Degenerate disc disease is a major cause of low back pain, yet its aetiology is still poorly understood. The intervertebral disc is the largest avascular structure in the body. Cells of the nucleus pulposus, therefore, rely on diffusion of oxygen & nutrients down concentration gradients from peripheral vessels in the cartilage end-plates. Thus, there is a low oxygen tension and cellular respiration is largely anaerobic.

The purpose of this study was to examine the effects of inflammation, hypoxia and acidosis on degeneration and pro-inflammatory mediator production in virgin porcine nucleus pulposus cultures.

Intervertebral discs were harvested from normal 6-month old agricultural pigs slaughtered for other purposes. Nucleus pulposus was contained within the annulus until further dissection under sterile conditions in the laboratory was performed. Nucleus pulposus was harvested, diced and divided into 200mg samples. Samples were incubated under optimal conditions.

Discs were cultured in 5μg/ml E. coli lipopolysaccharide, in a hypoxic environment or at low pH. IL-6, IL-8 and LDH assays were performed by ELISA, in accordance with manufacturer’s instructions.

Time and dose-response curves were generated for each experiment (results not shown). Results at 72 hours incubation are tabulated below:

These results confirm that nucleus pulposus is a biochemically active tissue capable of producing pro-inflammatory mediators in response to environmental stresses. IL-6 and IL-8 are both involved in the inflammatory cascade, causing chemotaxis of neutrophils and macrophages to the area. IL-8 itself causes hyperalgesia. Acidotic and inflammatory conditions, but not hypoxia, stimulated cytokine release. This may indicate a protective reduction in cellular activity in reduced oxygen environments. Necrosis, as measured by LDH production, was negligible.

Introduction: Since the introduction of joint arthroplasty major advances including the introduction of laminar airflow, have been made in reducing infection to current rates of 1 to 2%. Nonetheless infection remains a devastating complication, with major implications in terms of patient suffering, duration of hospital stay and financial burden. We undertook a study to examine the incidence of bacterial wound contamination occurring in the intra-operative period.

Materials and Methods: All patients admitted to our unit for elective hip and knee arthroplasty were entered into the study. On arrival in theatre a skin swab was taken. The patient was then prepared and draped in the anaesthetic room before final draping by the surgical team in the operating theatre. All procedures were performed in theatres equipped with laminar airflow, and all surgical personnel wore isolator suits. During the course of the procedure swabs were taken from the anterior aspect of the femur at 30-minute intervals. In addition the skin and inside blades and the suction tip were harvested at the end of the procedure. All samples were then sent for culture. Patient data including age, comorbid conditions and history of previous surgery were noted on a standardised pro forma. In addition, operative data including duration of the procedure, operating surgeon and type of drape and skin preparation used were noted.

Results: 65 patients have been examined to date. An incidence of contamination of 14% has been noted (9 patients) with the skin blade and suction tip being the most common source of contaminating organisms. Staphylococcus epidermis was cultured in 5 cases, with Gram negative organisms being cultured in the remaining samples. In all 9 cases only small numbers of organisms were identified. None of the patients with positive cultures developed clinical signs of deep or superficial wound sepsis, and all had an uncomplicated postoperative course.

Conclusions: While low levels of contamination are unavoidable in theatre, it is important that strict discipline be maintained in order to minimise this risk. In particular, careful attention to patient skin preparation, the use of prophylactic antibiotics and minimising use of the suction tubing help decrease contamination rates.

Aseptic loosening is currently the leading cause of failure of total hip arthroplasty. The aetiology of periprosthetic bone resorption is currently under intense investigation. Wear particles are produced from the articulating surface of the femoral and acetabular components. These particles gain access to the bone-cement interface where they are phagocytosed by macrophages. Particle stimulated macrophages differentiate into bone resorping osteoclasts. This leads to periprosthetic bone resorption and subsequent implant loosening.

Nuclear factor kappa B (NFκB) is a transcription factor known to be activated by pathogenic stimuli in a variety of cells. The activation of NFkB would appear to be the primary event in the activation of particle stimulated macrophages in the periprosthetic membrane. NFκB subsequently causes a cascade of events leading to the release of bone resorbing cytokines, namely interleukin-6 (IL-6) and tumour necrosis factor α (TNFα).

The aim of our study was to ascertain if bone resorption could be prevented in vitro by the addition of PDTC, an NFkB inhibitor to particle stimulated macrophages.

Human monocytes were isolated and cultured from healthy volunteers. The monocyte/macrophage cell line was differentiated into osteoclasts by the addition of alumina particles and allowed to adhere onto bone slices. The NFkB inhibitor, PDTC, has added to the cultured osteoclasts. Bone resorption was analysed by counting the number of resorption pits in each bone slice.

The addition of PDTC to stimulated macrophages reduced the number of resorption pits by greater than 40% compared to control.

This is a unique and promising finding that may offer a future therapeutic strategy for the prevention of periprosthetic bone resorption and therefore aseptic loosening in total hip arthoplasty.

The management of type two odontoid peg fractures remains controversial. The policy in our unit is to initially manage all of these injuries non-operatively. Patients with displaced fractures (0.2mm translation, > 15° angulation) are placed in halo vests followed by fracture reduction under radiological control. Undisplaced or minimally displaced fractures are treated in either custom-made minerva orthoses or halo vests.

We report the results of 42 consecutive cases of type two odontoid peg fractures. There were 24 males and 18 females with a mean age of 53 (range 18–89) years. Twenty-one (50%) of patients were > 65 years of age. In 29 cases the fracture was undisplaced or minimally displaced and in the remaining 13 cases it was displaced (> 2mm translation, > 15° angulation) either posteriorly (extension-type)(6) or anteriorly (flexion type) (7). All displaced cases were treated in halo vests while the remainder were treated in minervas (14) or halo vests (15).

Loss of reduction occurred in nine cases necessitating adjustment in five and C1/2 posterior fusion in four. Of these cases five were displaced extension type-fractures, two required fusion. Pin site infection necessitated early removal of halo vest and conversion to minerva in three cases. In all of these cases fracture union was achieved.

Overall, union was achieved in 37 patients giving a non-union rate of 12%. The mean age of the five non-unions was 42 years with only one patient over 65 years of age. Four of these patients had C1/2 posterior fusions and the remaining patient refused surgery.

Of the 29 patients with displaced or minimally displaced fractures five (17%) required surgery for either non-union (3) or displacement (2), whereas three (23%) of the displaced group required surgery for non-union (1) or displacement (2). All of these were extension type fractures.

We conclude that a policy of non-operative management of these fractures resulted in union in a high proportion of patients of all age groups except for those with extension type fractures. This fracture pattern may warrant primary surgical intervention.

Aseptic loosening has become the single most important long-term complication of total joint replacements. The pathophysiology of this loosening is multifactorial in origin ranging from mechanical wear, poor surgical technique, thermal damage and the inflammatory response to particulate wear debris. Cytokines are released in response to macrophage activation by particulate wear debris (PWD), the resultant inflammatory cascade stimulates osteoclastic resorption of bone. The failure of remodelling and repair mechanisms may be as a result of Osteonecrosis from cement (PMMA).

Hypothesis: That PMMA increases Osteoblast susceptibility to necrosis and apoptosis following inflammatory challenge.

Materials and Methods: Osteoblast cell cultures were grown on PMMA cement plates and assessed for apoptosis and necrosis by PI exclusion staining, morphological changes on light and electron microscopy and flow cytometry.

Results: PMMA induced osteonecrosis is highest at 1 hour (34.45) in comparison to control levels (4.55). There is no significant change in Apoptosis at 24 hours. Culture of the Osteoblasts on cement and delayed stimulation with TNF-α causes increased Apoptosis and Necrosis.

Conclusion: PMMA cement causes Osteoblast necrosis in the early stages of polymerisation, after 24 hours there is little increase in apoptosis/necrosis. However Osteoblasts that grow in contact with cement are more susceptible to apoptosis and necrosis following TNFα challenge. This may prove to be an important step in the pathogenesis of Aseptic loosening.

This study examines patient characteristics, indications for conversion, surgical and anaesthetic technique, peri-operative management and complications of surgery in this small and challenging group of patients. In the six years from 1994 to 1999, 33 conversion arthroplasties were performed for failed femoral hemiarthroplasty. The average age at conversion surgery was 75.5 years (range 65–90). The female to male ratio was 6:1. Primary hemiarthroplasties comprised 24 Austin-Moore, 6 Thompson & 3 Bipolar prostheses. The average interval from primary to conversion surgery was 50 months (6 months to 17 years). The average age at primary surgery was 71.2 years (62–88) – AMP:71.4 years, Thompson’s: 74.2 years, Bipolar: 63.5 years. All hemiarthroplasties were performed for fractured femoral necks. 62% of patients came from the Eastern Health Board area, while 38% were tertiary are referrals from other Health Boards. The average length of stay was 17.5 days (3–24). Indications for conversion included gross loosening/acetabular erosion in 9 cases, suspected infection in 4 cases and abscess/septicaemia in 1 case. All but 3 patients had significant pain (night pain etc.) and/or severely impaired mobility.

We also looked at anaesthetic and analgesic practice, surgical technique and prostheses used.

Post-operatively, mean total blood loss was 1430 ml (420–2280) with an average of 1.4 units of blood transfused (0–5). Intraoperative complications included acetabular & femoral perforation, periprosthetic fracture and cement reactions. Complications post-op (in hospital) included cardiac arrhythmia’s, cerebrovascular accidents, pulmonary embolus, myocardial infarct, respiratory & urinary tract infections, constipation, nausea & vomiting.

The elderly nature of these patients and the physiological stress of what is major surgery allied with multiple co-morbidities make their care especially challenging. A conversion arthroplasty is a procedure with a significant risk of considerable morbidity. Primary total hip replacement or bipolar hemiarthroplasty are options which, therefore, should be seriously considered in the case of fractured femoral necks to minimise the need for further surgery in the future, with all its attendant risks.