The August 2015 Children’s orthopaedics Roundup. 360 . looks at: Learning the Pavlik; MRI and patellar instability; Cerebral palsy and hip dysplasia; ‘Pick your poison’: elastic nailing under the spotlight; Club feet and surgery; Donor site morbidity in vascularised fibular grafting; Cartilage biochemistry with hip dysplasia; SUFE and hip decompression: a good option?

Aims. Several studies have reported the safety and efficacy of subcapital re-alignment for patients with slipped capital femoral epiphysis (SCFE) using surgical dislocation of the hip and an extended retinacular flap. Instability of the hip and dislocation as a consequence of this surgery has only recently gained attention. We discuss this problem with some illustrative cases. Materials and Methods. We explored the literature on the possible pathophysiological causes and surgical steps associated with the risk of post-operative instability and articular damage. In addition, we describe supplementary steps that could be used to avoid these problems. Results. The causes of instability may be divided into three main groups: the first includes causes directly related to SCFE (acetabular labral damage, severe abrasion of the acetabular cartilage, flattening of the acetabular roof and a bell-shaped deformity of the epiphysis); the second, causes not related to the SCFE (acetabular orientation and poor quality of the soft tissues); the third, causes directly related to the surgery (capsulotomy, division of the ligamentum teres, shortening of the femoral neck, pelvi-trochanteric impingement, previous proximal femoral osteotomy and post-operative positioning of the leg). Conclusion. We present examples drawn from our clinical practice, as well as possible ways of reducing the risks of these complications, and of correcting them if they happen. Cite this article: Bone Joint J 2017;99-B:16–21

In developmental dysplasia of the hip, a deficient acetabulum may be augmented by placing local autogenous iliac osseous graft, or the ilium itself, over the head of the femur with the expectation that the added bone will function as a bearing surface. We analysed this bone obtained en bloc during subsequent surgery which was performed for degenerative osteoarthritis in three patients at 6, 25 and 30 years after the initial augmentation procedure. In each patient, the augmentation comprised of red cancellous bone covered on its articulating surface by a distinct layer of white tissue. Microscopy of this tissue showed parallel rows of spindle-shaped cells lying between linearly arranged collagen bundles typical of joint capsule. Biochemical analysis showed type I collagen, the principal collagen of joint capsule and bone, with no significant quantity of type II collagen, the principal collagen of cartilage. While the added bone produced by acetabular augmentation was durable, histological and biochemical analyses suggested that it had not undergone cartilage metaplasia. The augmented acetabulum articulates with the head of the femur by means of an interposed hip joint capsule

Aims

Anterior cruciate ligament (ACL) rupture commonly leads to post-traumatic osteoarthritis, regardless of surgical reconstruction. This study uses standing MRI to investigate changes in contact area, contact centroid location, and tibiofemoral alignment between ACL-injured knees and healthy controls, to examine the effect of ACL reconstruction on these parameters.

Aims

The aim of this study was to inform the epidemiology and treatment of slipped capital femoral epiphysis (SCFE).

1. The hyaluronate of synovial fluid is an acidic linear polymer which can effectively resist the diffusion of other macromolecules into its domain. Gelatin was used as an experimental model for hyaluronate, to investigate its effect upon the diffusion of protein-polysaccharides from cartilage slices. 2. The concentration of protein-polysaccilaride in the extracting medium was quantitated by uronic acid estimation and liquid scintillation spectrometry of . 35. sulphate-labelled proteinpolysaccharide. 3. Concentrations of gelatin in excess of 20 per cent (W/v) significantly retarded diffusion of protein-polysaccharides out of cartilage slices, but evidently not the movement of these molecules within cartilage. 4. It is suggested that disaggregation of both the protein-polysaecharide molecules of cartilage and the hyaluronate of synovial fluid contribute to cartilage breakdown

Aims

There is conflicting evidence on the safety of intra-articular injections of hyaluronic acid (HA) or corticosteroids (CSs) before total knee arthroplasty (TKA). We performed a meta-analysis of the relationship between intra-articular injections and subsequent infection rates after TKA.

Objectives. Recent studies have shown that systemic injection of rapamycin can prevent the development of osteoarthritis (OA)-like changes in human chondrocytes and reduce the severity of experimental OA. However, the systemic injection of rapamycin leads to many side effects. The purpose of this study was to determine the effects of intra-articular injection of Torin 1, which as a specific inhibitor of mTOR which can cause induction of autophagy, is similar to rapamycin, on articular cartilage degeneration in a rabbit osteoarthritis model and to investigate the mechanism of Torin 1’s effects on experimental OA. Methods. Collagenase (type II) was injected twice into both knees of three-month-old rabbits to induce OA, combined with two intra–articular injections of Torin 1 (400 nM). Degeneration of articular cartilage was evaluated by histology using the Mankin scoring system at eight weeks after injection. Chondrocyte degeneration and autophagosomes were observed by transmission electron microscopy. Matrix metallopeptidase-13 (MMP-13) and vascular endothelial growth factor (VEGF) expression were analysed by quantitative RT-PCR (qPCR).Beclin-1 and light chain 3 (LC3) expression were examined by Western blotting. Results. Intra-articular injection of Torin 1 significantly reduced degeneration of the articular cartilage after induction of OA. Autophagosomes andBeclin-1 and LC3 expression were increased in the chondrocytes from Torin 1-treated rabbits. Torin 1 treatment also reduced MMP-13 and VEGF expression at eight weeks after collagenase injection. Conclusion. Our results demonstrate that intra-articular injection of Torin 1 reduces degeneration of articular cartilage in collagenase-induced OA, at least partially by autophagy activation, suggesting a novel therapeutic approach for preventing cartilage degeneration and treating OA. Cite this article: N-T. Cheng, A. Guo, Y-P. Cui. Intra-articular injection of Torin 1 reduces degeneration of articular cartilage in a rabbit osteoarthritis model. Bone Joint Res 2016;5:218–224. DOI: 10.1302/2046-3758.56.BJR-2015-0001

Aims

The aim of this study was to compare any differences in the primary outcome (biphasic flexion knee moment during gait) of robotic arm-assisted bi-unicompartmental knee arthroplasty (bi-UKA) with conventional mechanically aligned total knee arthroplasty (TKA) at one year post-surgery.

To study the anatomy of subarticular bone and cartilage, fresh specimens of cartilage on bone from the human shoulder, hip and knee were treated with bleach or papain, or were fixed and decalcified. All were compared using scanning electron microscopy. Papain digestion selectively removed cartilage to the tidemark. The tidemark contour was highly variable; irregularities were indirectly related to degenerative lesions and were most prominent in peripheral non-weight-bearing areas of joints with central fibrillation. Decalcification exposed the interface between the bone and calcified cartilage. Collagen fibrils in articular cartilage did not interdigitate with those of bone. The subchondral bone was appositional, avascular, smooth and very thin in most areas of human joints. Perforations through subchondral bone or calcified cartilage were rare. Bleach maceration destroyed important details

1. The changes resulting from superficial scarification of articular cartilage have been observed in the knee joint of adult rabbits. A reduction in the amount of stainable matrix ground substance occurred at the sites of damage. Particular attention was therefore paid to sulphated mucopolysaccharide synthesis by cartilage cells in or near the traumatised areas. 2. The femoral groove cartilage one week after scarification showed evidence of increased mucopolysaccharide synthesis, especially by the more superficial chondrocytes near the cuts, but three or four weeks later the enhanced chondrocyte activity tended to diminish, and after six weeks the superficial cells near the cuts were found to be inactive. From six to thirty-four weeks the loss of stainable ground substance extended more deeply, but cell degeneration in these deeper areas of matrix depletion was preceded by a period in which many of the deeper chondrocytes still showed evidence of active mucopolysaccharide synthesis. Cellular activity in tags of depleted cartilage was usually lost before the tags finally disintegrated. Chondrocyte clusters were often seen in the scarified areas, especially in the deeper zones. They seemed to be a reactive rather than degenerative phenomenon. 3. In the scarified cartilages of the patella examined after one week a reactive response by superficial chondrocytes was less evident than in the femoral cartilage from the same joint, and after six weeks areas of deeply extending matrix loss were exceptional. 4. The structural and functional changes in the rabbits' femoral articular cartilage after its scarification resembled those which have been observed in the developing cartilage lesion of human osteoarthritis–namely, loss of interstitial matrix and superficial fibrillation, a stimulated synthesis of chondroitin sulphate by the chondrocytes, and the appearance of cell clusters in the deeper zones. Within the period of the experiment, up to thirty-four weeks, the joint lesions remained strictly localised to the traumatised areas ofcartilage, and exposure of bone and joint remodelling, which are features of advanced osteoarthritis in man, were not seen

Autologous chondrocyte implantation (ACI) is used widely as a treatment for symptomatic chondral and osteochondral defects of the knee. Variations of the original periosteum-cover technique include the use of porcine-derived type I/type III collagen as a cover (ACI-C) and matrix-induced autologous chondrocyte implantation (MACI) using a collagen bilayer seeded with chondrocytes. We have performed a prospective, randomised comparison of ACI-C and MACI for the treatment of symptomatic chondral defects of the knee in 91 patients, of whom 44 received ACI-C and 47 MACI grafts. Both treatments resulted in improvement of the clinical score after one year. The mean modified Cincinnati knee score increased by 17.6 in the ACI-C group and 19.6 in the MACI group (p = 0.32). Arthroscopic assessments performed after one year showed a good to excellent International Cartilage Repair Society score in 79.2% of ACI-C and 66.6% of MACI grafts. Hyaline-like cartilage or hyaline-like cartilage with fibrocartilage was found in the biopsies of 43.9% of the ACI-C and 36.4% of the MACI grafts after one year. The rate of hypertrophy of the graft was 9% (4 of 44) in the ACI-C group and 6% (3 of 47) in the MACI group. The frequency of re-operation was 9% in each group. We conclude that the clinical, arthroscopic and histological outcomes are comparable for both ACI-C and MACI. While MACI is technically attractive, further long-term studies are required before the technique is widely adopted

Composites of chondrocytes and polymerised fibrin were supplemented with insulin-like growth factor-I (IGF-I) during the arthroscopic repair of full-thickness cartilage defects in a model of extensive loss of cartilage in horses. Repairs facilitated with IGF-I and chondrocyte-fibrin composites, or control defects treated with chondrocyte-fibrin composites alone, were compared before death by the clinical appearance and repeated analysis of synovial fluid, and at termination eight months after surgery by tissue morphology, collagen typing, and biochemical assays. The structure of cartilage was evaluated histologically by Toluidine Blue reaction and collagen type-I and type-II in situ hybridisation and immunohistochemistry. Repair tissue was biochemically evaluated by DNA assay, proteoglycan quantitation and characterisation, assessment of collagen by reverse-phase high-performance liquid chromatography, and collagen typing using cyanogen bromide digestion and peptide separation by polyacrylamide gel electrophoresis. The results at eight months showed that the addition of IGF-I to chondrocyte grafts enhanced chondrogenesis in cartilage defects, including incorporation into surrounding cartilage. Gross filling of defects was improved, and the tissue contained a higher proportion of cells producing type-II collagen. Measurements of collagen type II showed improved levels in IGF-I-treated defects, supporting in situ hybridisation and immunohistochemical assessments of the defects. IGF-I improves the repair capabilities of chondrocyte-fibrin grafts in large full-thickness repair models

1. Homografts of eighteen-day-old foetal femora in pure strains of mice showed no fundamental difference in behaviour from grafts of more mature bone and cartilage. 2. Growth of bone was limited to a short period after transplantation and was abolished by previous immunisation. Cartilage growth alone was responsible for the increase in size of these transplants and did not appear to be influenced by the presence of immunity. 3. There is no reason to suppose that bone from an immature source is likely to behave more favourably than more mature bone homografts in clinical use. 4. The limited growth of cartilage and the total failure of bone survival in the heterografts indicate an immune reaction ofa different order from that which develops against the homograft. 5. The different effect of the homograft immune reaction on cartilage and bone enabled certain conclusions to be drawn concerning the part played by these two tissues in determining the form of a bone. Cartilage growth and development is shown to be regulated in large part by intrinsic factors. Bone growth and form on the other hand is shown to be dependent largely upon extrinsic influences

Aims

Pelvic incidence (PI) is considered an important anatomical parameter for determining the sagittal balance of the spine. The contribution of an abnormal PI to hip osteoarthritis (OA) remains controversial. In this study, we aimed to investigate the relationship between PI and hip OA, and the difference in PI between hip OA without anatomical abnormalities (primary OA) and hip OA with developmental dysplasia of the hip (DDH-OA).

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The aim of this study was to explore the genetic correlation and causal relationship between blood plasma proteins and rheumatoid arthritis (RA).

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Slipped upper femoral epiphysis (SUFE) has well documented biochemical and mechanical risk factors. Femoral and acetabular morphologies seem to be equally important. Acetabular retroversion has a low prevalence in asymptomatic adults. Hips with dysplasia, osteoarthritis, and Perthes’ disease, however, have higher rates, ranging from 18% to 48%. The aim of our study was to assess the prevalence of acetabular retroversion in patients presenting with SUFE using both validated radiological signs and tomographical measurements.

The anatomy and microstructure of the menisci allow the effective distribution of load across the knee. Meniscectomy alters the biomechanical environment and is a potent risk factor for osteoarthritis. Despite a trend towards meniscus-preserving surgery, many tears are irreparable, and many repairs fail. . Meniscal allograft transplantation has principally been carried out for pain in patients who have had a meniscectomy. Numerous case series have reported a significant improvement in patient-reported outcomes after surgery, but randomised controlled trials have not been undertaken. It is scientifically plausible that meniscal allograft transplantation is protective of cartilage, but this has not been established clinically to date. Cite this article: Bone Joint J 2015; 97-B:590–4