Recently there has been considerable interest in the role of inflammatory mediator production by herniated degenerate discs. Modic has described MR endplate changes which have an inflammatory appearance and have been linked with discogenic back pain. To date there has been no biomechanical investigation of discs with associated Modic changes.

The aim of this study is to determine if degenerate discs with associated Modic changes have higher levels of pro-inflammatory mediator production than those without Modic changes.

Intervertebral disc tissue was obtained from 52 patients undergoing spinal surgery for sciatica [40] and discogram proven discogenic low back pain [12]. The tissue was cultured and the medium analysed for interleukin-6, interleukin-8 and prostaglandin E2 using an enzyme linked immunoabsorbetn assay method. Preoperative MR images of the patients were examined by a double blinded radiologist to determine the Modic status of the cultured disc level.

Forty percent of patients undergoing surgery for discogenic low back pain had a Modic 1 change compared to only 12.5% of patients undergoing surgery for sciatica [p< .05] There was a statistically significant difference between levels of IL-6, IL-8 and PGE2 production by both the Modic1 [M1] and Modic2 [M2] groups compared to the Modic negative [NEG] group. IL-6:NEGvM1 p< .001, NEG v M2 p< .05, IL-8: NEG v M1 p< .01, NEG v M2 p> .05, PGE2: NEG v M1 p< 01, NEG v M2 p< .05.

Modic changes have been associated with positive provocative discography by a number of authors. Pain generation requires the presence of nerves and hyperalgsia inducing mediators. Both IL-8 and PGE2 are known to induce hyperalgesia. The fact that Modic changes are associated with high levels of production of these mediators supports their role as an objective marker of discogenic low back pain.

Introduction: Increased levels of IL-6 and IL-8 have been found in intervertebral disc (IVD) tissue from patients undergoing fusion for discogenic low back pain. The stimuli that induce these mediators in degenerate discs remain unknown. Impaired diffusion of nutrients and wastes to and from the nucleus pulposus (NP) is believed to be an important factor in the degenerative process. The oxygen tension and pH in the NP of degenerating discs are significantly decreased.

Aims: The aims of this study were to (1) demonstrate the ability of porcine NP to respond to a proinflamma-tory stimulus (lipopolysaccharride) in vitro, (2) investigate the effects of pH, pO₂ and glucose concentration on NP proinflammatory mediator secretion and (3) determine if methylprednisolone or indomethacin can block NP proinflammatory mediator secretion.

Methods: IVDs were harvested from 6-month old pigs and dissected under sterile conditions in the laboratory. 200mg samples of NP were cultured under optimal conditions (control), in a 1% O₂ environment, at pH6 and in culture medium without glucose for 72 hours. Blocking experiments were performed by culturing LPS-stimulated samples with either methylprednisolone or indomethacin for 24 hours. IL-6 and IL-8 levels were estimated by ELISA.

Results: Time and dose-response curves were generated for each experiment (results not shown). Results for the optimum dose and at 72 hours incubation were note.

Data = mean ± standard deviation. Statistical analysis was by students t test. A significant result between control and stimulated groups is indicated by: * p=0.024m, † p=0.0007 or ‡ p=0.012.

Methylprednisolone (2mg/ml) caused a significant (p=0.044) 30-fold reduction in IL-6 production and a significant (p=0.00004) 500-fold reduction in IL-8 levels as compared with nucleus pulposus cultured with 5 μg/ml LPS alone for 24 hours.

Addition of 500 μM indomethacin significantly (p=0.04) decreased IL-6 production by a factor of 120 and IL-8 levels by a factor of 50 (p=0.00004).

Necrotic cell death, as measured by lactate dehydrogenase (LDH) concentration, was not significant in any of the experiments.

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.

This basic science study attempts to explain why patients with spinal cord injuries have been seen to display increased healing of attendant fractures.

For the main part, this has been a clinical observation with laboratory work confined to rats. While the benefits in relation to quicker fracture healing are obvious, this excessive bone growth (heterotopic ossification) also causes unwanted side effects, such as decreased movement around joints, joint fusion and renal tract calculi. However, the cause for this phenomenon remains unclear.

This paper evaluates two group with spinal column fractures – those with neurological compromise (n=10) and those without (n=11), and compares them with a control group with isolated long bone fractures (n=10). Serum was taken from these patients at five specific time intervals post injury (24hrs, 120hrs, 10 days, 6 weeks and 12 weeks). The time period most closely related to the end of the acute inflammatory reaction and the laying down of callus was the 10-day post injury time period.

Serum samples taken at this time period were analysed for IGF-1 and TGF-ß levels, both known to initiate osteoblastic activity, using ELISA kits. They were also exposed to an osteoblast cell culture line and cell proliferation was measured.

Results show that the group with neurology has increased levels of IGF-1 compared to the other groups (p< 0.14, p< 0.18 respectively, Student’s t-test) but had lower TGF-ß (p< 0.05, p< 0.006) and osteoblast proliferation levels (p< 0.002, p< 0.0001). When the neurology group is subdivided into complete (n=5) and incomplete (n=5), it was shown that the complete group had higher levels of both IGF-1 and TGF-ß. This trend is reversed in the osteoblast proliferation assay.

This work, for the first time in human subjects, identifies a factor which may be regulating this complication of acute spinal cord injuries, namely IGF-1. Furthermore, the observed trend in the two cytokines seen in the complete neurology group may suggest a role for TGF-ß. However, the results do show that a direct mediation of this unwanted side effect of spinal cord injuries is unlikely as seen in the proliferation assay. Further work remains to be done to fully understand the complexities of the excessive bone growth recognised in this patient group.

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.

Total knee arthroplasty has evolved considerably over the last thirty years. Early implant design achieved the short-term goals of pain relief and mobility, however loosening and polyethylene wear associated with over constraint was problematic. The Low Contact Stress total knee arthroplasty was developed in an attempt to address the problems of loosening and polyethylene wear. The highly congruent interface between the femoral component and the mobile insert minimises stress within the polyethylene and reduces the potential of wear and damage. Furthermore, the mobile bearing phenomenon minimises both torsional and shear stresses at the component bone interface. In our unit the impact of choice is the LCS rotating platform prosthesis, which is inserted with cruciate-sacrifice.

We reviewed 219 patients (272 knees) with an average follow-up of 6 years (5–8 years). In almost all cases the components were inserted with cement fixation. The patella was primarily resurfaced in 20 patients (21 knees). All operations were performed or supervised by the senior author. Female to male ratio was 2:1. Average age at surgery was 68 years (40–86) with osteoarthritis being the commonest primary diagnosis (89%). Postoperative range of motion ranges from 30–130° (average 103°). Average Oxford Knee, American Knee Society Score and Patellar Score was 19 (12–53), 160 (42–199) and 25 (4–30) respectively. Six patients (1.7%) required MUA at six weeks. Two patients (0.6%) required secondary patellar resurfacing. Three patients (0.8%) had revision of their components for persistent pain. At operation all components were noted to be well fixed. Spinout of the rotating platform occurred in one patient (0.3%). This was treated by exchange of the insert.

In conclusion, our early results of the LCS rotating platform prosthesis are encouraging with no cases of component loosening to date. This supports the continued use of the implant.

Introduction: Historically, it has been accepted that pain associated with arthritis of the hip is usually located in the groin and thigh with radiation to the anterior knee. However pain below the knee, and into the foot was not believed to be associated with arthritis of the hip. Patients complaining of thigh pain that extends below the knee are often considered to have a degenerative lumbar spine as the cause for their lower limb symptoms, and hip arthroplasty may not be offered. We examined the severity and location of pain in patients attending for arthroplasty and assessed how this altered following surgery.

Methods: 200 consecutive patients undergoing primary total hip arthroplasty completed a questionnaire regarding the location and severity of pain in the leg and also an Oxford hip score to assess functionality. These were completed approximately 4 weeks preoperatively and again at a 3-month review clinic.

Results: 57% (114/200) of patients complained of pain below their knee preoperatively. Only 9% (10/114) of these patients continued to complain of pain postoperatively, and of these patients their mean pain score decreased by 44% (9 to 5). Only 1% (2/200) of all patients complained solely of pain in the knee or more distally, and both of these had complete relief of pain 3 months postoperatively.

Conclusion: A significant number of patients with degenerative hip disease have pain below the knee. Patients who complain of pain in their back, buttock or thigh, which extends below the knee, may still benefit from total hip replacement. Careful consideration should be taken before labelling the pain as being referred from degenerative back disease.

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.

Rapidly progressive cases of primary idiopathic hip osteoarthrosis are well known and recognised. The prevalence reported in the literature varies from 4–18%. Three types have been identified- type 1 (rapid), type 2 (moderate) and type 3 (delayed) depending on the duration of chondrolysis and the subsequent rate of bone loss per year.

We reviewed the charts of all patients deemed to be RPO type 1 who had underwent hip arthroplasty under the care of the senior author (DEB) over a two-year period in an attempt to identify risk factors, which may have contributed to the rapid progression of their disease. All patients were treated using a custom femoral stem and a spiked Duraloc cementless socket following careful preparation of the acetabulum.

We identified 34 patients (40 hips) with type 1 rapidly progressive osteoarthrosis. Over the same time period 991 patients had underwent primary total hip arthroplasty, giving a prevalence of 4%. Of the 34 patients, 29 were female of average age 70.6 years (range, 51–83 years). All of the bilateral cases (6 patients) were female. Body mass index (BMI) for the female group ranged from 20.6 to 41.1Kg/m² (average, 28.2kg/m²) whilst that for the males was on average 25.8Kg/m² (range, 23.4–29.7Kg/m²).

Preoperative erythrocyte sedimentation rate (ESR) was 18mm/hr on average for the female group (range, 2–65mm/hr) and ranged from 3–52mm/hr (average, 20mm/hr) for the male patients. The preoperative Oxford Hip Score averaged 51 points for the female group and 48 points for the male group.

A detailed review of occupational history did not reveal any common occupational hazard. The majority of patients were non-smokers and denied any regular alcohol intake. Twenty-two patients (65%) had a history of hypertension. Twenty-seven patients (79%) had a history of non-steroidal anti-inflammatory use (most common preparation-diclofenac). Twenty-four patients (71%) resided in a rural area.

When compared to a cohort of patients undergoing primary total hip arthroplasty over the same time period, the only statistically significant risk factor identified was female gender.

We conclude, that patients who develop rapidly progressive osteoarthrosis of the hip are difficult to identify due to the absence of specific clinical features. We also outline our experience in the management of these technically challenging cases.

Background: Prospective population studies demonstrate that poor paraspinal muscle endurance increases the risk of developing first-time LBP and many CLBP studies also document excessive paraspinal muscle fatigability. The question arises as to whether this could have predisposed to chronic symptoms, through impaired spinal instability, especially in light of the wide inter-individual variation observed in the constitutionally determined paraspinal muscle fibre-type composition, which governs contractile performance.

Objective: To determine whether CLBP-associated excessive paraspinal fatigue results from a paucity in the type I fibre content.

Design: Control comparison using male subjects.

Subjects: Thirty-five CLBP patients with Von-Korff Chronic Pain Scores of ≤ III (high level of residual function, despite pain, to negate effects of disuse atrophy), and 32 controls of similar age.

Outcome measures: Fatigue-induced median frequency (MF) declines in the surface EMG signal, monitored bilaterally at L4 level during Biering-Sorensen- and 60%MVC- isometric fatigue tests. Percutaneous para-spinal muscle biopsies permitted histomorphometric comparisons.

Results: Between-group differences were assessed using independent t-tests (p < 0.05). There were no differences for MF decline during the Biering-Sorensen -0.37(0.16) vs. -0.36(0.12), and the 60% MVC test −0.42(0.31) vs −0.51(0.29), and in the percentage number of type I fibres, 63.6% vs 64.3%, or percentage area occupied by type I fibres, 69.4% vs 67.2%, in the paraspinal muscles for patients and controls respectively (p> 0.05).

Conclusion: Impaired CLBP-associated endurance is not the result of a constitutionally ‘adverse’ fibre-type composition.

Objective: To determine the factor structure of the Coping Strategies Questionnaire (CSQ)¹ in chronic low back pain patients (CLBP) presenting for physiotherapy.

Subjects: CLBP patients presenting for their first assessment at an outpatient physiotherapy department were used (N = 105; 60% male; M age = 41 yrs; SD ± 10).

Design: A factor analysis, using varimax rotation, was performed on patients’ responses to the CSQ. Factors emerging with eigenvalues of ≥1 were considered. A coping strategy was included in a factor if it correlated with the factor at a level greater than 0.6.

Results: Three factors accounted for 70% of the variance in questionnaire responses. Factor 1, labeled Adaptive Coping, accounted for 35% of the variance and comprised the subscales for reinterpreting pain sensations, ignoring pain sensations, and coping self-statements. Factor 2, labeled Maladaptive Coping, accounted for 23% of the variance and comprised the subscales for diverting attention, catastrophizing, praying or hoping, and behavioural coping styles. The final factor, labeled Efficacy of Pain Management, accounted for 12% of the variance and comprised the two single-item scales. Adaptive Coping was positively correlated with Maladaptive Coping (r = 0.37, P < 0.01). Efficacy of Pain Management was positively correlated with Adaptive Coping (r = 0.28, P < 0.01). A non-significant negative correlation was found between Maladaptive Coping and Efficacy of Pain Management (r = −0.03, P > 0.05).

Conclusion: Three underlying factors, labelled Adaptive Coping, Maladaptive Coping, and Efficacy of Pain Management accounted for 70% of the variance in questionnaire responses.

Patients with spinal cord injuries have been seen to have increased healing of attendant fractures. This for the main has been a clinical observation with laboratory work confined to rats. While the benefits in relation to quicker fracture healing are obvious, this excessive bone growth (heterotopic ossification) also causes unwanted side effects, such as decreased movement around joints, joint fusion and renal tract calculi. However, the cause for this phenomenon remains unclear.

This paper evaluates two groups with spinal column fractures – those with neurological compromise (n=10) and those without (n=11), and compares them with a control group with isolated long bone fractures (n=10). Serum was taken from these patients at five specific time intervals post injury (24hrs, 120hrs, 10 days, 6 weeks and 12 weeks). The time period most closely related to the end of the acute inflammatory reaction and the laying down of callus was the 10-day post injury time period.

Serum samples taken at this time period were analysed for IGF-1 and TGF-β levels, both known to initiate osteoblastic activity, using ELISA kits. They were also exposed to an osteoblast cell culture line and cell proliferation was measured.

Results show that the group with neurology has increased levels of IGF-1 compared to the other groups (p< 0.14, p< 0.18 respectively, Student’s t-test) but had lower TGF- (p< 0.05, p< 0.006) and osteoblast proliferation levels (p< 0.002, p< 0.001), despite having a significantly higher cell proliferation than a control group (p< 0.0001). When the neurology group is subdivided into complete (n=5) and incomplete (n=5), it was shown that the complete group had higher levels of both IGF-1 and TGF-. This trend is reversed in the osteoblast proliferation assay.

This work, for the first time in human subjects, identifies a factor which may be regulating this complication of acute spinal cord injuries, namely IGF-1. Furthermore, the observed trend in the two cytokines seen in the complete neurology group may suggest a role for TGF-β. However, the results do show that a direct mediation of this unwanted side effect of spinal cord injuries is unlikely as seen in the proliferation assay. Further work remains to be done to fully understand the complexities of the excessive bone growth recognised in this patient group.

Objective: To determine the extent to which coping strategies mediate chronic low back pain (CLBP) disability in patients presenting for physiotherapy.

Subjects: CLBP patients presenting for their first assessment at an outpatient physiotherapy department were used (N = 90; 60% male; M age = 41 yrs; SD ± 10).

Design: The mediating role of coping strategies was investigated after controlling for the influence of recorded demographics, healthcare variables and pain. Hierarchical multiple regression was employed with disability¹ as the dependent variable. Independent variables were entered in three separate steps. Demographics (sex, age and socioeconomic status) were entered in Step one. Healthcare and Pain variables (leg pain, previous surgery, history of back pain and current pain intensity [VAS]) were entered in Step two. Three coping dimensions (Adaptive Coping, Maladaptive Coping and Efficacy of Pain Management), derived from a factor analysis of the Coping Strategies Questionnaire², were entered in the final Step.

Results: Demographics accounted for 14% of the variance in disability [F (3, 86) = 4.81, P =. 004]. Healthcare and Pain variables accounted for an additional 17% of the variance [F (4, 82) = 5.11, P =. 001]. The three coping dimensions accounted for a further 6% of the variance [F (3, 79) = 2.71, P =. 05]. The model accounted for 38% of the variance in disability [F (10, 79) = 4.81, P =. 000].

Conclusion: Coping did mediate levels of CLBP disability. Moreover, disability is influenced more by Adaptive (Standardised β = −. 26, P =. 02) and Maladaptive (Standardised β =. 27, P =. 02) coping strategies than Efficacy of Pain Management (Standardised β =. 07, P > . 05).

Objective: To implement an early occupational intervention which tackles the psychosocial factors (yellow and blue flags) that influence recovery from occupational back pain.

Design: An early, psychosocial, occupational health nurse-led intervention using a basic ‘counselling’ technique that reinforces evidence-based messages and advice, along with availability of modified work.

Subjects: 206 workers from a sample of Glaxosmithkline sites who took absence due to back pain.

Outcome measures: Duration of presenting absence.

Results: The target for contacting the worker was achieved at Site 1 (mean 3 days), but not Site 2 (mean 12 days). Results showed that late contact of absent workers (> 1 week) was significantly associated with both longer presenting absence and fewer recipients of the psychosocial intervention, compared with early contact. Preliminary results show that the psychosocial intervention (irrespective of early or late contact) reduces the length of presenting absence by half.

Conclusions: The lack of early contact at Site 2 was due to local sickness absence management differences. This study reveals a third class of obstacles to recovery – organisational policies (black flags) – that can negate the effect of occupational rehabilitation programs.

Objective: To assess the psychometric properties of the Tampa Scale for Kinesiophobia (TSK)¹.

Subjects: Eighty-four chronic low back pain (CLBP) patients presenting for their first assessment at an outpatient physiotherapy department were used (57% female; M age = 45 yrs; SD ± 10 yrs).

Design: Eighty-four patients completed the TSK. Internal consistency, item-total correlations, distribution of scores on each item, three-day test-retest reliability and responsiveness were then calculated. To determine responsiveness, patients were categorised into two groups, namely meaningful change in pain-related fear (Group 1) and non-meaningful change in pain-related fear (Group 2). Patients were categorised based on their response to a thirteen-point global rating scale (GRS). Standardised Response Means (SRMs)² were computed for each group.

Results: Internal consistency was excellent (Cronbach α = 0.82). With the exception of items 8 and 16 all item-total correlations exceeded the level of 0.20. Scores were normally distributed for most items, however, items 4, 12 and 14 were positively skewed (Z-scores > 1.96). Test-retest coefficients were high (ICC = 0.91). SRMs were −0.96 and −0.44 for Groups 1 and 2, respectively, thus indicating good discriminatory power. An adapted version of the TSK (MTSK-12), constructed from the twelve most psychometrically robust items, had comparable reliability and validity (Cronbach α = 0.82; ICC = 0.91; SRM [Group 1] = 0.89; SRM [Group 2] = 0.39).

Conclusion: Overall the TSK has excellent psychometric properties. The MTSK-12 is a valid and reliable measure of pain-related fear and warrants further investigation.

Study design: Cross-sectional questionnaire-based workforce survey together with collection of retrospective data on work absence.

Objectives: To determine if psychosocial ‘blue flags’ are related to back pain and/or sickness absence due to back pain.

Summary of background: The original description of the psychosocial ‘yellow flags’ for back pain chronicity included a mixture of individual psychological parameters and parameters related to perceptions about work and the workplace. It has recently been suggested that these latter parameters should be considered separate and distinct from the individual parameters , and can be termed ‘blue flags’. To date, however, there has been no attempt to explore the specific relationship between the blue and yellow flags or their relative relationship to symptoms and disability.

Methods: The workforce of a large multi-site company was invited to complete a booklet of questionnaires, which included the standard Nordic instrument for obtaining back pain data, and specific instruments to obtain data on ‘yellow’ and ‘blue’ psychosocial flags. The blue flags included psychosocial aspects of work, attribution and elements from the demand/control model, with psychological distress used as a yellow flag comparator. Of the 7,500 workers, 60% responded. Sickness absence records identified workers who had taken absence for back pain. The exploration of the data involved determining statistically significant relationships between psychosocial scores and both back pain history and absence. Appropriate statistical procedures were then used to establish cut-off points for the psychosocial variables. Odds ratios were calculated for two particular outcome variables: self-reported back pain in the previous 12 months and recorded absence over the same period.

Results: Cut-off points were established for each variable, along with the odds ratio (OR) that this score or a score above or below (depending on the scale direction) is associated with reports of back pain or absence. The ORs for psychological distress were 1.9 and 2.4 respectively for LBP and absence in the last 12 months. The ORs for the blue flag variables varied from 1.1 to 1.5 for LBP and from 1.8 to 3.2 for absence.

Conclusions: The psychosocial blue flags reported here are statistically significantly related both to reported back pain and absence. The effect size is less than that for distress in respect of back pain, but variously higher and lower for absence. Whilst prospective studies are needed to determine cause/effect, the results offer tentative support for the suggestion that blue flags should be addressed in clinical interventions.

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.

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.

Traditional biomedical/ergonomic occupational interventions to reduce work loss show limited success. Attention is now focussing on tackling the psychosocial factors that influence occupational back pain.

A workforce survey of Glaxo Smith Kline (reported to the Society last year) established that clinical and occupational psychosocial factors (yellow & blue flags) act independently and may represent obstacles to recovery. Consequently, a nurse-led intervention was devised. Occupational nurses at two manufacturing sites were trained to identify both clinical and occupational psychosocial factors, and address them using a basic ‘counselling’ technique that reinforces evidence-based messages and advice, along with availability of modified work. The program should ideally be implemented within the first days of absence, with ‘case-management’ by the nurse for a further 4 weeks. Control sites simply offer ‘usual management’. Outcomes at 12-month follow-up are rates for work loss/work retention.

The target for contacting the worker (3 days) was achieved at one site, but not the other (mean 12 days), thus exerting a differential delay in delivering the intervention. The lack of early identification at the second site was due to local reporting/recording mechanisms. This study reveals a third class of obstacles to recovery – black flags – company policies/procedures that can impede occupational rehabilitation programs.