Tendinopathy can commonly occur around the foot and ankle resulting in isolated rupture, debilitating pain and degenerative foot deformity. The pathophysiology and key cells involved are not fully understood. This is partly because the dense collagen matrix that surrounds relatively few resident cells limits the ability of previous techniques to identify and target those cells of interest. In this study, we apply novel single cell RNA sequencing (CITE-Seq) techniques to healthy and tendinopathic foot/ankle tendons. For the first time we have identified multiple sub-populations of cells in human tendons. These findings challenge the view that there is a single principal tendon cell type and open new avenues for further study. Healthy tendon samples were obtained from patients undergoing tendon transfer procedures; including tibialis posterior and FHL. Diseased tendon samples were obtained during debridement of intractable Achilles and peroneal tendinopathy, and during fusion of degenerative joints. Single cell RNA sequencing with surface proteomic analysis identified 10 sub-populations of human tendon derived cells. These included groups expressing genes associated with fibro-adipogenic progenitors (FAPs) as well as ITGA7+VCAM1- recently described in mouse muscle but, as yet, not human tendon. In addition we have identified previously unrecognised sub-classes of collagen type 1 associated tendon cells. Each sub-class expresses a different set of extra-cellular matrix genes suggesting they each play a unique role in maintaining the structural integrity of normal tendon. Diseased tendon harboured a greater proportion of macrophages and cytotoxic lymphocytes than healthy tendon. This inflammatory response is potentially driven by resident tendon fibroblasts which show increased expression of pro-inflammatory cytokines. Finally, identification of a previously unknown sub-population of cells found predominantly in tendinopathic tissue offers new insight into the underlying pathophysiology. Further work aims to identify novel proteins targets for possible therapeutic pathways.

Background

Cam morphology develops during adolescence and predisposes individuals to future hip pain and osteoarthritis. An improved understanding of cam development is required to determine whether the process is modifiable.

Aims

The appropriate management for patients with a degenerative tear of the rotator cuff remains controversial, but operative treatment, particularly arthroscopic surgery, is increasingly being used. Our aim in this paper was to compare the effectiveness of arthroscopic with open repair of the rotator cuff.

Aims

A trial-based comparison of the use of resources, costs and quality of life outcomes of arthroscopic and open surgical management for rotator cuff tears in the United Kingdom NHS was performed using data from the United Kingdom Rotator Cuff Study (UKUFF) randomised controlled trial.

Objectives

High failure rates of metal-on-metal hip arthroplasty implants have highlighted the need for more careful introduction and monitoring of new implants and for the evaluation of the safety of medical devices. The National Joint Registry and other regulatory services are unable to detect failing implants at an early enough stage. We aimed to identify validated surrogate markers of long-term outcome in patients undergoing primary total hip arthroplasty (THA).

Introduction

Tendon healing begins with inflammation and results in an incomplete repair with fibrosis, culminating in tendon pathology along with tissue degeneration. Inflammatory mediators regulate the expression of growth factors, and members of the TGFβ superfamily including BMPs have been suggested to play a key role in the development of fibrosis. In established tendon diseases where inflammation and reparative processes persists, the cellular phenotype of tendon cells has been implied to undergo a transformation from that of normal tissue. This study investigates the inflammation-driven mechanisms of tendon pathology using an in vitro tendon cell model. We hypothesized that cells from diseased tendons will exhibit dysregulation of TGFβ superfamily members in response to inflammatory mediators when compared to cells derived from healthy tendons.

Summary Statement

Dickkopf-3 is upregulated in OA cartilage and synovial tissue. In vitro studies show Dkk3 can prevent cartilage degradation and antagonise Wnt signaling. We hypothesis that Dkk3 can protect against OA-related cartilage destruction.

Summary Statement

The effects of local glucocorticoid on tendon appear broadly negative and this supports the emerging clinical evidence which points toward significant long term harms associated with this treatment modality.

Summary Statement

The aim of this study was to compare patterns (aligned, random and grid) of electrospun polydioxanone scaffolds for tendon repair. The aligned design was optimal, directing cell shape, orientation and protein expression. Moreover, it naturally crimped, presenting tendon-like morphology.

Summary

The dGEMRIC index correlates more strongly with the pattern of radiographic joint space narrowing in hip osteoarthritis at five year follow-up than morphological measurements of the proximal femur. It therefore offers potential to refine predictive models of hip osteoarthritis progression.

Summary Statement

The peripheral neuronal phenotype is significantly altered in rotator cuff tendinopathy (RCT) with a clear upregulation of the Glutaminergic system being present in disease.

Summary Statement

This study describes the design and preliminary in vitro testing of a novel patch for the repair of rotator cuff tendon tears. The laminated design incorporates woven and electrospun components. The woven element provides the patch with excellent mechanical strength and the electrospun layer improves cell attachment and promotes cell orientation and diferentiation.

Summary Statement

A novel biomimetic polydioxanone tendon patch with woven and electrospun components is biocompatible, recapitulates native tendon architecture and creates a tissue-healing microenvironment directed by a subpopulation of regenerative macrophages. The woven component provides tensile strength while the tendon heals.

Introduction

Subtle deformities of the acetabulum and proximal femur are recognised as biomechanical risk factors for the development of hip osteoarthritis (OA) as well as a cause of hip and groin pain. We undertook this study to examine relationships between a number of morphological measurements of the acetabulum and proximal femur and the hip pain in a 20-year longitudinal study.

INTRODUCTION

There is increasing evidence for a multi-stage model of rotator cuff (RC) tendon tears, wherein healing is affected by tear size. The underlying pathophysiology however is not fully understood. Changes in the production and remodeling of the RC extracellular matrix (ECM) are likely to be important determinants of RC tendinopathy as they affect healing and the ability to bear loads. This study aimed to gain greater insight into size related tear pathogenesis by analyzing gene expression profiles from normal, small and massive RC tears.

INTRODUCTION

This study describes the prevalence of pain, functional loss and rotator cuff tears (RCTs) in a general population cohort. It is the first multidisciplinary assessment in such a cohort.

Introduction

The pathophysiology of high failure rates following rotator cuff tendon repairs, particularly massive tears, is not fully understood. Collagen structural changes have been shown to alter tendon thermal and mechanical properties. Thermal changes in small biopsies, detected by differential scanning calorimetry (DSC) can help to quantify collagen structural differences in torn rotator cuff tendons. This study aimed to form a quantitative rather than qualitative assessment, of whether differences in collagen structure and integrity existed between small biopsies of normal, small and massive rotator cuff tears using DSC.

INTRODUCTION

In order to address high failure rates following rotator cuff repairs, a greater understanding is required of the underlying structural changes so that treatments can be appropriately targeted and biomarkers of failure can be identified. As collagen is the primary constituent of tendon and determines force transmission, collagen structural changes may affect responses to loading. For example changes in collagen 1 and 5 are associated with the hyperelastic Ehlers-Danlos syndrome, which is diagnosed by looking for pathopneumonic altered collagen fibres or ‘collagen flowers’ in skin using transmission electron microscopy (TEM). To date no study has been performed on the microstructure of torn human rotator cuff tendons using TEM.

It was hypothesized that normal, small and massive human rotator cuff tendons tears will have altered microscopic structures. The unique study aimed to use TEM to compare the ultrastructure of small and massive rotator cuff tears, to normal rotator cuff tendons.

Purpose

The Oxford Knee Score (OKS) is a validated and widely used PROM that has been successfully used in assessing the outcome of knee arthroplasty (KA). It has been adopted as the nationally agreed outcome measure for this procedure and is now routinely collected. Increasingly, it is being used on an individual patient basis as a pre-operative measure of osteoarthritis and the need for joint replacement, despite not being validated for this use. The aim of this paper is to present evidence that challenges this new role for the OKS.

Objective

To investigate the effect of lab-based simulator training, on the ability of surgical trainees to perform diagnostic knee arthroscopy.

Background: Up to one third of adults have been estimated to have rotator cuff tendon (RCT) tears. Larger RCT tears are associated with poorer scores and function, and are more likely to re-rupture after surgical repairs, hence there is a need for earlier identification and treatment. The aim of this study was to identify biomarkers of RCT tear pathologies to aid accurate identification and monitoring of disease progression. FTIR provides unique biochemical fingerprints of tissue specimens. All molecules are excited to higher vibrational states at specific wavelengths, which can be used to identify the chemical composition of tissues.

Methods: The chemical composition of 55 formalin-fixed RCTs was measured from patients aged between 20 and 89. RCT tears were classified according to size (Post et al.); 10 each of small, medium, large and massive and 5 partial tears. These torn RCTs were compared to 10 uninjured RCTs. A diamond attenuated total reflectance accessory was used with a FTIR spectrometer to collect spectra for each sample. The spectra were reduced and classified using standard multivariate analysis; principal component analysis (PCA), partial least square (PLS) and discriminant function analysis (DFA). Data pre-processing was applied to ensure accurate quantitative data analysis.

Results: Hierarchical cluster (HCA) demonstrated that normal and torn tendons could be clearly differentiated, and RCT could also be distinguished by their tear size. Partial tears were clearly distinguishable from normal RCT. Using a genetic algorithm we identified the following spectral regions of importance which accounted for most of the features which discriminated between normal and torn tendons:

1030–1200cm-1: carbohydrates, phospholipids,

Partial tears were distinguishable from other stages of tendon pathology based on a spectral region which correlated with collagen III.

Conclusions: FTIR can clearly distinguish normal and different sized RCT tears. This prospective non-randomized study indicates that the onset of RCT tear pathology is mainly due to an alteration of the collagen structural arrangements, with associated changes in lipids and carbohydrates. Partial tears show early onset of chemical changes, particularly in collagen III, which could be used to identify earlier stages of disease. The approach described is rapid and has the potential to be used per-operatively to determine the quality of the tendon and extent of disease, thus guiding surgical repairs or allowing monitoring of disease progression or response to treatments.

The aim of this study was to find evidence of tissue hypoxia and apoptosis (programmed cell death) have on a human model of rotator cuff failure.

We studied twenty seven patients with no tear mild impingment (3), no tear moderate impingment (3), no tear severe impingment (3), partial tear (3), small tear (3), moderate tear (3), large tear (3), massive tear (3) and control (3) who were undergoing shoulder arthroscopy, subacromial decompression and potential rotator cuff repair. A supraspinatus tendon biopsy was taken during debridement/repair on all cases (ethics number C01.071). Control tendon was obtained from the subscapularis tendon of patients undergoing stabilization surgery.

Biopsies were analysed using two immunocytological techniques. A monoclonal antibody against BNIP-3 (a pro-apoptotic marker of hypoxia) and TUNEL (an apoptotic marker). An immunofluorescent nuclear counterstain DAPI (4 6-Diamidino-2-phenylindole dihy-drochloride) was used to stain all cells. Positive cells and total cell number were then counted in 10 high powered fields per section.

The results showed a significant increase in BNIP-3 expression in the cuff tears compared with intact tendons. This increase was least in the massive tears. Apoptosis increases from mild impingement to massive cuff tears (mean 7.3% to 21%)

Introduction: Femoroacetabular impingement (FAI) is an important cause of hip pain in young adults and a precursor to osteoarthritis. Morphological abnormality of either the acetabulum, proximal femur, or both, may result in FAI. The majority of patients however, have a cam deformity of the proximal femur. From a research perspective, FAI is an example of how subtle morphological abnormality results in a predictable pattern of cartilage damage, and thereby offers great potential as a model to study early degenerative disease and for clinical trials of joint preserving treatments. Accurate classification of the morphology of the hip is essential for this further study.

The aim of this study was to define normal, borderline, and abnormal parameters for the morphology of the proximal femur, in the context of the cam deformity, by studying asymptomatic individuals with normal clinical examination and no osteoarthritis from the general population.

Methods: 157 individuals (79 male, 78 female, mean age 46 years) with no previous history of hip problems were recruited. The participants were the spouses/partners of patients involved in a cohort study of osteoarthritis and FAI. All participants underwent clinical (interview, examination, and hip scores) and radiological assessment (standardised AP Pelvic and cross-table lateral radiographs of each hip). Radiographs were scored for the presence of osteoarthritis, and the morphology of the proximal femur was analysed. The alpha angle, anterior offset ratio, presence of a cam ‘bump’, synovial herniation pit were recorded in each hip.

Results: 21 subjects were excluded because they either had positive clinical features or radiological evidence of osteoarthritis (equivalent to a Kellgren and Lawrence grade of 2). From the remaining 136 subjects, with essentially ‘normal hips from the general population’, mean values for the alpha angle and anterior offset ratio were generated. Borderline and Abnormal values are suggested. Gender differences were noted with higher mean alpha angles and lower offset ratios occurring in men.

Discussion: Although it has limitations, standardised plain radiography remains the cheapest and most convenient way to screen an individual for the presence of a cam deformity. Despite the recent interest in FAI, our knowledge of what is normal in the general population, as assessed using appropriate radiographic techniques, is modest. The ranges provided by this study will facilitate the accurate classification of subjects with FAI, thereby providing guidance for surgeons treating such patients, and also enable the generation of refined cohorts for the study of the natural history of subtle morphological abnormalities of the hip, and for enrolment in clinical trials.

Introduction: Femoroacetabular impingement (FAI) is an important cause of hip pain in young adults and a precursor to osteoarthritis. Genetic factors are important in the aetiology of osteoarthritis of the hip. From a research perspective, FAI is an example of how subtle morphological abnormality results in a predictable pattern of cartilage damage, and thereby offers great potential as a model to study early degenerative disease.

Although many causes of FAI are described, the vast majority of patients give no history of previous hip disease. The purpose of this study was to investigate the extent to which FAI has an underlying genetic basis, by studying the siblings of patients undergoing surgery for FAI and comparing them with controls.

Methods: 66 patients (probands, 29 male, 37 female, mean age 39.1 years) treated surgically for FAI provided siblings for the study. These patients were classified as having cam, pincer or mixed FAI. 101 siblings (55 male, 56 female, mean age 38.2 years) were recruited. The control group consisted of the 77 partners of those siblings (40 male, 37 female, mean age 41.9 years). All subjects underwent clinical (interview, examination, and hip scores) and radiological assessment (standardised AP Pelvic and cross-table lateral radiographs of each hip). Radiographs were scored for the presence of osteoarthritis, and cam- and pincer-type abnormalities.

Results: Participants were classified as a) Normal morphology with no clinical features, b) Abnormal morphology but no clinical features c) Abnormal morphology with clinical signs but no symptoms, and d) Abnormal morphology with symptoms and signs. The sibling relative risks were significant for groups b, c, and d, supporting the hypothesis of an underlying genetic predisposition to FAI. Siblings usually demonstrated the same type of abnormal morphology as the proband. Gender specificity was apparent however, with pincer abnormalities which were usually apparent in female probands being common in sisters but less common in brothers. The brothers of probands with cam deformities almost universally demonstrated the same deformity, although only 50% of sisters did so.

Discussion: Genetic influences are important in the aetiology of FAI. Whether the morphological abnormality is determined at conception or by an inherited predisposition to an acquired event during maturity warrants further study. We have identified a spectrum of disease with a proportion of siblings with abnormal morphology currently asymptomatic. These cohorts present an opportunity to prospectively study the natural history of the condition, improve our understanding of the mechanisms and pathology in early degenerative disease, and potentially to be recruited into clinical trials of surgical and adjuvant treatments.

Introduction: Subtle deformity of the hip joint may cause osteoarthritis. In femoroacetabular impingement (FAI), cam deformities damage acetabular cartilage. Whether surgical removal of cam lesions halts progression is unknown. Sensitive, non-invasive assays of chondral damage are required to evaluate early treatment efficacy.

Delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) permits inference of glycosaminoglycan (GAG) distribution. We aimed to determine whether hips with cam deformities have altered GAG content, using dGEMRIC.

Methods: Subjects were recruited from a prospective cohort study. All were clinically and radiographically assessed. Hips with a normal joint space width (> 2.5mm) were eligible for dGEMRIC. 32 Hips (18 male, 14 female, mean age 51.7 years, none of whom had been investigated for hip pain) with (n=21) and without (n=11) cam deformities were scanned.

2 regions of interest (ROI) were studied:

acetabular cartilage from 12 to 3 O’Clock (T1-Index-acet).

The average of all pixels within the given ROI defined the T1-index.

For each hip, the ratio of the GAG content T1-Index-acet/T1-Indextotal was calculated. Mean T1-Indexto-tal and T1-Indexacet/T1-Indextotal were compared.

Results: T1-Indextotal were similar (689ms v 700ms, p=0.79) but T1-Indexacet/T1-Indextotal was lower in cam hips (0.93 v 1.01, p=0.017), indicating localised depletion of GAG content. Cam hips with positive clinical signs had lower T1-Indextotal than cam hips without (629ms v 717ms, p=0.055), and non-cam hips (629ms v 722ms, p=0.049).

Discussion: Cam hips have lower GAG content of their anterosuperior acetabular cartilage. dGEMRIC identified more generalised disease in cases with positive clinical findings. Ratios of GAG content for specific ROIs enable mapping of chondral damage. This may aid understanding of early disease mechanisms, track progression, and facilitate assessment of the efficacy of surgical procedures.

Introduction: Femoroacetabular impingement (FAI) causes pain in young adults and osteoarthritis. Genetic factors are important in the aetiology of osteoarthritis. We aimed to investigate the extent to which FAI has an underlying genetic basis, by studying the siblings of patients undergoing surgery for FAI and comparing them with controls.

Methods: 66 patients (probands, 29 male, 37 female, mean age 39.1 years) treated surgically for FAI provided siblings for the study. Probands were classified as having cam, pincer or mixed FAI. 101 siblings (55 male, 56 female, mean age 38.2 years) were recruited. The control group consisted of their 77 partners and was age and gender-matched. All subjects were assessed clinically and radiologically (standardised AP Pelvic and cross-table lateral radiographs of each hip). Radiographs were scored for the presence of osteoarthritis, and morphological abnormalities.

Participants were classified as:

Normal morphology, no clinical features

Results: The sibling relative risks were significant for groups b, c, and d (ranging between 2–5, p< 0.01). Pro-bands and siblings shared the same pattern of abnormal morphology. Gender specificity was apparent: pincer abnormalities common in sisters but not in brothers. The brothers of probands with cam deformities almost universally demonstrated the same deformity, but only 50% of sisters did.

Discussion: Genetic influences are important in the aetiology of FAI. Whether the morphological abnormality is determined at conception or by an inherited predisposition to an acquired event during development warrants further study. Symptoms are variable, indicating a spectrum of disease progression. These cohorts present an opportunity to prospectively study the natural history of the condition, improve understanding of the mechanisms and pathology, and potentially to be recruited into clinical trials.

The reproduction of ideal offset is an aim of hip replacement. Determining this measurement from traditional radiology techniques is inaccurate because femoral neck anteversion will foreshorten the femoral neck offset in a standard two dimensional x-ray making the measurement “apparent”. A novel method of determining offset is presented.

A computer software program has been developed for pre-operative planning of joint replacements, (Orthopaedic Work Station)

The program relies on using a CT scout film for magnification correction and to determine measurement parameters including leg length difference.

It was recognised that by collecting extra cross-sectional references that three-dimensional measurement of offset would be possible.

The CT scanner has software that allows determination of:

The location of the centre of the femoral head

For this study the line joining the two centroids is considered the longitudinal axis of the femur.

The CT scanner has software that also allows for the centroids to be moved along the longitudinal axis into the plane represented by a perpendicular line from the longitudinal axis to the centre of the femoral head.

It is a simple matter to measure the distance between the centroid and the centre of the femoral head to obtain a true offset.

A phantom femur was measured using the radiology method described and then measured directly. Exact correlation was established. A study of inter-observer measurement has shown statistically consistent agreement using six observers in twenty cadaver femurs.

The method is accurate and uses existing data collected as part of the pre-operative planning process. CT scanning prior to hip replacement, gives less radiation exposure and is more efficient with respect to radiology services than conventional radiology.

An intraoperative study may require ethics approval.

The aim of this study was to understand the role tissue hypoxia and apoptosis have on a human model of rotator cuff failure. We studied twenty seven patients with no tear mild impingment (3), no tear moderate impingment (3), no tear severe impingment (3), partial tear (3), small tear (3), moderate tear (3), large tear (3), massive tear (3) and control (3). A supraspinatus tendon biopsy was taken during debridement/repair in all cases (ethics no. C01.071). Control tendon was obtained from the subscapularis tendon of patients undergoing stabilization surgery. Biopsies were analysed using two immunocytological techniques. A monoclonal antibody against BNIP-III (a marker of hypoxia) and TUNEL (Terminal deoxynucleotidyl Transferase Biotin-dUTP Nick End Labeling – an apoptotic detection process). An immunoflorescent counterstain DAPI (4′,6-diamidino-2-phenylindol) was used to stain all cells. Positive cells and total cell number were then counted in 10 high powered fields. The results showed a significant increase in BNIP-III expression in the cuff tears compared with intact tendons. This increase was least in the massive tears. Apoptosis increases from mild impingment to massive cuff tears (mean 7.3% to 21%) In conclusion, as tear size increases, the viability of the tendon reduces with increasing hypoxia and apoptosis.

Aim: To investigate the capacity for retention of arthroscopic technical skills.

Methods: Six consultant lower limb surgeons were given standardized instruction on how to perform an arthroscopic Bankart suture on a lab-based ALEX shoulder model. Each surgeon then performed a suture repair three times and returned to repeat the process on four consecutive occasions, approximately two weeks apart. Six months later the same surgeons returned again to repeat the entire process. They received no further tuition or instruction. Their performance was objectively assessed throughout using validated motion analysis equipment to produce learning curves using time taken, number of movements and total path length.

Results: The initial learning curves and the learning curves at 6 months were the same.

Conclusions: Arthroscopic skills were not retained over a 6 month period. The same learning curves were identified suggesting the need for regular repetition of this simulated task if the level of learning is to be maintained. This has implications for technically difficult arthroscopic procedures suggesting a minimum level of frequency is needed to maintain optimum surgical performance.

A sibling risk study that shows a statistically significant increase in risk for anteromedial osteoarthritis of the knee.

Anteromedial osteoarthritis is a distinct phenotype of osteoarthritis. Previous studies have shown a genetic aetiology to both hip and knee osteoarthritis. The aim of this study was to determine the sibling risk of antero-medial osteoarthritis of the knee.

We conducted a retrospective cohort study of 132 probands with primary anteromedial osteoarthritis, who had undergone unicompartmental arthroplasty. Sibling were identified as having symptomatic knee problems by postal Oxford Knee Score (OKS). A positive OKS was defined as an OKS+/− 2SD of the mean of the proband group. Sibling spouses were used as controls. Those siblings & spouses that were symptomatic from the OKS were invited to undergo Knee X-rays, to look for radiological signs of osteoarthritis. Osteoarthritis was diagnosed as greater than Grade II on the Kell-gren Lawrence classification. The pattern of disease was noted and it was considered if the sibling were suitable for a unicompartmental knee arthroplasty. The prevalence and sibling risk of anteromedial osteoarthritis was determined using a randomly selected single sibling per proband family. The prevalence was determined in the 103 single proband sibling pairs.

There was a statistically significant risk within the sibling group P= 0.024 using the Chi square test. The relative risk of anteromedial osteoarthritis was. 3.21(95% CI 1.08 to 9.17)

Genetic factors play a major role in the development of anteromedial osteoarthritis.

The aim of this study was to determine cell viability in different stages of rotator cuff tendon tears using a cell viability molecular probe. Surgical biopsies taken from the edge of the Supraspinatus tendon tear from12 patients, 5 women and 7 men, mean age of 61 years were subjected to a cell viability assay using Molecular Probes Live/Dead cell viability assay. Specimens were then incubated with Calcein-AM and Ethidium Homodimer-1 and following snap freezing, sections were viewed under fluorescent microscopy. Cells which remained metabolically active fluoresced green, whereas dead cells were red. Populations of live and dead cells were counted for each specimen on ten high powered (x400 magnification) fields of view. The results show that the percentage of live cells is reduced in large chronic degenerate tears but greatest in acute traumatic tears. In addition, for those cases where tissue was assayed from the edge of the tear and 1 cm more proximally, there was a considerable increase in the percentage of viable cells in more proximal tissue. Use of this simple assay demonstrates high cell viability and consequently good quality tissue in traumatic tears, but lower quality tissue in larger more degenerate tears. This suggests that traumatic lesions have a high propensity to heal while larger more degenerate tears are less likely to heal but have better quality tissue more proximally.

Progressive arthritis can occur in association with massive tears of the rotator cuff. Altered joint kinematics are commonly proposed as the principle causative factor but this does not explain the absence of arthropathy in some patients. We have investigated the role of the ANKH gene in patients with cuff tear arthropathy. The transmembrane protein ANKH promotes intracellular to extracellular inorganic pyrophosphate channelling which regulates calcium pyrophosphate dihydrate and hydroxyapatite crystal deposition. Genomic DNA was prepared from peripheral blood leucocytes from 20 patients with cuff tear arthropathy diagnosed clinically and radiologically and 24 healthy matched controls. All 12 exons and exon-intron boundaries from the ANKH gene were PCR amplified and sequenced with BigDye version 3.1 terminator kit (ABI), and analysed using ABI PRISM ® 3100 Genetic Analyser. We have identified 5 single nucleotide polymorphisms (SNPs) including 4 that have previously been identified in patients with chondrocalcinosis. These are in exon 2 (GCC†’GCT 294), intron 2 (G†’A +8), exon 8 (GCA†’GCG 963) and intron 8 (T†’G +15). We also identified an A†’G variant in 3′-UTR, 30 base pairs after the stop codon which has not been reported before in crystal deposition diseases, and is also not seen in any of the healthy controls. Further elucidation is necessary to demonstrate a causal relationship between these ANKH mutations and cuff tear arthropathy, which will add to our understanding of pathogenic mechanisms in this condition.

The aim of this study was to observe cellular and vascular changes in different stages of full thickness rotator cuff tear.

Biopsies of the Supraspinatus tendon in 40 patients with chronic rotator cuff tears undergoing surgery were analysed using histological and contempary immunocytochemical techniques. Sections were stained with primary antibodies against PCNA (Proliferating cell nuclear antigen), CD34 (QBEnd 10), CD45 (Leucocyte Common Antigen), CD68, D2-40 (Lymphatic Endothelial Marker) and Mast Cell Tryptase. A histological analysis was performed with Mayer’s Haemotoxylin and Eosin, Congo Red and Toluidine Blue.

The reparative response and inflammatory component (figure 1) of the tissue was seen to diminish as the rotator cuff tear size increased. This was evidenced by increasing degeneration and oedema, reducing fibroblast proliferation, reduced thickening of the synovial membrane and reducing vascularity. Macrophage, other leucocyte and mast cell numbers also reduced as tear size increased. Large and massive tears revealed a higher degree of chondroid metaplasia and amyloid deposition when compared to smaller sized tears. There was no association with the patient’s age or duration of symptoms.

Small sized rotator cuff tears retain the greatest potential to heal and have a significant inflammatory component. Tissue from large and massive tears is of such a degenerate nature that it may never heal and this is probably a significant cause of re-rupture after surgical repair in this group. Selection of patients for reconstructive surgery should take into account the composition and healing potential of tendon tissue and its relationship to tear size in chronic tears of the rotator cuff.

Antero-medial osteoarthritis of the knee displays a well recognised pattern of cartilage damage on the medial tibial plateau. Anteriorly there is a full thickness cartilage defect, with transition to a partial thickness defect, becoming full thickness in the posterior third of the plateau. The retained posterior cartilage is macroscopically normal, but no previous study has assessed its histo-logical features. This study characterises the histological changes, to examine if antero-medial OA of the knee represents a model of progressive osteoarthritic cartilage damage.

Five unicompartmental resection specimens of patients with idiopathic single compartment antero-medial osteoarthritis were assessed. The samples were stained with H& E and Saffinin-O stains and reviewed using the Mankin system, an established method for scoring osteoarthritic changes in cartilage (range 0 [normal] to 14 [grossly osteoarthritic]) Digital images of the histology were reviewed by two observers to exclude inter and intra observer error. Each specimen was assessed at 4 interval points (A,B,C,D) along the A-P axis starting from the most posterior aspect of the exposed bone to the area of macroscopically normal cartilage. Three repeat measurements were taken from the macroscopically normal region (D1,D2,D3). The scores were compared to historical age matched controls of non-osteoarthritic cartilage, where a Mankin grade of < 3 suggests normal cartilage.

From anterior to posterior the H& E staining showed a consistent decrease in structural integrity and cellularity of the cartilage, matched by a qualitative decrease in GAG content (Saffinin-O staining). Mean Mankin scores showed a progressive decrease in score; A = 14.0 (95% CI 0), B = 5.8 (95%CI 2.4), C = 4.4 (95%CI 2.5), D = 1.0 (95%CI 0.9) {p=0.04 ANOVA}. Repeated measurements at the macroscopically normal area showed the Mankin grade was maintained; D1= 1.0 (95%CI 0.9), D2 = 0.6 (95%CI 0.5), D3 = 0.6 (95%CI 0.6).

The results show that the retained posterior cartilage in antero-medial arthritis has a consistently normal Mankin grade. We suggest the defect represents a model of progressive cartilage damage from near normal (posterior) to the grossly osteoarthritic state (anterior).

The aim of this study was to observe the macroscopic and microscopic appearance of the Coracoacromial ligament and Subacromial bursa during Subacromial decompression and correlate it with the outcome at 3 months. Twenty patients with Subacromial Impingement without Rotator Cuff tear and five patients with large/massive irreparable Rotator Cuff tears who underwent a Subacromial Decompression. Patients with other shoulder pathology were excluded. Patients completed an Oxford Shoulder Score pre-operatively and their injection history was noted. At operation the shape of the acromion was noted. The macroscopic appearance of the CA ligament and the Subacromial bursa was classified as normal, mild/moderate and severe. Biopsies of the Subacromial bursa and CA ligament were taken and were analysed using histological and contempory immunocytochemical techniques. A histological analysis was performed using Mayer’s Haemotoxylin and Eosin, Toluidine Blue and Congo Red. Sections were stained with primary antibodies against PCNA (Proliferating cell nuclear antigen), Mast Cell Tryptase, CD3 (T-cell), CD20 (B cell), CD 34 (QBEnd 10), CD45 (Leucocyte Common Antigen), CD68 and D2–40 (Lymphatic Endothelial Marker). Post operatively the patients completed an Oxford Shoulder Score at 3 months. All the patients demonstrated an improvement in their Oxford Shoulder Score. The histological analysis demonstrated thickening of the synovial membrane and increased vascularity within the bursa and ligament. Increased numbers of inflammatory cells were present within the ligament and bursa of patients with impingement compared with massive rotator cuff tears. There was a relationship between outcome and the appearance of the bursa and ligament.

The aim of this study was to use motion analysis to study a surgeon’s learning curve for an arthroscopic Bankart repair on a training model in a skills laboratory. Six fellowship trained lower limb surgeons unfamiliar with advanced shoulder arthroscopy performed an arthroscopic Bankart repair on an ALEX shoulder model. Standardised training was given and then an electromagnetic tracking system used to objectively assess hand movements, distance travelled by hands and time taken while the surgeons performed the technique. The arthroscopic repair was repeated three times on four consecutive occasions by each surgeon giving a total of 72 repair episodes. Analysis revealed improvement of all outcome parameters with less hand movements, less distance travelled and less time to complete the task. This study objectively demonstrates a learning curve for arthroscopic Bankart suture in a skills laboratory. It indicates the potential benefits of practicing aspects of arthroscopic techniques in a skills centre on appropriately selected models.

Cuff Tear Arthropathy is characterised by massive rotator cuff tears, glenohumeral joint destruction and joint effusions containing basic calcium phosphate and calcium pyrophosphate dihydrate crystals. We have investigated the role of the ANKH gene in patients with cuff tear arthropathy and the effect of mutations on protein function. The transmembrane protein ANKH transports inorganic pyrophosphate (PPi) from the intracellular to extracellular space. Control of the extracellular levels of PPi is crucial in preventing calcium crystal formation. Genomic DNA was prepared from peripheral blood leucocytes from 22 patients with cuff tear arthropathy diagnosed clinically and radiologically. All 12 exons and exon-intron boundaries from the ANKH gene were PCR amplified and sequenced with BigDye version 3.1 terminator kit (ABI), and analysed using ABI PRISM ® 3100 Genetic Analyser. ANKH complementary DNA (cDNA) was ligated with mammalian expression vector pcDNA3 and site directed mutagenesis was used to make the ANKH mutation detected in the cases. Human articular chondrocytes were transfected with the cDNA variants and PPi concentrations measured. A G-to-A single nucleotide polymorphism in the 3′ untranslated region (3′UTR) of ANKH was identified. The G/A genotype was seen more frequently in the cases (45%) when compared to controls (20%) (p= 0.0008). We observed altered levels of extracellular PPi in human chondrocytes transfected with ANKH cDNA with the 3′ UTR variant when compared with control cells and normal ANKH cDNA. Cuff Tear Arthropathy appears to be heritable via a G-to-A transition in the 3′UTR of ANKH that alters extracellular PPi concentrations in chondrocyte cells. This supports a hypothesis of a primary crystal mediated arthropathy in patients with Cuff Tear Arthropathy.

A prospective study was carried out to determine if recognised histological features seen at surgery could help predict those rotator cuff tendon repairs which re-ruptured. 40 rotator cuff tendon edge specimens from 40 patients’ shoulders were analysed histologically following routine mini-open rotator cuff repair. 32/40 underwent Ultrasonography, at a mean time of 35 months post-operatively, to determine repair integrity. The histological features seen at surgery were then compared to the repair integrity of the tendon from which it had been taken. Rotator cuff repairs that remained intact demonstrated a greater reparative response, in terms of increased fibrobast cellularity, cell proliferation and a thickened synovial membrane, than those repairs which reruptured. Larger tears which remained intact showed a higher degree of vasacularity and a significant inflammatory component than those that re-ruptured. Good tissue quality at the time of surgery allows the repair the best chance of remaining intact despite the size of the lesion. Routine histological analysis of the tissue biopsy, preformed in the post-operatively, can now aid the clinician in terms of early management and repair prognosis.

The aim of the study is to assess the use of patient-based questionnaires in the evaluation of shoulder surgery using a specifically designed database.

The patient based questionnaires used in this study were the Oxford Shoulder Score, used to assess shoulder pain and the Oxford Instability Score, used to assess shoulder instability.

Two hundred and ninety-five patients were recruited between October 2001 and October 2003. They were prospectively assessed prior to surgery and at regular intervals post operatively.

The results demonstrate a high degree of compliance with regard to completion of the questionnaires. Differences in outcome were noted between patients in different diagnostic groups. The specifically designed database allows presentation of outcome information either by individual patient (Figure1) or by procedure group.

Patient based questionnaires can be effectively used to audit shoulder practice. A customised database allows rapid and clear presentation of outcome results for both individual patients and groups of patients.

This is the largest reported natural history study of frozen shoulder. 500 patients were identified from a specialist shoulder clinic register with a diagnosis of frozen shoulder based on Codman’s criteria. 273 patients with primary frozen shoulder replied to a detailed postal questionnaire regarding their condition. Mean follow up from symptom onset was 52 months (range 12–240months), with 89% of shoulders followed up for a minimum of 3 years. A positive family history was identified in 20% (n=45) of 1st degree relatives. The relative risk to siblings compared with a control population was 4:1. Patients with mild to moderate symptoms recovered more quickly than those with severe or unbearable symptoms. The mean age of onset was 53 years (range27–85yrs). The female to male ratio was 1.6:1. The condition was bilateral in 20%, with no incidence of ipsilateral recurrence. 22% of patients reported a history of minor trauma to the upper limb prior to the onset of symptoms. 16% were diabetic and 4% reported a history of Dupuytren’s contracture. Right and left arms were affected equally with no relationship to hand dominance. 61% reported slow, and 39% reported sudden onset of symptoms. Generally pain and stiffness improved with time but at 3 and 4 years after onset 13% and 9% respectively still had symptoms.

Frozen shoulder affects people mainly in their 6th decade. Genetic factors play an important role in the aetiology. The natural history is for improvement with time, with the less severe symptoms at onset improving most quickly. 9% of patients were still symptomatic at 4 year follow up.

The purpose of this study was to investigate the role that genetics play in the aetiology and symptomatology of full thickness tears of the rotator cuff.

From a retrospective, cohort study of 205 patients diagnosed with full thickness rotator cuff tears, we determined, using ultrasound, the prevalence of full thickness tears in their 129 siblings. Using 150 spouses as controls, the relative risk of full thickness rotator cuff tear in siblings v controls was 2.42 (p< 0.0001, 95 % CI 1.77 to 3.31). The relative risk of symptomatic full thickness rotator cuff tear in siblings v controls was 4.65 (p< 0.0001, 95 % CI 2.42 to 8.63).

The significantly increased risk for tears in siblings implies that genetic factors play a major role in the development of full thickness tears of the rotator cuff.

Aim To determine if tissue metabolism varies in supraspinatus tendons with distance from the edge of the rotator cuff tendon tear and also with differing size of tear.

Background Tissue metabolism can be assessed by measuring oxygen and nitrous oxide concentrations within the tissue. Viable tendon tissue consumes oxygen and contains nitrous oxide (used in the general anaesthetic) from the blood stream. Non-viable tendon tissue will not consume oxygen but will contain nitrous oxide.

Methods Oxygen and Nitrous Oxide concentrations were measured amperometrically using silver needle microelectrodes.

The needle was inserted into the supraspinatus tendon of patients with massive, large, medium and small full thickness rotator cuff tears and patients with partial thickness and no tears. Patients undergoing open stabilisation were used as controls. Measurements were made at a number of quantifiable points from the tendon edge to allow the creation of a topographical map of tissue metabolism. Oxygen consumption was calculated using measured oxygen and nitrous oxide levels at each point.

Results In patients with rotator cuff tears oxygen consumption was significantly lower near to the edge of the tear.

Patients with impingement syndrome but no evidence of a rotator cuff tear also showed a decreased level of oxygen consumption in the anterior part of supraspinatus, but this was significantly higher than the levels seen in the torn tendon.

The control group showed no significant alteration in oxygen levels

Conclusion Patients with rotator cuff tendon tear demonstrate significantly reduced levels of tissue metabolism. This reduction in tissue viability is significantly greater at the edge of the tear and in larger tears. Patients with intact tendons and impingement syndrome also demonstrate minor reduction in tissue tendon viability compared with controls.

A systematic review of the English language literature has suggested that the performance of linked and unlinked elbow replacement implants differ in terms of function, survival and mode of failure; however, in this review, only one comparative series using contemporary implants was identified. We have performed a cohort study of Kudo, Souter-Strathclyde and Coonrad-Morrey elbow replacements performed at a single centre by or under the direct supervision of a single Consultant shoulder and elbow surgeon to see if these findings were reflected in clinical practice. The first forty implantations in patients with Rheumatoid arthritis for each device have been reviewed with respect to surgical complications, elbow function and implant survival. The follow-up was shorter for the Coonrad-Morrey cohort. In terms of pain relief and range of motion, the performance of the implants was comparable. The mode of failure was different, with no dislocations/ instability seen with the linked Coonrad-Morrey implants. The loosening rate of the Coonrad-Morrey implants (both clinical and radiographic) was lower, albeit with a shorter follow-up period. The loosening rates seen in this series were higher than those previously reported in the English language literature. We conclude that the functional performance of the implants, at similar stages of the surgical learning curves, are similar in patients with Rheumatoid arthritis, but that use of a linked implant removes the risk of post-operative instability and may reduce the risk of the radiographic and clinical loosening.

The purpose of this study was to investigate the association of endocrine disease with calcific tendinitis and the effects that such disease has on its natural history.

A retrospective observational cohort study of 102 consecutive patients (125 shoulders) with calcific tendinitis is presented. Seventy-three (71.6 %) female, 29 (28.4 %) male. Compared with population prevalences, significant levels of endocrine disorders were found in our study cohort. Sixty-six patients (81 shoulders, 62 female (93.9 %), 4 male (6.1 %), mean age 50.3 years) with associated endocrine disease were compared with 36 patients (44 shoulders, 11 female (30.6 %), 25 male (69.4 %), mean age 52.4 years) without endocrine disease. The endocrine cohort were significantly younger than the non-endocrine cohort when symptoms started (mean 40.9 years and 46.9 years respectively, p=0.0026), had significantly longer natural histories (mean 79.7 months compared with 47.1 months, p=0.0015) and a significantly higher proportion underwent operative treatment (46.9 % compared with 22.7 %, p=0.0014).

Disorders of thyroid and oestrogen metabolism may contribute to calcific tendinitis aetiology. Classifying calcific tendinitis into Type I idiopathic and Type II secondary or endocrine-related aids prognosis and management.

Between 1972 and 2002 74 patients were treated under the combined care of the orthopaedic oncology service and lymphoma clinic with primary bone lymphoma. We reviewed the seventeen cases affecting the upper limb (23%). Of the seventeen patients nine remain alive. Assessment of the patient’s clinical presentation, histopathological definition, treatment and function outcome was made. The nine survivors were assessed clinically and with the Oxford shoulder score and the Toronto extremity salvage score.

Average time from first presentation to diagnosis was 7 months. All seventeen were diagnosed as a B –cell non-Hodgkin’s lymphoma, fifteen cases were high grade and two cases were low grade. The scapula was involved in six, humerus eight and clavicle three cases. Seven patients sustained pathological fractures three of which were at presentation; of these two were treated surgically. Eight patients have subsequently died of their disease. Functional outcome in surviving patients after medical treatment was very good with average TESS score of 79% (52%–99%) and OSS of 27 (12–52).

The presentation of lymphoma of the shoulder girdle may mimic benign shoulder conditions and lead to a delay in radiological and histopathological diagnosis. Pathological fracture is a common presentation and complication of treatment, however these fractures have a high chance of healing with medical treatment alone. Although shoulder stiffness remains a problem following medical treatment, overall upper limb function is good. There is little evidence that these patients require surgery in the short to medium term.

From 1985 to 1998 we used the Souter implant for elbow replacement in the rheumatoid population. We have followed this cohort prospectively, and present simple outcome measures including initial pain relief, early complication rates, radiological changes with time, and survivorship.

We performed 71 Souter elbow replacements in 62 rheumatoid patients (51 female, 11 male). The average age at surgery was 61 (range 38–79). All patients had end stage arthropathy. Early results and complications were assessed in all patients. Subsequently, ten cases were revised for loosening, and eight patients (10 elbows) died before recent follow up, leaving 51 cases for long term study. Clinical and radiological data were obtained.

On early follow up, 94% had no or minimal pain. Thirty-one percent suffered a complication. Overall, 18% cases had ulnar nerve problems and 7% dislocated in the first year. Seven percent had wound problems, including two deep infections. At mean long term follow up of 6 years (range: 2–15 years) there were high rates of satisfaction in patients with retained prostheses. Progressive radiolucency around the humeral component was common and treated expectantly. Late instability was not seen. Pain relief was maintained.

There have been few long-term reports on the Souter elbow replacement. This group of patients from a single centre has been followed prospectively. Infection and ulnar nerve complications are comparable with other series, and are less related to prosthesis. The rate of humeral component loosening in this series is high. The rate of dislocation, however, is low. This prosthesis sacrifices stability to transmit forces through the soft tissues. Although stability is acceptable there is no beneficial reduction in loosening.

The purpose of this study was to evaluate the outcomes of treatment of rheumatoid elbows with Kudo Total Elbow Replacements.

Between 1993–1997 we performed 39 Kudo Total Elbow Replacements in 35 patients with Rheumatoid Arthritis, aged 39–81 years old (mean age: 60,7 yrs). Eleven patients (13 elbows) were male and 24 (26 elbows) were female. Twenty-eight (28) replacements were performed on the right side and eleven (11) on the left. All the patients were evaluated clinically (pre-op and post-op, using Mayo score system) and radiographically. In seven elbows another procedure (radial head excision (three), radial head excision & synovectomy (three), arthroscopy & interposition arthroplasty(one)) had been performed previously for the rheumatoid arthritis. Eight elbows seemed to have ulnar nerve problems pre-op. We followed-up 31 patients (35 elbows). Mean follow-up was 5years (range: 4–8 years).

The pre-operative pain had been reduced significantly in almost all patients. In the majority, the movement had also been improved post-operatively. Two elbows were unstable (one subluxated, one dislocated). Both presented early postoperatively. Only one patient developed a postoperative ulnar nerve problem and that resolved. One elbow had a delay in wound healing. Radiolucency appeared around both the humeral and ulnar components in five elbows, around humeral component in two and around ulnar component also in two. Five elbow replacements were revised. Four of them due to aseptic loosening and one due to instability problem (dislocation). No deep infection was noticed in any elbow.

In our hands, Kudo Elbow Replacements seemed to have aseptic loosening rates comparable to other series and low dislocation rates.

We carried out a prospective study of 93 patients undergoing surgery for conditions of the rotator cuff during 1994 and 1995. They were assessed before operation and after six months, and four years, using the patient-based Oxford Shoulder Score (OSS), the SF-36 questionnaire and the Constant shoulder score. The response rates were higher for the OSS and SF-36. The correlation coefficients were high (r > 0.5) between all scores at each stage of the study. While all scores improved substantially at six months, the Constant score was reduced significantly at four years. This did not correlate with the patients’ judgement of the change in symptoms or of the success of the operation. Our study suggests that patient-based measures of pain and function can reliably assess outcomes in the medium term after surgery to the shoulder.

We have developed a 12-item questionnaire for completion by patients presenting with shoulder instability. A prospective study of 92 patients was undertaken involving two assessments, approximately six months apart, performed in an outpatient department. Each patient completed the new questionnaire and the SF36 form. An orthopaedic surgeon completed the Constant shoulder score and the Rowe assessment.

The new questionnaire and the Rowe clinical score each achieved a large standardised effect size (≥0.8) and compared favourably with relevant items on the SF36. By contrast, the Constant score barely registered any effect, confirming that it may be relatively insensitive to changes in clinical status for this particular condition.

The questionnaire provides a measurement of outcome for shoulder instability which is short, practical, reliable, valid and sensitive to changes of clinical importance.

We have developed a 12-item questionnaire for patients having a total knee replacement (TKR). We made a prospective study of 117 patients before operation and at follow-up six months later, asking them to complete the new questionnaire and the form SF36. Some also filled in the Stanford Health Assessment Questionnaire (HAQ). An orthopaedic surgeon completed the American Knee Society (AKS) clinical score.

The single score derived from the new questionnaire had high internal consistency, and its reproducibility, examined by test-retest reliability, was found to be satisfactory. Its validity was established by obtaining significant correlations in the expected direction with the AKS scores and the relevant parts of the SF36 and HAQ. Sensitivity to change was assessed by analysing the differences between the preoperative scores and those at follow-up.

We also compared change in scores with the patients’ retrospective judgement of change in their condition. The effect size for the new questionnaire compared favourably with those for the relevant parts of the SF36. The change scores for the new knee questionnaire were significantly greater (p < 0.0001) for patients who reported the most improvement in their condition.

The new questionnaire provides a measure of outcome for TKR that is short, practical, reliable, valid and sensitive to clinically important changes over time.

We developed a 12-item questionnaire for completion by patients having shoulder operations other than stabilisation. A prospective study of 111 patients was undertaken before operation and at follow-up six months later. Each patient completed the new questionnaire and the SF36 form. Some filled in the Stanford Health Assessment Questionnaire (HAQ). An orthopaedic surgeon assessed the Constant shoulder score.

The single score derived from the questionnaire had a high internal consistency. Reproducibility, examined by test-retest reliability, was found to be satisfactory. The validity of the questionnaire was established by obtaining significant correlations in the expected direction with the Constant score and the relevant scales of the SF36 and the HAQ. Sensitivity to change was assessed by analysing the differences between the preoperative scores and those at follow-up. Changes in scores were compared with the patients’ responses to postoperative questions about their condition. The standardised effect size for the new questionnaire compared favourably with that for the SF36 and the HAQ. The new questionnaire was the most efficient in distinguishing patients who said that their shoulder was much better from all other patients.

The shoulder questionnaire provides a measure of outcome for shoulder operations which is short, practical, reliable, valid and sensitive to clinically important changes.

We developed a 12-item questionnaire for completion by patients having total hip replacement (THR). A prospective study of 220 patients was undertaken before operation and at follow-up six months later. Each completed the new questionnaire as well as the SF36, and some the Arthritis Impact Measurement Scales (AIMS). An orthopaedic surgeon assessed the Charnley hip score.

The single score derived from the questionnaire had a high internal consistency. Reproducibility was examined by test-retest reliability and was found to be satisfactory. The validity of the questionnaire was established by obtaining significant correlation in the expected direction with the Charnley scores and relevant scales of the SF36 and the AIMS. Sensitivity to change was assessed by analysing the differences between the preoperative scores and those at the follow-up. The standardised effect size for the new questionnaire compared favourably with that for the SF36 and the AIMS.

The new questionnaire provides a measure of outcome for THR which is short, practical, reliable, valid and sensitive to clinically important changes.

The clinical features, investigation, treatment and outcome of two adults with fibrogenesis imperfecta ossium are described. In this rare acquired disorder of bone, normal lamellar collagen is replaced by structurally unsound collagen-deficient tissue, which leads to extreme bone fragility and ununited fractures. Transmission microscopy and SEM showed striking ultrastructural changes in bone structure and mineralisation. Both patients had monoclonal IgG paraproteins in the plasma and one excreted monoclonal lambda light chains in the urine. No abnormal plasma cells were found in the bone marrow and there was no evidence of amyloid deposition in the tissues. In both patients initial treatment with 1 alpha-hydroxycholecalciferol appeared to be ineffective, but in one, repeated courses of melphalan and corticosteroids over three years together with 1 alpha-hydroxycholecalciferol produced striking clinical and histological improvement. The findings in these and other patients strongly suggest that paraproteinaemia is an integral feature of fibrogenesis imperfecta ossium, and this needs further investigation.

To assist surgeons to select a total hip replacement (THR) we present comparative information on all such implants on the market in the UK. We identified 62 different primary THRs, manufactured by 19 companies; half had been introduced in the last five years, and only 30% have any results published in peer-reviewed journals. The prices range from 250 pounds to 2000 pounds, and the two cheapest implants have the longest reported follow-up. The number of THR implants available in the UK, and presumably the rest of the world, is rapidly increasing, but there is little or no scientific evidence that the newer, more expensive, implants are better than established designs. Some will undoubtedly be worse. We believe that this situation is unsatisfactory and make recommendations for improvement, in particular that preference be given to implants with good results in published peer-reviewed long-term clinical trials.

Survival analysis is a powerful tool for analysing the results of total joint replacement, but it has major drawbacks when the failure rates are very low. We have reviewed 35 recent survival analyses of joint replacements to assess the magnitude of these problems and make recommendations as to how they may be avoided.

We describe 22 patients who presented between the ages of 4 and 14 years with gradual onset of malaise and pain at the sites of multiple bone lesions. The symptoms from the bone lesions were sometimes sequential in onset and often relapsing. The radiological findings were typical of osteomyelitis. Radioisotope bone scans identified some clinically silent lesions. Bone biopsies were performed in 20 patients and the changes of osteomyelitis were seen in 17; microbiological culture was positive in only one. Seven patients had polyarthritis, two had palmoplantar pustulosis and one had psoriasis. Some symptomatic relief was obtained with anti-inflammatory agents and, to a less extent, with antibiotics. No patient had primary immunodeficiency. The mean duration of symptoms from the bone lesions was two years (1 to 4). When arthritis was present the joint symptoms lasted considerably longer (mean 7 years; range 4 to 10). The long-term prognosis was generally good. There was no evidence of altered bone growth or abnormal joint development. One patient developed a progressive kyphosis requiring fusion, but no other surgical intervention was necessary.

We measured the range of rotation in both hips of 397 normal children and in the unaffected hip of 135 children with unilateral congenital dislocation of the hip. Both groups were assessed for generalised joint laxity. Joint laxity was more common in normal children with an internally centred arc of hip rotation than in normal children with a neutral or an externally rotated arc. The children with congenitally dislocated hips had significantly more joint laxity than did the control group and significantly more of them had an internally centred arc of hip rotation. We suggest that the lax joint capsule fails to mould away the neonatal anteversion of the femoral neck during the first few months of life.

The microvascular anatomy of the calcaneal tendon was investigated in cadaver tendons by injection of barium sulphate and indian ink and a quantitative study of intratendinous blood supply was made, using a computer-assisted image analysis system. There was a reduction in both the number and the mean relative area of vessels in the mid-section of the tendon. This area of reduced vascularity may be of significance in the pathogenesis of rupture.

The use of an osteocutaneous free fibular graft as a single-stage reconstructive procedure for composite tissue loss is increasingly common. Detailed anatomical study in cadavers of the blood supply to the graft demonstrates cutaneous arteries arising from the peroneal artery and then passing along the posterior surface of the lateral intermuscular septum. These vessels pierce the crural fascia and then ramify to supply the skin. Knowledge of the vascular anatomy of the skin overlying the fibula is essential to the success of the graft.