Four-corner fusion method using a bioabsorbable plate for scapholunate advanced collapse and scaphoid nonunion advanced collapse wrists: a case series study.

BACKGROUND: Scaphoid excision and four-corner arthrodesis is an acceptable salvage procedure for the treatment of scapholunate advanced collapse (SLAC) and scaphoid nonunion advanced collapse (SNAC) wrists, since first popularized in the 1980s. We investigated the potential application of novel bioabsorbable plates and screws made of un-sintered hydroxyapatite/poly-L-lactide composite for the treatment of metacarpal fractures. We used this material for the fixation of four-corner fusions for SLAC or SNAC wrists commencing from April 2009. The purpose of this study was to clarify the controversy in the literature regarding the use of these plates. METHODS: The surgical procedures and clinical outcomes of four-corner fusions using a bioabsorbable (poly-L-lactic acid and hydroxyapatite) plate were reported. Ten patients (mean age, 59.2 years) with SLAC or SNAC wrists underwent fusions between April 2009 and June 2016. The primary diseases were scapholunate ligament injury, Preiser disease, and scaphoid pseudarthrosis. The mean postoperative follow-up period was 45.9 months (range, 12-86). RESULTS: In all patients, bone union was achieved without dislocation or pain. The mean wrist flexion and extension arc improved from 78.5 degrees before surgery to 90.5 degrees after surgery. Mean grip strength improved from 51 to 69% after surgery, and the Quick Disabilities of the Arm, Shoulder, and Hand (QuickDASH) score improved from 53.5 to 14.3. No complications such as infection, avascular swelling, or tendon adhesion were observed. This implant requires no removal of internal fixation devices, produces stable outcomes, and is an effective fusion technique. CONCLUSIONS: We summarized the outcomes of four-corner arthrodesis using bioabsorbable plates. Satisfactory clinical results were shown, with no obvious complications. This novel plate also serves as a good alternative for patients who are allergic to metals. Furthermore, bioabsorbable plates are advantageous as they do not require removal.

Hook Plate Technique for Bony Mallet Thumb.

Bony mallet is a common sport injury, but bony mallet thumb is rarely encountered. We performed open reduction and fixation of bony mallet thumb using a hook plate procedure on a 27-year-old man under general anesthesia. The patient began working one day after surgery. Six months postoperatively, the patient had excellent dexterity according to Crawford's evaluation criteria and no difficulties at work or playing softball. Tension band fixation, compression pins, and the extension block technique are commonly used to manage bony mallet. Despite the anatomical reduction, rigid fixation, and early resumption of motion skills offered by the hook plate technique, to our knowledge, no previous reports of its application to bony mallet thumb were found. In this case, the hook plate technique was chosen and made an early return to work possible and brought about a successful result.

Radiographic Measurements as a Predictor of Correction Loss in Conservative Treatment of Colles' Fracture.

Dorsal displaced distal radius fracture (Colles' fracture) is very common and could occur from fragility in middle-aged and elderly people. Many Colles' fractures are still treated conservatively in clinics without hospitalization. Internal fixation using a palmar locking plate has been the standard treatment, but some complications have been reported. The aim of this study was to analyze changes in radiographic parameters over time in patients with conservatively treated Colles' fractures, and to establish whether the type of fracture influenced these changes. Prospective data collected included patient characteristics and radiological findings. The study was conducted at two private clinics and included 60 patients (13 men and 47 women; mean age, 72.5 years old; range, 55 to 96 years old) with a Colles' fracture (types of injury: intramedullary [n = 15], anatomical [n = 39], extramedullary [n = 2], and unknown [n = 4]) who were treated conservatively with manipulation and cast immobilization. Conservative, non-surgical treatment with manipulation was performed first, then, cast immobilization continued for 4 weeks. Loss of correction between the time of reduction and the final observation was defined by the following radiographic measurements: palmar tilt, radial inclination, and ulnar variance. The average final follow up period was 4.6 months (1.5-12 months). Immediately after reduction, 11 intramedullary fractures, 42 anatomical fractures and 7 extramedullary fractures were confirmed. Correction loss according to ulnar variance was significantly greater (P = 0.012) during the final observation for patients with an intramedullary injury at reduction than that for patients with extramedullary and anatomical injuries at reduction. We found that the correction loss for ulnar variance from immediately after reduction until the final observation was significantly greater in the intramedullary group, suggesting that an alternative to conservative treatment may be beneficial for patients with intramedullary fractures.

[An Experience of Using a Distraction Plate for an Elderly Patient with a Highly Communited Intraarticular Distal Radius Fracture].

We performed open reduction and internal fixation using a distraction plate in two cases of elderly patients with highly communited intraarticular open distal radius fractures. There was no corrective loss of intraarticular fracture fragment in either case. The implant was removed in one case because bone union was achieved. The plate was retained in the other case, without the hope of implant removal. Neither case complained of any marked disturbance of activities of daily living (ADL), and there was no pain at the time of the final follow up period. However, there is a high possibility of limitation of the range of motion (ROM) of the wrist after implant removal, therefore we need to judge the indications carefully.

Enhanced expression of Wnt9a in the flexor tenosynovium in idiopathic carpal tunnel syndrome.

This study aimed to clarify the association between abnormal Wnt signaling and the cause of idiopathic carpal tunnel syndrome (ICTS) and whether an association exists between Wnt signaling and cell proliferation in the flexor tenosynovium. The subjects included nine patients with ICTS; the controls were nine patients with distal radius fractures without any symptoms of carpal tunnel syndrome. We extracted mRNA from the flexor tenosynovium and compared the expression levels of genes encoding 17 types of Wnt in both subjects and controls via quantitative real-time polymerase chain reaction (PCR). Expression levels of factors involved in cell proliferation, such as estrogen-responsive finger protein, epidermal growth factor receptor, heparin binding-epidermal growth factor-like growth factor, insulin-like growth factor-1, and vascular endothelial growth factor (VEGF) were also measured using quantitative real-time PCR. In addition, we compared the Wnt and MIB-1 protein expression levels to clarify the effect of Wnt on cell proliferation. Quantitative real-time PCR revealed significantly greater expression of the gene encoding Wnt9a in subjects with ICTS than in controls and also revealed a positive correlation between the expression of genes encoding Wnt9a and VEGF in subjects with ICTS. Quantitative evaluation using immunohistochemical staining also indicated more marked Wnt9a expression in subjects than in controls. However, there was no relationship between the expression of Wnt9a and the cell proliferation index MIB-1. These results indicate that Wnt9a expression is enhanced in ICTS and that Wnt9a may be involved in VEGF expression in ICTS.

Mechanical stimulation suppresses phosphorylation of eIF2alpha and PERK-mediated responses to stress to the endoplasmic reticulum.

Cellular perturbations such as stress to the endoplasmic reticulum induce an integrated stress response, which activates phosphorylation of eIF2alpha and leads to alleviation of cellular injury or apoptosis. This study investigated the role of mechanical stimulation in the regulation of eIF2alpha and cell death. Mechanical stimulation was applied to mouse ulnae, MC3T3 cells, and mesenchymal stem cells. The results demonstrate that mechanical stimulation reduces phosphorylation of eIF2alpha through inactivation of Perk. Furthermore, flow pre-treatment reduces thapsigargin-induced cell mortality through suppression of phosphorylation of Perk. However, H(2)O(2)-driven cell mortality, which is not mediated by Perk, is not suppressed by mechanical stimulation. Taken together, our observations suggest a pro-survival role of mechanical stimulation in Perk-mediated stress responses.

Elcatonin injections suppress systemic bone resorption without affecting cortical bone regeneration after drill-hole injuries in mice.

It is assumed that there are systemic changes in mineral metabolism during fracture healing that may cause a predisposition to sequential fractures in osteoporotic patients who suffered from previous fractures. Initial therapies for patients with osteoporotic fractures are important to prevent disabilities in daily life consequent to bone and muscle atrophies, and sequential fractures, although systemic and local bone metabolism during fracture healing have not been well understood. We evaluated the effects of bone injury and elcatonin injection as an initial therapy on systemic and local bone turnover and bone wound healing. Two drill holes were made in the diaphysis of the left femur and tibia of 12-week-old male C57BL/6J mice. They were treated with three doses of elcatonin or a vehicle thrice a week until the end of the 28-day experiment. Urinary crosslinked C-telopeptide of type I collagen (CTX) increased and the bone mineral densities (BMDs) in the lumbar vertebrae decreased in the vehicle-treated mice. Elcatonin injection prevented increases in urinary CTX and reduction of the BMDs. In the noninjured femoral metaphysis, osteoclast surface increased until day 28, whereas elcatonin suppressed it. In the fracture site, elcatonin facilitated osteoblast proliferation and did not delay the healing of the bone defect. Bone injuries accelerated bone turnover systemically and locally, and the elcatonin injections suppressed the systemic acceleration of bone resorption without a delay of filling regenerated cortical bone in the bone defect.

Genetic disruption of all NO synthase isoforms enhances BMD and bone turnover in mice in vivo: involvement of the renin-angiotensin system.

INTRODUCTION: NO is synthesized by three different NO synthase (NOS) isoforms, including neuronal (nNOS), inducible (iNOS) and endothelial NOS (eNOS). The roles of NO in bone metabolism have been extensively investigated in pharmacological studies and in studies with NOS isoform-deficient mice. However, because of the nonspecificity of agents and compensation among the NOS isoforms, the ultimate roles of endogenous NO are still poorly understood. To address this point, we successfully generated mice in which all three NOS genes are completely disrupted. In this study, we examined whether bone metabolism is abnormal in those mice. MATERIALS AND METHODS: Experiments were performed in 12-wk-old male wildtype, singly nNOS(-/-), iNOS(-/-), and eNOS(-/-) and triply n/i/eNOS(-/-) mice. BMD was assessed by DXA. The kinetics of osteoblastic bone formation and those of osteoclastic bone resorption were evaluated by measurements of morphological and biochemical markers. RESULTS: BMD was significantly higher only in the triply NOS(-/-) mice but not in any singly NOS(-/-) mice compared with the wildtype mice. Markers of osteoblastic bone formation, including bone formation rate, mineral apposition rate, and serum alkaline phosphatase concentration, were also significantly larger only in the triply NOS(-/-) mice compared with wildtype mice. Furthermore, markers of osteoclastic bone resorption, including osteoclast number, osteoclast surface, and urinary deoxypyridinoline excretion, were again significantly greater only in the triply NOS(-/-) mice. Importantly, the renin-angiotensin system in bone was significantly activated in the triply NOS(-/-) mice, and long-term oral treatment with an angiotensin II type 1 (AT(1)) receptor blocker normalized this pathological bone remodeling in those mice. CONCLUSIONS: These results provide the first direct evidence that genetic disruption of the whole NOS system enhances BMD and bone turnover in mice in vivo through the AT(1) receptor pathway, showing the critical role of the endogenous NO/NOS system in maintaining bone homeostasis.

ApoE gene deficiency enhances the reduction of bone formation induced by a high-fat diet through the stimulation of p53-mediated apoptosis in osteoblastic cells.

UNLABELLED: Osteoblast apoptosis increased in the tibias of apoE(-/-) mice fed with a high-fat diet, decreasing bone formation. The expression of p53 mRNA in marrow adherent cells increased. LDL or oxidized LDL increased apoptosis in the calvarial cells of apoE(-/-) mice. The increase in p53-mediated apoptosis is apparently related to a high-fat diet-induced osteopenia in apoE(-/-) mice. INTRODUCTION: The effects of high-fat loading and the apolipoprotein E (apoE) gene on bones have not been elucidated. We hypothesized that apoE gene deficiency (apoE(-/-)) modulates the effects of high-fat loading on bones. MATERIALS AND METHODS: We assessed this hypothesis using wildtype (WT) and apoE(-/-) mice fed a standard (WTS and ApoES groups) or a high-fat diet (WTHf and ApoEHf groups). The concentration of serum lipid levels and bone chemical markers were measured. Histomorphometry of the femurs was performed using microCT and a microscope. Bone marrow adherent cells from the femurs were used for colony-forming unit (CFU)-fibroblastic (CFU-f) assay and mRNA expressions analysis. The apoptotic cells in the tibias were counted. TUNEL fluorescein assay and Western analysis were performed in cultures of calvarial cells by the addition of low-density lipoprotein (LDL) or oxidized LDL. RESULTS: In the ApoEHf group, the values of cortical bone volume and trabecular and endocortical bone formation of the femurs decreased, and urinary deoxypyridinoline increased. Subsequent analysis revealed that the number of apoptotic cells in the tibias of the ApoES group increased, and more so in the ApoEHf group. The ratio of alkaline phosphatase-positive CFU-f to total CFU-f was decreased in the ApoEHf group. p53 mRNA expression in adherent cells of the apoE(-/-) mice increased and had a significantly strong positive correlation with serum LDL. TUNEL fluorescein assay of osteoblastic cells revealed an increase of apoptotic cells in the apoE(-/-) mice. The number of apoptotic cells in the apoE(-/-) mice increased with the addition of 100 microg/ml LDL or oxidized LDL. The p53 protein expression in apoE(-/-) cells exposed to 100 microg/ml LDL or oxidized LDL increased. CONCLUSIONS: We concluded that apoE gene deficiency enhances the reduction of bone formation induced by a high-fat diet through the stimulation of p53-mediated apoptosis in osteoblastic cells.

Osteoclast development in immobilized bone is suppressed by parathyroidectomy in mice.

We tested the hypothesis that signaling of parathyroid hormone (PTH) facilitates osteoclastogenesis in bone marrow cells after immobilization, thereby reducing trabecular bone volume. We performed histomorphometric analyses in immobilized limbs after right sciatic neurectomy (IM) and in the contralateral limbs after sham surgery (M). Mice underwent thyroparathyroidectomy (TPTX) and then 0.2 microg/body of thyroxine was given three times a week, or the mice were subjected to sham surgery (sham). Six-week-old male ddY mice were assigned to four groups, as follows, after acclimatization for 1 week: M + sham, IM + sham; M + TPTX, and IM + TPTX. Bilateral tibial samples were used for analysis. Trabecular bone volume (BV/TV) in the secondary spongiosa of the proximal tibias in IM + sham was significantly reduced compared to that in M + sham. Osteoclast surface (Oc.S/BS) and number (Oc.N/BS) in IM + sham transiently increased at 3 and 4 weeks after IM. In contrast, TPTX partially prevented the IM-related reduction of BV/TV and completely suppressed the transient increases of Oc.S/BS and Oc.N/BS. In the bone marrow cells, the mRNA expression of RANKL was elevated in IM + sham, but not in IM + TPTX, compared to that in M + sham. The percentage of Mac-1-positive bone marrow cells, osteoclast precursors, was not altered after IM. There were no significant differences in the concentrations of interleukin (IL)-1alpha in the tibial bone marrow cell culture medium between M + sham and IM + sham. Our data demonstrated that significant increases in osteoclast surface and number after IM were suppressed in TPTX mice, closely associated with a reduction in the high expression of RANKL mRNA in the tibial bone marrow cells. We speculate that enhanced osteoclastogenesis due to limb immobilization may be related to the elevation of RANKL expression by the facilitation of parathyroid hormone signaling in bone marrow cells.