A Novel Method for Preoperative Positioning of Total Ankle Replacement Using 3D Digital Model.

Objective: To establish a digital model of the ankle joint through 3D imaging technology and explore the preoperative placement of ankle replacement prostheses.

Methods: Computed tomography images of intact ankle joints from 54 cases in the outpatient and inpatient departments of our hospital were collected; according to the INBONE® total ankle system surgery process, the surgery model and surgical osteotomy were finished using MIMICS based on computer simulation method. The shortest distance was measured between the center point and the anterior, posterior, medial, and lateral, respectively, to ensure the precise position of the ankle replacement prosthesis by digital simulation surgery.

MALDI-TOF-MS serum protein profiling for developing diagnostic models and identifying serum markers for discogenic low back pain.

Background: The identification of the cause of chronic low back pain (CLBP) represents a great challenge to orthopedists due to the controversy over the diagnosis of discogenic low back pain (DLBP) and the existence of a number of cases of CLBP of unknown origin. This study aimed to develop diagnostic models to distinguish DLBP from other forms of CLBP and to identify serum biomarkers for DLBP.

Methods: Serum samples were collected from patients with DLBP, chronic lumbar disc herniation (LDH), or CLBP of unknown origin, and healthy controls (N), and randomly divided into a training set (n = 30) and a blind test set (n = 30).

Expression profiles of genes involved in apoptosis and selenium metabolism in articular cartilage of patients with Kashin-Beck osteoarthritis.

Kashin-Beck disease (KBD) is a special type of endemic osteoarthritis. It has been suggested that alterations in selenium metabolism and apoptosis play a role in KBD. However, the underlying molecular mechanism remains largely unclear.

Association of clinical features of bone and joint lesions between children and parents with Kashin-Beck disease in Northwest China.

We investigated the clinical features of bone and joint lesions in children with Kashin-Beck disease (KBD) and the association of these features with their parents to determine specific clinical features for diagnosing KBD. A total of 2,248 children (4 to 18 years old) and their parents were examined by stratified cluster sampling from 33 villages in six endemic counties and from six villages in a non-endemic county. We collected individual information, clinical symptoms, and radiological signs of the right hand.

[Changes of death receptor regulator expression in the articular cartilage of patients with Kashin-Beck disease].

Objective: To investigate the changes in the expressions of Fas-associated death domain protein (FADD) and cellular-FLICE inhibitory protein (c-FLIP) in the articular cartilage of patients with Kashin-Beck disease (KBD) and the role of these proteins in the pathogenesis of KBD.

Methods: The cartilage samples were collected from patients with established diagnosis of KBD and osteoarthritis and from healthy control subjects undergoing amputation due to traffic accidents. The expressions of Fas-associated death domain protein (FADD) and cellular-FLICE inhibitory protein (c-FLIP) in the cartilage were detected by immunohistochemistry, and the positive chondrocytes were counted in different layers of the articular cartilage under microscope.

Association between Caspase-9 promoter region polymorphisms and discogenic low back pain.

Caspase-9 (CASP-9) is an initiator caspase protease for apoptosis, and plays an important role in the development and progression of lumbar disc disease (LDD). The expression and/or activity of CASP-9 are significantly enhanced in the degenerated disc. The polymorphism in the promoter region of CASP-9 enhances the transcriptional activity of this gene, thereby modulating the susceptibility to LDD.

Clinical diagnosis for discogenic low back pain.

Discogenic lower back pain (DLBP) is the most common type of chronic lower back pain (LBP), accounting for 39% of cases, compared to 30% of cases due to disc herniation, and even lower prevalence rates for other causes, such as zygapophysial joint pain. Only a small proportion (approximately 20%) of LBP cases can be attributed with reasonable certainty to a pathologic or anatomical entity. Thus, diagnosing the cause of LBP represents the biggest challenge for doctors in this field.