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Stem loosening and stress-shielding are problems encountered in cemented hip arthroplasty. Could proximal stem fixation by partial cementing solve the problem? More physiological transmission of forces with only proximal cement fixation seems to be possible with this recent development (Z-stem, Option 3000, Mathys Orthopaedics, Bettlach, Switzerland). In a prospective clinical trial, this new implant was used for total hip arthroplasty in human patients. One hundred and thirty-three (133) total hip replacements in 123 patients were performed between April 1996 and January 2003. All of them were followed up regularly; 53 were analysed with the EBRA-FCA method (Einzel Bild Röntgen Analyse--femoral component analysis), whereas the rest were analysed using conventional follow-up X-rays. Eighty-six (86) patients with 95 hips could be examined in August 2004 to obtain mid-term results. At this stage, the mean follow-up time was 61 months (5.08 years), with a maximum of 100 months (8.33 years). Up to October 2004, nine cases needed a revision. The clinical data collected reported an average Harris Hip Score of 89.3 (good). The EBRA-FCA analysis reported a mean subsidence of less than 1.5 mm after the first two years, under the EBRA threshold of predicted loosening. At the latest follow-up (at an average of 61 months), there was an average stable subsidence of 2.4 mm in general. Eight (8) patients presented with subsidence of more than 5 mm. The results of the new implant seem to be encouraging. Finally, comparing our results to other fixation concepts will require longer follow-up periods. [ABSTRACT FROM AUTHOR]

Surgical treatment of most displaced proximal humerus fractures is challenging due to osteoporosis. Locking plates are intended to provide superior mechanical stability. In a prospective multicentre study 131 patients were treated with second generation locked plating (NCB-PH, Zimmer, Inc.). The open procedure (n = 78) was performed using a deltopectoral approach; the minimally invasive technique (n = 53) involved percutaneous reduction and an anterolateral deltoid split approach. Clinical and radiological follow-up was obtained. Improvement in function (ROM) was statistically significant. Fracture type (AO) had the most significant impact on the incidence of complications. The most frequent complications detected were intra-articular screw perforation (15%) and secondary displacement (8%). Complication rate and functional outcome of the NCB-PH are comparable to reports in the literature. Not all problems are likely to be solved by this new generation of implants, i.e. secondary dislocation still occurred in 8% of our patients.

Platelet-rich plasma (PRP), a platelet concentrate made of autogenous blood, has been used in recent years to improve bone defect healing particularly in maxillofacial reconstructions. The aim of the present study was to assess the effect of PRP on new bone formation in a critical diaphyseal long bone defect. A critical size defect (2.5 cm) in the tibial diaphysis of 16 sheep was supplied either with autogenous PRP in a collagen carrier or with collagen alone (controls). Platelets were enriched about 3.5 fold compared to normal blood in the PRP. After 12 weeks, the explanted bone specimens were quantitatively assessed by X-ray, computed tomography (CT), biomechanical testing and histological evaluation. Bone volume, mineral density, mechanical rigidity and histology of the newly formed bone in the defect did not differ significantly between the PRP treated and the control group, and no effect of PRP upon bone formation was observed. It was suggested that PRP does not enhance new bone formation in a critical size defect with a low regenerative potential. Such bone defects might require more potent stimuli, e.g. combinations of functional biomaterials or autografts, precursor cells or osteoinductive growth factors.

Endoscopic minimally invasive techniques have become an established method of fracture stabilisation in the spine. In view of this fact, anterior stabilisation strategies must be reconsidered, as monosegmental A 3.1 compression fractures are increasingly being stabilised endoscopically from the anterior aspect using minimally invasive techniques. This study investigated the biomechanical necessity of anterior two-point or four-point stabilisation in the instrumentation of mono- and bisegmental fractures. In three biomechanical in vitro studies, burst fracture stabilisation was simulated, and anterior short fixation devices were tested under load with pure moments up to 3.75 Nm to evaluate the biomechanical stabilising characteristics of different kinds of instrumentations in flexion/extension, lateral bending, and axial rotation. Only anterior four-point stabilisation resulted in sufficient primary stability both in mono- and bisegmental instrumentation and therefore represents the standard procedure in open as well as in minimally invasive spinal surgery.

We investigated the osseointegration of solvent-preserved, xenogenous cancellous bone blocks in the treatment of unstable fractures of the thoracolumbar junction. In 22 patients, the anterior repair procedure was performed by thoracoscopy or minimally invasive retroperitoneal surgery. Twenty-two patients had undergone monosegmental anterior fusion and were surveyed prospectively. Solvent-preserved, bovine cancellous bone blocks were used in 11 patients; iliac crest bone graft was used in the others. Follow-up after 12 months included CT scans, which revealed successful osseointegration in eight out of 11 patients who had received autogenous iliac crest bone grafts, while three patients showed a partial integration. There were no graft fragmentations. In patients who had received solvent-preserved, xenogenous cancellous bone blocks, complete osseointegration was achieved at the graft-bone interface in only two out of 11 cases, after 1 year. Partial integration was found in three patients. In view of these results, autogenous iliac crest bone grafts are still the unrivalled standard for defect repair in spinal surgery.

The influence of additional dorsal structure damage on anterior stabilization of a thoracolumbar fracture is still unknown. Screw-cement enhancement can be used to reinforce the stability of anterior instrumentation. We have developed a new anchorage system for fixation of anterior stabilization devices, adapted through geometric optimization and the additional option of cementation after screw insertion. This study examines the question of whether this enhancement is strong enough to enable a single anterior procedure and still compensate for dorsal instability. Various spinal reconstruction procedures were evaluated biomechanically in an increasing ventrodorsal instability model for thoracolumbar fracture stabilization. A biomechanical in vitro study, simulating stabilized defect situations (corporectomy/vertebrectomy) with strut grafting and overbridging instrumentation, was performed on six human T10-L2 cadaveric specimens. The primary stability parameters, range of motion and neutral zone, were evaluated with or without anterior screw-cement enhancement. This was compared with a single conventional anterior stabilization without a dorsal defect (corporectomy). It was also compared with a single anterior, posterior or combined procedure in the presence of additional dorsal structure damage (vertebrectomy). The use of an additional cementable screw dowel enhanced the primary stability of the anterior instrumentation, compensating for dorsal instability. These results are warranted for the clinical use of minimally open or endoscopic techniques, creating the highest possible primary stability while performing a single anterior enhanced instrumentation with a tissue-preserving approach.

The anatomic proof of a spinal compartment and the clinical symptoms of compartment syndrome in patients with chronic back pain are inconsistent with the rarely met measuring criteria of intramuscular pressure (IMP). Previous studies assume a dependence of the IMP on spinal alignment (degree of lumbar spine flexion) and the degree of muscle activation. The significance of these disturbance variables in the interpretation of IMP could explain the above discrepancy. This study therefore investigates the influence of both a 30% increase in trunk flexion and alterations in muscle contraction from 100% to 60%. Sixteen healthy subjects participated in the study. The IMP and mean rectified amplitude of the multifidus surface EMG signal were determined at rest and 0 degrees and approximately 30 degrees of lumbar spine flexion, and they were compared. Subsequently, both parameters were measured during both 100% and 60% maximal voluntary contraction (MVC) of the muscle and then correlated. During rest and 0 degrees flexion, the median IMP was 9.3 mmHg (range 0.0-22.5) while the median mean rectified amplitude (MRA) of the EMG signal was 1.98 microV (range 1.32-7.38). In 30 degrees flexion, the median IMP went up to 24.3 mmHg (range 1.4-97.3) with hardly any increase in the median MRA of 2.32 microV (range 1.20-9.72). Under 60% MVC, the median IMP rose to 186.6 mmHg (range 15.4-375.4) and the median MRA to 21.02 microV (range 4.63-43.63). During 100% MVC, the median MRA increased to 34.38 microV (range 12.99-102.54) while the median IMP rose to 273.4 mmHg (range 90.4-395.1). Spearman's rank correlation coefficient for the IMP and MRA quotients of the 100/60% MVC values was r= -0.21. To sum up, it can be said that IMP was subject to great interindividual variation in all the experiments. This parameter is highly dependent on spinal alignment and muscular activity. Further studies are needed so that the IMP can be interpreted properly when diagnosing a chronic compartment of the erector spinae muscles.

Severe blunt chest trauma is frequently associated with multiple organ failure and sepsis. Posttraumatic immunosuppression seems to play a major role in their development. However, the immunologic alterations following pulmonary contusion are insufficiently elucidated. Specifically, it remains unknown whether immunocompetent cells located distant from the site of the impact are affected. We therefore aimed to characterize the influence of pulmonary contusion on lymphocytes and splenic macrophages. Male C3H/HeN mice (n = 8-10/group) were anesthetized and subjected to trauma or sham procedure. Blunt chest trauma was induced by a blast wave focused on the thorax. Two or 24 h later, splenocytes and splenic macrophages were isolated and stimulated for 48 h. The cytokine release (IFN-gamma, IL-2, IL-3, IL-10, IL-12, IL-18) from splenocytes as well as from splenic macrophages (TNF-alpha, IL-10, IL-12, IL-18) and plasma levels of TNF-alpha and IL-6 were quantified by ELISA. The results indicate that at 2 h after blunt chest trauma, plasma TNF-alpha and IL-6 were markedly increased. At the same time, no differences in splenocyte cytokine production were detectable. However, at 24 h a significantly depressed cytokine release was observed in trauma animals. Furthermore, splenic macrophages showed a significantly decreased production of TNF-alpha, IL-10, and IL-12 at 24 h and markedly increased release of IL-18 at 2 h after trauma. These results indicate that blunt chest trauma causes severe immunodysfunction of lymphocytes and splenic macrophages. Thus, lung contusion as a localized type of trauma causes dysfunction of immunocompetent cell populations, which are located distant from the site of injury.

A new instrumentation system for ventral stabilization of the spine that can be used for an endoscopic and minimally invasive approach was developed. We describe the implantation technique and report on the first clinical results. This prospective study covers the first 45 patients to undergo this new technique since it was introduced in 1999. In all patients the operation was successfully performed in a completely minimally invasive procedure. Mono- and bisegmental stabilization was performed mainly at the thoracolumbar junction after initial posterior instrumentation in most cases. Lesions varied from fresh/old fractures to metastases (T5-L3). Pre- and postoperative follow-up included clinical examination and radiological visualization via X-ray and computed tomographic scan. Our experience with this minimally invasive procedure demonstrated the feasibility of the method.

The cause for the high morbidity of blunt chest trauma is not fully understood. It is still unclear if and to what extent a second insult, e.g., apoptotic tissue damage initiated by the primary insult itself, may contribute to the development of serious complications. This study was done to elucidate whether a pulmonary contusion may induce programmed cell death. Sixty-four Wistar rats were evenly randomized to eight experimental groups: four sets were subjected to a standardized blast wave injury and sacrificed 6, 24, 48, and 72 h after the trauma; four groups served as controls for the same time points. Lung and liver samples were stained (H & E; TUNEL), and PMN infiltration was determined by myeloperoxidase (MPO) activity. Caspase 8 was analyzed by Western blot, and TNF-alpha plasma levels by ELISA. Postmortem examination revealed bilateral pulmonary contusion in trauma animals with higher (P < 0.05) numbers of apoptotic cells in lung but not in liver tissue as early as 6 h after the injury. This amount gradually increased and reached a maximum after 48 h: 6.8 +/- 1.1 apoptotic cells/hpf vs. 0.6 +/- 0.06 in controls. Chest trauma caused an increased expression of active caspase 8 in lung but not in liver tissue at 48 and 72 h. TNF-alpha plasma levels were not different. MPO activity in lung tissue of trauma animals increased (P < 0.05) after 6 h and peaked at 72 h. This study has provided the first evidence that apoptotic cell death in lung tissue is initiated following (experimental) pulmonary contusion. The exact mechanism remains, however, unclear and has to be elucidated further.

We studied a 4-year-old boy from Angola who presented with 2 cutaneous ulcerations of the right hip and osteomyelitis of the left knee and right ankle. Mycobacterium ulcerans disease was confirmed by direct smear examination and by polymerase chain reaction. The patient was treated with antimycobacterial drugs, repeated surgical debridement, skin grafting, and daily hyperbaric oxygenation. Despite significant improvement of the local lesions in response to hyperbaric oxygenation, swelling of the right knee, without associated skin lesions, was noted. Radiological evaluation and open biopsy revealed extensive metaphyseal osteomyelitis of the right distal femur. A 99technetium bone scan revealed an additional focus in the diaphysis of the left humerus, without soft-tissue involvement. This case documents, for the first time (to our knowledge), the systemic spread of M. ulcerans, with subsequent multifocal osteomyelitis and secondary involvement of soft tissues and supports the hypothesis that low tissue oxygen levels promote hematogenous spread of M. ulcerans. Sickle cell anemia, with associated microthrombosis and microinfarction, may have contributed to tissue hypoxia.

Severe blunt chest trauma remains an important injury with high morbidity and mortality. However, the associated immunological alterations are poorly understood. Existing big animal models require large-scale settings, are often too expensive, and research products for immunological studies are limited. In this study we aimed to establish a new model of blunt, isolated and bilateral chest trauma in mice and to characterize its effects on physiological and inflammatory variables. Male C3H/HeN mice (n = 9-10/group) were anesthetized and a femoral artery was catheterized. The animals were subjected to trauma or sham procedure and monitored for 180 min. Blunt chest trauma was induced by a blast wave focused on the thorax. Trauma intensity was optimized by varying the exposure distance. Blood pressure, heart rate, respiratory rate, arterial blood gases and plasma cytokine levels were measured. Macroscopic and microscopic examinations were performed. In addition, outcome was evaluated in a 10-day survival study. Chest trauma caused a drop (P < 0.05) in blood pressure and heart rate, which partly recovered. Blood gases revealed hypoxemia and hypercarbia (P < 0.05) 180 min after trauma. There was marked damage to the lungs but none to abdominal organs. Histologically, the characteristic signs of a bilateral lung contusion with alveolar and intrabronchial hemorrhage were found. Plasma interleukin-6 and tumor necrosis factor alpha were considerably increased after 180 min. Blunt chest trauma resulted in an early mortality of 10% without subsequent death. On the basis of these findings, this novel mouse model of blunt chest trauma appears suitable for detailed studies on immunological effects of lung contusion.

The aim of this prospective study was to determine the local concentrations of inflammatory mediators in various tissue types frequently affected by trauma to estimate the role of prestored cytokine release by mechanical tissue trauma in the induction of a systemic inflammatory response syndrome. The degree of tissue damage, evaluated by its systemic release of inflammatory mediators, represents an important factor concerning the outcome of trauma patients. Clinical trials indicate that the kind of traumatized tissue influences the cytokine pattern measured in patients blood afterwards. However, the tissue-specific mediator composition underlying this systemic mediator release is rarely elucidated. Upon approval of the local IRB/EC, skin, subcutaneous fat, muscle, cancellous bone, and lung tissue were obtained during standard surgical procedures. The protein-based concentrations of Interleukin (IL)-6, IL-8, IL-10, and IL-12 were determined in tissue homogenates by enzyme-linked immunoabsorbant assay (ELISA; n = 60 samples). Albumin was measured to evaluate the degree of blood contamination of tissue samples. IL-6 and IL-8 were consistently detectable in more than 95% of the tissue specimens. Lung and cancellous bone presented by far the highest concentrations of these cytokines, whereas skin, subcutaneous fat, and muscle showed significantly lower levels. IL-10 was not detectable in 88%; IL-12 could not be measured in 63% of the samples. Cytokine concentrations did not correlate with the amount of albumin measured in tissue specimens. Due to their consistent presence at the tissue level, high systemic concentrations of IL-6 and IL-8 in patients blood, seen after pulmonary trauma, long bone fractures, or soft tissue injury, may be interpreted as an overspill of local trauma mediators. This indicates their relevance in post-traumatic monitoring. Furthermore, albumin is a suitable and necessary indicator to evaluate influences of possible blood contamination in tissue samples.

Chemokines mediate the migration of leukocytes to sites of inflammation. Changes in the plasma concentration of interleukin (IL)-8 and macrophage inflammatory protein (MIP)-1beta have not been investigated in the very early phase starting immediately after unintentional trauma. Enrolled in the study were 94 patients with multiple blunt injuries. Blood samples were collected at the scene of accident, then at regular intervals for 24 h. IL-8 and MIP-1beta plasma levels were determined by commercial test kits. Patients were grouped according to trauma severity, pattern of injury, as well as survivors vs. nonsurvivors. Serious casualties [Injury Severity Score (ISS) > or = 32] revealed a significant increase in IL-8 compared to only a slight elevation in individuals with an ISS < 32. Nonsurvivors showed a highly significant (P < 0.005) increase in IL-8 levels beginning immediately after admission. Trauma resulted in a modest activation of MIP-1beta production without differences regarding trauma severity, pattern of injury, or survival. A very strong trauma stimulus is necessary to activate IL-8 production. In contrast to MIP-1beta, IL-8 levels were significantly elevated in nonsurvivors compared to survivors. Therefore, IL-8 might be an early predictor of survival.

Trauma may cause a relevant reduction in antithrombin (AT) III activity, which is associated with adverse events. The very early changes in AT III activity after accident trauma are still unclear and possible relations with Interleukin (IL)-6, which is known to interact with AT III, have not been investigated so far. Upon approval of the IRB/IEC, 30 patients were enrolled with multiple injuries (ISS 9-75). Groups were performed according to injury severity, IL-6 concentration, and survivors versus non-survivors. Blood samples were collected at the scene of accident then at 2, 4, 6, 12, and 24 h and at day 3, 5, 10 and 15. No patient received AT III concentrates. In all groups a reduction in AT III activity occurred, which was most pronounced in very severe injuries. The activity re-increased spontaneously and steadily in all groups regardless of the IL-6 concentration. There was no clear impact of the AT III activity on survival.