Neurological Analysis Based on the Terminal End of the Spinal Cord and the Narrowest Level of Injured Spine in Thoracolumbar Spinal Injuries.

This study aimed to clarify neurological differences among the epiconus, conus medullaris, and cauda equina syndromes. Eighty-seven patients who underwent surgery for acute thoracolumbar spinal injuries were assessed. We defined the epiconus as the region from the terminal end of the spinal cord to the proximal 1.0 to 2.25 vertebral bodies, the conus medullaris as the region proximal to < 1.0 vertebral bodies, and the cauda equina as the distal part of the nerve roots originating from the spinal cord. On the basis of the distance from the terminal end of the spinal cord to the narrowest level of the spinal canal, the narrowest levels were ordered as follows: the epiconus followed by the conus medullaris and cauda equina. The narrowest levels were the epiconus in 22 patients, conus medullaris in 37 patients, and cauda equina in 25 patients. On admission, significantly more patients had a narrowed epiconus of Frankel grades A-C than a narrowed cauda equina. At the final follow-up, there were no significant differences in neurological recovery among those with epiconus, conus medullaris, or cauda equina syndrome. Anatomically classifying the narrowest lesion is useful for clarifying the differences and similarities among these three syndromes.

Causes and Clinical Outcomes of Patellar Post Impingement.

BACKGROUND: Patellar post impingement (PPI), which occurs when the post impinges on the patella, may reportedly cause poor total knee arthroplasty (TKA) outcomes. The causes of PPI and its effect on clinical outcomes and symptoms were investigated. MATERIAL AND METHODS: The study subjects were 100 patients who underwent TKA (65 posterior stabilized TKA, 35 bi-cruciate stabilized [BCS] TKA). Whether PPI occurred during surgery was investigated; the patients were then classified into a PPI+ group and a PPI- group, and whether the implant or patellar shape was related to the occurrence of PPI was examined. The measurement parameters included patellar shape, joint range of motion (ROM), and clinical outcome using the new Knee Society Score. RESULTS: There were 38 knees in the PPI+ group and 62 knees in the PPI- group. There was no difference in patellar shape between the 2 groups, but PPI was more frequent in patients with short patellar tendon and those with low patellar height. In terms of implant type, the PPI+ group included 12 patients (18.5%) who underwent posterior stabilized TKA and 26 (74.3%) who underwent BCS TKA. There was no difference between the 2 groups in either joint ROM or new Knee Society Score. These results suggest that the position of the patella and implant shape that causes the post to be positioned anteriorly may contribute to PPI. CONCLUSION: PPI occurred more frequently in knees with low patellar height and in patients who had undergone BCS TKA. PPI had no effect on joint ROM or clinical outcome.

Long-term effect of immobilization in external rotation after first-time shoulder dislocation: an average 18-year follow-up.

BACKGROUND: Immobilization in external rotation (ER) after a first-time shoulder dislocation was introduced to reduce the risk of recurrence compared with immobilization in internal rotation (IR), but its efficacy remains controversial. The purpose of this study was to determine the long-term effect of immobilization in ER after a first-time shoulder dislocation. METHODS: Between October 2000 and March 2004, 198 patients with a first-time anterior dislocation of the shoulder (average age 37) were randomly assigned to immobilization in ER (ER group = 104 shoulders) or IR (IR group = 94 shoulders) for 3 weeks. At an average 2-year follow-up, 159 patients (80.3%) were available for evaluation. In the current study, these 159 patients were further followed up and interviewed by telephone. The following items were evaluated: recurrent instability, apprehensive feeling, surgical intervention, limitation in the range of motion, return to sports, and the Single Assessment Numeric Evaluation (SANE) score. RESULTS: The average follow-up period was 18.2 years (range, 16-20 years). Fifty-six patients were available for follow-up with the follow-up rate of 35%. The number of recurrent patients was 6 of 27 (22%) in the ER group and 6 of 29 (21%) in the IR group (P = .889). The number of surgically stabilized patients was 3 of 27 (11%) in the ER group and 10 of 29 (34%) in the IR group (P = .038). In total, the recurrence rate was 33% (9 of 27) in the ER group and 55% (16 of 29) in the IR group (P = .100). Adding the surgical cases and those with the SANE score ≤70% as failure cases, the failure rate in the ER group (26%) was significantly lower than that in the IR group (52%) (P = .048). Among those who survived without surgical intervention, there were no significant differences in apprehensive feeling, return to sports, limited range of motion, and the SANE score between the groups. CONCLUSIONS: Immobilization in ER reduced the risk of surgical intervention compared with IR in the long term.

Immunohistochemical study of amelogenin binding proteins in an amelogenin point mutation mouse / Estudio inmunohistoquímico de proteínas de unión de la amelogenina en un ratón con mutación puntual de amelogenina

Amelogenin is one of the enamel matrices secreted by ameloblasts. A mutation of the amelogenin gene can cause hereditary dental enamel defects known as amelogenesis imperfecta (AI). Since lysosome-associated membrane protein-1 (LAMP-1), -3 (LAMP-3), and 78kDa glucose-related protein (Grp78) were identified as binding proteins of amelogenin, several studies have suggested the involvement of these binding proteins with the cell kinetics of ameloblasts in normal or abnormal conditions. The purpose of this study is to investigate the distribution of these amelogenin binding proteins in the ameloblast cell differentiation of mice with a point mutation of the amelogenin gene (Amelx*). The incisors of Amelx* mice had a white opaque color and the tooth surface was observed to be rough under a scanning electron microscope. Among the sequential ameloblast cell differentiation in the Amelx* mice, the shape of ameloblasts at the transition stage was irregular in comparison to those in wild-type (WT) mice. Immunostaining of Grp78 revealed that the whole cytoplasm of the transition stage ameloblasts was immunopositive for Grp78 antibody, while only the distal part of cell was positive in the WT mice. Furthermore, in the Amelx* mice, the cytoplasm of the transition stage ameloblasts was immunopositive for LAMP-1 and LAMP-3. These results suggest that Amelx* may cause the abnormal distribution of amelogenin binding proteins in the cytoplasm of ameloblasts.

La amelogenina es una de las matrices de esmalte secretadas por los ameloblastos. Una mutación del gen de amelogenina puede causar defectos hereditarios del esmalte dental conocidos como amelogénesis imperfecta (AI). Dado que la proteína de membrana asociada a lisosoma-1 (LAMP-1), -3 (LAMP-3) y la proteína relacionada con la glucosa de 78 kDa (Grp78) se identificaron como proteína de unión a amelogenina, varios estudios han sugerido la participación de estas proteínas con la cinética celular de los ameloblastos en condiciones normales o anormales. El objetivo del estudio fue investigar la distribución de LAMP-1, LAM-3 y Grp78 durante la diferenciación celular de ameloblastos de ratones con una mutación puntual del gen de amelogenina (Amelx*). Los incisivos de los ratones Amelx* presentaron un color blanco opaco y se observó en microscopio electrónico de barrido que la superficie del diente era áspera. La diferenciación celular secuencial y la forma de los ameloblastos en la etapa de transición en los ratones Amelx* fue irregular en comparación con los ratones silvestres (RS). La inmunotinción de Grp78 reveló que todo el citoplasma de los ameloblastos en etapa de transición fue inmunopositivo para el anticuerpo Grp78, mientras que solo la parte distal de la célula fue positiva en los ratones RS. Además, en ratones Amelx*, el citoplasma de los ameloblastos en etapa de transición fue inmunopositivo para LAMP-1 y LAMP-3. Estos resultados sugieren que Amelx* puede causar distribución anormal de proteínas de unión a amelogenina en el citoplasma de los ameloblastos.

Quantitative measurements of hip abduction strength in lumbar surgery patients.

BACKGROUND: We sought to evaluate the hip abduction strength in patients before and after lumbar surgery. MATERIALS AND METHODS: Eighty-four patients (51 males and 33 females) undergoing surgery for lumbar disc herniation or lumbar canal stenosis were selected. Mean age was 64.7 ± 13.8 years. Seven patients (8.3%) had surgery at multiple levels, including L2-L3 (group A), 27 (32.1%) patients had surgery at multiple levels including L3-L4 (group B), 32 (38.1%) patients had surgery at the L4-L5 level only (group C), and 18 (21.4%) patients had surgery at the L5-S1 level only (group D). Hip abduction strength was measured in the 84 patients preoperatively and in 49 patients postoperatively. RESULTS: In all patients, preoperative mean hip abduction strength on the symptomatic side and the asymptomatic side was 71.4 ± 34.5 N and 90.7 ± 36.5 N, respectively (p = 0.0008). In groups A and B, there were no significant differences between the mean hip abduction strength on the symptomatic and contralateral side. In group C, those on the symptomatic and contralateral side were 68.0 ± 33.5 N and 89.3 ± 34.8 N, respectively (p = 0.0181). In group D, those on the symptomatic and contralateral side were 74.3 ± 42.4 N and 101.7 ± 44.7 N, respectively (p = 0.0314). In the 49 patients of all groups that could be measured postoperatively, there were no significant differences between the mean hip abduction strength on both sides. CONCLUSIONS: It was confirmed that the gluteus medius, which was main hip abductor, was mainly innervated by L5 and its mean strength significantly improved postoperatively. The possibility of improvement of hip abduction strength, especially with unchanged tibialis anterior strength, could be very useful for operative decisions.

Limaprost or Pregabalin: Preoperative and Postoperative Medication for Pain due to Lumbar Spinal Stenosis.

PURPOSE: We aimed to evaluate the incidence of (and risk factors for) postoperative pregabalin and/or limaprost to treat persistent numbness and/or pain of the lower extremities after lumbar spinal stenosis (LSS) surgery. METHODS: Medical records of 329 patients (168 men, 161 women; average age 70 years) were retrospectively reviewed for data on the duration of LSS diagnosis; LSS disease; preoperative medication (limaprost, pregabalin, or combined limaprost/pregabalin; duration); symptoms; preoperative/postoperative intermittent claudication (IC); operation type; and postoperative medication and period. RESULTS: Limaprost, pregabalin, and combined limaprost/pregabalin were prescribed preoperatively for 43%, 7%, and 5% of patients, respectively. At an average of 21 months postoperatively, limaprost, pregabalin, and combined therapy were prescribed in 11%, 8%, 4% of patients, respectively. Medication requirement was significantly lower postoperatively than preoperatively (P < 0.0001). Significant risk factors for required postoperative medication were required preoperative medication (odds ratio [OR] 3.088, 95% confidence interval [CI] 1.679 to 5.681]; postoperative period (OR 1.063, 95% CI 1.031 to 1.096); and postoperative IC (OR 3.868, 95% CI 1.481 to 10.103). A negative impact from postoperative medication was seen in patients who had undergone decompression surgery (OR 0.589, 95% CI 0.377 to 0.918). CONCLUSIONS: Overall, 23% of LSS patients required medication for pain and/or numbness at 21 months postoperatively. Significant factors portending required postoperative medication were preoperative medication, longer postoperative period, and postoperative IC. A negative influence from postoperative medication was seen in patients who had undergone decompression surgery without fusion.

Factors related to curved femur in elderly Japanese women.

BACKGROUND: Multiple factors are involved in the development of atypical femoral fractures, and excessive curvature of the femur is thought to be one of them. However, the pathogenesis of femoral curvature is unknown. We evaluated the influence of factors related to bone metabolism and posture on the development of femoral curvature. METHODS: A total of 139 women participated in the present study. Curvatures were measured using antero-posterior and lateral radiography of the femur. We evaluated some bone and vitamin D metabolism markers in serum, the bone mineral density (BMD), lumbar spine alignment, and pelvic tilt. RESULTS: We divided the women into two groups, curved and non-curved groups, based on the average plus standard deviation as the cut-off between the groups. When univariate logistic regression analysis was performed to detect factors affecting femoral curvature, the following were identified as indices significantly affecting the curvature: age of the patients, serum concentrations of calcium, intact parathyroid hormone, pentosidine, homocysteine and 25-hydroxyvitamin D (25(OH)D), and BMD of the proximal femur (P < 0.05) both in the lateral and anterior curvatures. When we used multivariate analyses to assess these factors, only 25(OH)D and age (lateral and anterior standardized odds ratio: 0.776 and 0.385, and 2.312 and 4.472, respectively) affected the femoral curvature (P < 0.05). CONCLUSION: Femoral curvature is strongly influenced by age and serum vitamin D.

Immunohistochemical study of amelogenin and lysosome-associate membrane proteins (LAMPs) in cartilage / Estudio inmunohistoquímico de la amelogenina y proteínas de membrana asociadas a lisosomas (LAMPs) en el cartílago

Amelogenin is one of the enamel matrix proteins secreted by ameloblasts during enamel formation in tooth development. Recent studies showed that the amelogenin is expressed in chondrocyte. Lysosome-associated membrane proteins (LAMPs) have been identified as binding partner proteins to amelogenin and it has been suggested they act as signaling receptors of amelogenin. The purpose of this study is to clarify the localization of amelogenin and LAMPs in growth plate cartilage and cartilaginous nodules in micromass culture. Mouse knee joints including tibia growth plate at 4 weeks old and micromass cultures of limb bud mesenchymal cells after 2 weeks were fixed in paraformaldehyde, routinely processed, sections were cut and immunostained with amelogenin, collagen type II and type X, LAMP-1 and -3. The positive immunoreaction of amelogenin was observed both in proliferation and hypertrophic zone cartilage of growth plate after enzymatic pretreatment in immunostaining. Furthermore, cartilaginous nodules in micromass culture were immunopositive to amelogenin. The chondrocytes in the proliferation zone of the growth plate were immunopositive to LAMP-1 but weakly stained in the chondrocytes of hypertrophic zone. These observations indicate that amelogenin may be present in cartilage matrix produced in vivo and in vitro and amelogenin may involve cartilage formation through the LAMP-1 signaling pathway.

La amelogenina es una de las proteínas de la matriz del esmalte secretadas por ameloblastos durante la formación del esmalte en el desarrollo dentario. Estudios recientes demuestran que la amelogenina se expresa en los condrocitos. Las proteínas de membrana asociadas a lisosomas (LAMPs) se han identificado como proteínas de unión asociadas a la amelogenina; se ha sugerido que actúan como receptores de señalización de la amelogenina. El propósito de este estudio fue aclarar la localización de la amelogenina y las LAMPs en el cartílago de crecimiento y nódulos cartilaginosos en cultivos de micromasa. Articulaciones de la rodilla del ratón, que incluían la placa de crecimiento tibial de 4 semanas de edad y cultivos de micromasa de células mesenquimales del brote del miembro después de 2 semanas se fijaron en paraformaldehído y procesaron rutinariamente. Los cortes fueron sometidos a inmunotinción con amelogenina, colágeno tipo II y X, LAMP-1 y LAMP-3 . Se observó inmunorreacción positiva de amelogenina tanto en la zona proliferación e hipertrófica del cartílago de crecimiento después del pretratamiento enzimático. Además, los nódulos cartilaginosos en el cultivo de micromasa eran inmunopositivos para la amelogenina. Los condrocitos en la zona de proliferación de la placa de crecimiento fueron immunopositivos a LAMP-1, mientras que los condrocitos de la zona hipertrófica se tiñeron débilmente. Estas observaciones indican que la amelogenina puede estar presente en la matriz del cartílago producida tanto in vivo e in vitro, además la amelogenina puede estar implicada en la formación de cartílago mediante la vía de señalización de LAMP-1.

Expression of toll-like receptor 2 in glomerular endothelial cells and promotion of diabetic nephropathy by Porphyromonas gingivalis lipopolysaccharide.

The toll-like receptor (TLR) has been suggested as a candidate cause for diabetic nephropathy. Recently, we have reported the TLR4 expression in diabetic mouse glomerular endothelium. The study here investigates the effects of the periodontal pathogen Porphyromonas gingivalis lipopolysaccharide (LPS) which is a ligand for TLR2 and TLR4 in diabetic nephropathy. In laser-scanning microscopy of glomeruli of streptozotocin- and a high fat diet feed-induced type I and type II diabetic mice, TLR2 localized on the glomerular endothelium and proximal tubule epithelium. The TLR2 mRNA was detected in diabetic mouse glomeruli by in situ hybridization and in real-time PCR of the renal cortex, the TLR2 mRNA amounts were larger in diabetic mice than in non-diabetic mice. All diabetic mice subjected to repeated LPS administrations died within the survival period of all of the diabetic mice not administered LPS and of all of the non-diabetic LPS-administered mice. The LPS administration promoted the production of urinary protein, the accumulation of type I collagen in the glomeruli, and the increases in IL-6, TNF-α, and TGF-ß in the renal cortex of the glomeruli of the diabetic mice. It is thought that blood TLR ligands like Porphyromonas gingivalis LPS induce the glomerular endothelium to produce cytokines which aid glomerulosclerosis. Periodontitis may promote diabetic nephropathy.

Inhibition of extracellular signal-regulated kinase downregulates claudin-2 expression and alters paracellular permeability in mouse rectum CMT93-II cells.

The morphological and physiological properties of tight junctions (TJs) are determined by the combination and mixing ratios of claudin species. Mouse rectum carcinoma cell lines, CMT93-I and -II cells, expressed claudin-4, -6, -7, and -12, and CMT93-II cells further expressed claudin-2. Although there were no differences in the morphology and number of TJ strands between the two cell lines, transepithelial electrical resistance (TER) of CMT93-II cells was approximately one-seventh that of CMT93-I cells. In this study, we aimed to determine whether claudin-2 expression in CMT93-II cells caused the reduction of TER. Inhibition of the extracellular signal-regulated kinase (ERK) pathway by U0126 treatment for 24 and 48h in CMT93-II cells markedly decreased claudin-2 from the apical junctional region and increased TER. However, claudin-4, -6, and -7 were still continuously localized at the apical junctional region by U0126 treatment. Moreover, the claudin-2 expression recovered at the apical junctional region after the removal of U0126 and TER decreased almost to the baseline level. These results suggest that the ERK pathway positively regulates claudin-2 protein expression and claudin-2 is involved in lowering TER in CMT93-II cells.

Immobilization in external rotation after shoulder dislocation reduces the risk of recurrence. A randomized controlled trial.

BACKGROUND: An initial anterior dislocation of the shoulder becomes recurrent in 66% to 94% of young patients after immobilization of the shoulder in internal rotation. Magnetic resonance imaging and studies of cadavera have shown that coaptation of the Bankart lesion is better with the arm in external rotation than it is with the arm in internal rotation. Our aim was to determine the benefit of immobilization in external rotation in a randomized controlled trial. METHODS: One hundred and ninety-eight patients with an initial anterior dislocation of the shoulder were randomly assigned to be treated with immobilization in either internal rotation (ninety-four shoulders) or external rotation (104 shoulders) for three weeks. The primary outcome measure was a recurrent dislocation or subluxation. The minimum follow-up period was two years. RESULTS: The follow-up rate was seventy-four (79%) of ninety-four in the internal rotation group and eighty-five (82%) of 104 in the external rotation group. The compliance rate was thirty-nine (53%) of seventy-four in the internal rotation group and sixty-one (72%) of eighty-five in the external rotation group (p = 0.013). The intention-to-treat analysis revealed that the recurrence rate in the external rotation group (twenty-two of eighty-five; 26%) was significantly lower than that in the internal rotation group (thirty-one of seventy-four; 42%) (p = 0.033) with a relative risk reduction of 38.2%. In the subgroup of patients who were thirty years of age or younger, the relative risk reduction was 46.1%. CONCLUSIONS: Immobilization in external rotation after an initial shoulder dislocation reduces the risk of recurrence compared with that associated with the conventional method of immobilization in internal rotation. This treatment method appears to be particularly beneficial for patients who are thirty years of age or younger.

A new method of immobilization after traumatic anterior dislocation of the shoulder: a preliminary study.

This preliminary prospective study was conducted to determine whether immobilization with the arm in external rotation would decrease the rate of recurrence after initial traumatic anterior dislocation of the shoulder. Forty patients with initial shoulder dislocations were assigned to (1) conventional immobilization in internal rotation (IR group, n = 20) or (2) a new method of immobilization in external rotation (ER group, n = 20). The recurrence rate was 30% in the IR group and 0% in the ER group at a mean 15.5 months. The difference in recurrence rate was even greater among those who were aged less than 30 years (45% in the IR group and 0% in the ER group). Immobilization with the arm in external rotation is effective in reducing the rate of recurrence after initial dislocation of the shoulder.

Smad signaling in mesenchymal and chondroprogenitor cells.

BACKGROUND: Bone morphogenetic proteins (BMPs) are pleiotropic differentiation factors that regulate cell fate determination by orchestrating the activities of downstream signal transducers. Although BMP ligands can elicit signal transduction from heterodimeric combinations of several type-I and type-II receptors, cytoplasmic transducers of the BMP signal include only three known BMP-specific regulatory Smad proteins: Smad1, 5, and 8. In order to determine the combination of signals that regulate chondrogenesis by BMPs, we analyzed the functions of BMP Smad subtypes. METHODS: Multipotential mesenchymal C3H10T1/2 cells and monopotential chondroprogenitor MC615 cells were placed in micromass culture in the presence or absence of BMP4. Chondrogenic differentiation was assayed by measuring Sox9 and type-II collagen gene expression and by alcian blue staining. Transactivation of type-II collagen by regulatory Smads singly, or in combination with Smad4, which partners with regulatory Smads, was assayed by luciferase activity. RESULTS: In the absence of BMP4, mesenchymal cells did not exhibit chondrogenic differentiation, whereas chondroprogenitor cells showed increased cartilage marker expression. In the presence of BMP4, the rate and extent of chondrogenesis increased in a dose-dependent manner for both cell types. We further determined that Smad1 or Smad5, but not Smad8, synergized with Smad4 in the transactivation of the type-II collagen promoter in chondroprogenitor cells. In contrast, Smad8 and Smad4 presented modest synergy in mesenchymal cells. CONCLUSIONS: Taken together, our data suggest that uncommitted mesenchymal cells do not have the cellular competence to respond to the rate-limiting chondroinductive factor BMP. However, in chondroprogenitor cells, BMP stimulates differentiation through mechanisms mediated by Smad1 or Smad5 in combination with Smad4.

The receptor activator of nuclear factor-kappa B ligand-mediated osteoclastogenic pathway is elevated in amelogenin-null mice.

Amelogenins, major components of developing enamel, are predominantly involved in the formation of tooth enamel. Although amelogenins are also implicated in cementogenesis, their precise spatial expression pattern and molecular role are not clearly understood. Here, we report for the first time the expression of two alternate splice forms of amelogenins, M180 and the leucine-rich amelogenin peptide (LRAP), in the periodontal region of mouse tooth roots. Lack of M180 and LRAP mRNA expression correlated with cementum defects observed in the amelogenin-null mice. The cementum defects were characterized by an increased presence of multinucleated cells, osteoclasts, and cementicles. These defects were associated with an increased expression of the receptor activator of the nuclear factor-kappa B ligand (RANKL), a critical regulator of osteoclastogenesis. These findings indicate that the amelogenin splice variants, M180 and LRAP, are critical in preventing abnormal resorption of cementum.