degeneration after anterior cervical fusion found with those fusing C5-6 and C6-7 than those leaving C5-6 or C6-7 as an adjacent level.

Study Design Retrospective analysis of adjacent disc degeneration (ADD) after anterior cervical decompression and fusion (ADF). Objectives To elucidate the influence of the number of levels fused in ADF on the incidence of ADD. Summary of Background Data ADD is known as a complication associated with ADF. However, how the number of levels fused affects the incidence of ADD is not well understood. Methods One hundred and two patients with cervical degenerative disease, who underwent ADF and were followed for more than 24 months, were retrospectively analyzed. They were classified into 2 groups, a long group (L group) consisting of 50 cases with ADF of 4 or more disc levels, and a short group (S group) consisting of 52 cases with ADF of 3 or fewer disc levels. Furthermore, the patients were also divided into 2 groups according to inclusion or exclusion of C5-6 and C6-7 (C group: including both, NC group: not including both). The incidence of ADD, and that of symptomatic ADD (sADD), was compared between the 2 classifications. Results In the L group, there were 13 cases of ADD (26.0%), including 1 case of sADD (2.0%), whereas in the S group, there were 22 cases of ADD (42.3%), including 11 cases of sADD (21.2%). The incidence of sADD was significantly lesser in the L group (P=0.024). Three cases with sADD in the S group required revision surgery, whereas no additional surgery related to ADD was performed on patients in the L group. In addition, in the C group, ADD occurred in 20 of 71 cases (28.2%) and sADD occurred in 4 of 71 cases (5.6%), whereas in the NC group, ADD occurred in 15 of 31 cases (48.4%) and sADD occurred in 8 of 31 cases (25.8%). The incidence of ADD and sADD were significantly lesser in the C group (P=0.048). Conclusions ADD occurs less frequently among patients in whom C5-6 and C6-7 are fused than among those in whom C5-6 or C6-7 is left at an adjacent level, irrespective of the length of the fusion.

Incidence and Characteristics of Carpal Fractures Occurring Concurrently With Distal Radius Fractures

PURPOSE To investigate the incidence and characteristics of carpal fractures occurring concurrently with distal radius fractures and to determine the risk factors for this combination. METHODS We retrospectively analyzed 161 consecutive patients with 170 distal radius fractures who were treated between 2007 and 2011. Posteroanterior, lateral, and oblique radiographs of the wrist were examined, as were computed tomography scans when available. We evaluated the incidence and characteristics of carpal fractures occurring concurrently with distal radius fractures and the patient factors of gender, age, AO/ASIF classification, and energy of the injury. RESULTS Of the 170 distal radius fractures, 11 (7%) also had 1 or 2 carpal fractures. Of the 15 carpal fractures, 8 were scaphoid, 2 triquetrum, 2 pisiform, 1 capitate, 1 trapezium, and 1 hamate. Eleven of the 15 carpal fractures were diagnosed by computed tomography alone. Male gender, patients of lower mean age, AO/ASIF type B, and high-energy trauma significantly raised the risk of simultaneous fractures of the distal radius and carpals. CONCLUSIONS The incidence of carpal fractures occurring concurrently with distal radius fractures was not negligible, and almost all carpal fractures had no or minimal displacement. Suspicion of carpal fractures occurring concurrently with distal radius fracture should be high, and computed tomography should be considered, in males, young patients, and those with AO/ASIF type B fractures and high energy trauma.

Activin-A enhances mTOR signaling to promote aberrant chondrogenesis in fibrodysplasia ossificans progressiva

Fibrodysplasia ossificans progressiva (FOP) is a rare and intractable disease characterized by extraskeletal bone formation through endochondral ossification. Patients with FOP harbor point mutations in ACVR1, a type I receptor for BMPs. Although mutated ACVR1 (FOP-ACVR1) has been shown to render hyperactivity in BMP signaling, we and others have uncovered a mechanism by which FOP-ACVR1 mistransduces BMP signaling in response to Activin-A, a molecule that normally transduces TGF-β signaling. Although Activin-A evokes enhanced chondrogenesis in vitro and heterotopic ossification (HO) in vivo, the underlying mechanisms have yet to be revealed. To this end, we developed a high-throughput screening (HTS) system using FOP patient-derived induced pluripotent stem cells (FOP-iPSCs) to identify pivotal pathways in enhanced chondrogenesis that are initiated by Activin-A. In a screen of 6,809 small-molecule compounds, we identified mTOR signaling as a critical pathway for the aberrant chondrogenesis of mesenchymal stromal cells derived from FOP-iPSCs (FOP-iMSCs). Two different HO mouse models, an FOP model mouse expressing FOP-ACVR1 and an FOP-iPSC-based HO model mouse, revealed critical roles for mTOR signaling in vivo. Moreover, we identified ENPP2, an enzyme that generates lysophosphatidic acid, as a linker of FOP-ACVR1 and mTOR signaling in chondrogenesis. These results uncovered the crucial role of the Activin-A/FOP-ACVR1/ENPP2/mTOR axis in FOP pathogenesis.

An EWS-FLI1-Induced Osteosarcoma Model Unveiled a Crucial Role of Impaired Osteogenic Differentiation on Osteosarcoma Development

Summary EWS-FLI1, a multi-functional fusion oncogene, is exclusively detected in Ewing sarcomas. However, previous studies reported that rare varieties of osteosarcomas also harbor EWS-ETS family fusion. Here, using the doxycycline-inducible EWS-FLI1 system, we established an EWS-FLI1-dependent osteosarcoma model from murine bone marrow stromal cells. We revealed that the withdrawal of EWS-FLI1 expression enhances the osteogenic differentiation of sarcoma cells, leading to mature bone formation. Taking advantage of induced pluripotent stem cell (iPSC) technology, we also show that sarcoma-derived iPSCs with cancer-related genetic abnormalities exhibited an impaired differentiation program of osteogenic lineage irrespective of the EWS-FLI1 expression. Finally, we demonstrate that EWS-FLI1 contributed to secondary sarcoma development from the sarcoma iPSCs after osteogenic differentiation. These findings demonstrate that modulating cellular differentiation is a fundamental principle of EWS-FLI1-induced osteosarcoma development. This in vitro cancer model using sarcoma iPSCs should provide a unique platform for dissecting relationships between the cancer genome and cellular differentiation.

Traumatic closed index extensor tendon rupture at the musclotendinous junction: a report of two cases.

This report describes two cases of traumatic closed index extensor tendon rupture at the musclotendinous junction. Both patients were injured when their work gloves were caught in the revolving parts of machines, and both were treated surgically. One of the patients completely ruptured the index extensor digitorum communis (EDC) and the extensor indicis proprius (EIP) tendons at the musclotendinous junction of dorsal forearm. In this patient, the distal stump of the index EDC tendon was sutured to the middle EDC tendon in an end-to-side juncture. The other patient completely ruptured the EIP tendon and partially ruptured the index EDC tendon at the musclotendinous junction. In this patient, tendon transfer of the extensor digiti minimi (EDM) to the EIP tendon and plication of the index EDC tendon were performed. In both cases, surgical intervention enabled the patients to extend their index fingers almost normally; however, the former complained of inability to extend his index finger independently. Tendon transfer of the EDM in cases of index extensor tendon rupture at the musclotendinous junction is a good method to restore ability to independently extend the index finger. However, consideration should be given to anatomical variation in the little finger. The EDC tendon is sometimes absent leaving the EDM tendon as the only extensor tendon to the little finger.

Palmar-divergent dislocation of the scaphoid and the lunate

We describe a patient with palmar-divergent dislocation of the scaphoid and lunate. After successful closed reduction, the scapholunate and lunotriquetral ligaments were sutured through the dorsal approach, and the anterior capsule was sutured through the palmar approach. The scapholunate and lunotriquetral joints were fixed with Kirschner wires for 7 weeks. At the 1-year follow-up, magnetic resonance imaging showed no evidence of avascular necrosis of the scaphoid or lunate, and radiographs showed no evidence of the dorsal and volar intercalated segment instability patterns associated with carpal instability. However, flexion of the scaphoid and a break in Gilula’s line remained. To our knowledge, this is the first report showing treatment of palmar-divergent dislocation of the scaphoid and lunate by suturing the carpal interosseous ligaments.

Simultaneous fracture of the waist of the scaphoid and the hook of the hamate.

A case of simultaneous fracture of the waist of the scaphoid and the hook of the hamate is presented. The scaphoid fracture was treated surgically with a headless compression screw, while the hook fracture was treated conservatively with cast immobilisation for eight weeks. Both fractures achieved bone union and the patient returned to work without any symptoms or complications. Only two cases of fractures of the scaphoid and hamate have been reported previously. However, both of them involved fracture of the body of the hamate. This is the first report of simultaneous fracture of the scaphoid and the hook of the hamate.

In vivo reprogramming drives Kras -induced cancer development

The faithful shutdown of the somatic program occurs in the early stage of reprogramming. Here, we examined the effect of in vivo reprogramming on Kras-induced cancer development. We show that the transient expression of reprogramming factors (1–3 days) in pancreatic acinar cells results in the transient repression of acinar cell enhancers, which are similarly observed in pancreatitis. We next demonstrate that Kras and p53 mutations are insufficient to induce ERK signaling in the pancreas. Notably, the transient expression of reprogramming factors in Kras mutant mice is sufficient to induce the robust and persistent activation of ERK signaling in acinar cells and rapid formation of pancreatic ductal adenocarcinoma. In contrast, the forced expression of acinar cell-related transcription factors inhibits the pancreatitis-induced activation of ERK signaling and development of precancerous lesions in Kras-mutated acinar cells. These results underscore a crucial role of dedifferentiation-associated epigenetic regulations in the initiation of pancreatic cancers.Cellular reprogramming and cancer development share properties. Here, the authors examine the impact of in vivo reprogramming on Kras-induced cancer and show reprogramming-mediated repression of somatic cell enhancers in conjunction with Kras mutation results in rapid PDAC development.

Comments on “Flexor Tendon Rupture Due to Previously Undiagnosed Kienböck Disease: A Case Report”:

To the Editor: We read with interest the article by Turner et al in the 2017 issue of HAND. The authors reported a case of flexor tendon rupture due to Kienböck disease and stated that no prior cases have been reported. However, flexor tendon rupture associated with Kienböck disease has indeed been previously reported. In 1942, James reported a case of rupture of the flexor pollicis longus (FPL) and flexor profundus tendons of the index finger secondary to Kienböck disease. Niwa et al reported 6 cases of closed tendon rupture as a result of Kienböck disease and also reviewed 11 reported cases in English and 48 cases in Japanese. According to their article, flexor tendon rupture has been reported in a total of 14 cases. Recently, we also encountered a case with FPL rupture caused by Kienböck disease in a 74-year-old woman without marked wrist pain. Plain radiographs revealed Lichtman stage IV, and computed tomography (CT) showed protrusion of the collapsed lunate fragment toward the volar side (Figure 1). In intraoperative findings, the joint capsule was perforated by lunate fragments, as in previous reports 795511 HANXXX10.1177/1558944718795511HANDHirakawa et al letter2018

Recurrent atraumatic acute carpal tunnel syndrome due to hematoma caused by distal radioulnar joint arthritis during anticoagulant treatment with apixaban

Atraumatic acute carpal tunnel syndrome is a rare type of median nerve neuropathy caused by etiologies that increase compartment pressure in the carpal tunnel. This report describes a patient with flexor tendon abrasion as an unusual complication of distal radioulnar joint arthritis. This abrasion caused a hematoma to form in the carpal tunnel during anticoagulant treatment with apixaban, resulting in recurrent acute carpal tunnel syndrome.