We conducted a multicentre two arm double blind randomised controlled trial to assess efficacy of pulsed ultrasound for accelerating the rate of bone healing. Sixty-two skeletally mature adults undergoing limb lengthening, of between 2.5cm to 10cm by distraction osteogenesis, at the proximal tibia using an Ilizarov frame were randomised to either an active or a placebo (control) ultrasound device. Primary outcome measure was time ready for removal of frame after adjusting for distraction length (days/cm) for both intension to treat (ITT) and per protocol (PP) patients. The time at which the frame was removed was determined by the maturation of the regenerate bone. Secondary outcomes were return to weight bearing and covariates affecting time to frame removal. The baseline characteristics of the two groups were well balanced, and 90% of patients were managed and followed up as PP. There was no difference in the time to frame removal between the two groups for the ITT (5.0days/cm, p=0.23) or the PP (10.1days/cm, p=0.054). There was no difference in return to weight bearing between the two groups, after adjusting for distraction length, for the ITT or PP patients (p>0.5). Smoking was the only covariate identified to increase the frame removal time (hazard ratio 0.46, 95% confidence interval 0.22 to 0.96; p=0.04). This trial demonstrated no difference in bone healing between those who underwent pulsed ultrasound and those who did not. Smoking was observed to have a significant inhibitory effect on bone healing.
To assess efficacy of pulsed ultrasound for accelerating regenerate consolidation. A multicentre two arm patient and assessor double blind RCTObjective:
Design:
With an ageing population comes an increased prevalence of osteoporosis and associated fracture. Whilst treatment of the condition following such a fracture is partially effective, primary prevention through screening and appropriate follow-up is the ideal. In order to assess a population's risk of fracture, paper questionnaires would traditionally have to be sent, however this is an wasteful and costly. A more efficient method may be to have patients assess their own FRAX score through a modified computer application. To investigate the feasibility of patients self-reporting their FRAX score from the use of a touch screen application.Introduction
Aim
To analyse the pain distribution in the acute and chronic phase following thoracolumbar fractures. Prospective observational study 39 patients with fractures between T11 and L2, with no neurological deficit, were treated conservatively. Strict inclusion and exclusion criteria were applied. All had X-rays and MR imaging (whole spine) at post-injury and one-year follow-up. The patients documented their pain distribution using pain drawing, along with 10 other domains of pain and functional outcomes for a period over 12 months. The pain distribution was analysed. The association of distal pain distribution to - other associated injury, resultant kyphosis, Pre-existing or increase in disc degeneration at the lower non-injured disc levels – were analysed and reviewed The most common site of the pain distribution in both the acute (90%) and chronic phase (97%) was distal to the fracture (regions - iliac crest, lumbosacral junction and buttock). Factors mentioned above that could be related to distal pain distribution did not show any significant correlation (P>0.5) with different domains of pain outcome. Some of the commonly believed reasons for distal pain distribution like resultant kyphosis and associated disc/facet pathologies were not supported by our study findings. The distal pain distribution corresponds to the scelerotomal referred pain mapping, which could be the probable explanation. Thoracolumbar pathologies could be the source of pain in patients complaining of low back symptoms. Distal pain distribution of spine pathologies should not be attributed as functional.
Stable thoracolumbar fracture is a common injury. The factors that determine its outcome are unclear. Aspects of injury severity were analysed for their ability to predict outcome by controlling other outcome-affecting factors (patient's pre-injury health status, legal aspects, associated injuries, etc.). No reliable disc injury severity grading system was available and therefore a new system was developed. A prospective observational study of 44 conservatively treated patients with stable fractures between T11 and L5 was conducted. Bony injury severity was scored based on comminution, apposition and kyphosis parameters. Disc injury severity was scored by the new scale based on variables – Herniation, Indentation, Height decrease and Signal change – seen in MRI. Ten outcome domains (five domains of pain and function each) were assessed at 1 to 2 years from injury. The data was analysed by non-parametric correlation and stepwise-linear regression analysis to assess the predictive value of different variables (patient factors, injury factors and social factor) to outcome. The correlation coefficients between injury severity and outcome were consistently higher with disc injury severity than bony. Disc injury severity showed highest predictive value for both pain (29%) and functional (16%) outcomes, whereas the bony injury severity parameters (kyphosis, etc.) and the posterior ligament injury severity provided no prediction of outcome. According to AO classification, the fractures were A1, A2, A3 and B1; in this spectrum of injuries, the AO classification had no prediction of outcome. The disc injury score also had a good predictive value for final disc degeneration. Disc injury severity should be gauged in advising prognosis and treatment. The new disc injury severity grading system showed good construct validity.
Ten percent of fractures end in delayed or non-union. NSAIDs have been linked to an inhibitory action on fracture repair for three decades yet the mechanism of action remains to be elucidated. Cancer research has identified that NSAIDs impede cell proliferation by inhibiting angiogenesis. It is proposed that a similar mechanism occurs in the induction of NSAID induced non-union. We have investigated this hypothesis in a randomised placebo control trial of the NSAID rofecoxib using a murine femoral fracture. All animals had an open femoral fracture treated using an external fixator. Outcomes measures included x-ray, histology and biomechanical testing, with laser Doppler used to assess blood flow across the fracture gap. Radiology showed similar healing patterns in both groups; however, at the later stages (day 32) the NSAID group had significantly poorer healing. Histological analysis showed that controls healed quicker (days 24 and 32), with more callus (day 8) and less fibrous tissue (Day 32). Biomechanical testing showed controls were stronger at day 32. Both groups exhibited a similar pattern of blood flow; however NSAIDs exhibited a lower median flow from day 4 onwards (significant at days 4, 16 and 24). Positive correlations were demonstrated between both histological and radiographic assessments of healing, with increasing blood flow. NSAID animals exhibited lower flows and poorer healing by all outcomes. Regression analysis demonstrates, however, that the negative effect of NSAIDs on fracture repair is independent of its inhibitory action on blood flow. COX-2 inhibitors are marketed as having cleaner side effect profiles and are widely used in trauma patients. Following development of a novel method of analysing functional vascularity across a fracture gap, we have demonstrated that the COX-2 inhibitor rofecoxib has a significant negative effect on blood flow at the fracture gap alongside inhibiting fracture repair.
no treatment (control); administration of alendronate (ALN) from 14 days after osteotomy; ALN from the time of osteotomy. Fracture repair was assessed weekly with the use of standardised radiography, DEXA scan and in vitro peripheral quantative computed tomography (pQCT). The rats were sacrificed 42 days post-osteotomy and the femora underwent mechanical testing.
A stastical analysis of intra and inter-observer variability was tested using the linearly-weighted kappa statistic for each of the 240 pixel density graphs taken and for the summation total in the 48 radiographs.
On analysis of the summation scores we expected an agreement of 75.54% and observed an actual agreement of 96.30%. This showed a kappa statistic of 0.8545 and a standard error of 0.0849.
Thrombin related peptide (TP 508) is a 23 amino-acid synthetic peptide that mimics a portion of the receptor-binding domain of the human thrombin molecule. Thrombin triggers both proteolytic activated receptors and non proteolytic activated receptors to bring about a mixture of responses ranging from tissue breakdown and clot formation, to new vessel formation and tissue repair. TP 508 stimulates only the non proteolytic activated receptors, and this initiates repair and angiogenesis but not clot formation or tissue breakdown Previous studies have shown that TP508 can stimulate repair in the dermal and musculoskeletal tissues by promoting angiogenesis and enhancing the proliferation and migration of cells. High energy fractures are associated with a delay in healing. We hypothesized that high energy fracture healing would be improved with the use of TP508, and that the dose and site of application would have importance.
24 animals were sacrificed on day 21 and the remaining 56 mice on day 35. Of the 35 day old animals 8 in each group had both femora harvested and the biomechanical properties were tested using the 3-point bending technique. Specimens from the 21 day old animals and remaining 35 day old animals were used for histological analysis. All 80 animals had digital radiographs taken each week. Using image analysis software five pixel density graphs were generated across each fracture gap. A validated semi quantitative analysis was used to score each graph and the total accumulated for each radiograph. The width of the fracture calus was measured and expressed as a ratio of the femur diameter.
Radiographic analysis showed greater healing of fracture and callus formation in Group I compared to Groups II, III, and IV, at both three and five weeks post-fracture (P<
0.05). Histological analysis showed an increase in bone formation in group I compared to the other groups.
We investigated the effect of neck dimension upon cervical range of movement. Data relating to 100 subjects healthy subjects aged between 20 and 40yrs was recorded with respect to age, gender and ranges of movement in three planes. Additionally two commonly used methods of measuring neck motion, chin-sternal distance and uniplanar goniometer, were assessed against a validated measurement tool the CROM goniometer (Performance Attainment Associates, Roseville, MN). Using multiple linear regression analysis it was determined that sagittal flexion (P= 0.0021) and lateral rotation (P<
0.0001) were most closely related to neck circumference alone whereas lateral flexion (P<
0.0001) was most closely related to a ratio of circumference and length. The uniplanar goniometer has some usefulness when assessing neck motion, comparing favourably to chin-sternal distance that has almost no role. Neck dimension should be incorporated into cervical functional assessment. One should be wary about recorded values for neck motion from non-validated measurement tools.
The first aim of the study was to investigate if bacteria were implicated in non-union of fractures of the tibia and femur, which had been treated with intramedullary nailing. The second aim was to evaluate the antimicrobial susceptibility of bacteria isolated from the retrieved intramedullary nails. Forty intramedullary nails removed from tibial and femoral fractures were retrieved for the purpose of the study. Twenty of these nails were from fractures, which had successfully united and 20 were removed from fractures which had failed to unite prior to further operative intervention. There was no evidence of clinical infection in either of the two groups. The nails were subjected to ultrasound in the research laboratory to dislodge adherent bacteria formed as biofilm from the surface of the nail. Using both standard culture techniques and non-culture techniques (Immunofluorescence microscopy and PCR analysis) any dislodged bacteria were isolated and identified. Isolated bacteria were tested for antimicrobial susceptibility to commonly used antibiotics in orthopaedic practice according to NCCLS guidelines. Bacteria were detected in 15 out of 20 [75%] of the nails removed from fractures, which had developed a non-union, and in 5 out of 20 [25%] of fractures that had united, using both standard culture techniques and non-culture techniques. The bacterial isolates identified were mainly Staphylococcus epidermidis and the Gram-positive anaerobe Proprionibacterium acnes. Vancomycin was the most effective antibiotic, with 2 out of 34 [6%] isolates being resistant. Erythromycin was the least effective, with 21 out of 34 [62%] isolates being resistant. Based on overall Minimum Bactericidal Concentrations at which 90% of all strains were killed, Vancomycin was the most active bactericidal agent tested followed in decreasing order by fucidic acid, ciprofloxacin, gentamicin, cefamandole and erythromycin. Bacteria were detected more commonly in the fracture non-union group than in the union group [p<
0.01]. Of the antibiotic agents tested Vancomycin was the most effective and Erythromycin was the least effective.
NSAIDs inhibit fracture repair, yet the mechanism behind this effect is unknown. It is recognised that NSAIDs impede tumour growth via an inhibition of angiogenesis, primarily via a COX-2 pathway. We propose that the inhibition of fracture repair is via a similar mechanism and have investigated this hypothesis using a murine fracture model. 225 animals were randomised into either treatment (rofecoxib) or control groups and underwent a standard open femoral fracture treated using an external fixator. Outcomes measures involved assessment of healing using radiographic, histolological and biomechanical means; and measurement of blood flow across the fracture gap using Laser Doppler Flowmetry. X-ray analysis showed a similar healing pattern in both groups, however at days 16 and 32 the NSAID group had significantly poorer healing. Histological analysis showed that controls healed quicker (significant at days 24 and 32); and had more bone but less cartilage at day 8. Biomechanical testing showed controls were statistically stronger and stiffer at day 32, while NSAID animals had a significantly greater rate of fixation failure, leading to loss of pin-bone osseointegration; this occurred primarily before day 16. There was no difference in blood flow between the groups on the day of surgery, and both groups exhibited a similar flow pattern; NSAID animals however, exhibited a lower median flow from day 4 onwards, which was significantly poorer at days 4, 16 and 24. Positive correlations were demonstrated between a higher blood flow and both the histological and radiographic results. While NSAIDs were seen to inhibit fracture repair in all outcome measures; and were also noted to decrease blood flow at the fracture, with strong negative correlations being noted between NSAID prescription and fracture repair; multiple regression analysis suggest that this negative effect of NSAIDs on healing is independent of its inhibitory action on blood flow. COX-2 inhibitors are marketed as having cleaner side effect profiles and prescribing is on the rise. Recently however some of the newer COX-2 specific inhibitors have been removed from the market as their seemingly clean side effect profile has come under scrutiny. We have demonstrated that the COX-2 specific inhibitor rofecoxib does has a significant negative effect on fracture repair; and as hypothesised that it also has a significant negative effect on blood flow at the fracture site. While these outcomes strongly correlate, the mechanism behind the effect remains to be elucidated, as we have also demonstrated that these modalities are independent of each other.
Several studies document what we all know – that, in the vast majority of patients treated in fracture units for low-trauma fractures, there is no attempt to identify and treat factors predisposing to further fractures. We treat Equally, it is completely unrealistic to expect orthopaedic surgeons, focused on surgically treating a tide of challenging osteoporotic fractures, to assess the risk in each patient of further falls and the degree to which bone strength is compromised, and be responsible for prescribing treatments which will reduce risk in a cost-effective way. Yet the fracture unit is absolutely the best (and most cost-effective) place to identify the group of patients who will benefit most from preventive measures. The answer is to work in a system, which connects up the right people to give each patient what they need. Surgeons to heal the current fracture (together with rehabilitationists to restore function and confidence) and physicians to assess and treat falls risk and osteoporosis. Making this happen in practice requires answers to questions only you can answer:
who are the best physicians for our fracture unit to work with? what is the best mechanism for selecting the appropriate patients to refer? how do we persuade the commissioners to pay for it? This is an issue in which it is worth us investing a lot of effort: we will ourselves soon be old and we must get this right in time for when we need it!
We hypothesised that in response to fracture, some integral osteoblasts are recruited via the circulation from remote bone marrow sites.
All animals had bone marrow harvested from their right tibia by saline flush. The mononuclear cells were isolated and culture-expanded in osteogenic medium for 3 weeks. Fluorescent reporter molecules were incorporated into the cell membranes, 24 hours prior to re-implantation of the cells into the fracture model. A 3 mm ulnar defect was preformed in all the animals. In groups I–III this was established 48 hours prior to cell re-implantation. The animals were sacrificed at least 3 weeks after fracture surgery. Representative samples of the fracture callous, lung, liver, spleen and kidney were harvested from all animals and cryo-sectioned. Using confocal microscopy, the labelled cells were expressed as the average in 5 high power fields for each solid tissue. In addition, cyto-spins were made from blood and marrow and the cell number expressed as a percentage of the total cells.
In all sections, these labelled cells appeared on trabecular surfaces in an osteoblastic fashion, but occasionally they were surrounded by osteoid, corresponding to osteocytes. A small number of labelled cells were found in the blood, bone marrow, lung, liver and spleen of all animals in groups I–III. No labelled cells were identified in the kidney tissue.
That fracture callus with overlying muscle crush would contain raised expression of acute inflammatory cytokines (IL-1β, IL-6 and TNF-α). That application of locally applied blocking antibodies to these inflammatory cytokines might negate excessive cytokine release and modulate fracture healing in this model.
Injection of anti-TNF-α antibodies into MC mice caused more new bone formation on day 16 (p=0.03) and day 24 (p=0.06), stiffer calluses at day 24 (p=0.01) and faster fracture gap obliteration at day 16 (p=0.05) and day 24 (p=0.001). IL-1β blockade had slightly less effect, more new bone formationd ay 16 (p=0.01) and day 24 (p=0.03), slightly stiffer (p=0.08), but no significant difference in fracture gap obliteration from controls.
The burden of non vertebral fractures on the National Health Service is enormous. Osteoporotic fractures have an associated morbidity and mortality and as a consequent incur heavy financial burden with a current cost to the National Health Service of some £1.7 billion per year, hip fractures accounting for the greater part. We know from our own local experience in the North of Ireland that this previous service had failed to target these fracture patients for secondary prevention of osteoporosis (Northern Ireland Colles Fracture Study). Although hip fractures account for only 7% of all fractures they result in the utilisation of 25% of acute orthopaedic beds. The silent nature of osteoporosis makes a diagnosis prior to fracture difficult and attendance at a fracture clinic may be the first opportunity to diagnose this condition and to intervene with anti-resportive treatment. An osteoporosis service commenced in Greenpark Health Care Trust in 1996. In 2001, guidelines (Crest guidelines) for the prevention and treatment of osteoporosis were established and in April 2003 a pilot study for the fracture liaison service commenced with the appointment of a Fracture Liaison Nursing Sister. The responsibility of this Nurse included:
Liaison and attendance at Out-Patient Fracture Clinic to ensure that all patients presenting with a low trauma fragility fracture were assessed and referred appropriately for bone densitometry. An education and awareness role for patients regarding osteoporosis and fall prevention. To conduct additional nurse led osteoporosis clinic at Green Park Healthcare Trust for patients referred from the Out-Patient Fracture Service at the Royal Victoria Hospital. Current activity levels include 18 fracture clinics per week at the Royal Victoria Hospital site with approximately 35 patients per clinic. To date, the Fracture Liaison Nurse has been able to attend 54% of these clinics. The patients were identified by Fracture Clinic chart reviews to identify those greater than fifty years of age with a low trauma fracture and approximately 115 charts were reviewed weekly. At risk patients were interviewed with approximately 35 interviews carried out weekly. Patients were then recruited first for assessment and dexa scanning, measurements were made at both lumbar spine L1-L4 and at the femoral neck with approximately 22 patients weekly recruited. An assessment of osteoporosis risk was made, a plain bed dexa scanner (lunar prodigy scanner) and treatment options were decided depending on the patients T score and according to the CREST Guidelines. The patients were given bone health advice at their scanning visit. Clinic activity was recorded on a database (Gismo) and a computer generated letter to the GP was produced. Provisional outcomes included arrangements to rescan after 24 months, referral to falls assessment and referral to a Consultant Specialist Osteoporosis Clinic.
- Normal (0 to −1 SD) 16.6% - Osteopenic (−1 to −2.5 SD) 46.7% - Osteoporotic (>
−2.5 SD) 36.7% The mean age for those scanned was 66 years and 3 months. Osteoporotic risk factors identified include a previous fracture (18%). Early menopause (19%), fall history (12%), Back pain and height loss (18%), smokers (11%), family history of osteoporosis (13%), alcohol excess (5%). Outcome – no treatment recommended 26%, 13% were already on treatment, 17% were prescribed treatment, 43% were prescribed Calcium and Vitamin D, 27% a Bisphosphonate, 20% a Bisphosphonate and Calcium and Vitamin D and 12% Evista (serm). Patient follow-up outcome included a follow-up of dexa scan at 24 months 20%, no hospital review planned 74%, 7% referred to a Specialist Osteoporosis Clinic and 6% were referred for a FALLS assessment.
Analysis revealed no significant difference in complication rates between the calendar years. However, there was a significant difference between complication rates in frames applied for acute trauma, late presentation of trauma, and elective surgery. This difference did not appear to relate to time spent in the frame, and therefore seems to represent a separate variable. There was a disproportionate increase in complications in Ilizarov frames applied for upper limb problems.
During the process of distraction osteogenesis new bone is formed rapidly and undergoes remodelling almost immediately. Little is known about the regulatory mechanisms governing the removal of the redundant callus in this process. Tissue homeostasis is achieved by a delicate balance between the processes of cell death (apoptosis) and cell proliferation. The aim of this study was to test the hypothesis that apoptosis is involved during distraction osteogenesis. Mid-tibial osteotomies were performed in 6 adult male NZW rabbits (age; 24 weeks, weight; 3.0 −3.5 kg), and the tibiae stabilised with unilateral external fixators (Orthofix M-100). 7 days later, twice daily distraction was initiated at rates of 0.7 mm/day for 3 weeks. BrdUrd (40mg/kg) was injected intravenously to the rabbit 1h before killing. The regenerate bone was collected, fixed in 10% buffered formalin and decalcified for paraffin embedding. Some fresh regenerate bone tissues were also prepared for examination under transmission electronic microscopy (TEM). BrdUrd immunohistochemistry has been used to detect proliferating cells and the terminal deoxynucleotidyl transferase (TDT)-mediated dUTP-biotin nick end-labelling (TUNEL) method was used to identify cells undergoing apoptosis. To detect bone-resorbing cells, tartrate-resistant acid phosphatase (TRAP) staining was also performed. BrdUrd positive cells and TUNEL-positive cells were shown to coexist in most of the areas in the regenerates. In the mineralisation front, the majority of the TUNEL-positive cells were present in the transitional region between the fibrous tissue and the new bone. The TUNEL-positive cells were close to or on bone surfaces, and some of the newly formed osteocytes in the new trabeculae were also positive. The TUNEL-positive cells were also seen in the cartilage region of the regenerate. However, the TUNEL labelling was greatly reduced in the new bone close to the osteotomised bone ends, TUNEL-positive labelling were not detected in the cortical bone of the osteotomised bone ends and in the adjacent surrounding periosteum. TRAP staining in the regenerate revealed similar patterns of distribution to those of the TUNEL staining. There were more TRAP-positive cells in the new bone near the mineralisation front than in that of the new bone region, which was close to the osteotomised bone ends. TEM examinations have demonstrated characteristic signs of apoptotic changes in the fibroblast, osteoblast and osteocytes in the specific regions of the distraction regenerate. The study provided evidence that in the process of rapid bone formation during distraction osteogenesis, superfluous cells are removed by apoptotic mechanisms. The demonstration of a mixture of proliferative and apoptotic cell populations in the regenerating tissue, indicates that apoptosis and cell proliferation may be regulated by local factors. The neovascularisation of the regenerate and withdrawal of growth factors and cytokines may be responsible for apoptosis occurring in some parts of the regenerating tissue. The changes of distribution of apoptotic cells in the different regions of the regenerate, together with the observed patterns of osteoclast activities, suggest that bone cells undergoing apoptosis may initiate rapid bone remodelling seen during distraction osteogenesis.
Fracture repair is a complex physiological process during which bone shows the remarkable ability to mount a repair process, restoring its mechanical integrity and anatomical configuration by original osseous tissue. Programmed cell death, or apoptosis, is a naturally occurring cell suicide pathway with a homeostatic function in the maintenance of continuously renewing tissues. The present study investigated the relation between cell proliferation and cell death (apoptosis) during fracture healing in a mouse femoral model. Left femoral osteotomies were performed in 20 male CFLP mice (35–45g), immobilised with uniplanar external fixators. 4 animals were sacrificed on days 2, 4, 8, 16 and 24 post-fracture and fracture callus collected for paraffin embedding. Localisation of cell proliferation was examined using immunohistochemistry with proliferating cell nuclear antigen (PCNA) monoclonal antibody. Apoptotic cells were visualised with the terminal deoxynucleotidyl transferase (TdT)–mediated dUTP-biotin nick end-labelling (TUNEL) method. Random images of each time specific specimen were captured via a digital camera and the positive labelling indices of PCNA and TUNEL labelling were calculated and statically compared. Cell proliferation and apoptosis were found co-existing during the entire period of fracture healing studied. Cell proliferation was predominant in the early phases of fracture healing (days 2–8). PCNA positive labelling index peaked at day 8 (p<
0.01, t-test) and PCNA-positive cells were not limited to the fracture gap mesenchymal tissues but extended in the periosteum along most of the fractured femur. TUNEL positive labelling was minimal in the early stages (days 2–8). In later stages of fracture healing (days 16–24), PCNA expression declined as intramembranous and endochondral ossification spread within the fracture site and apoptosis was the dominant cell activity with the TUNEL positive labelling index peaked at day 16 (p<
0.05, t-test) and then declined sharply at day 24. The current study indicated that apoptosis was a normal concomitant during fracture repair, confirming programmed cell death in chondrocytes and bone cells, and that cell proliferation and apoptosis were tempero-spatially dependent. These findings support the view that apoptosis is a natural process, genetically programmed and active during fracture repair. The demonstration of a mixture of proliferative and apoptotic cell populations in the regenerating tissues of fracture callus, suggests that apoptosis and cell proliferation may be regulated by local factors during fracture healing.
The age of the patient had little impact on the Kerr-Atkins score but a large effect on PCS. Conversely the pre-op Bohlers angle, a measure of fracture severity, had a large effect on the Kerr-Atkins score but little impact on the PCS. The AOFAS was responsive to both these predictors: 41% of the variance in AOFAS score was explained by Bohlers angle and the age of the patient. We did not find any significant difference in outcome between operative and non-operatively treated patients.
This study does not demonstrate any significant advantage of operative treatment in Sanders type 2 fractures of the Os Calcis.
The overall 1-year mortality was 31.4% (235/748) and the sex distribution (male 73/153 [47.7%] female 162/595 [27.2%]). 27/748 patients who did not undergo surgical intervention had a 1-year mortality of 85.2%. Factors which were associated with an increased 1 year mortality were: male sex (p<
0.0005), High ASA score (p<
0.0005), low Barthel score (p<
0.0005), poor mental score (p<
0.0005), decreased mobility (p<
0.0005), increased dependency in home circumstances (p<
0.0005), increased age (p<
0.0005), increased delay to surgery (p<
0.0005) and living alone (p<
0.0005). Marital status, fracture type and type of operative intervention had no statistical effect on mortality. Using logistic regression male sex, high ASA score, increased age, increased delay to surgery and poor mental score all remained independently associated with an increased mortality at 1 year.
On day 24, day 0 treated specimens demonstrated significantly more mesenchymal tissue. No correlation was demonstrated between post-operative motion and callus area or new bone area. The care of cartilage present however, was significantly correlated to the amount of post-operative movement in all groups.