Discogenic low back pain affects 42% of patients suffering low back pain. Degenerative disc disease is described as failure in cellular response to external stresses leading to physiologic dysfunction. Glycosylation patterns of tissues give insights into the spatially and temporally regulated inflammatory and degenerative processes. These glycoconjugates participate in many key biological processes including molecular trafficking and clearance, receptor activation, signal transduction, and immunomodulation. We hypothesise that glycoprofile of the the intervertebral disc(IVD) is temporally and spatially distinct in health and degeneration. The glycoprofile of the IVD has been studied in murine, bovine and ovine models for injury and aging. In this study, healthy(n=2) and degenerated(n=2) human IVD samples received from Utrecht(UU, ND) with ethical approval(NUIG), were compared using lectin histochemistry. The N-glycan profile of human degenerated IVD samples was characterised by high resolution quantitative UPLC-MS. Healthy and degenerated human discs present distinct glycosylation trends intracellularly/extracellularly in annulus fibrosus(AF) and nucleus pulposus(NP) tissue. There are quantitative and spatial differences in glycosylation in healthy and degenerated tissue. These findings are consistent with previous studies of IVD in murine, bovine and ovine models. The human N-glycan profile of degenerated surgical tissues is distinct from other cited tissue profiles such as human plasma⁵. These studies offer validation of previous animal models of IVD injury and degeneration, demonstrating similar changes in the glycoprofile in both animals and humans. Glycoprofiling may offer insight into disease progression, offering new realms of disease classification in patient specific manner while also elucidating potentials therapeutic targets, inhibiting disease progression.

The use of platelet-leukocyte gel (PLG), made from platelet rich plasma, to stimulate bone formation and wound healing has been investigated extensively. As leukocytes play an important role in the innate host-defence, we hypothesised that PLG might also have antimicrobial properties.

The purpose of this study was to investigate the antimicrobial activity of PLG against Staphylococcus aureus in an in vitro experiment. To determine the contribution of myeloperoxidase (MPO), present in leukocytes, in this process, MPO release was measured.

Platelet rich plasma (PRP) was prepared from whole blood of 6 donors. In this process platelet poor plasma (PPP) was obtained as well. PLG was prepared by mixing PRP with either autologous (PLG-AT) or bovine thrombin (PLG-BT). The antimicrobial activity of PLG-AT, PLG-BT, PRP and PPP was determined in a bacterial kill assay, containing 1x106 CFU/ml of Staphylococcus aureus, during a 24-hour period. MPO release was measured by ELISA.

Cultures showed a rapid decrease in the number of bacteria in the presence of both PLG-AT and PLG-BT, which was maximal between 4 and 8 hours, to approximately 1% of the bacteria in controls. Also PRP and PPP induced a statistically significant bacterial kill, but the effect of PLG-AT was the largest (p=0.093 vs. PLG-BT; p=0.004 vs. PRP and p< 0.001 vs. PPP). PLG-AT, PLG-BT and PRP showed a comparable, gradually increasing MPO release for 8 to 12 hours. Some MPO was also measured in the PPP samples. No correlation between MPO release and bacterial kill could be found.

PLG appears to have potent antimicrobial capacity, but the role of MPO in this activity is questionable. PLG might represent a useful strategy against postoperative infections. Further research should investigate its antimicrobial capacity in the in vivo situation.