Aims. Insufficient treatment response in rheumatoid arthritis (RA) patients requires novel treatment strategies to halt disease progression. The potential benefit of combination of cytokine-inhibitors in RA is still unclear and needs further investigation. To explore the impact of combined deficiency of two major cytokines, namely interleukin (IL)-1 and IL-6, in this study double deficient mice for IL-1αβ and IL-6 were investigated in different tumour necrosis factor (TNF)-driven inflammatory bone disorders, namely peripheral arthritis and sacroiliitis, as well as systemic bone loss. Methods. Disease course, histopathological features of arthritis, and micro-CT (µCT) bone analysis of local and systemic bone loss were assessed in 15-week-old IL1-/-IL6-/-hTNFtg in comparison to IL1-/-hTNFtg, IL6-/-hTNFtg, and hTNFtg mice. µCT bone analysis of single deficient and wild-type mice was also performed. Results. Combined deficiency of IL-1/IL-6 markedly ameliorated TNF-mediated arthritis and bilateral sacroiliitis, but without additive benefits compared to single IL-1 deficiency. This finding confirms the important role of IL-1 and the marginal role of IL-6 in TNF-driven pathways of local joint damage, but questions the efficacy of potential combinatorial therapies of IL-1 and IL-6 in treatment of RA. In contrast, combined deficiency of IL-1/IL-6 led to an additive protective effect on TNF-driven systemic bone loss compared to single IL-1 and IL-6 deficiency. This finding clearly indicates a common contribution of both IL-1 and IL-6 in TNF-driven systemic bone loss, and points to a discrepancy of cytokine dependency in local and systemic TNF-driven mechanisms of inflammatory arthritis. Conclusion. Combinatorial treatments in RA might provide different benefits to inflammatory local arthritis and systemic comorbidities. Cite this article: Bone Joint Res 2022;11(7):484–493

We have developed a novel technique to analyse bone, using imaging mass cytometry (IMC) without the constraints of using immunofluorescent histochemistry. IMC can measure the expression of over 40 proteins simultaneously, without autofluorescence. We analysed mitochondrial respiratory chain (RC) protein deficiencies in human bone which are thought to contribute to osteoporosis with increasing age. Osteoporosis is characterised by reduced bone mineral density (BMD) and fragility fractures. Humans accumulate mitochondrial mutations and RC deficiency with age and this has been linked to the changing phenotype in advancing age and age-related disease. Mitochondrial mutations are detectable from the age of 30 onwards, coincidently the age BMD begins to decline. Mitochondria contain their own genome which accumulates somatic variants at around 10 times the rate of nuclear DNA. Once these mutations exceed a threshold, RC deficiency and cellular dysfunction occur. The PolgD257A/D257A mouse model expresses a proof-reading deficient version of PolgA, a mtDNA polymerase. These mice accumulate mutations 3-5 times higher than wild-type mice showing enhanced levels of age-related osteoporosis and RC deficiency in osteoblasts. Bone samples were analysed from young and old patients, developing a protocol and analysis framework for IMC in bone tissue sections to analyse osteoblasts in-situ for RC deficiency. Samples from the femoral neck of 10 older healthy volunteers aged 40 – 85 were compared with samples from young patients aged 1-19. We have identified RC complex I defect in osteoblasts from 6 of the older volunteers, complex II defects in 2 of the older volunteers, complex IV defect in just 1 older volunteer, and complex V defect in 4 of the older volunteers. These observations are consistent with the PolgD257A/D257A mouse-model and suggest that RC deficiency, due to age-related pathogenic mitochondrial DNA mutations, may play a significant role in the pathogenesis of human age-related osteoporosis

Objectives. Congenital cruciate ligament deficiency is a rare condition that may occur in isolation or in association with longitudinal limb deficiencies such as fibular hemimelia or proximal femoral focal deficiency. Often anomalies of the menisci and their attachments can be very abnormal and impact on surgical management by standard techniques. Arthroscopic surgical knee reconstruction is undertaken to improve symptomatic instability and/or to stabilise and protect the knee for future planned limb lengthening surgery. The aim of this study is to evaluate the arthroscopic findings of patients undergoing surgery for congenital cruciate ligament deficiency, and specifically to determine the frequency and types of meniscal anatomical variations seen in these cases. Methods. Patients undergoing surgery for congenital cruciate ligament deficiency were identified from a prospectively collated database. Diagnosis was confirmed through review of the clinical notes and imaging. Operative notes and 4K saved arthroscopic images and video recordings for these cases were reviewed. Results. Over a six-year period (July 2017 – September 2023), 42 patients underwent surgery for congenital ligament deficiency and tibiofemoral instability (45 surgical episodes). Median age of patients at time of surgery was 10 years (range 4 – 17 years). The most frequent diagnosis was congenital longitudinal limb deficiency syndromes in 27 cases, with the most frequent being fibular hemimelia. Isolated congenital ligament deficiency without any other associated extra-articular manifestations occurred in 11 cases. Absence of meniscal root attachments or hypertrophy of meniscofemoral ligaments acting as ‘pseudo-cruciates’ were seen in over 25% of patients. In isolated ACL deficiency these were injured causing onset of instability symptoms and pain following trauma. Often these abnormal structures required addressing to allow surgical reconstruction. Conclusions. Our findings demonstrate that there are often meniscal variations seen in association with congenital absence or hypoplasia of the cruciate ligaments. In these patients hypertrophied meniscofemoral ligaments may act as cruciate-like structures and play a role in providing a degree of sagittal plane stability to the knee. However, when the knee becomes unstable to the point that cruciate ligament reconstruction is indicated, these meniscal variants may often require stabilisation using complex meniscal root repair techniques or variations to standard cruciate ligament reconstruction techniques to accommodate the variant anatomy

The aims were to assess whether vitamin D deficiency influenced mortality risk for patients presenting with a hip fracture. A retrospective study was undertaken including all patients aged over 50 years that were admitted with a hip fracture to a single centre during a 24-month period. Serum vitamin D levels were assessed. Patient demographics and perioperative variables and mortality were collected. Cox regression analysis (adjusting for confounding) was utilised to determine the independent association between serum vitamin D level and patient mortality. The cohort consisted of 2075 patients with a mean age of 80.7 years and 1471 (70.9%) were female. 1510 (72.8%) patients had a serum vitamin D level taken, of which 876 (58.0%) were deficient (<50nmol/l). The median follow up was 417 (IQR 242 to 651) days. During follow up there were 464 (30.7%) deaths. Survival at 1 year was significantly (p = 0.003) lower for patients who were vitamin D deficient (71.7%, 95% confidence intervals (CI) 68.6 to 74.9) compared to those who were not (79.0%, 95% CI 75.9 to 82.3). Vitamin D deficiency was also independently associated with an increased mortality risk at 2-years (HR 1.42, 95% CI 1.17 to 1.71, p = 0.03), but not at 1-year (p = 0.08). Hip fracture patients with vitamin D deficiency had an increased mortality risk. This risk was independent of confounders at 2 years. The role of measuring vitamin D levels in these patients is unclear. Improved public health policy about vitamin D may be required to reduce deficiency in this patient population

The aims were to assess whether vitamin D deficiency influenced mortality risk for patients presenting with a hip fracture. A retrospective study was undertaken including all patients aged over 50 years that were admitted with a hip fracture to a single centre during a 24-month period. Serum vitamin D levels were assessed. Patient demographics and perioperative variables and mortality were collected. Cox regression analysis (adjusting for confounding) was utilised to determine the independent association between serum vitamin D level and patient mortality. The cohort consisted of 2075 patients with a mean age of 80.7 years and 1471 (70.9%) were female. 1510 (72.8%) patients had a serum vitamin D level taken, of which 876 (58.0%) were deficient (50nmol/l). The median follow up was 417 (IQR 242 to 651) days. During follow up there were 464 (30.7%) deaths. Survival at 1 year was significantly (p=0.003) lower for patients who were vitamin D deficient (71.7%, 95% confidence intervals (CI) 68.6 to 74.9) compared to those who were not (79.0%, 95% CI 75.9 to 82.3). Vitamin D deficiency was also independently associated with an increased mortality risk at 2-years (HR 1.25, 95% CI 1.03 to 1.53, p=0.025), but not at 1-year (p=0.057). Hip fracture patients with vitamin D deficiency had an increased mortality risk. This risk was independent of confounders at 2 years. The role of measuring vitamin D levels in these patients is unclear. Improved public health policy about vitamin D may be required to reduce deficiency in this patient population

Abstract. Introduction. Vitamin D deficiency in the UK is well documented − 30–40% of the population. It is an essential component of calcium metabolism and adequate levels are important for bone healing. Studies have demonstrated an overall prevalence of vitamin D deficiency/insufficiency at 77% in trauma patients aged >18, deficiency alone was 39%. Adequate vitamin D levels have a positive effect on bone mineral density and callus formation at fracture sites. Methods. We conducted a retrospective consecutive case series of all patients aged 0–50 undergoing surgical management for any fracture in October 2021 to March 2022. We assessed if vitamin D levels were checked and if patients were prescribed replacement as per local guidelines. Results. A total of 131 patients were identified, (mean 29 years; 83 male and 48 female). Most cases were upper limb fractures (n=78, 60%), as opposed to lower limb (n=53, 40%). Only 20 (15%) had their levels checked, of which 13 (65%) were insufficient/deficient (10 insufficiency, 2 deficiency, 1 severe deficiency). Of these 13 patients, only 3 (23%) were prescribed replacement therapy. Conclusions. Only a small proportion of patients had their levels checked, however the majority were insufficient/deficient. The prevalence in our study is consistent with larger epidemiology studies, which reflect a higher rate of deficiency in fracture patients compared to the general population. Thus, we propose that all patients in this age group should undergo a vitamin d level check upon time of clerking and this should be accurately treated as per trust guidance

Aim. Reconstruction of composite soft-tissue defects with extensor apparatus deficiency in patients with periprosthetic joint infection (PJI) of the knee is challenging. We present a single-centre multidisciplinary orthoplastic treatment concept based on a retrospective outcome analysis over 20 years. Method. One-hundred sixty-seven patients had PJI after total knee arthroplasty. Plastic surgical reconstruction of a concomitant perigenicular soft-tissue defect was indicated in 49 patients. Of these, seven presented with extensor apparatus deficiency. Results. One patient underwent primary arthrodesis and six patients underwent autologous reconstruction of the extensor apparatus. The principle to reconstruct missing tissue ‘like with like’ was thereby favoured: Two patients with a wide soft-tissue defect received a free anterolateral thigh flap with fascia lata; one patient with a smaller soft-tissue defect received a free sensate, extended lateral arm flap with triceps tendon; and three patients received a pedicled medial sural artery perforator gastrocnemius flap, of which one with Achilles tendon. Despite good functional results 1 year later, long-term follow-up revealed that two patients had to undergo knee arthrodesis because of recurrent infection and one patient was lost to follow-up. In parts, results have been published under doi: 10.7150/jbji.47018. Conclusions. A treatment concept and its rationale, based on a single-centre experience, is presented. It differentiates between various types of soft-tissue defects and shows reconstructive options following the concept to reconstruct ‘like with like’. Despite good results 1 year postoperatively, PJI of the knee with extensor apparatus deficiency remains a dreaded combination with a poor long-term outcome

Aims. This study investigated the effects of β-caryophyllene (BCP) on protecting bone from vitamin D deficiency in mice fed on a diet either lacking (D-) or containing (D+) vitamin D. Methods. A total of 40 female mice were assigned to four treatment groups (n = 10/group): D+ diet with propylene glycol control, D+ diet with BCP, D-deficient diet with control, and D-deficient diet with BCP. The D+ diet is a commercial basal diet, while the D-deficient diet contains 0.47% calcium, 0.3% phosphorus, and no vitamin D. All the mice were housed in conditions without ultraviolet light. Bone properties were evaluated by X-ray micro-CT. Serum levels of klotho were measured by enzyme-linked immunosorbent assay. Results. Under these conditions, the D-deficient diet enhanced the length of femur and tibia bones (p < 0.050), and increased bone volume (BV; p < 0.010) and trabecular bone volume fraction (BV/TV; p < 0.010) compared to D+ diet. With a diet containing BCP, the mice exhibited higher BV and bone mineral density (BMD; p < 0.050) than control group. The trabecular and cortical bone were also affected by vitamin D and BCP. In addition, inclusion of dietary BCP improved the serum concentrations of klotho (p < 0.050). In mice, klotho regulates the expression level of cannabinoid type 2 receptor (Cnr2) and fibroblast growth factor 23 (Fgf23) through CD300a. In humans, data suggest that klotho is connected to BMD. The expression of klotho is also associated with bone markers. Conclusion. These data indicate that BCP enhances the serum level of klotho, leading to improved bone properties and mineralization in an experimental mouse model. Cite this article: Bone Joint Res 2022;11(8):528–540

Introduction:. Vitamin D plays an important role in bone turnover. Deficiency (including borderline deficiency, or insufficiency) has a known association with fractures and has been linked to delayed or nonunion of fractures. We therefore routinely test vitamin D in cases of nonunion. Noting a high rate of vitamin D deficiency in this group, we instituted a policy to routinely screen for and treat vitamin D deficiency in both post-operative and pre-operative patients. We hypothesised that, in the post-operative patients, levels would correlate with rates of union. Methods:. We sent serum vitamin D levels on consecutive post-operative patients seen in clinics between January and May 2014. They included those with an arthrodesis of the ankle, triple joint or first MTPJ. Union was deemed to have occurred when the patient was comfortable full weight bearing and radiographs showed trabeculae crossing the fusion site. Nonunions were all confirmed with computed tomography. Results:. Ten patients were treated for nonunion, and had a mean serum vitamin D of 58nmol/L. Fourteen patients (collected over a shorter time period) had confirmed union, with a mean vitamin D of 90nmol/L. This was statistically significant on a one tailed Student's t test (p=0.038). Vitamin D was deficient in five (50%) of nonunions and in three (21%) of unions, giving an odds ratio of 3.67. Conclusions:. Our early results show a significant association of serum vitamin D levels with likelihood of nonunion, and we continue to collect data. There is a high prevalence of vitamin D deficiency in our patient population. This is of concern both for the outcome of their surgery and for their lifetime fracture risk. We recommend either screening for or presumptively treating vitamin D deficiency

Abductor deficiency commonly contributes to total hip dislocation. Successful treatment of the deficiency can improve function, decrease pain, and decrease reliance on implants to cure recurrent dislocation. The defining physical exam findings are dependence on ambulatory assistive devices, severe limp, positive Trendelenberg sign, and inability to abduct against gravity. Three techniques have been described for chronic abductor discontinuity in which the abductors have retracted or are absent and cannot reach the greater trochanter: Vastus lateralis muscle shift, Achilles tendon allograft, and gluteus maximus muscle transfer. None of the techniques were specifically performed for dislocation. The vastus lateralis shift transfers the entire muscle proximally maintaining the neurovascular bundle. The procedure requires an incision from the hip to the knee, isolation of the neurovascular bundle, and elevation of the muscle from the femur. The authors admitted that the technique is demanding and not easily applicable to many surgeons. Repair with an Achilles allograft requires an identifiable contractile abductor mass. The allograft is looped through the abductors to bridge the gap to the trochanter. Two variations of a gluteus muscle transfer for abductor deficiency after total hip have been described. A portion of the gluteus maximus with its distal fascial portion are transferred to the greater trochanter. As far as dislocation is concerned an advantage of this technique is the use of the posterior maximus flap to fill a posterior and superior capsular defect not addressed with the other techniques. In addition the technique is easy to perform in almost all cases

The expression of the mechanosensor, integrin αvβ3, is reduced in osteoporotic bone cells compared to controls. MLO-Y4 osteocytes experience altered mechanotransduction under estrogen deficiency and it is unknown whether this is associated with defective αvβ3 expression or signalling. The objectives of this study are to (1) investigate αvβ3 expression and spatial organisation in osteocytes during estrogen deficiency, and (2) establish whether altered responses of osteocytes under estrogen deficiency correlate to defective αvβ3 expression and functionality. MLO-Y4 cells were cultured as follows: Ctrl (no added estradiol), E+ (10nM 17β-estradiol for 5 days), and Ew (10nM 17β-estradiol for 3 days and withdrawal for 2 days). Cells were cultured with/without 0.5µM IntegriSense750 (αvβ3 antagonist). Laminar oscillatory fluid flow of 1Pa at 0.5Hz was applied for 1hr. αvβ3 content was quantified using an ELISA. The location and quantity of αvβ3 and focal-adhesions was determined by immunocytochemistry. Estrogen withdrawal under static conditions led to lower cell and focal-adhesion area (p<0.05), compared to E+ cells. Fluid flow led to higher αvβ3 content (p<0.05) in all groups, compared to static counterparts, with αvβ3 blocking altering this response. Fluid flow on Ew cells had the highest αvβ3 levels (p<0.05), but αvβ3 did not localise at focal-adhesions sites. Cell morphologies were similar after treatment with the αvβ3 antagonist to the Ew group. These results suggest there are fewer functional focal-adhesion sites at which αvβ3 integrins localise to facilitate mechanotransduction. To further understand these results, we are analysing osteocyte mechanotransduction by quantifying PGE2 and gene expression (COX-2, RANKL, OPG, SOST)

Proximal femoral focal deficiency is a congenital disorder of malformation of the proximal femur and/or the acetabulum. Patients present with limb length discrepancy and clinical features along a spectrum of severity. As these patients progress through to skeletal maturity and on to adulthood, altered biomechanical demands lead to progression of arthropathy in any joint within the lower limb. Abnormal anatomy presents a challenge to surgeons and conventional approaches and implants may not necessarily be applicable. We present a case of a 62-year-old lady with unilateral proximal femoral focal deficiency (suspected Aitken Class A) who ambulated with an equinus prosthesis for her entire life. She presented with ipsilateral knee pain and instability due to knee arthritis but could not tolerate a total knee arthroplasty due to poor quadriceps control. A custom osteointegration prosthesis was inserted with a view to converting to the proximal segment to a total hip replacement if required. The patient went on to develop ipsilateral symptomatic hip arthritis but altered acetabular anatomy required a custom tri-flange component (Ossis, Christchurch, New Zealand) and a custom proximal femoral component to link with the existing osseointegration component (Osseointegration Group of Australia, Sydney, Australia) were designed and implanted. The 18 month follow up of the custom hip components showed that the patient had Oxford hip scores that were markedly improved from pre-operatively. Knee joint heights were successfully restored to equal when the patient's prosthesis was attached. The patient describes feeling like “a normal person”, walks unaided for short distances and can ambulate longer distances with crutches. Advances in design and manufacture of implants have empowered surgeons to offer life improving treatments to patients with challenging anatomy. Using a custom acetabular tri-flange and osseointegration components is one possible solution to address symptomatic ipsilateral hip and knee arthropathy in the context of PFFD in adulthood

Integrin α2β1 is one of the major transmembrane receptors for fibrillary collagen. In native bone we could show that the absence of this protein led to a protective effect against age-related osteoporosis. The objective of this study was to elucidate the effects of integrin α2β1 deficiency on fracture repair and its underlying mechanisms. Standardised femoral fractures were stabilised by an intramedullary nail in 12 week old female C57Bl/6J mice (wild type and integrin α2. -/-. ). After 7, 14 and 28 days mice were sacrificed. Dissected femura were subjected to µCT and histological analyses. To evaluate the biomechanical properties, 28-day-healed femura were tested in a torsional testing device. Masson goldner staining, Alizarin blue, IHC and IF staining were performed on paraffin slices. Blood serum of the animals were measured by ELISA for BMP-2. Primary osteoblasts were analysed by in/on-cell western technology and qRT-PCR. Integrin α2β1 deficient animals showed earlier transition from cartilaginous callus to mineralized callus during fracture repair. The shift from chondrocytes over hypertrophic chondrocytes to bone-forming osteoblasts was accelerated. Collagen production was increased in mutant fracture callus. Serum levels of BMP-2 were increased in healing KO mice. Isolated integrin deficient osteoblast presented an earlier expression and production of active BMP-2 during the differentiation, which led to earlier mineralisation. Biomechanical testing showed no differences between wild-type and mutant bones. Knockout of integrin α2β1 leads to a beneficial outcome for fracture repair. Callus maturation is accelerated, leading to faster recovery, accompanied by an increased generation of extra-cellular matrix material. Biomechanical properties are not diminished by this accelerated healing. The underlying mechanism is driven by an earlier availability of BMP-2, one main effectors for bone development. Local inhibition of integrin α2β1 is therefore a promising target to accelerate fracture repair, especially in patients with retarded healing

Background. The cruciate ligaments are important structures for biomechanical stability of the knee. For total knee arthroplasty (TKA), understanding of the exact function of the (PCL) and anterior (ACL) cruciate ligament during walking is important in the light of recent designs of bicruciate TKAs. However, studies evaluating in vivo function of the PCL during daily activities such as walking are scarce. We aimed to assess the role of the PCL during gait by measuring kinematics and kinetics of individuals with PCL deficiency and compare them with individuals with ACL deficiency and healthy young adults. Methods. Individuals with unilateral PCL deficiency (PCLD; n=9), unilateral ACL deficiency (n=10) and healthy young adults performed (n=10) 10 walk trials (5 for each leg) in which they walked over a force platform. Motion analysis (Vicon Motion Capture System) was used to calculate joint angles and internal moments around the knee, hip and ankle in the sagittal plane. Joint angles and moments of the injured knee (in PCLD and ACLD) or left knee (in HYA) were compared between groups at weight acceptance, mid-stance and push-off phases (see Fig. 1). Clinical assessment included passive knee laxity (Kneelax) for anterior (in 20–30° knee flexion) and posterior tibia translation (in 70–90° knee flexion) and Lysholm questionnaires. Results. Lysholm scores were significantly lower in PCLD and ACLD individuals compared to HYA (p's ≤ .001). PCLD subjects had more passive anterior (p = .001) and posterior tibia translation (p = .041) compared to HYA, but no significant differences were found in both directions between ACLD and HYA (p's > .10). During gait, knee angles at weight acceptance, late stance and around toe-off were not significantly different between the PCLD and HYA, and between ACLD and HYA (all p's > .06). However, the knee extension moment during mid-stance was significantly lower in the PCLD group when compared to the HYA group (p = .001; Fig. 2). Interestingly, the knee moment in the PCLD group remained positive (i.e. extension moment) throughout the stance phase, whereas HYA and ACLD groups created a substantial flexion moment around the knee at this instant. We did not observe any significant differences in hip and ankle joint angles and moments between groups. Discussion. We observed a difference in gait pattern in individuals with PCL deficiency compared to HYA, that was confined to an absence of knee flexion moments during the mid-stance phase. We hypothesize that this difference reflects a compensation strategy employed by individuals with PCL deficiency to avoid external knee (hyper)extension moments. Gait adaptations related to PCL deficiency might also have implications for design of total knee prosthesis and calls for careful evaluation of gait patterns after TKA with a specific focus on the role of the PCL. For any figures or tables, please contact the authors directly

Femoral head deformity can be a devastating outcome in a small percentage of patients with Perthes' disease. Deformities usually start during the fragmentation stage. In this study, we aimed to determine the effects of Vitamin D deficiency on the natural history of Perthes' disease. Patients with Perthes' disease and Vitamin D deficiency presenting to our unit in the last 3 years were identified. All X-rays were reviewed retrospectively to determine the duration of the fragmentation and ossification stages. Treatment methods were obtained from the notes. Late presenters (i.e. after fragmentation stage) were excluded. In our unit, Vitamin D deficiency is diagnosed if levels <72 nmol/L. Fifteen patients (17 hips) with Perthes' disease were found to be Vitamin D deficient. Levels ranged from (18–71 nmol/L). The mean length of the fragmentation stage was 15.7 months which is significantly higher than quoted literature figures (8 months). Ossification stage duration was 18.8 months which was comparable to quoted figures. However, patients with severe Vitamin D deficiency (< 52 nmol/L) were found to have longer ossification stage (20.6 months) compared with patients with mild deficiency (52–72 nmol/L) (16.4 months). Seven out of 16 patients (44%) required surgical containment which is significantly higher than the usually low rates of surgical intervention. The critical fragmentation stage in Vitamin D deficiency is significantly longer putting the femoral head at higher risk of deformity and extrusion. This leads to higher rates of surgical containment. Also the severity of Vitamin D deficiency might be an important determinant of the period of time required for ossification and healing. Vitamin D level is an important prognostic factor and must be measured in all patients with Perthes' disease. Prescribing Vitamin D supplements is advisable in this group of patients. However, the effects of these supplements on the course of the disease requires further research. Level of evidence: III

Abductor deficiency after THA can result from proximal femoral bone loss, trochanteric avulsion, muscle destruction associated with infection, pseudotumor, ALTR to metal debris, or other causes. Constrained acetabular components are indicated to control instability after THA with deficient abductors. However, the added implant constraint also results in greater stresses at the modular liner-locking mechanism of the constrained component and bone-implant fixation interface, which can contribute to mechanical failure of the constrained implant or mechanical loosening. Use of large heads has been effective in reducing the rate of dislocation after primary THA. However, relatively large (36mm) heads were not found to be effective in controlling dislocation in patients with abductor deficiency. Dual mobility implants which can provide considerably larger head diameters than 36mm may offer an advantage in improving stability in patients with abductor deficiency. However the utility of these devices in controlling instability after THA with deficient abductors has not been established. Whiteside has described a transfer of the tensor muscle and anterior gluteus maximus to the greater trochanter for treatment of absent abductors after THA. Transposition of the tensor muscle requires raising an anterior soft tissue flap to the lever of the interval between the tensor muscle and sartorius, which is the same interval used in an anterior approach to the hip. The muscle is transected distally and transposed posteriorly to attach to the proximal femur. This can result in soft tissue redundancy between the posterior tensor muscle and anterior gluteus maximus. This interval is separated and the anterior gluteus maximus also attached to the proximal femur. The transposed tensor muscle provides muscle coverage over the greater trochanter, which may be beneficial in controlling lateral hip pain. In our practice, 11 patients were treated with Whiteside's tensor muscle transfer. Six patients had absent abductors, one had an avulsed greater trochanter, and four intact but weak abductors. One patient had a muscle transposition alone, one had an ORIF of the greater trochanter and muscle transposition, two had a muscle transposition and head/liner exchange, three had a muscle transposition and cup revision, two had a femoral revision and liner exchange with muscle transposition, and two had a muscle transposition with both component revision. None of the patients had constrained components. The mean pre-operative abductor strength was 2.2 (0/5 in four patients 3/5 in four patients, and 4/5 in three patients). Pre-operative lateral hip pain was none or mild in two patients, moderate in three, and severe in six patients. Mean post-operative abductor strength was 3.2 (2/5 in four patients, 3/5 in three, 4/5 in two, 5/5 in two patients). Post-operative lateral hip pain was none in five and mild in six patients. One patient sustained a dislocation four weeks after surgery which was treated with open reduction. All of the other hips have remained stable. Treatment of patients with hip instability and abductor deficiency has generally required use of a constrained acetabular component. In our experience, transfer of the tensor muscle and anterior gluteus maximus to the greater trochanter can improve abductor strength by one grade and also reduce lateral hip pain. The combination of a large head and tensor muscle transposition may be a viable alternative to use of a fully constrained component in patients with deficient abductors after THA. However, the need for implant constraint should also be individualised and based on factors such as the viability of the transposed muscle, patient compliance with post-operative activity restrictions, femoral head/neck ratio, and cup position

Hip abductor deficiency (HAD) associated with hip arthroplasty can be a chronic, painful condition that can lead to abnormalities in gait and instability of the hip. HAD is often confused with trochanteric bursitis and patients are often delayed in diagnosis after protracted courses of therapy and steroid injection. A high index of suspicion is subsequently warranted. Risk factors for HAD include female gender, older age, and surgical approach. The Hardinge approach is most commonly associated with HAD because of failure of repair at the time of index surgery or subsequent late degenerative or traumatic rupture. Injury to the superior gluteal nerve at exposure can also result in HAD and is more commonly associated with anterolateral approaches. Multiple surgeries, chronic infection, and chronic inflammation from osteolysis or metal debris are also risk factors especially as they can result in bone stock deficiency and direct injury to muscle. Increased offset and/or leg length can also contribute to HAD, especially when both are present. Physical exam demonstrates abductor weakness with walking and single leg stance. There is often a palpable defect over the greater trochanter and palpation in that area usually elicits significant focal pain. Note may be made of multiple incisions. Increased leg length may be seen. Radiographs may demonstrate avulsion of the greater trochanter or significant osteolysis. Significant polyethylene wear or a metal-on-metal implant should be considered as risk factors, as well as the presence of increased offset and/or leg length. Ultrasound or MRI are helpful in confirming the diagnosis but false negatives and positive results are possible. Treatment is difficult, especially since most patients have failed conservative management before diagnosis of HAD is made. Surgical options include allograft and mesh reconstruction as well as autologous muscle transfers. Modest to good results have been reported, but reproducibility is challenging. In the case of increased offset and leg length, revision of the components to reduce offset and leg length may be considered. In the case of significant instability, abductor repair may require constrained or multi-polar liners to augment the surgical repair. HAD is a chronic problem that is difficult to diagnose and treat. Detailed informed consent appropriately setting patient expectations with a comprehensive surgical plan is required if surgery is to be considered. Be judicious when offering this surgery

Abductor deficiency after THA can result from proximal femoral bone loss, trochanteric avulsion, muscle destruction associated with infection, pseudotumor, ALTR to metal debris, or other causes. Whiteside has described a transfer of the tensor muscle and anterior gluteus maximus to the greater trochanter for treatment of absent abductors after THA. Transposition of the tensor muscle requires raising an anterior soft tissue flap to the lever of the interval between the tensor muscle and sartorius, which is the same interval used in an anterior approach to the hip. The muscle is transected distally and transposed posteriorly to attach to the proximal femur. This can result in soft tissue redundancy between the posterior tensor muscle and anterior gluteus maximus. This interval is separated and the anterior gluteus maximis also attached to the proximal femur. Relatively large unconstrained (36 mm heads) were not found to be effective in controlling dislocation in patients with abductor deficiency. In our practice, 11 patients with abductor deficiency were treated with Whiteside's tensor muscle transfer and an unconstrained large diameter femoral head. The mean pre-operative abductor strength was 2.2 and improved to 3.2 post-operatively. One patient sustained a dislocation four weeks after surgery which was treated with open reduction. All of the other hips have remained stable. The combination of a large head and tensor muscle transposition may be a viable alternative to use of a fully constrained component in patients with deficient abductors after THA

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

Aim. In an earlier study we identified severe Vitamin D deficiency as a problem in institutionalised children with cerebral palsy (CP), which resulted in rickets and a high incidence of fractures. The purpose of this study was to establish whether a cohort of non-ambulatory children with CP, living at home, presented with Vitamin D deficiency. Method. The participants were a consecutive sample (N=100) of non-ambulatory children with CP attending a CP outpatient clinic. Their ages ranged from 2 to 15 years (mean 5.8, SD 3.3 years). There were 57 males and 43 females. Nineteen were on Level IV of the Gross Motor Function Classification System (GMFCS), and 81 were on Level V. 66% were on anticonvulsant therapy (ACT). Basic demographic data was collected, and measurements included blood sample analysis and wrist radiographs. There was radiographic evidence of osteopenia and delayed ossification of the carpal bones. Results. Three participants had Vitamin D deficiency rickets confirmed by wrist changes and serology. There was a significantly higher level of Alkaline Phosphatase (p=0.04) in children on ACT than in those who did not receive ACT. Preliminary results show that one third of the children had Vitamin D deficiency. Conclusion. Non ambulatory children with CP are at risk of developing rickets. We recommend regular exposure to sunlight or Vitamin D supplementation as preventative measures. NO DISCLOSURES