Cannulated hip screws are frequently used in the management of hip fractures. There have been concerns over the failure rate of the technique and the outcomes of those that subsequently require conversion to total hip replacement (THR).

This study utilised a database of over 600 cannulated hip screw (CHS) fixations performed over a 14-year period and followed up for a minimum of one year (1-14). We identified 57 cases where a conversion to THR took place (40 females, 17 males, mean age: 71.2 years). Patient demographics, original mechanism of injury, fracture classification, reason for fixation failure, time until arthroplasty, implant type and post-arthroplasty complications were recorded. Clinical outcomes were measured using the Oxford Hip Score.

The failure rate of cannulated screw treatment was 9.4% and the mean time from initial fixation to arthroplasty was 15.4 (16.5) months. Thirty six fractures were initially undisplaced and 21 were displaced. As one might expect the displaced cases tended to be younger but this didn't reach statistical significance [66.5(14.3) vs 72.7(13.1), p=0.1]. The commonest causes of failure were non-union (25 cases, 44%) and avascular necrosis (17 cases, 30%). Complications after THR consisted of one leg length discrepancy and one peri-prosthetic fracture. The mean Oxford score pre-arthroplasty was 12.2 (8.4), improving to 38.4 (11.1) at one-year. Although the pre op Oxford scores tended to be lower in patients with undisplaced fractures and higher ASA scores, the improvement was the same whatever the pre-op situation. The one-year Oxford score and the improvement in score are comparable to those seen in the literature for THR in general.

In conclusion, CHS has a high success rate and where salvage arthroplasty is required it can provide good clinical outcomes with low complication rates.

Background: Osteoarthritis (OA) is a progressive degenerative condition that causes pain and impairs the mobility of more than 10% of the UK population. Over 50,000 total knee replacements (TKR) are carried out each year for patients with the most severe symptoms. The aim of this study was to assess if markers of protein damage in the synovial fluid and plasma of patients with OA increase with severity of symptoms. These markers may then be of use in assessing disease presence and progression to assist with subsequent management. Proteins damaged by glycation (modified by sugars) and oxidation undergo cellular proteolysis. The proteolytic debris thereby formed - called glycation and oxidation free adducts (glycated and oxidised amino acids) - is released into the synovium and plasma for urinary excretion. In this study the concentrations of the glycation free adducts, Nε-carboxymethyl-lysine (CML) and methylglyoxal-derived hydroimidazolone (MG-H1), and the oxidation free adduct methionine sulfoxide (MetSO) were measured in the synovial fluid and plasma of patients with severe OA (sOA) and early-stage OA (eOA).

Methods: Patients were recruited from those attending the Rheumatology clinics at Ipswich Hospital, Ipswich and the Orthopaedic clinics at University Hospital, Coventry. Volunteer subjects were recruited to the normal healthy control group. The age (years; mean ± SD) for patient and control subject groups was: controls 45 ± 6 (n = 8), sOA 70 ± 12 (n = 8), eOA 50 ± 14 (n = 6). Patients found to have eOA changes (Outerbridge grade I/II) during routine arthroscopy were recruited to the eOA group. Synovial fluid and venous blood samples were taken with informed consent. All synovial fluid samples were taken from the knee joint. The concentrations of glycation and oxidation free adducts were assayed by stable isotopic dilution analysis liquid chromatography with tandem mass spectrometric detection (LC-MS/MS) in ultrafiltrate of synovial fluid and plasma. Significance of difference between study groups was assessed by ANOVA and Student’s t-test.

Results: The concentrations (nM; mean ± SD) of MetSO, CML and MG-H1 in synovial fluid were all markedly increased in OA patients with more severe disease. MetSO free adduct: eOA 459 ± 107 and sOA 2889 ± 1064 (p< 0.001). CML free adduct: eOA 77 ± 24 and 224 ± 51 (p< 0.001). MG-H1 free adduct: eOA 387 ± 182 and sOA 674 ±199 (p< 0.05). Analysis of plasma of these patients also showed increases in the concentrations of corresponding glycation and oxidation free adducts compared to those of normal healthy controls.

Discussion: The concentration of glycation and oxidation free adducts increased with severity of symptoms in the synovial fluid of patients with OA. This probably occurs by down regulation of protective gene expression in OA. Measurement of plasma protein glycation and oxidation free adducts may be useful in assessing progression and severity of OA. In the future, these markers may guide non-operative management and facilitate earlier joint-preserving surgery.

The aim of this study was to try to elucidate the increased susceptibility of the neck of femur to fracture. Quantitative polarised light microscopy has been applied to fresh, undecalcified sections of samples of bone taken from the site of fracture, in specimens taken at operation from patients with fractures of the femoral neck or osteoarthritic femoral heads or from the equivalent site from otherwise normal subjects at necropsy. In all 21 specimens of fractured necks of femur, but in none of the other specimens, relatively large crystals (up to 2.5 X 0.5 micrometres) were found close to the site of fracture; the properties of these crystals were compatible with their being apatite. Measurement of the natural birefringence of the collagen showed no difference in the orientation of the collagen in all three types of specimen. However, the orientation of acidic glycosaminoglycans, measured by the birefringence of alcian blue bound to these moieties, was 45 per cent lower in the specimens from fractured necks of femur than in the other specimens, even though the total content of acidic glycosaminoglycans was unchanged. Although the decreased orientation was most marked close to the site of fracture, it was still apparent 15 millimetres from that site. These changes were unlikely to be simply the sequelae of fracture since they were not found in traumatic fractures of other bones. Thus it is conceivable that changes in the orientation of the ground substance allow formation of relatively large crystals of apatite and that such crystals, in the microcrystalline mass of apatite, are the cause of the increased fragility of such bones.