Introduction: The magnitude of the initial chondral injury and the residual articular step-off are amongst prognostic factors implicated in outcome following intra-articular fractures. The alignment of an intra-articular fracture line may be an as yet unrecognised prognostic variable.

Hypothesis: That fractures in the coronal plane of the medial femoral condyle result in worse outcomes than those in the sagittal plane.

Aim: To compare the effect of displaced intra-articular osteotomies (ie simulating fractures fixed in an incongruent position) of the medial femoral condyle – in one group performed in the sagittal plane, in the other in the coronal plane.

Materials and Methods: The study was conducted in two arms: in vitro and in vivo.

In vitro study: A pneumo-electric rig was designed and built. Ten freshly harvested porcine knee joints underwent osteotomy (test specimens: 5 sagittal, 5 coronal). 5 control specimens underwent no osteotomy. Specimens were mounted on the rig and subjected to cyclical flexion and extension under load (40,000 cycles over 11 hours). Transarticular pressure measurements were performed before and after testing. Surface roughness was measured following testing using laser interferometry.

In vivo study: Three groups (A to C), each comprising 15 New Zealand white rabbits were utilised. Rabbits from each group were consigned to a control (5), coronal osteotomy (5) or sagittal osteotomy (5) group. Rabbits in group A were sacrificed at 3 weeks (early outcome), group B at 10 weeks (immediate) and group C at 20 weeks (long term). The knee was then harvested en bloc and prepared for light microscopy. A further 10 specimens underwent electron microscopy of the medial meniscus.

Results:

In vitro study: A significant difference in loading patterns was noted between the sagittal, coronal and control groups. Specimens from the sagittal group sustained significantly more wear on the apposing medial tibial articular surface (p=0.04), with the meniscus having a protective effect on the underlying articular surface.

In vivo study: Light microscopy confirmed degenerative changes in the apposing tibial articular cartilage, being more marked in sagittal specimens. On the femoral side of the knee, the healing response of the femoral osteotomy was significantly better in sagittal test specimens than coronal (p< 0.05).

Conclusion: In contrast to the hypothesis, sagittal femoral step-offs gave rise to more tibial wear. This can be explained by the short duration of exposure of the coronal incongruity to the apposing joint during the flexion extension cycle. The sagittal step-off was constantly exposed, giving rise to persistently elevated tibial joint loading pressures opposite the high side of the step-off.

In contrast, the coronal femoral osteotomies had a worse healing response. The alignment of the fracture line perpendicular to the plane of motion of the joint exposes the repair tissue within it to increased shear and tensile stresses. This may play a negative role in the repair of these coronal defects when compared to sagittal osteotomies, which are relatively protected from the high transarticular pressures and showed a greater tendency to remodel their articular surface.

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 (1 day, 5 days, 10 days, 42 days (6 weeks) and 84 days (12 weeks)). These samples were then analysed for levels of Transforming Growth Factor-Beta (TGF-ß) using the ELISA technique. This cytokine has been shown to stimulate bone formation after both topical and systemic administration.

Results show TGF-ß levels of 142.79+/−29.51 ng/ml in the neurology group at 84 days post injury. This is higher than any of the other time points within this group (p< 0.001 vs day 1, day 5 and day 10 and p=0.005 vs 42 days, ANOVA univariate analysis). Furthermore, this level is also higher than the levels recorded in the non neurology (103.51+/−36.81 ng/ml) and long bone (102.28=/−47.58 ng/ml) groups at 84 days post injury (p=0.011 and p=0.021 respectively, ANOVA univariate analysis). There was statistically significant difference in TGF-ß levels seen between the clinically more severely injured patients, ie complete neurological deficit and the less severely injured patients, ie incomplete neurological deficit.

In conclusion, the results of this work, carried out for the first time in humans, offers strong evidence of the causative role of TGF-ß in the increased bone turnover and attendant complications seen in patients with acute spinal cord injuries.

Metallic implants are used frequently in the operative repair of joints and fractures in orthopaedic surgery. 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 up to 500 times more resistant than planktonic strains of bacterial flora to antibiotics. 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, antibacterial layers of silver on orthopaedic stainless steel and titanium K-wires and to investigate the effect of these coatings when exposed to Staphylococcus Aureus biofilms in an in vitro and in vivo environment.

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 and titanium 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. Silver leaching experiments were carried out in phosphate buffered saline at 37°C for 48 hours 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 minutes to allow biofilm initiation and adhesion. Wires were then culturing for 24 hours at 37°C in RPMI. Subsequently, wires were sonicated at 50Hz in ringer’s solution and gently vortexed to dislodge biofilm. Sonicate was plated out by log dilution method on Columbia blood agar plates. Bacterial colonies were then counted and changes expressed in log factors.

K-wires were coated with 1 to 50 nm of silver by running the magnetron sputtering at low currents. These coatings showed excellent adhesive properties within the 48 hours exposed with only 3.7% of silver leaching in buffered saline. The silver coated stainless steel wires showed a log 2.31 fold reduction in biofilm formation as compared to control wires (p< .001), Student t-test), the silver coated titanium wires showed a log reduction of 2.06, (p< .001, Student t-test). Animal studies demonstrated enormous difficulty in reproducing biofilm formation and showed a 0.49 log fold reduction in the titanium group when exposed to Staph Aureus (p< .01, Student t-test), the other groups showed no statistically significant reduction.

We have perfected a method of depositing tiny layers of anti-bacterial silver onto stainless steel and titanium, which is anti-infective in vitro but not in vivo. Further studies involving other metal coatings such as platinum and copper are warranted.

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.

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.