H erniated intervertebral disc tissue has been shownto produce a number of proinflammatory mediators and cytokines, but there have been no similar studies using discs from patients with discogenic low back pain.We have compared the levels of production of interleukin-6 (IL-6), interleukin-8 (IL-8) and prostaglandin E 2 (PGE 2 ) in disc tissue from patients undergoing discectomy for sciatica (63) with that from patients undergoing fusion for discogenic low back pain (20) using an enzyme-linked immunoabsorbent assay.There was a statistically significant difference between levels of production of IL-6 and IL-8 in the sciatica and low back pain groups (p < 0.006 and p < 0.003, respectively).The high levels of proinflammatory mediator found in disc tissue from patients undergoing fusion suggest that production of proinflammatory mediators within the nucleus pulposus may be a major factor in the genesis of a painful lumbar disc. [Br] 2002;84-B:196-201. J Bone Joint Surg Received 8 June 2001; Accepted 3 August 2001The pathophysiology of discogenic low back pain is incompletely understood. 1 The changes which occur as a disc degenerates are well documented, but are unhelpful in determining whether a degenerate disc will cause pain.2 It is known that disc tissue from patients undergoing discectomy for sciatica synthesises proinflammatory mediators and cytokines. 3-12 Sequestrated and extruded discs produce higher levels of these mediators than specimens in which the annulus is intact. 5,10,12,13 To date, there have been no studies of the production of inflammatory mediators in disc tissue from patients undergoing operations for discogenic low back pain. It has been shown, however, that degenerate discs in these patients contain more nociceptive nerve endings in the endplates of the disc and in the nucleus pulposus than do degenerate discs which do not cause low back pain. 14, 15 We have therefore compared levels of production of the proinflammatory mediators tumour necrosis factor alpha (TNF␣), interleukin-1beta (IL-1␤), interleukin-6 (IL-6), interleukin-8 (IL-8) and prostaglandin E 2 (PGE 2 ), in disc tissue from patients undergoing discectomy for sciatica with those from patients undergoing fusion for discogenic low back pain. Patients and MethodsWe obtained specimens of intervertebral disc from 63 patients undergoing primary lumbar discectomy for sciatica. Intraoperative assessment of the morphology of the disc herniation revealed 25 in which the annulus was intact (AI), 30 in which a nuclear extrusion was present (EXT) and eight in which the nucleus was sequestrated (SEQ). The mean ages were 42 years in the AI group, 39.5 years in the EXT group and 42 years in the SEQ group. The male: female ratio in the AI, EXT and SEQ groups was 17:8, 20:10 and 6:2, respectively. Three specimens were from the L3/L4 level, 28 from the L4/L5 level and 32 from the L5/ S1 level.We also obtained disc specimens from 20 patients undergoing primary lumbar interbody fusion for discogenic low back pain, which had been confirmed by discograph...

Herniated intervertebral disc tissue has been shown to produce a number of proinflammatory mediators and cytokines, but there have been no similar studies using discs from patients with discogenic low back pain. We have compared the levels of production of interleukin-6 (IL-6), interleukin-8 (IL-8) and prostaglandin E2 (PGE2) in disc tissue from patients undergoing discectomy for sciatica (63) with that from patients undergoing fusion for discogenic low back pain (20) using an enzyme-linked immunoabsorbent assay. There was a statistically significant difference between levels of production of IL-6 and IL-8 in the sciatica and low back pain groups (p < 0.006 and p < 0.003, respectively). The high levels of proinflammatory mediator found in disc tissue from patients undergoing fusion suggest that production of proinflammatory mediators within the nucleus pulposus may be a major factor in the genesis of a painful lumbar disc.

Factors in circulating air may play a role in immune responses after surgery through induction of gut-derived lipopolysaccharide (LPS) translocation across the gut. CD-1 mice were randomized to one of four treatment groups: controls, laparoscopy with carbon dioxide inflation, laparoscopy with air inflation and laparotomy. The peritoneal and systemic immune response was assessed by evaluating peritoneal macrophage, blood monocyte and neutrophil activity. In a second study, the effect of each of the treatments on fluorescein isothiocyanate (FITC)-LPS translocation across the gut was assessed. There were significant (P < 0.05) increases in peritoneal tissue macrophage release of superoxide and tumour necrosis factor after laparoscopy with air and laparotomy compared with control procedures and carbon dioxide laparoscopy. However, peritoneal macrophage FITC-Candida albicans ingestion was significantly decreased after air laparoscopy and laparotomy compared with controls and carbon dioxide laparoscopy (P < 0.05). These findings correlated with a significant (P < 0.05) decrease in CD11b expression. Significant translocation into the peritoneal cavity and systemic circulation occurred after air laparoscopy and laparotomy only. Factors in circulating air can induce LPS translocation and subsequent stimulation of postoperative immune responses. The beneficial effects of laparoscopic surgery may be explained by the minimal air contamination of the peritoneal cavity.

This study demonstrates that laparoscopic surgery appears to be associated with similar metabolic responses compared with open surgery, while immune parameters vary greatly between groups. The beneficial effects of laparoscopic surgery may relate, in part, to preservation of immune function in the postoperative period.