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.

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.

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. 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: 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.

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.

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.

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.

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).

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.

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.