Measuring quality of life: Using quality of life measures in the clinical setting.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to A J Carr.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
There is increasing interest in the potential of composites of hydroxyapatite with phosphate- or silicate-based bioactive glasses, and certain of these glass additions have been found, in previous work, to aid densification and form a mechanically-reinforced, bioactive material; in particular, large improvements in flexural strength and fracture toughness were obtained through the addition of small amounts of phosphate glass. Less is known about the mechanical behavior of HA/bioglass composites, although in vivo studies by other workers have shown encouraging biological results. In this investigation, the sintering behavior, mechanical properties, and microstructure of composites of HA with up to 50 wt % glass, were analyzed. X-ray diffraction showed the phase composition of sintered composites with up to 5 wt % added bioglass to be non-stoichiometric HA with alpha-TCP or beta-TCP. Phase analysis of composites containing higher glass additions was impracticable due to peak broadening and overlap, although reaction products, at the highest glass additions and sintering temperatures, may include wollastonite-2M and beta-Na2Ca4(PO4)2SiO4. Sintered density, and mechanical properties other than fracture toughness, showed no significant improvement over HA.
Age-related localised deposition of amyloid in connective tissue has been found in degenerative articular and periarticular tissue. Biopsies of the supraspinatus tendon of 28 patients undergoing repair of the rotator cuff were analysed histologically for the presence of localised deposition of amyloid. There was a long history of impingement in 20 patients, and eight patients had suffered an acute traumatic tear with no preceding symptoms. Localised deposition of amyloid identified by Congo Red staining was detected in 16 samples (57%). Amyloid was present in 14 (70%) of the degenerative tears, but in only two (25%) of the acute tears. Immunohistochemical staining showed that the amyloid deposits were positive for P component, but negative for kappa and lambda light chains, prealbumin, and beta2 microglobulin. Critical electrolyte staining revealed highly-sulphated glycosaminoglycans at sites of deposition of amyloid. The presence of localised deposition of amyloid in tears of the rotator cuff is likely to represent irreversible structural changes. These findings support the theory that impingement and tears are due to intrinsic degenerative changes within the tendons of the rotator cuff.
This retrospective study confirms the benefit of arthroscopic removal of loose bodies from the elbow, and documents the accuracy of history and plain radiographs. In contrast to previous reports, patients with a diagnosis of osteoarthritis had a similar outcome to those with an alternative diagnosis.
OBJECTIVE: To examine 11 candidate genes as susceptibility loci for osteoarthritis (OA). METHODS: A total of 481 families have been ascertained in which at least two siblings have had joint replacement surgery of the hip, or knee, or hip and knee for idiopathic OA. Each candidate gene was targeted using one or more intragenic or closely linked microsatellite marker. The linkage data were analysed unstratified and following stratification by sex and by joint replaced (hip or knee). RESULTS: The analyses revealed suggestive linkage of the type IX collagen gene COL9A1 (6q12-q13) to a subset of 132 families that contained affected females who were concordant for hip OA (female-hip) with a P-value of 0.00053 and logarithm of the odds (LOD) score of 2.33 [corrected P-value of 0. 0016, corrected LOD score of 1.85]. CONCLUSIONS: COL9A1 may therefore be a susceptibility locus for female hip OA. In addition, there was weak evidence of linkage to HLA/COL11A2 (6p21.3) in female hip OA with a corrected P-value of 0.016.
BACKGROUND: In independent linkage studies chromosome 2q11-q24 and chromosome 2q23-35 have previously been implicated as regions potentially harbouring susceptibility loci for osteoarthritis (OA). OBJECTIVE: To test chromosome 2q for linkage to idiopathic osteoarthritis. METHODS: Using a cohort of 481 OA families that each contained at least one affected sibling pair with severe end-stage disease (ascertained by hip or knee joint replacement surgery), we conducted a linkage analysis of chromosome 2q using 16 polymorphic microsatellite markers at an average spacing of one marker every 8.5 cM. RESULTS: Our results provide suggestive evidence for a locus at 2q31 with a maximum multipoint logarithm of the odds score (MLS) of 1.22 which increased to 2.19 in those families concordant for hip-only disease (n = 311). This suggestive linkage was greater in male-hip families (MLS = 1.57, n = 71) than in female-hip families (MLS = 0.71, n = 132). CONCLUSIONS: Chromosome 2q is likely to contain at least one susceptibility locus for OA.
OBJECTIVES: To determine and compare the aetiological background, clinical patterns and radiological features of idiopathic osteoarthritis (OA) of the hip and the knee warranting arthroplasty. METHODS: A total of 402 Caucasians consecutively undergoing total hip replacement (THR) or total knee replacement (TKR) for idiopathic OA at a major centre was surveyed. RESULTS: Previous joint injury was more common in the TKR group (P < 0.0001). However, both groups manifested a mixed occupational background, body mass indices similar to the general population and a predominance of females (F:M = 1.3-1.4:1). The TKR group had a significantly younger age of symptom onset (56 yr) than the THR group (61 yr) but both groups had a tendency to bilateral arthroplasty (33%), nodal involvement (54-59%), a significant excess of right-sided replacements (1.8:1, THR; 2.2:1, TKR) and similar levels of pre-operative pain and disability. Up to 40% of hips manifested acetabular dysplasia and 10% possible previous slipped upper femoral epiphyses. Eighty-five per cent with end-stage coxarthrosis or gonarthrosis had an identical pattern of radiographic disease contralaterally. CONCLUSIONS: Our data suggest the importance of a constitutional tendency to idiopathic, end-stage OA, a disorder traditionally associated with environmental factors leading to 'wear and tear'.
One of the first stages in developing an accurate biomechanical representation of the elbow joint is to model realistically the geometry of the joint. In particular, given the complex anatomy of the articular surfaces, the relationship between surface topography and joint contact must be fully understood in order to model the contact conditions. As the joint articulates, the location and size of the contacts between the mating surfaces change, altering the distribution and magnitude of load transmission. In this paper, a geometric model of the anatomical elbow joint in the coronal plane is described. The contours of the articulating surfaces are represented algebraically by a series of connecting lines and circular arcs. It is shown that the location and size of the contact between the surfaces change significantly due to small changes in the topography of one or more of the mating surfaces. The surface topography-joint contact relationship is modelled for a number of different clinical conditions for the joint. The model is relevant to clinical studies of joint degeneration and to the design of prosthetic components for the elbow joint.
We present three cases of recurrent instability of the elbow in association with the Ehlers-Danlos syndrome. The pattern of instability has not previously been reported. We describe our procedure for achieving stability using a bone graft to the olecranon fossa which gave a functional range of movement.
We assessed the inter- and intraobserver variation in classification systems for fractures of the distal humerus. Three orthopaedic trauma consultants, three trauma registrars and three consultant musculoskeletal radiologists independently classified 33 sets of radiographs of such fractures on two occasions, each using three separate systems. For interobserver variation, the Riseborough and Radin system produced 'moderate' agreement (kappa = 0.513), but half of the fractures were not classifiable by this system. For the complete AO system, agreement was 'fair' (kappa = 0.343), but if only AO type and group or AO type alone was used, agreement improved to 'moderate' and 'substantial', respectively (kappa = 0.52 and 0.66). Agreement for the system of Jupiter and Mehne was 'fair' (kappa = 0.295). Similar levels of intraobserver variation were found. Systems of classification are useful in decision-making and evaluation of outcome only if there is agreement and consistency among observers. Our study casts doubt on these aspects of the systems currently available for fractures of the distal humerus.
OBJECTIVE: Evidence has accumulated supporting a role for genes in the etiology of osteoarthritis (OA). Several candidates have been targeted as potential susceptibility loci including genes that are involved in the regulation of bone density. Genetic association analysis has suggested a role for the vitamin D receptor gene (VDR) and the estrogen receptor gene (ER) in susceptibility. Such findings must be tested in additional independent cohorts. We tested for association of these 2 genes, plus a third gene implicated in bone density, COL1A1, with idiopathic OA. METHODS: A case-control cohort of 371 affected probands and 369 unaffected spouses was used. Association was tested using 4 intragenic single nucleotide polymorphisms (SNP), one each for the VDR and COL1A1 genes, and 2 for the ER gene. The VDR and ER SNP are the same SNP that have been associated with OA. All 4 SNP affect restriction enzyme sites and were genotyped using polymerase chain reaction and enzyme digestion. Allele and genotype distributions for each SNP were compared between cases and controls and analyzed using Fisher's exact test. RESULTS: There was no evidence of association of the VDR or the ER gene SNP to OA. There was weak evidence of association of the COL1A1 SNP in female cases (p = 0.017), reflected by a difference in the distribution of genotypes at this SNP between female cases and controls (p = 0.027). However, when corrected for multiple testing, these results were not significant. CONCLUSION: If the VDR, ER, or COL1A1 genes do encode predisposition to OA then the 4 SNP tested are not associated with major susceptibility alleles at these 3 loci.
OBJECTIVE: Measuring the impact of osteoarthritis has traditionally focused on the disease (measures of impairment), functional disability and latterly, general health status or quality of life. This paper highlights the importance of measuring the wider personal and social consequences of OA both at a population and an individual patient level. DESIGN: The World Health Organisation definition of handicap is used to describe this wider impact of disease and measures of handicap, both generic and disease-specific are reviewed. The measurement of handicap in OA is illustrated by the use of the Disease Repercussion Profile in a clinical trial of orthopaedic out-patients with OA and low back pain. These data are compared to routine clinical handicap data collected on consecutive patients with rheumatoid arthritis attending a different outpatient clinic. RESULTS: OA patients reported handicap in six areas of their lives: functional and social activities, relationships, socio-economic status, emotional well-being and body image. The prevalence was similar to that reported by RA patients. OA patients reported more severe handicap than RA patients in each of the 6 areas (F ratios 4. 97-55.67) and the differences were statistically significant (P values 0.03-0.0001) for all dimensions except functional and social handicap. The LBP patients scored slightly more severe handicap on all dimensions than the OA patients but these differences did not reach statistical significance. However, they scored significantly more severe handicap than the RA patients (F ratios 8.49-174.72, P< 0.0001). CONCLUSIONS: These data suggest that the psychosocial impact of OA may have been underestimated and highlight the importance of going beyond disability in assessing the impact of OA. Measurement of the wider impact of OA can be achieved using disease-specific and generic measures of handicap. The choice of tool will depend upon the setting (research or clinical practice) and the purpose of measurement.
We present a two-stage genomewide scan for osteoarthritis-susceptibility loci, using 481 families that each contain at least one affected sibling pair. The first stage, with 272 microsatellite markers and 297 families, involved a sparse map covering 23 chromosomes at intervals of approximately 15 cM. Sixteen markers that showed evidence of linkage at nominal P</=.05 were then taken through to the second stage, with an additional 184 families. This second stage confirmed evidence of linkage for markers on chromosome 11q. Additional markers from this region were then typed to create a denser map. We obtained a maximum single-point LOD score, at D11S901, of 2.40 (P=.0004) and a maximum multipoint-LOD score of 3.15, between markers D11S1358 and D11S35. A subset of 196 of the 481 families, comprising affected female sibling pairs, generated a corrected LOD score of 2.54 (P=.0003) for marker D11S901, with evidence for linkage extending 12 cM proximal to this marker. When we stratified for affected male sibling pairs there was no evidence of linkage to chromosome 11. Our data suggest that a female-specific susceptibility gene for idiopathic osteoarthritis is located on chromosome 11q.
Explore the source record for details and available documents.
OBJECTIVE: To determine the clinical efficacy of sclerosing injections in patients with chronic low back pain. METHODS: Randomized, double-blind, placebo-controlled trial of three, once weekly injections of dextrose-glycerine-phenol with lignocaine vs saline plus lignocaine in patients with mechanical back pain of more than 6 months' duration. All patient assessments were performed blind by an experienced physiotherapist. The injections to the ligaments of the L4-5 and L5-S1 lumbar motion segments were given by an orthopaedic physician experienced in the technique, blinded to the nature of the injection solution according to a standard protocol. Demographic and clinical data, the short-form McGill Pain Questionnaire, the modified Somatic Pain Questionnaire, the Zung Depression Inventory, Oswestry Disability Scale and the modified Schober method of measuring spinal flexion were undertaken at 0, 1, 3 and 6 months. RESULTS: Seventy-four patients [mean (S.D.) age 45(11) yr, female:male ratio 1:1, median pain duration >10 yr] were recruited and there were no drop-outs over the study period. There were no statistically significant differences in patient characteristics between the placebo and treatment groups at baseline or for any measure at follow-up. CONCLUSIONS: Three, weekly sclerosant injections alone may not be effective treatment in many patients with undifferentiated chronic back pain. Patient selection and combination with other treatment modalities may be factors in determining treatment success.
OBJECTIVE: To evaluate the effectiveness and cost effectiveness of specially trained physiotherapists in the assessment and management of defined referrals to hospital orthopaedic departments. DESIGN: Randomised controlled trial. SETTING: Orthopaedic outpatient departments in two hospitals. SUBJECTS: 481 patients with musculoskeletal problems referred for specialist orthopaedic opinion. INTERVENTIONS: Initial assessment and management undertaken by post-Fellowship junior orthopaedic surgeons, or by specially trained physiotherapists working in an extended role (orthopaedic physiotherapy specialists). MAIN OUTCOME MEASURES: Patient centred measures of pain, functional disability and perceived handicap. RESULTS: A total of 654 patients were eligible to join the trial, 481 (73.6%) gave their consent to be randomised. The two arms (doctor n = 244, physiotherapist n = 237) were similar at baseline. Baseline and follow up questionnaires were completed by 383 patients (79.6%). The mean time to follow up was 5.6 months after randomisation, with similar distributions of intervals to follow up in both arms. The only outcome for which there was a statistically or clinically important difference between arms was in a measure of patient satisfaction, which favoured the physiotherapist arm. A cost minimisation analysis showed no significant differences in direct costs to the patient or NHS primary care costs. Direct hospital costs were lower (p < 0.00001) in the physiotherapist arm (mean cost per patient = 256 Pounds, n = 232), as they were less likely to order radiographs and to refer patients for orthopaedic surgery than were the junior doctors (mean cost per patient in arm = 498 Pounds, n = 238). CONCLUSIONS: On the basis of the patient centred outcomes measured in this randomised trial, orthopaedic physiotherapy specialists are as effective as post-Fellowship junior staff and clinical assistant orthopaedic surgeons in the initial assessment and management of new referrals to outpatient orthopaedic departments, and generate lower initial direct hospital costs.
We have investigated the role of 23 candidate genes in the control of bone mineral density (BMD) by linkage studies in families of probands with osteoporosis (lumbar spine [LS] or femoral neck [FN] BMD T score < -2.5) and low BMD relative to an age- and gender-matched cohort (Z score < -2.0). One hundred and fifteen probands (35 male, 80 female) and 499 of their first- or second-degree relatives (223 males and 276 females) were recruited for the study. BMD was measured at the LS and FN using dual-energy X-ray absorptiometry and expressed as age- and gender-matched Z scores corrected for body mass index. The candidate genes studied were the androgen receptor, type I collagen A1 (COLIA1), COLIA2, COLIIA1, vitamin D receptor (VDR), colony-stimulating factor 1, calcium-sensing receptor, epidermal growth factor (EGF), estrogen receptor 1 (ESR1), fibrillin type 1, insulin-like growth factor 1, interleukin-1 alpha (IL-1alpha), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-11 (IL-11), osteopontin, parathyroid hormone (PTH), PTH-related peptide, PTH receptor type 1 (PTHR1), transforming growth factor-beta 1, and tumor necrosis factors alpha and beta. Sixty-four microsatellites lying close to or within these genes were investigated for linkage with BMD. Using the program MapMaker/Sibs there was suggestive evidence of linkage between BMD and PTHR1 (maximum LOD score obtained [MLS] 2.7-3.5). Moderate evidence of linkage was also observed with EGF (MLS 1.8), COLIA1 (MLS 1.7), COLIIA1/VDR (MLS 1.7), ESR1 (MLS 1.4), IL-1alpha (MLS 1.4), IL-4 (MLS 1.2), and IL-6 (MLS 1.2). Variance components analysis using the program ACT, correcting for proband-wise ascertainment, also showed evidence of linkage (p </= 0.05) at markers close to or within the candidate genes IL-1alpha, PTHR1, IL-6, and COLIIA1/VDR. Further studies will be required to confirm these findings, to refine the location of gene responsible for the observed linkage, and to screen the candidate genes targeted at these loci for mutations.