Effects of Tobacco Smoking on the Degeneration of the Intervertebral Disc: A Finite Element Study

Abstract

Tobacco smoking is associated with numerous pathological conditions. Compelling experimental evidence associates smoking to the degeneration of the intervertebral disc (IVD). In particular, it has been shown that nicotine down-regulates both the proliferation rate and glycosaminoglycan (GAG) biosynthesis of disc cells. Moreover, tobacco smoking causes the constriction of the vascular network surrounding the IVD, thus reducing the exchange of nutrients and anabolic agents from the blood vessels to the disc. It has been hypothesized that both nicotine presence in the IVD and the reduced solute exchange are responsible for the degeneration of the disc due to tobacco smoking, but their effects on tissue homeostasis have never been quantified. In this study, a previously presented computational model describing the homeostasis of the IVD was deployed to investigate the effects of impaired solute supply and nicotine-mediated down-regulation of cell proliferation and biosynthetic activity on the health of the disc. We found that the nicotine-mediated down-regulation of cell anabolism mostly affected the GAG concentration at the cartilage endplate, reducing it up to 65% of the value attained in normal physiological conditions. In contrast, the reduction of solutes exchange between blood vessels and disc tissue mostly affected the nucleus pulposus, whose cell density and GAG levels were reduced up to 50% of their normal physiological levels. The effectiveness of quitting smoking on the regeneration of a degenerated IVD was also investigated, and showed to have limited benefit on the health of the disc. A cell-based therapy in conjunction with smoke cessation provided significant improvements in disc health, suggesting that, besides quitting smoking, additional treatments should be implemented in the attempt to recover the health of an IVD degenerated by tobacco smoking.

The Impact of Tobacco Cigarette Smoking on Spinal Cord Stimulation Effectiveness in Chronic Spine–Related Pain Patients

“…52,53 Nicotine also affects intervertebral disk health through down-regulation of the proliferation rate and glycosaminoglycan biosynthesis. 54 From another perspective, smoking stimulates neutrophils in the pulmonary capillaries to release elastase and protease enzymes into the systemic circulation. 55 This is in addition to cigarette smoking inhibiting α1 antiprotease, which is the most potent protease inhibitor.…”

Prognostic factors in the progression of intervertebral disc degeneration: Which patient should be targeted with regenerative therapies?

“…The most surprising outcome of this study is probably that strong evidence was found that age, gender, body weight, BMI, smoking, car driving, the type of occupation (ie, working as a nurse or construction carpenter) nor recreational activities at leisure time were associated with the progression of DD. This was unexpected, as several studies show that heavy physical activity or work and smoking are key factors in the onset of DD . For smoking, however, there is one high‐quality study (out of five) that finds that smoking during follow‐up to a greater reduction in disc height .…”

“…show that heavy physical activity or work and smoking are key factors in the onset of DD. 11,[54][55][56] For smoking, however, there is one highquality study (out of five) that finds that smoking during follow-up to a greater reduction in disc height. 42 This is in contrast to a study by the same authors 2 years earlier, in which they found that smoking did not have any effect on the change in degeneration.…”

Detection of apoptosis and matrical degeneration within the intervertebral discs of rats due to passive cigarette smoking

“…Wang et al suggested that the occurrence of Fas-mediated apoptosis, which is promoted within the CEP, is not unidirectional, but indeed represents mutual interactions between these tissues and cells [35]. Recently, Elmasry et al suggested that both direct and indirect effects of smoking play significant roles in IVD degeneration: the nicotine-mediated down-regulation of cell proliferation and anabolism mainly affects GAG levels in the CEP, and the reduction of solute exchange between blood vessels and disc tissue mainly affects GAG levels and cell density in the NP [24]. Thus, there are possible alternative mechanisms responsible for the effects of cigarette smoke on the CEP and NP: the direct effects of nicotine on the CEP and the reduction of transport of nutrients through the CEP to the NP.…”