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 (p <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 (p <0.001), while conservative treatment rates slightly decreased from 76.5% in 2012 to 74.7% in 2016 (p <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.

Cervical myelopathy is a clinical syndrome resulting in symptoms of neurologic deficits due to prolonged spinal cord compression or ischemia in the cervical spine. Spinal cord compression can be caused by ossification of the posterior longitudinal ligament and hypertrophy of ligamentun flavum in addition to degenerative cervical spondylosis, degenerative disc disease, and progressive cervical kyphosis. Degenerative cervical myelopathy (DCM) is a series of disease entities caused by spinal cord compression by various nontraumatic and non-infectious causes. The pathophysiology of DCM includes spinal cord structure and function abnormalities caused by both static and dynamic factors. Surgical decompression for patients with moderate to severe cervical myelopathy not only inhibits the progression of neurological deterioration, but also improves functional status, pain, and quality of life. However, the role of nonsurgical treatment in patients with mild spinal cord compression is controversial. In general, patients with cervical myelopathies who do not undergo surgery have a poor prognosis. Appropriate surgical treatment is recommended when spinal cord compression is confirmed on image study in patients with reasonable symptoms of cervical myelopathy. The patient’s overall health, degree of compression, presence of concurrent cervical radiculopathy, and cervical spine alignment, in addition to lesion location and etiology, should be considered when determining an appropriate surgical procedure. This review covers the updated issues, including pathophysiology, clinical manifestations, differential diagnosis, and available treatments for DCM.

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 (2012-2015) 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 644500 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 (p<0.0011. 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;,p<0.001, while conservative treatment rates slightly decreased from 76.5% in 2012 to 74.7% in 2016 (p<0.001). The total health insurance cost was $193,210,353.55 in 2012 and $281,968,877.65 in 2016. Conclusiens: 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.

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.

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.