Effect of total disc replacement on atypical symptoms associated with cervical spondylosis

Sun, Yin; Zheng, Shuguo; Yu, Jie; Ke, Yan; Tian, Wei

doi:10.1007/s00586-013-2785-6

Cited by 32 publications

(22 citation statements)

References 11 publications

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“…Hypertrophic chondrocytes die through the induction of programmed cell death (apoptosis) in the background of cervical spondylosis or the joint disorder containing osteoarthritis (OA) characterized by progressive breakdown of articular cartilage [3,4]. Reactive oxygen species (ROS) generated from the hypoxia/ischaemia trigger apoptotic cell death [5].…”

Section: Introductionmentioning

confidence: 99%

RhoA inhibits the hypoxia-induced apoptosis and mitochondrial dysfunction in chondrocytes via positively regulating the CREB phosphorylation

Zhang

Jiang

2017

Bioscience Reports

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Chondrocytes that are embedded within the growth plate or the intervertebral disc are sensitive to environmental stresses, such as inflammation and hypoxia. However, little is known about the molecular signalling pathways underlining the hypoxia-induced mitochondrial dysfunction and apoptosis in chondrocytes. In the present study, we firstly examined the hypoxia-induced apoptosis, mitochondrial dysfunction and the activation of cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) signalling in human chondrocyte cell line, C28/I2 and then investigated the regulatory role of RhoA, a well-recognized apoptosis suppressor, in such process, with gain-of-function strategy. Our results indicated that hypoxia induced apoptosis and inhibited CREB phosphprylation in chondrocytes, meanwhile, the dysfunctional mitochondria with up-regulated mitochondrial superoxide and reactive oxygen species (ROS) levels, whereas with a reduced mitochondrial membrane potential (MMP) and Complex IV activity were observed in the hypoxia-treated C28/I2 cells. However, the overexpressed RhoA blocked the hypoxia-mediated reduction in CREB phosphprylation and inhibited the apoptosis induction, along with an ameliorated mitochondrial function in the hypoxia-treated C28/I2 cells. In conclusion, the present study confirmed the reduced CREB phosphorylation, along with the apoptosis induction and mitochondrial dysfunction in the hypoxia-treated chondrocyte cells. And the overexpression of RhoA ameliorated the hypoxia-induced mitochondrial dysfunction and apoptosis via blocking the hypoxia-mediated reduction in CREB phosphorylation.

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Section: Introductionmentioning

confidence: 99%

RhoA inhibits the hypoxia-induced apoptosis and mitochondrial dysfunction in chondrocytes via positively regulating the CREB phosphorylation

Zhang

Jiang

2017

Bioscience Reports

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“…Chondrocyte dysfunction results in the cervical spondylosis associated with degeneration of the intervertebral disc, or the joint disorder osteoarthritis (OA), which is characterized by progressive breakdown of articular cartilage (1)(2)(3). Chondrocytes are sensitive to environmental and multiple cellular stresses, including inflammation, mechanical loading, stress to the endoplasmic reticulum and hypoxia (4)(5)(6).…”

Section: Introductionmentioning

confidence: 99%

Ascorbic acid provides protection for human chondrocytes against oxidative stress

Chang

Huo

et al. 2015

Molecular Medicine Reports

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Abstract. Oxidative stress is considered to be an important cause of dysfunction in chondrocytes and articular cartilage degradation, which leads to the pathogenesis of osteoarthritis (OA) and cartilage aging. The present study aimed to assess the effects of the widely applied antioxidant, ascorbic acid (AA), on human chondrocytes against hydrogen peroxide (H 2 O 2 ) in vitro. Using annexin V-fluorescein isothiocyanate, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and senescence-associated β-galactosidase assays, the present study identified that AA reduced apoptosis, reduced the loss of viability and markedly decreased H 2 O 2 -mediated senescence in cells treated with H 2 O 2 . Furthermore, AA not only stimulated the expression levels of collagens and proteoglycans, but also inhibited the differentiation of chondrocytes under conditions of oxidative stress. In addition, reverse transcription-quantitative polymerase chain reaction and western blotting demonstrated that AA decreased the activity of nrf2, NF-κB, AP1 and matrix metalloproteinase-3, which is stimulated by H 2 O 2 . In conclusion, AA efficiently protected human chondrocytes against damage induced by H 2 O 2 by regulating multiple regulatory pathways.

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“…11 Because no typical abnormalities have been found so far by radiologic and pathologic studies that may cause those symptoms, it might be appropriate to call this set of symptoms "atypical." 12 Although there are many reports on the treatment of cervical spondylosis, there is little discussion on the atypical symptoms of cervical spondylosis in the current literature. In patients with such symptoms, cervical disk degeneration is normally the only abnormality that can be observed by imaging studies.…”

Section: Discussionmentioning

confidence: 99%

Effect of Anterior Cervical Discectomy and Fusion on Patients with Atypical Symptoms Related to Cervical Spondylosis

Muheremu

Sun

et al. 2016

J Neurol Surg A Cent Eur Neurosurg

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Background A considerable number of patients with cervical spondylosis complain about one or multiple atypical symptoms such as vertigo, palpitations, headache, blurred vision, hypomnesia, and/or nausea. It remains unclear whether surgical intervention for cervical spondylosis can also effectively alleviate those symptoms. The current study was performed to see if anterior cervical diskectomy and fusion (ACDF) offers such an extra benefit for patients with cervical spondylosis. Objective To investigate if patients who received ACDF for the treatment of cervical spondylotic myelopathy and/or radiculopathy can also achieve alleviation of certain atypical symptoms associated with cervical spondylosis after the surgery in the long run. Methods Sixty-seven patients who underwent ACDF for the treatment of cervical spondylotic myelopathy and/or radiculopathy were involved in this study. All these patients also complained about various associated atypical symptoms. They were followed up for 26 to 145 months after the surgery. Severity and frequency scores of the atypical symptoms before the surgery and at last follow-up were compared by paired t tests. Results Most patients reported significantly alleviated symptoms at the last follow-up compared with before the surgery. The severity of vertigo, headache, nausea, and palpitations were significantly alleviated at the last follow-up (with p values of p < 0.001, p = 0.001, p = 0.022, p = 0.004, respectively). There were no significant changes in the severity of tinnitus (p = 0.182), blurred vision (p = 0.260), and hypomnesia (p = 0.821). Conclusion ACDF can significantly alleviate vertigo, headache, nausea, and palpitations in most patients with cervical spondylotic myelopathy and/or radiculopathy, but it is not effective in alleviating symptoms such as tinnitus, blurred vision, and hypomnesia. It can be considered for alleviating atypical symptoms when other treatment options prove ineffective.

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Effect of total disc replacement on atypical symptoms associated with cervical spondylosis

Abstract: TDR may have a positive effect on atypical symptoms associated with cervical spondylotic myelopathy and/or radiculopathy.

Cited by 32 publications

References 11 publications

RhoA inhibits the hypoxia-induced apoptosis and mitochondrial dysfunction in chondrocytes via positively regulating the CREB phosphorylation

RhoA inhibits the hypoxia-induced apoptosis and mitochondrial dysfunction in chondrocytes via positively regulating the CREB phosphorylation

Ascorbic acid provides protection for human chondrocytes against oxidative stress

Effect of Anterior Cervical Discectomy and Fusion on Patients with Atypical Symptoms Related to Cervical Spondylosis

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