Skeletal fractures, including those resulting from osteoporosis, result in significant healthcare and societal costs on an annual basis. Therefore, it is important to understand the mechanisms by which these fractures occur. Incremental compression testing combined with micro-CT imaging has been used to visualize the progression of failure in trabecular bone samples; however, these studies have ignored the potential contributions of the cortical shell. In the current study, incremental compression testing with simultaneous micro-CT imaging was performed on rat vertebrae from multiple disease states (healthy control, osteoporotic, osteoporotic + treatment). These tests allowed the progression of failure through an entire vertebral body to be visualized for the first time. Three distinct failure modes were observed throughout all specimens, independent of disease state. Two of these failure modes (types I and II), which were observed in 93% of all specimens, were associated with the vascular apertures in the vertebrae's dorsal and ventral surfaces. This behaviour is likely caused by the stress concentrations in the cortical shell resulting from the apertures themselves, coupled with the reduced trabecular bone volume adjacent to them. These results suggest that the combined contributions of both the cortical shell and trabecular bone must be considered when studying the compressive failure behaviour of rat vertebrae.
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http://dx.doi.org/10.1016/j.jmbbm.2017.11.021 | DOI Listing |
Cell Signal
January 2025
Department of Orthopedics, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107 Yanjiang West Road, Guangzhou 510120, PR China. Electronic address:
Intervertebral disc degeneration (IVDD) is a leading cause of low back pain, primarily driven by inflammatory processes within the disc, particularly involving the infiltration and activity of macrophages. High Mobility Group Box 1 (HMGB1) has been identified as a crucial mediator in this inflammatory cascade, yet its precise role in macrophage-induced disc degeneration remains unclear. In this study, we employed a combination of in vivo and in vitro models, including genetically engineered mice with macrophage-specific overexpression of HMGB1, a rat model of IVDD, and cultured macrophages and nucleus pulposus cells (NPCs), to elucidate the role of HMGB1 in IVDD.
View Article and Find Full Text PDFSpine (Phila Pa 1976)
January 2025
Department of Orthopedics, the First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, People's Republic of China.
Study Design: Subgroup analysis of a retrospective clinical and animal trial [Study of different doses of methylprednisolone on functional recovery of spinal cord injury].
Objective: The aimed to investigate the efficacy of low-dose methylprednisolone regimens in promoting neural repair after SCI.
Summary Of Background Data: Spinal cord injury (SCI) can result in sensory, motor, and autonomic nerve dysfunction, often leading to disability or death.
Mol Med
January 2025
Division of Spine Surgery, Department of Orthopedics, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Ave, Guangzhou, 510515, People's Republic of China.
Background: Neuropathic pain (NP) is a debilitating condition caused by lesion or dysfunction in the somatosensory nervous system. Accumulation of advanced oxidation protein products (AOPPs) is implicated in mechanical hyperalgesia. However, the effects of AOPPs on NP remain unclear.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Azriele Faculty of Medicine in the Galilee, Bar-Ilan University, Safed 1311502, Israel.
Provoked vulvodynia (PV) is the leading cause of vulvar pain and dyspareunia. The etiology of PV is multifactorial and remains poorly understood. PV is associated with a history of repeated vulvar inflammation and is often accompanied by sensory neuromodulation as a result of activation of the metabotropic glutamate receptor 5 (mGluR5) in the sensory nerve terminals.
View Article and Find Full Text PDFBiomedicines
January 2025
Jaseng Spine and Joint Research Institute, Jaseng Medical Foundation, Seoul 135-896, Republic of Korea.
Background/objectives: Lumbar spinal stenosis (LSS) is a degenerative condition characterized by the narrowing of the spinal canal, resulting in chronic pain and impaired mobility. However, the molecular mechanisms underlying LSS remain unclear. In this study, we performed RNA sequencing (RNA-seq) to investigate differential gene expression in a rat LSS model and identify the key genes and pathways involved in its pathogenesis.
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