Introduction: Stress increases proinflammatory cytokine levels in the periphery and brain. Elevated levels of inflammatory mediators have been described in pathologic intervertebral disc (IVD) tissue, and these levels increase with the severity of the degeneration. Therefore, there is a probable link between emotional stress and disk degeneration.The present study was designed to evaluate the effects of chronic unpredictable stress(CUS)on the IVD of rats.
Methods: The cellular events involved in the injury- and stress-induced disc degeneration were investigated in male Wistar rats. Disc degeneration and apoptosis were evaluated using microscopic (light and electron) and molecular (immunoblotting and immunohistochemistry) methods. Corticosterone levels were used as markers of stress and measured by radioimmunoassay.
Results: The data gathered in this study showed that CUS can significantly increase corticosterone levels. Furthermore, biochemical markers of apoptosis [i.e., increases in the Bax to Bcl2 ratio and TUNEL reactivity (P<0.05)] were observed in the stressed animals. Electron and light microscopy also showed disc degeneration and apoptotic cells in the experimental groups.
Conclusions: Taken together, these data demonstrated that chronic stress is most likely a risk factor for creating IVD degeneration and that programmed cell death may be one of the mechanisms of stress-induced disc degeneration.
Patient Care: Stress is an unavoidable effect of daily life. If the results of this study attributable to human,change of patient's life style concerning chronic stress can help patients with back pain due to herniated disc.
Learning Objectives: By the conclusion of this session, participants should be able to: 1)describe a common but unfamiliar risk factor for disc degeneration: chronic stress. 2) present its presumptive mechanisms i.e. programmed cell death.