Treatment of bone infection often includes a burdensome two-stage revision. After debridement, contaminated implants are removed and replaced with a non-absorbable cement spacer loaded with antibiotics. Weeks later, the spacer is exchanged with a bone graft aiding bone healing. However, even with this two-stage approach infection persists. In this study, we investigated whether a novel 3D-printed, antibiotic-loaded, osteoinductive calcium phosphate scaffold (CPS) is effective in single-stage revision of an infected non-union with segmental bone loss in rabbits.

A 5 mm defect was created in the radius of female New Zealand White rabbits. The bone fragment was replaced, stabilized with cerclage wire and inoculated with Staphylococcus aureus (MSSA). After 4 weeks, the infected bone fragment was removed, the site debrided and a spacer implanted. Depending on group allocation, rabbits received: 1) PMMA spacer with gentamycin; 2) CPS loaded with rifampin and vancomycin and 3) Non-loaded CPS. These groups received systemic cefazolin for 4 weeks after revision. Group 4 received a loaded CPS without any adjunctive systemic therapy (n=12 group1-3, n=11 group 4). All animals were euthanized 8 weeks after revision and assessed by quantitative bacteriology or histology. Covariance analysis (ANCOVA) and multiple regression were performed.

All animals were culture positive at revision surgery. Half of the animals in all groups had eliminated the infection by end of study. In a historical control group with empty defect and no systemic antibiotic treatment, all animals were infected at euthanasia. There was no significant difference in CFU counts between groups at euthanasia.

Our results show that treating an osteomyelitis with segmental bone loss either with CPS or PMMA has a similar cure rate of infection. However, by not requiring a second surgery, the use of CPS may offer advantages over non-resorbable equivalents such as PMMA.

Purpose:

To explore clinicians' perceptions of empathy during musculoskeletal clinical consultations.

Introduction: Bone loss occurs as a consequence of disuse. Using the hindlimb-unloaded (HU) rat, the purpose of this study was to determine whether skeletal unloading and reloading alters regional bone blood flow (microspheres) and PNA vasodilator responsiveness (in vitro).

Results: Femoral bone and marrow perfusion were reduced after 10 minutes, 7 days and 28 days of HU. Further, when the hindlimb skeleton is reloaded for 10 minutes following 14 days HU, bone and marrow perfusion were lower than that in standing control animals (e.g., femoral proximal metaphysis: Control, 20 ± 3 ml/min/100g; HU, 13 ± 3 ml/min/100g). PNA endothelium-dependent vasodilation was attenuated with 14 days of HU (Control, 84 ± 5% maximal relaxation; HU, 55 ± 7% maximal relaxation).

Discussion: The HU-associated changes bone perfusion and endothelium-dependent vasodilation correspond to unloading-induced changes in bone structure. These results support the hypothesis that alterations in bone blood flow and vascular signaling may modulate bone remodeling.

Introduction: The purpose of this study was to determine whether regional blood flow (microspheres) in the femur is diminished with aging, and whether a reduction in flow is associated with impaired endothelium-dependent vasodilation.

Materials and Methods: Blood flow and PNA endothelium-dependent vasodilation was measured in young (4–6 months old) and aged (24–26 months old) male Fischer-344 rats.

Results: Blood flow in the aged rats was ~25% lower in femoral bone and 45% lower in diaphyseal marrow. Endothelium-dependent vasodilation was lower with old age (young: 83 ± 6% maximal relaxation; aged: 62 ± 5% maximal relaxation) and was mediated through impairment of the NOS signaling pathway, which resulted in a lower nitric oxide bioavailability (young: 168 ± 56 nM nitric oxide; aged: 50 ± 7 nM nitric oxide).

Discussion: Such age-related changes in bone perfusion and nitric oxide signaling could impact clinical bone loss, increase risk of fracture, and impair fracture healing in the elderly.

Introduction: Tumor necrosis factor-alpha (TNF-a) has been shown to be a potent stimulator of bone resorption in vitro and in vivo, and has been identified as an important factor in aseptic loosening of total joint replacements. In order to investigate the effects of TNF-a at the bone-cement interface, we developed a rabbit model in which a slow-release pellet containing a known amount of TNF-a was inserted adjacent to a polymethylmethacryate (PMMA) implant in the distal femur.

Methods: 25 male New Zealand white rabbits were used in this IACUC-approved study. After routine exposure of the distal femur, a 3 mm drill bit was used to drill through the intercondylar region into the medullary canal of the distal femur. A resorbable pellet containing 0, 420, 4200, 42 000 or 420 000 pg of TNF-a (n=5 animals per dose level) was inserted into the drill hole, immediately followed by a cylindrical PMMA implant (20 mm long). Animals were euthanized 42 days after surgery. The right femora were excised, radiographed, and processed for histology. Ground sections were prepared at the level of the proximal implant. Semi-automated image analysis was used to quantify cortical bone area, porosity and fractional surfaces (quiescent, osteoid and eroded). Data from control and treatment animals were compared with a one-way analysis of variance (ANOVA) using p< 0.05.

Results: All of the animals recovered well after surgery. Radiographically, all of the implants appeared to be stable, with no evidence of linear or cystic osteolysis. Local delivery of TNF-a for 6 weeks had no effect on cortical bone area or porosity. However, TNF-a stimulated bone resorption and decreased new bone formation at the endosteal surface (p< 0.05); these effects were not dose-dependent but were seen in all of the TNF-a groups.

Discussion: Our data provide direct evidence that local release of TNF-a is capable of inducing endosteal bone resorption in vivo. Additional studies are now needed to determine the effects of other proinflammatory cytokines in this animal model. However, based on these results, it appears that targeted blockade of TNF-a release or activity may provide a rational therapeutic approach to osteolysis and aseptic loosening.

In ten male rats we inserted ceramic ‘drawing-pin’ implants in weight-bearing positions within the right proximal tibia. Two animals were killed 6 weeks after surgery and two more 14 weeks after surgery. The remaining six received intra-articular injections of either high-density polyethylene (4 rats) or saline (2 rats) at 8, 10 and 12 weeks after surgery. These animals were killed two weeks after the last injection.

Histological examination of the bone-implant interface in the control animals showed appositional bone growth around the implant at both 6 and 14 weeks. Polyethylene, but not saline, caused a chronic inflammatory response with numerous foreign-body giant cells in periprosthetic tissues.

Our model of a stable, weight-bearing bone-implant interface provides a simple and reliable system in which to study in vivo the effects of particulate materials used in orthopaedic surgery.

We measured pressures in the anterior and deep posterior compartments continuously for up to 72 hours in 20 patients with closed fractures of the tibial shaft treated primarily in plaster casts. All were examined independently after periods of three to 14 months. Pressures above 40 mmHg occurred in seven (35%) and above 30 mmHg in 14 (70%). No patient had the symptoms of compartment syndrome during monitoring. Abnormalities at review did not correlate with the maximum consecutive time periods during which the compartment pressures were raised. Thus, in the absence of symptoms the monitored pressures did not relate to outcome. Routine monitoring in this type of patient is therefore of doubtful benefit.

We assessed 16 patients before and after high tibial osteotomy by electrophysiological recordings, creatine phosphokinase levels, radiographs and intracompartmental pressure monitoring. We found mild electrophysiological abnormalities pre-operatively in 12 of the 16 patients, but postoperatively these had deteriorated in 11 of the 14 patients studied. Creatine phosphokinase levels, compartment pressure and radiological deformity were not predictive of the development of postoperative common peroneal nerve palsy. Patients who also had a proximal fibular osteotomy had greater electrical abnormalities postoperatively and two of them developed common peroneal palsies. Proximal fibular osteotomy appears to be a causative factor in the development of common peroneal nerve palsy; more work is needed on the blood supply of the nerve.

The aetiology of pain in the lower leg during exercise has been studied in 110 athletes by monitoring intracompartmental pressure during exercise and by technetium bone scans. Patients were assigned to three diagnostic groups: chronic compartment syndrome, medial tibial syndrome and those with non-specific findings. Our results indicate that subcutaneous fasciotomy of the affected compartment(s) is the treatment of choice for chronic compartment syndrome. The treatment of patients with medial tibial syndrome, either by operation or conservatively, has been unsuccessful; non-specific symptoms have been treated conservatively with success.

Weakness of dorsiflexion of the foot is a common complication of proximal tibial osteotomy and it has been suggested that this may be caused by an anterior tibial compartment syndrome. A prospective study of 20 patients undergoing tibial osteotomy was undertaken, in which compartment pressures were recorded and related to clinical signs. In 10 of the patients, the operation site was drained, and in 10 no drainage was employed. The undrained group showed significant elevation (greater than 45 mmHg) of the anterior compartment pressure in seven patients, and five of these had transient clinical signs. Only one patient had any permanent deficit, a minor asymptomatic weakness of extensor hallucis longus. In the drained group the pressures remained below 30 mmHg in all except two patients, who both had only a minor pressure rise and no significant early clinical signs. However, two patients from this group later developed weakness of dorsiflexion, probably due to common peroneal nerve injury, the cause of which is not clear.

Acute compartment syndromes often develop insidiously and are often recognised too late to prevent permanent disability. Management is difficult as the compartment involved is seldom clinically apparent. By continuously monitoring the intracompartmental pressure these problems can be avoided: transient compartment syndromes can be differentiated from established ones and the correct compartment can be surgically decompressed. Pressure monitoring techniques were used in 28 patients; three developed a compartment syndrome requiring surgical intervention, seven had a temporary increase of pressure and in 18 the pressure remained unaltered. Of the three with compartment syndromes, one was unusual in that it affected the thigh and another, unique in our experience, affected both the thigh and the calf. Intracompartmental pressure monitoring significantly altered the management of two cases giving successful results with minimal intervention.