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IntroductionThe pathogenetic mechanism of low back pain and nerve root damage in lumbar disc herniation is the subject of ongoing debate. In particular, given that the mechanicalischaemic hypothesis alone cannot explain the cause-effect relationship between disc degeneration and neurological impairment, a biochemical mechanism is likely to be involved. It has recently been demonstrated that the autologous nucleus pulposus can induce histological and functional changes in spinal nerve roots when applied epidurally [17]. Cells of the nucleus pulposus can produce prostaglandin E2, interleukin-1 and interleukin-6 (IL-6) [31], phospholipase A2 [26], and growth factors like fibroblast-like growth factor (FGF) [32] and insulin-like growth factor-1 (IGF-1) [18]. These factors are known to control cell metabolism and to promote inflammatory processes. Moreover, recent studies suggest a critical role for IL-6 and its receptor in the modulation of pain [8]. The mechanisms of action underlying the possible effect of these factors on spinal nerve root structure and function are, however, still unknown. In addition, the fact that nerve roots differ from peripheral nerves in their anatomical, biomechanical, and physiological properties prevents extrapolation from the extensive literature and the numerous experimental models of peripheral nerve compression to the pathophysiology of root injury [5,23,25]. The working hypothesis of the present study is that transforming growth factor-β1 (TGF-β1), IGF-1, IL-6 and IL-6-receptor (IL-6R) can be produced at the site of herniation. This hypothesis was immunohistochemically explored by analysing normal and protruded intervertebral disc tissue for these factors.Abstract Nerve root irritation induced by factors produced by the intervertebral disc may play a crucial role in the pathophysiology of sciatic pain production. In this study we used immunohistochemistry to investigate the presence of transforming growth factor-β1 (TGF-β1), insulinlike growth factor-1 (IGF-1), interleukin-6 (IL-6), IL-6-receptor (IL-6R) and fibronectin in lumbar disc bioptic specimens from 30 patients with disc herniation (protrusion type). Chondrocytes of herniated discs stained positive for TGF-β1, IGF-1, IL-6 and fibronectin. We demonstrated for the first time the presence of IL-6-R in the chondrocytes of herniated tissue. Specimens from autoptic healthy tissue were used as controls. In these sections no immunoreaction for TGF-β1, IL-6, or IL-6R was found, while they expressed IGF-1 and fibronectin, but in lower quantities than herniated discs. These results demonstrated the production of factors such as TGF-β1, IGF-1, IL-6, IL-6R and fibronectin at the site of lumbar disc herniation.

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Carpal tunnel syndrome (CTS) is a compression median nerve neuropathy common in women at menopausal age. The aim of this work was to study immunohistochemically the expression of estrogen (ER) and progesterone (PR) receptors in CTS and control specimens. Biopsies of transverse carpal ligament (TCL) and flexor tendon synovitis were collected from 23 women and from 7 men undergoing surgery for median nerve decompression at the wrist for CTS. In TCL and synovial tissue, cells expressed ER and PR with statistically significant differences related to the age and sex of patients. Immunoreactivity was observed in fibroblasts of TCL, and in lining cells and fibroblasts of synovial tissue. In women, the number of ER-positive cells in the TCL and synovial tissue increased with the age, peaking at 55-70 years, and then decreasing. PR-immunoreactivity was observed only in fibroblasts of TCL and its expression decreased with age, while no immunolabeling was found in the synovial tissue. In TCL samples, the number of ER- and PR-positive cells in non-CTS patients was significantly lower than in CTS patients. These results demonstrate that ER and PR are present in TCL and flexor tendon synovitis, suggesting a role for sex steroid hormones in the pathogenesis of CTS disease.