Refine
Language
- English (16)
Is part of the Bibliography
- yes (16)
Keywords
- osteoporosis (4)
- inflammation (3)
- CHOP (2)
- GADD153 (2)
- GRP78 (2)
- IL-6 (2)
- biomechanics (2)
- bone mineral density (2)
- bone pathologies (2)
- bone–brain–nervous system interactions (2)
Bone pathology is frequent in stressed individuals. A comprehensive examination of mechanisms linking life stress, depression and disturbed bone homeostasis is missing. In this translational study, mice exposed to early life stress (MSUS) were examined for bone microarchitecture (μCT), metabolism (qPCR/ELISA), and neuronal stress mediator expression (qPCR) and compared with a sample of depressive patients with or without early life stress by analyzing bone mineral density (BMD) (DXA) and metabolic changes in serum (osteocalcin, PINP, CTX-I). MSUS mice showed a significant decrease in NGF, NPYR1, VIPR1 and TACR1 expression, higher innervation density in bone, and increased serum levels of CTX-I, suggesting a milieu in favor of catabolic bone turnover. MSUS mice had a significantly lower body weight compared to control mice, and this caused minor effects on bone microarchitecture. Depressive patients with experiences of childhood neglect also showed a catabolic pattern. A significant reduction in BMD was observed in depressive patients with childhood abuse and stressful life events during childhood. Therefore, future studies on prevention and treatment strategies for both mental and bone disease should consider early life stress as a risk factor for bone pathologies.
Study Design. A nonrandomized, prospective, and single-center clinical trial. Objective. The aim of this study was to determine whether the prosthesis design, and especially changes in the primary anchoring mechanism between the keel-based ProDisc C and the spike-based ProDisc Vivo, affects the frequency of heterotopic ossification (HO) formation over time. Summary of Background Data. The occurrence of motion-restricting HO as well as underlying risk factors has so far been a widely discussed, but not well understand phenomenon. The anchoring mechanism and the opening of the anterior cortex may be possible causes of this unwanted complication. Methods. Forty consecutive patients treated with the ProDisc C and 42 consecutive patients treated with the ProDisc Vivo were compared with respect to radiological and clinical outcome, with 2 years of follow-up. Clinical outcome scores included the Neck Disability Index (NDI), Visual Analogue Scale (VAS), and arm and neck pain self-assessment questionnaires. Radiological outcomes included the segmental lordosis and range of motion (ROM) of the index-segment as well as the occurrence of HO. Results. The clinical outcome parameters improved in both groups significantly. [ProDisc C: VAS arm and neck pain from 6.3 and 6.2 preoperatively to 0.7 and 1.3; NDI from 23.0 to 3.7; ProDisc Vivo: VAS arm and neck pain from 6.3 and 4.9 to 1.4 and 1.6, NDI from 34.1 to 8.7; 2-year follow-up (FU)]. The ProDisc Vivo cohort demonstrated a significantly lower incidence of HO than the ProDisc C group at 1-year FU (P = 0.0005) and 2-year FU (P = 0.005). Specifically, high-grade HO occurred in 9% versus 31%. Conclusion. These findings demonstrate that prosthesis designs that allow primary anchoring without violation of the cortical surface help to reduce the incidence of severe ossification, possibly affecting the functionality and mobility of the artificial disc device over of time.
Degeneration of the intervertebral disc – triggered by ageing, mechanical stress, traumatic injury, infection, inflammation and other factors – has a significant role in the development of low back pain. Back pain not only has a high prevalence, but also a major socio-economic impact. With the ageing population, its occurrence and costs are expected to grow even more in the future. Disc degeneration is characterized by matrix breakdown, loss in proteoglycans and thus water content, disc height loss and an increase in inflammatory molecules. The accumulation of cytokines, such as interleukin (IL)-1 , IL-8 or tumor necrosis factor (TNF)-, together with age-related immune deficiency, leads to the so-called inflammaging – low-grade, chronic inflammation with a crucial role in pain development. Despite the relevance of these molecular processes, current therapies target symptoms, but not underlying causes. This review describes the biological and biomechanical changes that occur in a degenerated disc, discusses the connection between disc degeneration and inflammaging, highlights factors that enhance the inflammatory processes in disc pathologies and suggests future research avenues.
Decades of research have demonstrated that physical stress (PS) stimulates bone remodeling and affects bone structure and function through complex mechanotransduction mechanisms. Recent research has laid ground to the hypothesis that mental stress (MS) also influences bone biology, eventually leading to osteoporosis and increased bone fracture risk. These effects are likely exerted by modulation of hypothalamic–pituitary–adrenal axis activity, resulting in an altered release of growth hormones, glucocorticoids and cytokines, as demonstrated in human and animal studies. Furthermore, molecular cross talk between mental and PS is thought to exist, with either synergistic or preventative effects on bone disease progression depending on the characteristics of the applied stressor. This mini review will explain the emerging concept of MS as an important player in bone adaptation and its potential cross talk with PS by summarizing the current state of knowledge, highlighting newly evolving notions (such as intergenerational transmission of stress and its epigenetic modifications affecting bone) and proposing new research directions.
Decades of research have demonstrated that physical stress (PS) stimulates bone remodeling and affects bone structure and function through complex mechanotransduction mechanisms. Recent research has laid ground to the hypothesis that mental stress (MS) also influences bone biology, eventually leading to osteoporosis and increased bone fracture risk. These effects are likely exerted by modulation of hypothalamic–pituitary–adrenal axis activity, resulting in an altered release of growth hormones, glucocorticoids and cytokines, as demonstrated in human and animal studies. Furthermore, molecular cross talk between mental and PS is thought to exist, with either synergistic or preventative effects on bone disease progression depending on the characteristics of the applied stressor. This mini review will explain the emerging concept of MS as an important player in bone adaptation and its potential cross talk with PS by summarizing the current state of knowledge, highlighting newly evolving notions (such as intergenerational transmission of stress and its epigenetic modifications affecting bone) and proposing new research directions.