This retrospective matched cohort study tested the hypothesis that an incomplete periacetabular acetabuloplasty, as an added step to delayed open reduction, diminishes the risk of developing acetabular dysplasia.

29 hips from 23 patients with idiopathic DDH that underwent intentionally delayed open reduction and acetabuloplasty at our institution from 2003 to 2010 were matched for age at presentation and bilaterality to historic controls. These were 29 hips from 26 patients, treated with open reduction alone from 1989 to 2003. Residual dysplasia treated with pelvic osteotomy, AVN grade II-IV, and rate of re-intervention were the outcome measures.

The mean ages at diagnosis and at surgery were 8.62 weeks and 12.97 months, respectively. At latest follow-up, 27 hips in the acetabuloplasty group and 22 in the open reduction alone group had satisfactory radiographic outcome (Severin class Ia, Ib or II) (p=0.16). 18 of the 58 hips (31.0%) had AVN, 7 (24.14%) in the case group and 11(37.93%) in the control group. Further surgery was required in 15 of the 29 hips in the open reduction alone group. These included 2 revision of open reductions, 5 pelvic osteotomies, 3 varus derotation osteotomies, and 5 apo or epiphysiodesis whilst only one patient in the acetabuloplasty group required a medial screw epiphysiodesis for late lateral growth arrest. There is a positive association between the need for further surgery and open reductions alone: the odds ratio is 14.00 and the 95% confidence interval (1.97, 99.63), p=0.0017. The five hips in the open reduction alone group that required a pelvic osteotomy were intervened at an average of 31.45 (±9.07) months.

The addition of an incomplete periacetabular periacetabuloplasty to all hips undergoing open reduction eliminated residual acetabular dysplasia in this cohort whilst it does not appear to have deleterious effects, as evidenced by the similar Severin and McKay scores.

Aim

With the link between obesity and Slipped Upper Femoral Epiphysis (SUFE) well established and a rising number of paediatric orthopaedic patients presenting with vitamin D deficiency, the aim of our study was to establish the incidence of vitamin D deficiency in SUFE patients and whether low vitamin D levels increases the time to proximal femoral physeal fusion post surgical fixation.

Aim

Shelf acetabuloplasty is part of the armamentarium for the treatment of Legg-Perthes-Calve disease. Surgeons have used it to increase the anterolateral cover of the deformed head in advanced stages of the disease. However, others, including the senior author, advocate its use for containment of the diseased femoral head earlier in the disease, for both the prevention of further femoral head extrusion and as an aid in the remodelling process. The current study presents the results of this procedure performed from August 1999 to February 2010.

Aim

This study presents the early results of a novel procedure, both in timing and surgical technique, aimed to treat those cases of congenital hip dysplasia that present late or fail conservative treatment.

Background

Vitamin D deficiency may increase predisposition to a number of paediatric orthopaedic conditions and the prevalence of vitamin D deficiency is increasing in children in developed countries. The aim of this study was to determine the epidemiology of vitamin D deficiency and insufficiency in children presenting to a regional paediatric orthopaedic service. We also examined the relationships between vitamin D status, social deprivation and ethnicity

AIMS

We present a retrospective study of bilateral CDH. We analysed the correlation of complications to the confounding factors.

Purpose

We describe two recent cases of intraosseous (IO) access resulting in amputation in critically ill infants and make contemporary recommendations on the safe practice of this technique.

Purpose This was an observational study to determine the prevalence of 25-hydroxyvitamin D (25[OH]D deficiency in our paediatric orthopaedic patient population.

Methods We have measured serum 25(OH)D levels in 44 paediatric patients who presented with bone pain. None of these patients had a pre-existing diagnosis of 25(OH)D deficiency. The age of patients ranged from 11 months to 16.5 years. There were 23 female and 21 male patients. The range of diagnoses included hip pain/irritable hip (4), Blount's disease (4), developmental hip dysplasia (7), genu valgum (3), Legg Calve Perthes’ disease (6), slipped capital femoral epiphysis (11), knee pain (3), other (6).

Those found to be 25(OH)D deficient underwent further biochemical investigation and were referred for paediatric endocrinology review with a view to vitamin D supplementation.

Results We found 9 patients (20%) with serum 25(OH)D levels of <20ng/mL indicating 25(OH)D deficiency. 17 patients (39%) had serum 25(OH)D levels in the range 20-30ng/mL indicating possible deficiency. The remaining 18 patients (41%) had a normal level of 25(OH)D. There was no association between low serum 25(OH)D level and any specific diagnosis, nor with gender or age of patient. There was, however, a statistically significant difference between the serum 25(OH)D level in those patients with unexplained joint pain (mean 22.5ng/mL) and those with other diagnoses (mean 30.7ng/ml) (P<0.05).

Conclusion Our results are consistent with other recent prevalence studies showing a concerning level of 25(OH)D deficiency among the paediatric population, and may suggest an increasing burden of disease in the coming years arising from the problem.

Purpose of Study

To assess the radiological outcomes of medial screw epiphyseodesis of the proximal femoral physis in the management of lateral growth arrest following treatment of developmental dysplasia of the hip.

Purpose

Clinical coding is used to record information from patient admissions in the form of coded data used for monitoring the provision of health services and trends, research, audit and NHS financial planning.

Osteoarthrosis (OA) is often considered to be due to “wear and tear”, aggravated by obesity. However, if developmental dysplasia of the hip (DDH) is treated incorrectly, osteoarthrosis can also occur at a very young age. We obtained cartilage from the femoral head a 23 year-old female after arthroplasty for DDH; from a 14 year-old male, resected for paralytic dislocation, and from OA and control patients. This provided a unique opportunity to compare the cellular and epigenetic features of OA in older patients with those in a young control as well as a DDH patient. We have recently defined the cellular and epigenetic features of idiopathic OA, in particular the association between induction of proteases and loss of DNA methylation in the respective promoter regions (Arthritis Rheum2005; 52: 3110–3124). We had shown that these proteases were silenced in normal articular chondrocytes, but “unsilenced” in OA chondrocytes. The present study determined whether the phenotypic changes of idiopathic OA also take place in juvenile OA and whether loss of DNA demethylation is also associated with the abnormal expression of proteases in juvenile OA. Paraffin sections were immunostained with antibodies to MMP-3, -9, and ADAMTS-4. DNA was extracted from freezer milled cartilage. The methylation status of specific CpG sites (at which methylation occurs) was established using methylation-sensitive restriction enzymes followed by PCR. From the 23 year old female, we only obtained a 1cm thick transverse slice of femur, taken near the femoral neck. However, this contained sufficient reasonably thick cartilage in the perimeter for histology and DNA extraction.

The cartilage of the 14-year old showed high cellularity and absence of immunostaining for all proteases investigated. Apart from the higher cellularity, this was similar to the ‘control’ cartilage obtained from patients with a fracture of the femoral neck. We had previously shown that, as OA progresses, more chondrocytes become immunopositive for the degradative enzymes and these cells divide so that in the typical clones of OA all cells synthesize the proteases. The cartilage from the 23-year old DDH patient showed extensive loss of proteoglycans from the superficial zone and fibrous repair tissue covered some areas. Nearly all chondrocytes produced the proteases and clones had formed, as in idiopathic OA. Since these sample were from the base of the femoral neck, where in idiopathic OA good cartilage often remains even in severe OA, the disease process must have reached an early end-stage in this young patient. The findings indicate that severe OA, as defined by the presence of clones that produce degradative enzymes, can develop very quickly. Interestingly, the expression and synthesis of degradative enzymes by OA chondrocytes was the same in juvenile and old-age OA. and their abnormal expression was associated with “unsilencing” via DNA demethylation in both juvenile and old-age OA. The results thus suggest that age per se is not a major determinant of OA progression.

The majority of diaphyseal forearm fractures in children are treated by closed reduction and plaster immobilisation. There is a small subset of patients where operative treatment is indicated. Recent reports indicate that elastic intramedullary nailing (EIN) is gaining popularity over plate fixation. We report the results of EIN for diaphyseal fractures of the forearm in 44 children aged between 5 and 15 years during a three-year period. The indications were instability (26), redisplacement (14), and open fractures (4). Closed reduction and nailing was carried out in 18 cases. A single bone had to be opened in 16 cases and in 10 cases both bones were opened for achieving reduction. Out of the 39 both bone forearm fractures, 35 patients had stabilisation of both radius and ulna and in 4 cases only a single bone was nailed (Radius 3, Ulna 1).

Union was achieved in all the 44 cases at an average time of 7 weeks with one delayed union. All patients regained full flexion and extension of the elbow and wrist. Pronation was restricted by an average of 20° in 30% patients.

Complications were seen in 10 patients (20%). 4 patients had prominent metal work which required early removal. There was refracture in one case, which was treated by nail removal and re-fixation. Two patients developed post operative compartment syndrome requiring fasciotomy. EIN of the radius alone in a patient with fractures of both the bones of forearm, led to secondary displacement of the ulna. This resulted in ulnar malunion and a symptomatic distal radio-ulnar joint subluxation. This was successfully treated by ulnar osteotomy.

Compared to forearm plating EIN involves minimal scarring, easier removal and less risk of nerve damage. We therefore recommend EIN for the treatment of unstable middle and proximal third forearm fractures.

Idiopathic osteoarthritis (OA) is a complex, late-onset disease whose causes are still unknown. In spite of tremendous efforts, the search for the genes pre-disposing towards osteoarthritis has so far met with little success. We hypothesize that epigenetic changes play a major role in the pathology of OA. Epigenetics refers to stable, heritable, but potentially reversible modifications of gene expression that do not involve mutations in the DNA sequence, for example DNA methylation or histone modification. Epigenetic changes are gene and cell-type specific, may arise sporadically with increasing age or be provoked by environmental factors. To investigate whether epigenetic changes are significant factors in OA, we examined the DNA methylation status of the promoter regions of three genes that are expressed by OA, but not by normal, articular chondrocytes, namely MMP-3 (stromelysin-1), MMP-9 (gelatinase B) and MMP-13 (collagenase3). We hypothesized that these genes are silenced in normal chondrocytes by methylation of the cytosines of CpG dinucleotides in the respective promoter regions, but that abnormal expression is associated with a de-methylation, leading to eunsilencing f of gene expression. Cartilage was obtained from the femoral heads of 16 OA and 10 femoral neck fracture (#NOF) patients, which served as controls due to the inverse relationship between osteoporosis and OA. The cartilage was milled in a freezer mill with liquid nitrogen, DNA was extracted with a Qiagen kit, digested with methylation sensitive restriction enzymes, followed by PCR amplification. These enzymes will cut at their specific cleavage sites only if the CpGs is not methylated and thus allow us to determine methylation status of specific CpG sites.

Results. Less than 5% of the chondrocytes in superficial layer from #NOF cartilage expressed degradative enzymes, whereas all cloned chondrocytes from advanced-stage OA cartilage were immunopositive. The overall % of CpG demethylation in the promoters of control patients (whose chondrocytes did not express the enzymes) was 20.1%, whereas 48.6% of CpG sites were demethylated in degradative chondrocytes of OA patients (p< 0.001). For MMP-13, the increase in demethylation between control and OA was from 4 ^..20%; for MMP-9 from 47 ^..81% and for MMP-3 from 30 ^..57%. However, not all available CpG sites were equally demethylated. Some sites were uniformly methylated in both OA and controls, others were demethylated even in controls. However, there was at least one crucial site for each degradative enzyme, where the differences in the degree of methylation were greatest and statistically different. These sites were at −110 for MMP-13; −36 for MMP-9; −635 for MMP-3. There was no relation between the % demethylation and the patient fs age and no apparent difference between males and females.

Conclusions: We have demonstrated an association between abnormal gene expression of MMP-3, MMP-9 and MMP-13 and promoter DNA demethylation. This epigenetic dysregulation of genes appeared to be clonally inherited by daughter cells and may be typical for osteoarthritis and other complex, late-onset diseases.

Clonal chondrocytes of osteoarthritic (OA) cartilage express an aberrant set of genes. We hypothesize that this aberrant gene expression may be due to clonally inherited epigenetic changes, defined as altered gene expression without changes in genetic sequence. The major epigenetic changes are due to altered DNA methylations in crucial parts of the promoter region. If the cytosines of CpG dinucleotides are methylated, the gene will be silenced, even if the right transcription factors are present. Similarly, de-methylations may activate previously silenced genes. Our aims were to provide ‘proof-of-concept’ data by examining the methylation status of genes in OA vs non-OA chondrocytes. Articular cartilage was obtained a) from the cartilage of fracture-neck-of-femur (#NOF) patients and b) from or around the eroded regions of OA samples. The former was full thickness cartilage, the latter was partially degraded cartilage, which contained mostly clonal chondrocytes as confirmed by histology. The cartilage samples were ground in a freezer mill (Glen Creston, UK) and DNA was extracted with a Qiagen DNeasy maxi kit. To assess DNA methylation status, the genomic DNA was treated overnight with methylation-sensitive restriction enzymes. Cleavage of selected sites was detected by PCR amplifications with primer pairs designed to bracket selected promoter regions. Loss of the PCR band after digestion with the enzymes indicated absence of methylations, whereas presence of the band indicated methylated cytosine. We selected MMP-9 as one of genes that is activated in OA. Transcription of mmp-9 is regulated by a 670 bp sequence at the 5′-end flanking region, which contains 6 CpGs and a further 21 CpGs within the 1.5 kb region further upstream. A PCR primer pair was designed to bracket a 350bp sequence upstream from the transcription start site of mmp-9, which contained four of the six potential methylation sites, cleaved by the methylation-sensitive enzymes AciI and HhaI. DNA from 9 OA patients, 5 #NOF patients and 1 rheumatoid arthritic (RA) patient were digested with HhaI or AciI and examined for the presence or absence of PCR bands. In all patients, digestion with HhaI abolished the PCR band, indicating that the HhaI site was never methylated in either #NOF or OA patients. However, a remarkable difference was found after digestion with AciI: in 8/9 OA patients, the PCR band was no longer detectable, while in 4/5 #NOF patients the PCR band was still present. This suggested that all three AciI cleavage sites were methylated in the majority of chondrocytes from #NOF patients, while at least one of the three AciI cleavage sites was unmethylated in OA patients. Interestingly, the PCR band was present in the RA patient, suggesting methylation of the AciI cleavage sites. The present study provides the first ‘proof-of-concept’ data that suggest epigenetic changes may play a role in the etiology of osteoarthritis. Clearly further work is required to establish the generality of the present findings and whether de-methylations are also found in the promoter regions of other genes that are aberrantly expressed in OA.

Introduction: Chondro-epiphyseal cartilage is generally resistant to vascular invasion. At the time of formation of the secondary ossification center in skeletal ‘long’ bones, the anti-angiogenic nature of cartilage is altered in favor of angiogenesis and vascular invasion takes place. We studied the control of this angiogenic ‘switch’ by experimentally investigating two factors which might influence vascular invasion. MMP 9 is a 92Kda gelatinase which degrades collagen types IV, V and X and gelatin (denatured collagen). It has been implicated in the control of endochondral ossification at the growth plate and has been shown to modulate endothelial cell morphogenesis. Basic Fibro-blast Growth Factor (b-FGF) is a cytokine with well established angiogenic capability and has also been implicated in the development of the growth plate. We investigated whether MMP-9 caused an effect on the development of the vasculature of the chondro-epiphysis of neo-natal rabbits and compared this to the effects of b-FGF.

Materials and Methods: The CAM Culture consists of placing a small tissue explant onto the the chorioallantoic membrane of 10 day-old chick embryos and continuing culture for a further 10 days. CAM derived vessels will invade the tissue, unless anti-angiogenic factors are present. Hence, CAM culture is used as an assay system for angiogenesis and factors that will influence it. We utilized the CAM culture model to investigate vascular in-growth into explants of femoral and humeral heads from 4 day old postnatal rabbits to test the influence of MMP-9 and b-FGF. A small nylon membrane, pre-soaked in a solution containing the factor, was placed on to a tangential cut across the perichondrium. The explant was then cultured on the CAM for 3–10 days.

Results: In control epiphyses, the in-growth of CAM derived blood vessels was rare and invasion of cartilage canals through the perichondrium seldom occurred, thus confirming the anti-angiogenic nature of epiphyseal cartilage. The initial presence of MMP 9 caused a tremendous increase in the de novo vascular invasion. MMP 9 treated epiphyses contained numerous large cartilage canals. In b-FGF treated epiphyses, a greater level of vascular in-growth was seen compared with controls, but this was not as marked as with MMP 9.

Our findings indicate that b-FGF and perhaps, more interestingly, MMP-9 are implicated in the activation of the angiogenic ‘switch’ at the chondroepiphysis leading to vascular invasion. The fact that MMP-9 can act as a stimulator to angiogenesis is a novel finding. The mechanism of action remains unclear although it is possible that it is involved in the deactivation of inhibitors of vasculogenesis or the activation of angiogenic factors, or both.

A 12 year old girl presented with a history of intermittent pain in her left knee since she started walking. She was seen in the vascular clinic due to engorged veins in her left leg and was diagnosis of Klippel-Trenaunay syndrome was made. Her knee pain worsened and an orthopaedic opinion was obtained. A history of repeated knee effusion and swelling was noted.

Examination revealed partial gigantism of the left leg and reduced range of motion of the knee. There was soft tissue swelling of the knee with no effusion. Blood investigations were normal. X-rays showed an arthritic joint. MRI scans revealed synovial thickening and a vascular malformation suggesting a synovial haemangioma. She underwent Radical Open Synovectomy and excision of the haemangioma. Blood loss was minimal. Extensive haemosiderin deposition was noted along with Grade IV arthritic changes. Postoperative recovery was uneventful. Surgeons have been reluctant to excise synovial hemangiomas due to the risk of haemorrhage.

A recent paper from Switzerland suggested excision was possible with minimal blood loss. Haemosiderin deposition due to recurrent haemarthrosis may predispose to articular damage. We recommend early excision of synovial haemangiomas to minimise articular damage.

The use of designer scaffolds to deliver biologically active osteogenic growth factors such as recombinant human bone morphogenetic protein-2 (rhBMP-2) to the sites of tissue regeneration in for example orthopaedics, has tremendous therapeutic implications. The aims of this study were to generate biomimetic biodegradable porous osteogenic scaffolds using a supercritical fluid process to encapsulate rhBMP-2, and to examine the ability of the scaffolds to promote human osteoprogenitor differentiation and bone formation in vitro and in vivo.

The rhBMP-2 encapsulated in Poly(-lactic acid) (PLA) scaffolds (100ng/mg PLA) were generated using an innovative supercritical fluid mixing method. The bioactivity of rhBMP-2 encapsulated PLA scaffolds were confirmed by induction of the C2C12 promyoblast cell line into the osteogenic lineage as detected by alkaline phosphatase expression. No induction of alkaline phosphatase-positive cells was observed using blank scaffolds. BMP-2 released from encapsulated constructs promoted adhesion, migration, expansion and differentiation of human osteoprogenitor cells on 3-D scaffolds. Enhanced matrix synthesis and cell differentiation on growth factor encapsulated scaffolds was observed following culture of human osteoprogenitors on explants of chick femoral bone wedge defects in an ex vivo model of bone formation developed using the chick chorioallantoic membrane model. In vivo studies using diffusion chamber implantation and subcutaneous implantation of human osteoprogenitors on rhBMP-2 encapsulated scaffolds showed morphologic evidence of new bone matrix and cartilage formation in athymic mice as assessed by x-ray analysis, immunocytochemistry and birefringence. These studies provide evidence of controlled release of BMP-2 from biodegradable polymer scaffolds initiating new bone formation in vivo.

The generation of 3-D biomimetic structures incorporating osteoinductive factors such as BMP-2 indicates their potential for de novo bone formation that exploits cell-matrix interactions and, significantly, realistic delivery protocols for growth factors in musculo-skeletal tissue engineering.

Introduction: To review the medium term outcome of staged surgery for treating recalcitrant idiopathic talipes equinovarus.

Methods: Between 1988 and 1995, we studied 91 club feet from a series of 120 recalcitrant feet in 86 patients requiring surgical treatment. The initial results have been reported previously and this cohort has been subsequently followed up for between 7 and 15years. The mean age at initial operation was 8.9 months. Surgery consisted of an initial plantar medial release followed two weeks later by a posterolateral release. This strategy was used specifically to address the problems of wound healing associated with single-stage surgery and to ascertain the rate of relapse after a two-stage procedure. The feet were classified preoperatively and prospectively into four grades according to the system suggested by Dimeglio et al. Reported relapse at last review was 0.0% in grade 2, 20.4% in grade 3 and 65.4% in grade 4 feet. The rate of overall relapse was 30.8%. At 7 to 15 year review an additional 9.1% in grade 2, 7.4% in grade 3, 11.5% in grade 4 had relapsed. Overall a further 8.8% had relapsed and were treated with further surgery. Functional outcome of the group remains good with 95.6% overall finding no restrictions to activities.

Conclusion: This review confirms that the strategy of staged surgery is supported in the medium term when considering rates of relapse and functional outcome.

Aims: There are no large published studies examining the complication rates associated with use of Kirschner wires in þxation of a wide variety of paediatric fractures. The aim of this study is to analyse the outcomes of fracture þxation using K-wire in upper limb fractures in children and to critically assess the incidence and type of complications. Methods: This study is a retrospective review of a consecutive series of 107 fractures in 105 paediatric trauma cases treated with K-wire in between 01.09.99 to 10.09.01. Results: The fractures were fractures around Wrist (47%) and around elbow (45%). 66 (61.68%) were performed by closed percutaneous technique, 27 (25.23%) by open method and in 14 (13.08%) combined approach was used. Around there were 13 cases with over-granulation at wound site, 6 cases of Soft tissue infection, 2 cases with tendinitis, 1 case of Osteo-myelitis and 1 case with hyper-sensitive scar. 3 cases found to have postoperative neurapraxia and 1 case with axonotmesis. Metal migration was detected in 4 cases and 14 cases found to have shown wire loosening. 10 fractures have lost position in postoperative period out of which 2 cases were reoperated for Re K-wire, 1 had undergone Re-MUA and 7 left for remodelling. Conclusions: K-wires are versatile but are not inherently benign. We conclude that best results could be achieved if total life of K-wire can be restricted to 3–4 weeks. We recommend one should explain all these risks and complications during consenting for K-wiring procedures.

Background: The necessity for radiographic follow up of infants with hip clicks and normal ultrasound is not clear.

Materials and methods: Infants referred to a paediatric hip clinic whose sole risk factor for DDH was a soft tissue hip click who had a normal ultrasound scan on initial assessment were identified. A follow up six month AP pelvis radiograph was assessed and acetabular index(A.I), position of femoral ossific nucleus and Shen-ton’s line measured. Infants with rotated pelvis Xrays were excluded. Inter-observer variability for acetabular index was measured and dysplasia defined according to Tonnis.

Results: 171 infants (193 clicking hips) met the criteria for inclusion. 48 male and 109 female with unilateral clicks (57 right, 64 left) and 36 bilateral clicks. 10 were excluded due to rotation of the AP pelvis Xray. Inter-observer error for A.I. was 4°. All A.I. were within normal ranges. Shenton’s line was unbroken and all hips were located.

Conclusion: In this study infants with soft tissue hip clicks and a normal ultrasound scan on initial assessment had a normal Xray at six months.