Abstract
Intervertebral disc degeneration (IDD) is an important cause of low back pain. Recent evidence suggests that in addition to abnormal and excessive mechanical loading, inflammation may be a key driver for both IDD and low back pain. Obesity, a known mechanical risk factor of IDD, is now increasingly being recognized as a systemic inflammatory state with adipokines being postulated as likely inflammatory mediators. The aim of this review was to summarize the current literature regarding the inflammatory role of adipokines in the pathophysiology of IDD. A systematic literature search was performed using the OVID Medline, EMBASE and PubMed databases to identify all studies assessing IDD and adipokines. Fifteen studies were included in the present review. Leptin was the most commonly assessed adipokine. Ten of 15 studies were conducted in humans; three in rats and two in both humans and rats. Studies focused on a variety of topics ranging from receptor identification, pathway analysis, genetic associations, and proteonomics. Currently, data from both human and animal experiments demonstrate significant effects of leptin and adiponectin on the internal milieu of intervertebral discs. However, future studies are needed to determine the molecular pathway relationships between adipokines in the pathophysiology of IDD as avenues for future therapeutic targets.
Highlights
Intervertebral disc degeneration (IDD), an important cause of low back pain (LBP), has traditionally been considered as an age-related process of ‘drying and cracking’ of the disc tissue caused by decreased proteoglycan content, leading to the classic radiological signs of decreased intervertebral height, end-plate sclerosis and osteophytosis [1,2]
The results from the present study indicate that obesity exerts important inflammatory effects on the homeostasis of intervertebral discs that are mediated via adipokines, mainly leptin and adiponectin
Work on resistin by Li et al found the expression of resistin in degenerated disc tissue [42]. These results indicate that adipokines may play a key role in disc homeostasis; their role in disc degeneration needs further exploration
Summary
Intervertebral disc degeneration (IDD), an important cause of low back pain (LBP), has traditionally been considered as an age-related process of ‘drying and cracking’ of the disc tissue caused by decreased proteoglycan content, leading to the classic radiological signs of decreased intervertebral height, end-plate sclerosis and osteophytosis [1,2]. While many patients with radiological evidence of IDD remain asymptomatic [7], some exhibit clinical symptoms of LBP Initial management of these symptomatic patients includes conservative measures such as back exercises, pain killers, anti-inflammatories and/or injections. Since these measures do not address the underlying etiology of disc degeneration, disease progression and/or development of neurological symptoms often necessitate the need for back surgery in some [8].
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