Mechanisms of Intervertebral Disk Degeneration/Injury and Pain: A Review

Abstract

Degeneration of the intervertebral disk and its treatments are currently intensely investigated topics. Back pain is a condition whose chronic and debilitating nature combined with its prevalence make it a major health issue of substantial socioeconomic importance. Although researchers, and even sometimes clinicians, focus on the degenerated disk as the problem, to most patients, pain is the factor that limits their function and impacts their well-being. The purpose of this review is to delineate the changes associated with disk degeneration and to outline mechanisms by which they could be the source of back pain. Although the healthy disk is only innervated in the external layer of its annulus fibrosus, adjacent structures are plentiful with nociceptive receptors. Stimulation of such structures as a consequence of processes initiated by disk degeneration is explored. The concept of discogenic pain and possible mechanisms such as neoinnervation and solute transport are discussed. Finally, how such pain mechanisms may relate to current and proposed treatment strategies is discussed.

The role of transient receptor potential channels in joint diseases

“…Although DDD does not always correlate with the presence and severity of LBP, an IVD-related problem is generally accepted to be the most common cause of LBP (Schwarzer et al, 1995), as degenerated IVDs are frequently invaded by newlyformed nociceptive nerves (Sivan et al, 2014;Urban et al, 2004). Discogenic nociceptive pain is caused by a neuronal sensitisation, due to internal IVD disruption (Roberts et al, 2006), while neuropathic pain arises from neuronal damage and inflammation caused by IVD-related compression of nerve roots (Cramer and Darby, 1997;Ito and Creemers, 2013).…”

“…Interestingly, in both OA and DDD, the severity of pain does not always correlate with macroscopic structural evidence of joint/IVD damage. This is explained by the fact that pain perception comprises a complex series of neurophysiologic events involving stimulation, tissue response, transmission of pain signal and subsequent modulation of these at both peripheral and central levels (Ito and Creemers, 2013;Schaible, 2012). Inflammatory cytokines are important regulators of these pain mechanisms and their presence is associated with inflammatory pain arising from articular joints and IVDs (Ito and Creemers, 2013;Wuertz et al, 2012;Zhang et al, 2013).…”

Low back pain: possibilities of pathogenetic treatment

“…Здесь они взаимодействуют с ноцицептивными рецепторами и способствуют прораста-нию нервных волокон через разрывы внутрь фиброзного кольца вплоть до структур пульпозного ядра, что в сово-купности и вызывает БНС [22,23]. Разрывы фиброзного кольца -частый феномен в процессе дегенерации дисков [9,10].…”

“…Нервные волокна имеют тенденцию распростра-няться вдоль фиброзного кольца во внутреннюю его часть, даже в ткани пульпозного ядра. В результате разры-вов усиливается транспорт воспалительных цитокинов и ноцицептивных стимуляторов из пределов пульпозного ядра к ноцицептивным рецепторам фиброзного кольца [23]. Обнаруживаемая в этих случаях зона высокоинтен-сивной плотности на МРТ рассматривается как феномен, отражающий локусы разрывов фиброзного кольца [24].…”

“…Основываясь на данных исследования уровня про-воспалительных цитокинов при дегенеративной болезни дисков, было высказано предположение, что собственно дегенеративный процесс может инициировать нейроим-мунные каскады с нарушением регуляции цитокинов в поврежденной области, что может вызывать экспрессию большого числа алгогенных медиаторов, способных про-дуцировать боль [23,25]. В исследовании D. Kraychete и соавт.…”