The role of nucleus pulposus (NP) biology in the genesis of sciatica is being increasingly investigated.

The aim of this study was to examine the ability of control and degenerate human nucleus pulposus to respond to an exogenous pro-inflammatory stimulus.

Control disc material was obtained from surgical procedures for scoliosis and degenerate disc tissue from surgical procedures for sciatica and low back pain. Disc specimens were cultured using a serumless technique under basal and lipopolysaccharride (LPS) stimulated conditions and the media harvested, aliquoted and stored at –80°C for subsequent analysis. Levels of IL-1β,TNFα, LTB4, GM-CSF, IL-6, IL-8, MCP-1, PGE2, bFGF and TGFβ-1 in the media were estimated using commercially available enzyme linked immunoabsorbent assay kits.

Neither basal nor LPS stimulated control or degenerate NP produced detectable levels of IL-1β, TNFα, LTB4 or GM-CSF. Control disc IL-8 secretion increased significantly with LPS stimulation, p< .018. Degenerate disc IL-6, IL-8 and PGE2 production increased significantly with LPS stimulation, p< .01, p< .001 and p< .005 respectively. LPS stimulated degenerate NP secreted significantly more IL-6, IL-8 and PGE2 than LPS stimulated control NP, p < 0.05, 0.02 and 0.003 respectively.

LPS induces an increase in both control and degenerate NP mediator production demonstrating the ability of human NP to react to a noxious stimulus by producing pro-inflammatory mediators. The difference in levels of basal and LPS stimulated mediator production between control and degenerate discs show that as a disc degenerates it increases both its level of inflammatory mediator production and its ability to react to a pro-inflammatory stimulus. The increased sensitivity of degenerating human NP to noxious stimuli and increased ability to respond with inflammatory mediator production support the role of NP as an active participant in the genesis of lumbar radiculopathy and discogenic back pain.

Aim: To investigate the effect of manipulation of the electrochemical environment around metallic implants on bacterial biofilm formation.

Background: The inability to prevent and treat prosthetic bacterial infection is a significant orthopaedic problem. Current antimicrobials are ineffective against bacterial biofilm communities. It is hypothesised that the alteration of the micro-environment could inhibit bacterial adhesion sufficiently to prevent biofilm formation allowing normal tissue integration to occur. Previous work by this group using zinc caused increased bacterial biofilm formation. Platinum being at the opposite end of the galvanic spectrum should cause the opposite effect.

Materials and Methods: Titanium 2mm Kirschner (K) wires (N=14) and Stainless Steel K wires (N=14) were cut into 50mm segments and sterilised. These were inoculated with either Staphylococcus Epidermitis (NC011047) or Staphylococcus Aureus (NC012973) suspensions. Superficial, non-adherent bacteria were removed by serial rinsing in phosphate buffered solution (PBS).

The K wires were added to either the culture media alone or the culture media containing platinum and incubated at 37 degrees for 24 hours. The wires were then removed from the media and rinsed in PBS. Samples were subjected to sonication, to fragment biofilms thereby releasing the bacteria, which were then quantified by serial log dilution technique and manual counting.

The presence of platinum reduced the adhesion of both Staph Aureus and Staph Epidermidis to stainless steel. This reduction was statistically significant using paired t-test (SPSS version 6.0). There was a significant reduction of adhesion with platinum in the Staph Aureus and titanium group while the reduction in the Staph Epidermidis and titanium group did not reach statistical significance.

Conclusion: The use of platinum to manipulate the microcurrent around metallic implants reduces bacterial biofilm formation in vitro. This has obvious clinical implications in prevention of implant infections.

Metallic implants are used frequently in the operative repair of joints and fractures in orthopaedic surgery. Metal infection is a catastrophic complication of the surgery with patients loosing their newfound mobility and independence, associated morbidity and mortality is high. Orthopaedic implant infection is chronic and biofilm based. Present treatment focuses on removing the infective substratum and implant surgically as well as prolonged anti-microbial therapy. Biofilms are 500 times more resistant than planktonic strains of bacterial flora to antibiotics, and with evolving resistant strains this form of therapy is loosing ground. Silver coatings on polymers and nylon (catheters, heart valve cuffs, burn dressings) have shown inhibition of this biofilm formation in its adhesion stage. Our aim was to deposit effective, minute, biocompatible, anti-bacterial layers of silver on orthopaedic stainless steel K-wires.

Combining magnetron sputtering with a neutral atom beam (Saddle Field) plasma source at 10⁻⁴ mbar in argon gas at temperatures of 60°C, a silver coating of 99.9% purity was deposited onto stainless steel orthopaedic K-wires. Coating thickness measurements were obtained using glancing angle x-ray diffraction of glass slides coated adjacent to wires. Magnetron parameters were modified to produce varying thickness of silver. Adhesiveness was examined using Rockwell punch tests and tape tests. Silver leaching experiments were carried out in phosphate buffered saline at 37°C for 48hrs and using inductive coupled plasma spectrometry to assess leached silver ions. Surface microscopy visualised physical changes in the coatings. Biofilm adhesion was determined by exposing wires to Staphylococcus aureus ATCC 29213 -NCTC 12973 for 15 min to allow biofilm adhesion and initiation. Wires were then cultured for 24h at 37°C in RPMI. Subsequently wires were sonicated at 50Hz in ringer’s solution and gently vortexed to dislodge biofilm. Sonicate was plated by the log dilution method on blood agar plates. Bacterial colonies were then counted and changes expressed in log factors. Surface biofilms were visualised using scanning electron microscopy. Cytotoxicity was assessed using fibroblast cell cultures lines.

K-wires were coated with 5 to 50 nm of silver by running the magnetron sputtering at low currents. These coatings showed excellent adhesive properties within the 48hr exposed with only 5% of silver leaching in buffered saline. The silver coated wires showed a log 3–4 fold reduction in biofilm formation as compared to control wires. The coatings showed no cytotoxic effects.

Silver coating of medical implants has been shown in urological catheters to reduce biofilm infection. We have perfected a method of depositing thin layers of anti-bacterial silver onto stainless steel, which is both anti-infective and biocompatible. This coating could potentially add to the armourary of anti-infective agents in the elimination of infection related orthopaedic implant failure.

Dupuytren’s contracture is characterised by abnormal fibroblast proliferation and extracellular matrix deposition in the palmar fascia. Fibroblast proliferation and matrix deposition in connective tissues are regulated by cytokines. A number of cytokines including transforming growth factor beta (TGFβ), basic fibroblast growth factor (bFGF), platelet derived growth factor (PDGF) and epidermal growth factor (EGF) are known to have potent anabolic effects on connective tissue. The aim of this study was to investigate the role played by anabolic cytokines in the pathogenesis of Dupuytren’s disease.

Twelve specimens of Dupuytren’s contracture and six control specimens of palmar fascia obtained from patients undergoing carpal tunnel release were cultured using a serumless method under standard conditions for 72 h. Levels of TGFβ-1, bFGF, PDGF and EGF in the medium were estimated using an enzyme linked immunoabsorbent assay technique.

Neither Dupuytren’s tissue nor control palmar fascia produced any EGF. The mean (±S.D.)levels of bFGF, PDGF and TGFβ-1 produced by cultured palmar fascia were: 1270 ± 832, 74 ± 24, < 7, and for Dupuytren’s tissue were 722 ± 237, 139 ± 76.6, 645 ± 332, respectively. The levels of PDGF and TGFβ-1 were significantly higher in Dupuytren’s tissue.

PDGF is produced in increased amounts by Dupuytren’s tissue. This may contribute to the fibroblast proliferation and increased ECM deposition observed in this condition. TGFβ-1 is not produced by normal palmar fascia but is produced in large amounts by Dupuytren’s tissue. The major physiologic role of TGFβ-1 is to stimulate formation of fibrous tissue. It plays a major role in wound healing and also in pathological conditions where fibrosis is a prominent feature. Inappropriate production of TGFβ-1 in the palmar fascia in Dupuytren’s disease may play a central role in initiating and stimulating the abnormal fibroblast proliferation and collagen synthesis seen in this condition.

The pathophysiology of discogenic low back pain is poorly understood. The morphological changes occurring in disc degeneration are well documented but unhelpful in determining if a particular degenerate disc will be painful or not.

Herniated intervertebral disc tisssue has been shown to produce a number of pro-inflammatory mediators and cytokines. No similar studies have to date been done utilising disc material from patients with discogenic low back pain.

The aim of this study was to compare 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 with that from patients undergoing fusion for discogenic low back pain.

Tissue from 50 patients undergoing discectomy for sciatica and 20 patients undergoing fusion for discogenic low back pain was cultured and the medium harvested for subsequent analysis using an enzyme linked immunoabsorbent assay method. Statistical analysis of the results was performed using the Mann-Whitney test.

Disc specimens from both experimental groups produced measurable levels of all three mediators. Mean production of IL-6, IL-8 and PGE2 in the sciatica group was 26.2±75.7, 247±573 and 2255±3974 respectively. Mean production of IL-6, IL-8 and PGE2 in the low back pain group was 92±154, 776±987 and 3221±3350 respectively (data = mean production pg/ml ± 1 standard deviation).

There was a statistically significant difference between the levels of IL-6 and IL-8 production in the sciatica and low back pain groups (p< 0.006 and p< 0.003 respectively).

The high levels of pro-inflammatory mediator production found in disc tissue from patients undergoing fusion for discogenic LBP may indicate that nucleus pulposis pro-inflammatory mediator production is a major factor in the genesis of a painful lumbar disc. This could explain why some degenerate discs cause LBP while other morphologically similar discs do not.

Infection around implanted biomaterials in humans is a major healthcare issue and current ability to effectively prevent and treat such infections using antibiotics is limited. The hypothesis of the study was that surface charge could be manipulated to a positive state and thus moderate bacterial adhesion to the implant. The surface charge was manipulated by creating a galvanic cell using a zinc strip in a standard suction drain.

Adhesion of Staph. aureus and Staph. Epidermidis to stainless steel and titanium implants in vitro and in vivo was quantified by sonication and log dilution technique. The response to this surface manipulation of charge varied for both the bacterial species and the type of metallic implant. In vitro studies produced an 88% reduction in Staph. aureus adhesion to stainless steel and a 36% reduction in adhesion to titanium. However Staph. epidermidis showed an increased adhesion to stainless steel (Log 1.81 ± 1.12 in vitro) and to titanium (log 1.80 ± 0.12). Staph aureus demonstrated a log increase of 1.56± 0.09 in adhesion to titanium in vivo while Staph. epidermidis generated a log increase of 3.97± 0.10 in adherent bacteria.

In this experiment we have shown that alteration of the electrochemical environment around an implant influences bacterial adhesion. While our technique is not therapeutically viable, further manipulation of surface charge of an implant is possible using other electroactive materials. This may be explored in the prophylactic treatment of implant infection

Cervical orthoses are currently used in the pre-hospital stabilization of trauma patients and also as part of the definitive non-operative treatment of injuries of the cervical spine. The construct stability of orthoses is compromised by virtue of the fact that the cervical spine exhibits the greatest range of movement amongst the spinal segments and also because of the complex composite nature of neck movements.

To date, data has been difficult to attain comparing the various orthoses, in the various planes of movement of the cervical spine. Various methods including the use of inclinometers, goniometers, radiography, computerized tomography and cineroentgenography have been used in an attempt to measure these movements but none have provided satisfactory triplanar data.

This paper uses the Zebris ultrasonic 3-D motion analysis system to measure flexion, extension, range of lateral bending and range of axial rotation in five similar male and five similar female subjects with no history of neck injuries. The subjects were tested in a soft and hard collar, Philadelphia, Miami J and Minerva.

Results show that the Minerva is significantly the most stable construct for restriction of movement in all planes in both groups (p< 0.002 vs. all groups, Student’s t-test), but more impressively in the female group. In the male group, the standard hard collar performs second best in flexion, lateral bending and axial rotation. In the female group, the second most stable orthosis is the Philadelphia in flexion/extension and the hard collar in lateral bending and axial rotation (p< 0.05 vs. next most stable in all cases, Student’s t-test). The soft collar in both groups offered only minimal resistance to movement in any plane, e. g. 45.07° vs. 46.45° extension vs. normal in males and 40.15° vs. 41.8° extension vs. normal in females.

Looking at these results together allows the ranking of the measured orthoses in order of the three-dimensional stability they offer. Furthermore, they validate the Zebris as a reliable and safe method of measurement of the complex movements of the cervical spine with low intersubject variability.

In conclusion, this paper, for the first time presents reproducible data incorporating the composite triplanar movements of the cervical spine thus allowing comparative analysis of the three-dimensional construct stability of the studied orthoses.

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.