Abstract
Intervertebral disc degeneration (IVDD) is a chronic, expensive, and high-incidence musculoskeletal disorder largely responsible for back/neck and radicular-related pain. It is characterized by progressive degenerative damage of intervertebral tissues along with metabolic alterations of all other vertebral tissues. Despite the high socio-economic impact of IVDD, little is known about its etiology and pathogenesis, and currently, no cure or specific treatments are available. Recent evidence indicates that besides abnormal and excessive mechanical loading, inflammation may be a crucial player in IVDD. Furthermore, obese adipose tissue is characterized by a persistent and low-grade production of systemic pro-inflammatory factors. In this context, chronic low-grade inflammation associated with obesity has been hypothesized as an important contributor to IVDD through different, but still unknown, mechanisms. Adipokines, such as leptin, produced prevalently by white adipose tissues, but also by other cells of mesenchymal origin, particularly cartilage and bone, are cytokine-like hormones involved in important physiologic and pathophysiological processes. Although initially restricted to metabolic functions, adipokines are now viewed as key players of the innate and adaptative immune system and active modulators of the acute and chronic inflammatory response. The goal of this review is to summarize the most recent findings regarding the interrelationships among inflammation, obesity and the pathogenic mechanisms involved in the IVDD, with particular emphasis on the contribution of adipokines and their potential as future therapeutic targets.
Highlights
Intervertebral disc degeneration (IVDD) is a chronic, complex and multi-factorial musculoskeletal disorder characterized by metabolic and structural changes that progressively lead to the loss of mechanical stability and shock absorber function of the intervertebral disc [1]
This review provides a systematic overview of the current understanding of obesity, inflammation and IVDD interrelationships
Adiponectin treatment had no effect on IL-6 expression in IL-1β stimulated IVD cells [50]. These findings indicated that adiponectin may act as an anti-inflammatory adipokine by suppressing the expression of pro-inflammatory mediators, including tumor necrosis factor (TNF)-α, contributing to IVD homeostasis and protecting it from degeneration [49,50]
Summary
Intervertebral disc degeneration (IVDD) is a chronic, complex and multi-factorial musculoskeletal disorder characterized by metabolic and structural changes that progressively lead to the loss of mechanical stability and shock absorber function of the intervertebral disc [1]. IVDD is a chronic and irreversible process characterized generally by increased matrix degradation, loss of proteoglycans and hydration in NP, angiogenesis/neovascularization, nerve ingrowth, and expression of catabolic cytokines These pathological features of IVDD lead to multiple anatomic, mechanical, and biochemical disc changes, including disc desiccation, disc bulging and reduced disc height, with resultant decrease of mechanical stability and shock absorber functions, which contributes to osteophyte formation, annular fissures, and decreased motion of spinal segments [2,15] (Figure 1). Interventional procedures, including fusion, discectomy, and total disc replacement, are highly intrusive and have a great risk of relapse, neighbouring segment degeneration and a loss of mechanical properties [2] Both conservative treatments and surgical interventions are only directed to the clinical symptoms of the disease, being largely ineffective and with no long-term action. Cell and gene therapies are promising, further research and well-designed clinical trials are of utmost importance for its safe application on IVDD treatment [2,3]
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