In osteoporosis treatment, current interventions, including pharmaceutical treatments and exercise protocols, suffer from challenges of guaranteed efficacy for patients and poor patient compliance. Moreover, bone loss continues to be a complicating factor for conditions such as spinal cord injury, prescribed bed-rest, and space flight. A low-cost treatment modality could improve patient compliance. Electrical stimulation has been shown to improve bone mass in animal models of disuse, but there have been no studies of the effects of electrical stimulation on bone in the context of bone loss under hormone deficiency such as in post-menopausal osteoporosis. The purpose of this study was to explore the effects of electrical stimulation on changes in bone mass in the ovariectomized rat model of post-menopausal osteoporosis. All animal protocols were approved by the institutional Animal Research Ethics Board. We developed a custom electrical stimulation device capable of delivering a constant current, 15 Hz sinusoidal signal. We used 30 female Sprague Dawley rats (12–13 weeks old). Half (n=15) were ovariectomized (OVX), and half (n=15) underwent sham OVX surgery (SHAM). Three of each OVX and SHAM animals were sacrificed at baseline. The remaining 24 rats were separated into four equal groups (n=6 per group): OVX electrical stimulation (OVX-stim), OVX no stimulation (OVX-no stim), SHAM electrical stimulation (SHAM-stim), and SHAM no stimulation (SHAM-no stim). While anaesthetized, stimulation groups received transdermal electrical stimulation to the right knee through bilateral skin-mounted electrodes (10 × 10 mm) with electrode gel. The left knee served as a non-stimulated contralateral control. The no-stimulation groups had electrodes placed on the right knee, but not connected. Rats underwent the stim/no-stim procedure for one hour per day for six weeks. Rats were sacrificed (CO2) after six weeks. Femurs and tibias were scanned by microCT focussed on the proximal tibia and distal femur. MicroCT data were analyzed for trabecular bone measures of bone volume fraction (BV/TV), thickness (Tb.Th), and anisotropy, and cortical bone cross-sectional area and second moment of area. Femurs and tibias from OVX rats had significantly less trabecular bone than SHAM (femur BV/TV = −74.1%, tibia BV/TV = −77.6%). In the distal femur of OVX-stim rats, BV/TV was significantly greater in the stimulated right (11.4%, p < 0 .05) than the non-stimulated contralateral (left). BV/TV in the OVX-stim right femur also tended to be greater than that in the OVX-no-stim right femur, but the difference was not significant (17.7%, p=0.22). There were no differences between stim and no-stim groups for tibial trabecular measures, or cortical bone measures in either the femur or the tibia. This study presents novel findings that electrical stimulation can partially mitigate bone loss in the OVX rat femur, a model of human post-menopausal bone loss. Further work is needed to explore why there was a differential response of the tibial and femoral bone, and to better understand how bone cells respond to electrical stimulation. The long-term goal of this work is to determine if electrical stimulation could be used as a complementary modality for preventing post-menopausal bone loss

Background. Acromegaly, which stems from high level of serum growth hormone secreted by a benign tumour in the anterior pituitary gland, is likely to cause severe peripheral joint pains due to hypertrophic changes in such joints. Recently, the life expectancy of such patients has been improved and more patients with acromegaly have undergone joint surgeries to mitigate joint pain and malfunctions. However, little is known about to what extent surgical procedures can improve the joint functions of acromegalic patients compared to non-acromegalic cases. Methods. First, we qualitatively analysed prognosis of total hip arthroplasty (THA) of acromegalic patients by investigating 11 cases in which direct anterior approach (DAA) THAs were performed to 8 acromegalic patients in our hospital between 2012 and 2015. Second, we quantitatively compared the functional prognosis of the 11 cases with that of 107 non-acromegalic cases. Technically, to control the difference in age, sex, height, and weight between the two patient groups, we first identified a model that could predict 3month-/6month-/12month-functional prognosis in the control cases. We estimated differences in functional outcomes between the two groups by calculating how accurately the control-case-based model could predict the prognosis of the acromegalic cases. Results. In the qualitative analysis, we found that compared to the control, the most acromegalic cases had atypically advanced degenerative arthritides with osteophytes and enthesophytes proliferations. In addition, some cases showed other signs, such as flattering of femoral head and arthritis with slight osteophytes. Regarding surgical procedures, acromegalic cases were likely to require longer operation time and larger amounts of blood loss compared to the control. In the quantitative analysis, we first identified a model in which age and body height could predict the functional prognosis of DAA THA in the non-acromegalic cases (F[2,104] = 6.7, P = 0.0017). We then found that the actual functional outcomes of the acromegalic cases were not significantly different from those predicted by this control-case-based model (P = 0.18). Conclusions. The qualitative analysis shows the atypical joint structures and resultant prolonged operation time and blood loss in the acromegalic cases. However, the quantitative analysis could not find significant differences in prognosis between the acromegalic and non-acromegalic cases. Although these observations and analyses need to be examined in studies with large sample sizes, this work suggests that functional outcomes of DAA THA to acromegalic patients can be comparable to that to non-acromegalic patients

Aims

This study explored the shared genetic traits and molecular interactions between postmenopausal osteoporosis (POMP) and sarcopenia, both of which substantially degrade elderly health and quality of life. We hypothesized that these motor system diseases overlap in pathophysiology and regulatory mechanisms.

Introduction:. Blount's disease can be defined as idiopathic proximal tibial vara. Several etiologies including the mechanical theory have been described. Obesity is the only causative factor proven to be associated with Blount disease. Varus deformity is also a clinical feature of rickets and 31% of children with vitamin D deficiency rickets presented with varus deformities to the local Metabolic Bone clinics. The aim of this study is to assess if there is an association between vitamin D and Blount's disease. We hypothesize that children with Blount disease are more likely to be vitamin D deficient. Method:. This a retrospective study of pre-operative and post-operative patients with Blount's disease who were screened for vitamin D deficiency. Patients with known vitamin D deficiency and rickets were excluded. The study patients had the following blood tests: calcium, phosphate, alkaline phosphatase, parathyroid hormone and 25-hydroxyvitamin D. Body mass index (BMI) was also assessed. Results:. We recruited 50 patients. The mean age of these patients was 10.4 years (SD 3.88) with average BMI of 28.7 (SD 10.2). Fifty two % were overweight. Thirty (60%) patients were diagnosed with infantile, 16(32%) adolescent and 4(8%) juvenile Blount disease. Eight (16%) patients were found to be vitamin D depleted (less than 20 ng/ml). Of these eight patients, six had insufficient 25-hydroxyvitamin D levels (12–20 ng/ml) and while the other two were vitamin D deficient (less than 12 ng/ml). Conclusion:. Vitamin D deficiency is a public health problem worldwide. This study confirms that the prevalence of Vitamin D deficiency in children with Blount's disease is similar to healthy children and infants living in Johannesburg. There is no evidence that Vitamin D deficiency is a factor in causing Blount's disease. Routine screening for Vitamin D deficiency in children with Blount disease is not recommended

Purpose of the study. Fibromatosis is a benign, but locally aggressive tumour. We had a series of patients who had a high rate of recurrence though they had a wide surgical excision. The question raised was whether there are newer treatment modalities with a higher success rate. We did a retrospective study and review of the literature in order to see if there was anything new that can help us reduce recurrences. Materials and Methods. A retrospective study of all patients who presented with histologically confirmed fibromatosis at an orthopaedic practice in the past 19 years was conducted. Age of the patient at first presentation; sex; tumour site; surgery performed; histological results; first line of treatment and recurrence rate were reviewed. Patients were also contacted telephonically in order to know if they had any recurrence that was managed by another orthopaedic surgeon. Results. We evaluated 17 patients of which 8 were males and 9 females. The mean age was 25.87 years (range 2–52 years). All of the primary sites were extra abdominal. Median follow up was 3.9 years (0–9) with a mean recurrence rate of 2.3 times. All the patients were treated with a wide marginal surgical excision without adjuvant therapy. Conclusion. Fibromatosis has a high recurrence rate with our current treatment modalities. Complete surgical excision does not guarantee a good outcome. A wide variety of treatment modalities are available. Non-surgical treatment includes: hormonal therapies; NSAIDs; chemotherapy; and radiotherapy. Wide surgical excision is the mainstay of treatment but a multidisciplinary approach is necessary in order to optimize the efficacy of our treatment. Level of evidence: Level III. NO DISCLOSURES

Aims

Orthopaedic infection is a potentially serious complication of elective and emergency trauma and orthopaedic procedures, with a high associated burden of morbidity and cost. Optimization of vitamin D levels has been postulated to be beneficial in the prevention of orthopaedic infection. This study explores the role of vitamin D in orthopaedic infection through a systematic review of available evidence.

Estrogen fluctuations have been implicated in the soft tissue injury gender-bias due to the hormones effect on the viscoelastic properties. The isolated effect of estrogen on the mechanical behaviour of human tendon is unknown. The purpose of this study was to elucidate the effect of circulating levels of estrogen on the strain properties of the human Achilles tendon. Twenty females (18–35 years) who were using the pill together with 20 matched, non-pill users, participated in this study. Non-pill users were tested at the time of lowest (menstruation) and highest (ovulation) estrogen whilst pill users, who exhibited constant and attenuated estrogen levels, were tested at menstruation and two weeks later. At each test session, maximal isometric plantarflexion efforts were performed on a calf-raise apparatus whilst synchronous real-time ultrasonography of the triceps surae aponeurosis was recorded. Connective tissue length (Lo) of the triceps surae complex was measured and tendon strain was calculated by dividing aponeurosis displacement during plantarflexion by Lo. Repeated measures ANOVA revealed a significant (p < 0.05) main effect of subject group with significantly higher Achilles strain rates (16.1%) in the non-pill users compared to the pill users. Augmented Achilles tendon strain was associated with higher average estrogen levels in non-pill users. Those results suggest that higher estrogen levels diminish the joint stabilising capacity of the triceps surae musculotendinous unit and may alter the energy storage capacity of the Achilles tendon during stretch-shorten cycle activities. This may result in a higher incidence of injuries during periods of high estrogen concentration

The effect of head injury on systemic physiology, including bone healing is still a topic of vivid discussion. We aimed to investigate whether in patients with long bone fractures the presence of head injury is associated with excessive callus formation. Data on patients with head injury and femoral diaphyseal fracture admitted to our trauma unit between 1997- 2002 were collected and analysed. Patients with factors that could influence bone healing such as smoking, NSAIDs and hormonal disorders were excluded. The severity of head injury was quantified using GCS, AIS and CT scan reports. Patients matched for age, sex and ISS with femoral shaft fractures and no head injury formed the control group of the study. All the fractures were stabilised with reamed femoral nail. The quantification of fracture healing response was estimated by taking the radiological ratio of the largest diameter of callus formed into two planes and the adjacent normal diameter of femoral canal. The minimum follow-up of the patients was 12 months. In total 42 patients were studied, 17 with head injury and femoral fracture and 25 with an isolated femoral fracture, (control group). Both groups were comparable in terms of age, sex, ISS. The difference between the mean callus to diaphyseal ratio was statistically significant for both the AP and Lateral projections (AP – mean difference 0.462, 95% CI 0.312 to 0.602, p<0.0001, LAT – mean difference 0.289, 95% CI 0.142 to 0.436, p<0.001) with the head injured patients having more florid callus compared to the control group. This study supports the view that head injury leads to exuberant callus formation in patients with long bone fractures. The mechanisms of this response could be both central and local. Research is ongoing to elucidate the pathways involved in this biological phenomenon

Purpose. Up to 70% of the differences in human bone mass have been attributed to genetic background. These differences are associated with alterations in the biomechanical properties, micro-architecture and remodeling of bone as well as its susceptibility to fracture and its capacity for repair. In previous work it was shown that C57Bl6 mice carrying one copy of the parathyroid hormone related protein (PTHrP+/−) gene developed osteopenia by four months of age. The current study was designed to determine if the haploinsufficient phenotype was maintained on a C3H background. Method. PTHrP+/+ and PTHrP+/− mice on C57Bl6 and C3H backgrounds were euthanised between 6 and 18 months of age. The femurs were harvested, fixed in 4% paraformaldehyde overnight and scanned on a Skyscan 1172 equipped with a 10kV X-ray source and a 10 megapixel camera at a resolution 5μm. The amount and quality of cortical and trabecular bone was quantified from 2D images and 3D reconstructions using CTAn, CTvol and CTVox software. The undecalcified specimens were embedded at low temperature in MMA, sectioned at 5 μm and stained with Von Kossa and Toluidine Blue to distinguish mineralized from unmineralized tissue. Results. A novel application of CTAn was developed to automatically and consistently separate cortical from trabecular bone for high throughput, independent quantification. At all ages, PTHrP+/− mice on the C57Bl6 background had less trabecular bone, which was of poorer quality, than their wild type counterparts. In contrast, no difference was seen between PTHrP+/− and PTHrP+/+ mice on the C3H background at any age. No difference in cortical thickness was seen between PTHrP+/− and PTHrP+/+ mice on either background at any age, although the femoral cortices of the C3H mice were consistently thicker than those of the C57Bl6 mice. Conclusion. The osteopenic phenotype of young adult PTHrP+/− mice on a C57Bl6 background is lost when the mutation is bred onto a C3H background. This suggests that some other osteogenic agent can compensate for the lack of PTHrP during bone development in the C3H mice

Introduction. Problematic bone defects are encountered regularly in orthopaedic practice particularly in fracture non-union, revision hip and knee arthroplasty, following bone tumour excision and in spinal fusion surgery. At present the optimal source of graft to ‘fill’ these defects is autologous bone but this has significant drawbacks including harvest site morbidity and limited quantities. Bone marrow has been proposed as the main source of osteogenic stem cells for the tissue-engineered cell therapy approach to bone defect management. Such cells constitute a minute proportion of the total marrow cell population and their isolation and expansion is a time consuming and expensive strategy. In this study we investigated human bone marrow stem cells as a potential treatment of bone defect by looking at variability in patient osteogenic cell populations as a function of patient differences. We produced a model to predict which patients would be more suited to cell based therapies and propose possible methods for improving the quality of grafts. Methods. Bone marrow was harvested from 30 patients undergoing elective total hip replacement surgery in Musgrave Park Hospital, Belfast (12 males, 18 females, age range 52-82 years). The osteogenic stem cell fraction was cultured and subsequently analysed using colony forming efficiency assays, flow cytometry, fluorescence activated cell sorting and proteomics. Results. The number and proliferative capacity of osteogenic stem cells varied markedly between patients. Statistical analysis revealed significantly better osteogenic capacity in:. male patients. samples in which the growth hormone Fibroblastic Growth Factor-2 was added to culture medium. patients who used the cholesterol lowering agent simvastatin. Patient use of inhaled steroids and NSAIDs were found to have detrimental effects. A statistical model to predict marrow profiles based on these variables was produced. Conclusions. Stem cell based tissue engineering represents the future of the treatment of bone defect. This study provides evidence that inter-patient variability in marrow cell colony forming and proliferation ability can in some way be explained by patient associated factors. Using this knowledge, we can identify which patients would be best suited to this method of treatment and propose techniques for enhancement of their graft profiles

Introduction

Studies have addressed the issue of increasing prevalence of work-related musculoskeletal (MSK) pain among different occupations. However, contributing factors to MSK pain have not been fully investigated among orthopaedic surgeons. Thus, this study aimed to approximate the prevalence and predictors of MSK pain among Saudi orthopaedic surgeons working in Riyadh, Saudi Arabia.

Construction of a functional skeleton is accomplished through co-ordination of the developmental processes of chondrogenesis, osteogenesis, and synovial joint formation. Infants whose movement in utero is reduced or restricted and who subsequently suffer from joint dysplasia (including joint contractures) and thin hypo-mineralised bones, demonstrate that embryonic movement is crucial for appropriate skeletogenesis. This has been confirmed in mouse, chick, and zebrafish animal models, where reduced or eliminated movement consistently yields similar malformations and which provide the possibility of experimentation to uncover the precise disturbances and the mechanisms by which movement impacts molecular regulation. Molecular genetic studies have shown the important roles played by cell communication signalling pathways, namely Wnt, Hedgehog, and transforming growth factor-beta/bone morphogenetic protein. These pathways regulate cell behaviours such as proliferation and differentiation to control maturation of the skeletal elements, and are affected when movement is altered. Cell contacts to the extra-cellular matrix as well as the cytoskeleton offer a means of mechanotransduction which could integrate mechanical cues with genetic regulation. Indeed, expression of cytoskeletal genes has been shown to be affected by immobilisation. In addition to furthering our understanding of a fundamental aspect of cell control and differentiation during development, research in this area is applicable to the engineering of stable skeletal tissues from stem cells, which relies on an understanding of developmental mechanisms including genetic and physical criteria. A deeper understanding of how movement affects skeletogenesis therefore has broader implications for regenerative therapeutics for injury or disease, as well as for optimisation of physical therapy regimes for individuals affected by skeletal abnormalities.

Cite this article: Bone Joint Res 2015;4:105–116

Recent recommendations by the National Institute for Health and Care Excellence (NICE) suggest that all patients undergoing elective orthopaedic surgery should be assessed for the risk of venous thromboembolism (VTE).

Little is known about the incidence of symptomatic VTE after elective external fixation. We studied a consecutive series of adult patients who had undergone elective Ilizarov surgery without routine pharmacological prophylaxis to establish the incidence of symptomatic VTE.

A review of a prospectively maintained database of consecutive patients who were treated between October 1998 and February 2011 identified 457 frames in 442 adults whose mean age was 42.6 years (16.0 to 84.6). There were 425 lower limb and 32 upper limb frames. The mean duration of treatment was 25.7 weeks (1.6 to 85.3).

According to NICE guidelines all the patients had at least one risk factor for VTE, 246 had two, 172 had three and 31 had four or more.

One patient (0.23%) developed a pulmonary embolus after surgery and was later found to have an inherited thrombophilia. There were 27 deaths, all unrelated to VTE.

The cost of providing VTE prophylaxis according to NICE guidelines in this group of patients would be £89 493.40 (£195.80 per patient) even if the cheapest recommended medication was used.

The rate of symptomatic VTE after Ilizarov surgery was low despite using no pharmacological prophylaxis. This study leads us to question whether NICE guidelines are applicable to these patients.

Cite this article: Bone Joint J 2014;96-B:426–30.

Tendinopathy is a debilitating musculoskeletal condition which can cause significant pain and lead to complete rupture of the tendon, which often requires surgical repair. Due in part to the large spectrum of tendon pathologies, these disorders continue to be a clinical challenge. Animal models are often used in this field of research as they offer an attractive framework to examine the cascade of processes that occur throughout both tendon pathology and repair. This review discusses the structural, mechanical, and biological changes that occur throughout tendon pathology in animal models, as well as strategies for the improvement of tendon healing.

Cite this article: Bone Joint Res 2014;3:193–202.