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Chronic compression or ischemia of the spinal cord in the cervical spine causes a clinical syndrome known as cervical myelopathy. Recently, a new term “degenerative cervical myelopathy (DCM)” was introduced. DCM encompasses spondylosis, intervertebral disk herniation, facet arthrosis, ligamentous hypertrophy, calcification, and ossification. The pathophysiology of DCM includes structural and functional abnormalities of the spinal cord caused by static and dynamic factors. In nonoperative patients, cervical myelopathy has a poor prognosis. Surgical treatments, such as anterior or posterior decompression accompanying arthrodesis, arthroplasty, or laminoplasty, should be considered for patients with chronic progressive cervical myelopathy. Surgical decompression can prevent the progression of myelopathy and improve the neurologic status, functional outcomes, and quality of life, irrespective of differences in medical systems and sociocultural determinants of health. The anterior surgical approach to the cervical spine has the advantage of removing or floating the intervertebral disk, osteophytes, and ossification of the posterior longitudinal ligament that compress the spinal cord directly. The posterior surgical approach to the cervical spine is mainly used for multisegment spinal cord compression in patients with cervical lordosis. In this review article, we addressed the pathophysiology, clinical manifestations, differential diagnosis, and treatment options for DCM.

Introduction: Anterior cervical corpectomy and fusion (ACCF) for cervical ossification of the posterior longitudinal ligament (OPLL) is associated with a high incidence of surgery-related complications. A novel anterior decompression technique (vertebral body sliding osteotomy [VBSO]) has been developed to prevent such complications. This study attests the efficacy and safety of VBSO versus those of standard ACCF. Methods: Patients requiring surgery for cervical OPLL underwent VBSO (24 patients) or ACCF (38 patients). Operating time, estimated blood loss, neurologic outcomes, complications, and various radiographic parameters were investigated. Results: The VBSO group showed a shorter mean operating time and less estimated blood loss versus the ACCF group. Sixteen patients in the ACCF group experienced various complications, namely neurologic deficit (two patients), cerebrospinal fluid leakage (four patients), graft migration (three patients), and pseudarthrosis (seven patients). In the VBSO group, only pseudarthrosis was reported (two patients). Conclusions: VBSO provides similar neurologic outcomes with a shorter operating time and less bleeding compared with ACCF. Surgeons do not need to directly manipulate the OPLL mass or dissect the interspace between the OPLL and dura mater. Therefore, this technique may decrease the incidence of surgery-related complications. Study Design: Retrospective comparative study.

Study Design: A nationwide population-based study.Purpose: Osteoporotic vertebral compression fracture (OVCF) is a major public health issue. This study examined the incidence and management trends of OVCF in South Korea. Overview of Literature: The incidence rates, management trends, and patterns of OVCF differ in different parts of the world. The age-standardized OVCF incidence rate in 2015 was higher in the United States and Asia than in Europe.Methods: A nationwide database (2012–2016) acquired from the Korean Health Insurance Review and Assessment Service was analyzed. International disease categories in the 10th revision of the International Statistical Classification of Diseases and Related Health Problems codes, medical procedure codes, and examination codes were used to identify and sort OVCF patients aged >50 years.Results: There were 644,500 OVCF cases from 2012 to 2016. OVCF was most common in patients in their seventies (45%) and the number of patients increased from 117,361 in 2012 to 139,889 in 2016 (<i>p</i> <0.001). During 2012–2016, 8.9% of patients visited the emergency department; of those, 54.3% were hospitalized and 35% underwent magnetic resonance imaging. In OVCF treatment, bone cement augmentation rates increased from 23.4% in 2012 to 25.2% in 2016 (<i>p</i> <0.001), while conservative treatment rates slightly decreased from 76.5% in 2012 to 74.7% in 2016 (<i>p</i> <0.001). The total health insurance cost was $193,210,353.55 in 2012 and $281,968,877.65 in 2016.Conclusions: The 5-year incidence of OVCF per 100,000 persons was 852.24 cases, and 45% of OVCF in South Korea occurred in patients in their seventies. The bone cement augmentation rate and total cost of OVCF are continuously increasing.

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Transforming growth factor β1 (TGFβ1) is a major mediator in the modulation of osteoblast differentiation. However, the underlying molecular mechanism is still not fully understood. Here, we show that TGFβ1 has a dual stage-dependent role in osteoblast differentiation; TGFβ1 induced matrix maturation but inhibited matrix mineralization. We discovered the underlying mechanism of the TGFβ1 inhibitory role in mineralization using human osteoprogenitors. In particular, the matrix mineralization-related genes of osteoblasts such as osteocalcin (OCN), Dickkopf 1 (DKK1), and CCAAT/enhancer-binding protein beta (C/EBPβ) were dramatically suppressed by TGFβ1 treatment. The suppressive effects of TGFβ1 were reversed with anti-TGFβ1 treatment. Mechanically, TGFβ1 decreased protein levels of C/EBPβ without changing mRNA levels and reduced both mRNA and protein levels of DKK1. The degradation of the C/EBPβ protein by TGFβ1 was dependent on the ubiquitin–proteasome pathway. TGFβ1 degraded the C/EBPβ protein by inducing the expression of the E3 ubiquitin ligase Smad ubiquitin regulatory factor 1 (SMURF1) at the transcript level, thereby reducing the C/EBPβ-DKK1 regulatory mechanism. Collectively, our findings suggest that TGFβ1 suppressed the matrix mineralization of osteoblast differentiation by regulating the SMURF1-C/EBPβ-DKK1 axis.

ObjectiveThe purpose of this study was to determine, when measuring prostate volume by TRUS, whether height is more accurately determined by transaxial or midsagittal scanning.Materials and MethodsSixteen patients who between March 1995 and March 1998 underwent both preoperative TRUS and radical prostatectomy for prostate cancer were included in this study. Using prolate ellipse volume calculation (height × length × width × π/6), TRUS prostate volume was determined, and was compared with the measured volume of the specimen .ResultsProstate volume measured by TRUS, regardless of whether height was determined transaxially or midsagittally, correlated closely with real specimen volume. When height was measured in one of these planes, a paired t test revealed no significant difference between TRUS prostate volume and real specimen volume (p = .411 and p = .740, respectively), nor were there significant differences between the findings of transaxial and midsagittal scanning (p = .570). A paired sample test, however, indicated that TRUS prostate volumes determined transaxially showed a higher correlation coefficient (0.833) and a lower standard deviation (9.04) than those determined midsagittally (0.714 and 11.48, respectively).ConclusionProstate volume measured by TRUS closely correlates with real prostate volume. Furthermore, we suggest that when measuring prostate volume in this way, height is more accurately determined by transaxial than by midsagittal scanning.

1α,25-dihydroxyvitamin D3 (1,25D3), the most popular drug for osteoporosis treatment, drives osteoblast differentiation and bone mineralization. Wnt/β-catenin signaling is involved in commitment and differentiation of osteoblasts, but the role of the Dickkopf-related protein 1 (DKK1), a Wnt antagonist, in osteoblasts remains unknown. Here, we demonstrate the molecular mechanism of DKK1 induction by 1,25D3 and its physiological role during osteoblast differentiation. 1,25D3 markedly promoted the expression of both CCAAT/enhancer binding protein beta (C/EBPβ) and DKK1 at day 7 during osteoblast differentiation. Interestingly, mRNA and protein levels of C/EBPβ and DKK1 in osteoblasts were elevated by 1,25D3. We also found that C/EBPβ, in response to 1,25D3, directly binds to the human DKK1 promoter. Knockdown of C/EBPβ downregulated the expression of DKK1 in osteoblasts, which was partially reversed by 1,25D3. In contrast, overexpression of C/EBPβ upregulated DKK1 expression in osteoblasts, which was enhanced by 1,25D3. Furthermore, 1,25D3 treatment in osteoblasts stimulated secretion of DKK1 protein within the endoplasmic reticulum to extracellular. Intriguingly, blocking DKK1 attenuated calcified nodule formation in mineralized osteoblasts, but not ALP activity or collagen synthesis. Taken together, these observations suggest that 1,25D3 promotes the mineralization of osteoblasts through activation of DKK1 followed by an increase of C/EBPβ.