In this context, we hypothesize that BMSC-CM has further favoured the activated state of resident microglia and invading macrophages, conferring a phenotype beneficial for tissue preservation, without affecting the number of inflammatory cells within the lesion. This hypothesis is in accordance with the fact that 
IL-1b and IL-6 do indirectly promote axonal outgrowth and protect neurons from death. In the literature, contradictory results have been described concerning the effect of BMSC transplantation on post-injury inflammatory reaction, going from reduced inflammation to enhanced macrophage/microglia response. Some authors also suggest that microglial activation after SCI is linked to the reduction of the lesion size. Indeed, microglia can be involved in neuroprotection via secretion of factors such as NGF, IGF-1 or via up-regulation of FGF-2 in neurons. In conclusion, our data show that the use of BMSC-CM in the context of SCI is beneficial and not deleterious, and leads to improved motor recovery. This treatment constitutes a novel promising therapeutic perspective in SCI context. More Mepiroxol investigations are needed to evaluate the potential of this treatment in chronic lesion models, and its future clinical application. According to the Bureau of Labor Statistics report entitled Nonfatal Occupational Injuries and Illnesses Requiring Days Away from Work, 2011, musculoskeletal disorders accounted for 33 percent of all lost work time workplace injuries and illnesses in the U.S. and required a median of 11 days away from work. Studies in humans with upper extremity work-related musculoskeletal disorders find evidence of inflammation, fibrosis and degeneration in serum and musculotendinous tissues, changes thought to induce concurrent motor dysfunction. However, the pathophysiological responses are still under investigation, particularly responses associated with chronic myopathies and tendinopathies, as are serum biomarkers that might aid in pinpointing the stage of these disorders. An inflammatory response in musculoskeletal tissues has been considered an important element in the pathogenesis of upper extremity soft tissue disorders. A small number of studies have searched for and detected serum biomarkers of inflammation in patients with upper extremity musculoskeletal disorders of short duration, including C-reactive protein, interleukin- 6, tumor necrosis factor-alpha, and members of the IL-1 family. The results of these studies suggest a role for inflammatory cytokines early in the course of upper extremity MSDs. However, tissues collected from patients with upper extremity MSDs at the time of surgical intervention show increased IL-1b immunoreactive fibroblasts and IL-6, but few acute inflammatory responses. Interestingly, IL-6, IL-1b and TNF-a have also been deemed as pro-fibrotic cytokines due to their mitogenic and chemotactic effects on fibroblasts and induction of fibrogenic proteins. A few studies examining serum of workers have also detected increased serum biomarkers of collagen turnover in response to prolonged Benzethonium Chloride exposure to heavy physical loads. Increased serum markers of collagen type I synthesis and degradation were identified in workers employed in heavy manual lifting jobs, although the overall ratio of these synthesis to degradation markers remained the same in male construction workers as in workers with sedentary jobs. These results indicate that stressed tissues can adapt to the needs of a particular job, increasing collagen synthesis to match that of collagen degradation. However, studies examining tendosynovial tissues collected from patients with upper extremity musculoskeletal disorders during surgical intervention show increased tissue fibrogenic and degradative.