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In this written conversation, the staff of a small rural school embark on an exploration of their developing pedagogies. They consider some of the sources of their individual theories and practice, and show how they work together to challenge and support each other. They acknowledge the community of adults and children to which they belong and from which their pedagogy grows. They explore the nature of relationships within this community of learners and consider how they might describe the knowledge that teachers need and develop in the course of their work. Throughout the conversation runs the thread of trust and the part it plays in releasing adults and children to work at the furthest limits of possibility.

BackgroundThe aim was to describe the population of patients with moderate rheumatoid arthritis (RA) in the United Kingdom and the burden of disease from the perspectives of the patient, caregiver, and health service.MethodsIn this descriptive study, retrospective patient-level data were extracted from hospital medical records to assess healthcare resource utilisation and validated outcome measures were administered via questionnaire to patients with moderate RA (Disease Activity Score [DAS28] between 3.2 and 5.1) from eight secondary care centres, and their caregivers. Patient-reported outcome instruments were scored according to licensed manuals.ResultsOutcome measures were completed by 102 patients and 38 caregivers. The mean EuroQoL-5 dimension-5 level crosswalk index value for patients was 0.62 (SD 0.24) compared to an England population norm of 0.82. Mean pain VAS score was 37.7 (SD 24.0) and mean Health Assessment Questionnaire Disability Index was 1.1 (SD 0.8). In employed patients who completed the Work Productivity and Activity Impairment questionnaire (n = 26), a mean 29% (SD 26%) reduction in work productivity was recorded. Patients experienced significant fatigue as a result of their RA (median Functional Assessment of Chronic Illness Therapy fatigue score 17.2 of a possible 52, interquartile range [IQR] 11.0–28.8). Over 50% of caregivers reported providing > 7 h of support care per week to the patient with RA, and 16 and 11% took paid/unpaid leave or reduced working hours, respectively. Mean Caregiver Reaction Assessment subscale scores were 1.9 (SD 0.9) for finance, 1.7 (SD 0.8) for health, 2.3 (SD 1.0) for schedule disruption, and 1.9 (SD 0.8) for family support. Patients had a mean 5.5 (SD 4.1) outpatient attendances and a median 9.0 (IQR 2.0–20.0) diagnostic and monitoring tests in the 12 months prior to enrolment.ConclusionsThis study shows that moderate RA has a considerable impact on healthcare resources and on patients’ and caregivers’ lives. There is scope to improve the management of patients with moderate RA.

Introduction Giant cell arteritis (GCA) is the most common form of vasculitis in adults with visual complications, in particular loss of vision, constituting the most feared manifestation. Tocilizumab (TCZ), an IL-6 receptor blocker, has been shown to induce lasting remission. However, the optimal duration of treatment with tocilizumab and risk of relapse once treatment is stopped, is currently unknown. We present an unusual case of a patient with GCA who developed visual loss after stopping a three year course of tocilizumab for surgical indications. Case description A 73-year-old lady presented to her GP in 2011 with headache and lower limb stiffness. At that time CRP was greater than 200 and ESR was 126. The GP commenced her on high dose prednisolone with an excellent response. A temporal artery biopsy was not done. She was then referred 14 months later to the rheumatology clinic due to bilateral hip pain and difficulty weaning off steroids, with an increase in inflammatory markers and return of symptoms, upon dose reduction. She was still on 30mg prednisolone at the time of referral. Methotrexate was introduced as a steroid sparing agent, but was stopped a few months later due to side effects. In 2012, while on prednisolone, she developed avascular necrosis of both hips requiring bilateral total hip replacements. An IFR was granted to start TCZ in 2014. She remained well on it with good clinical and serological response and eventually came off steroids completely in 2016. In July 2017, TCZ was stopped for aortic valve replacement for 4 months. This was then restarted at the beginning of December 2017. In February 2018, she developed frontal headaches and PMR-like symptoms. CRP was 2 and ESR 27 at this time. She was commenced on 15 mg daily of prednisolone and TCZ was continued at 8mg/kg. Unfortunately, a few days after her TCZ infusion, she was admitted to hospital with anterior ischaemic optic neuropathy (AION) in the left eye, resulting in partial blindness. Inflammatory markers were found to be completely normal. Intravenous methyl prednisolone was commenced. The patient was referred to a tertiary referral centre and TCZ 162 mg subcutaneously weekly was commenced in combination with leflunomide while tapering the dose of prednisolone. She is currently well with no new visual symptoms. Discussion This is an unusual case as the patient developed AION whilst on 15 mg of prednisolone following cessation and then re-institution of tocilizumab. The GiACTA trial showed that treatment with TCZ, while extremely efficacious, did not prevent disease flares in all patients, with 24% of patients in TCZ groups experiencing at least 1 or more disease flares. The trial proposed that the flares might be attributable to Th-1 cells, which are not affected directly by IL-6 receptor blockade, and may play an important role in some patients with GCA. Recently, the long-term safety and maintenance of efficacy in GCA patients was assessed in a 2-year extension of the GiACTA trial. Among the 81 patients in the once weekly TCZ arm, who were in clinical remission at week 52, 38 (47%) maintained clinical remission through part 2. However, only 25 of these 38 patients (66%) were treatment-free (no TCZ and no glucocorticoid treatment) at the end of the trial. Similarly, the risk of relapse after discontinuation of TCZ in GCA was assessed in a study by Adler et al. 17 of 20 patients randomised to the TCZ treatment arm were in remission after 12 months. Only half stayed in clinical remission after cessation of TCZ. No clinical or laboratory marker was found to be a reliable predictor of relapse. These two studies show that the odds of relapse after discontinuation are very high, as seen in our case. Furthermore, Adler et al reported that the mean time to relapse was 6.3 months. This shows that the risk of relapse is highest in the first few months, as is the case in our patient. Key learning points The optimal strategies for monitoring disease progress in GCA remain uncertain, and currently rely on assessing clinical features and measuring inflammatory markers. However, this has become even more challenging with the use of TCZ, which suppresses the acute phase response via IL-6 receptor blockade. CRP and ESR remain low in nearly all TCZ-treated patients who experience disease flares. This underlines the importance of clinical assessment, particularly poignant history-taking and clinical experience in assessing whether GCA activity might be present. Clinicians should have a very low threshold for suspecting a flare-up, as even the mildest of symptoms could be a harbinger of a full blown flare. As discussed above, studies have shown that effectively half the patients relapse after TCZ is discontinued and most do so within the first few months. This emphasizes the need for careful clinical observation during this time and immediate resumption of treatment in those with new symptoms. Furthermore, it raises the possibility that patients may need to be on TCZ long term and in certain cases indefinitely, given the very high risk of recurrence once the patient is off the drug. Further research and deeper understanding is needed of the pathways that lead to a flare of GCA while on optimal treatment. Finally, this case underscores the dire need for advances in the development of clinically useful biomarkers to help monitor disease activity and predict relapses in patients on TCZ. This case brings to light the fact that AION is possible following cessation and re-institution of tocilizumab. It is axiomatic that clinicians keep a close eye on patients stopping TCZ after the NICE guideline 12 month recommended course. Conflict of interest The authors declare no conflicts of interest.

Studies in childhood suggest that both body composition and early postnatal growth are associated with bone mineral density (BMD). However, little is known of the relationships between longitudinal changes in fat (FM) and lean mass (LM) and bone development in pre-pubertal children. We therefore investigated these associations in a population-based mother-offspring cohort, the Southampton Women's Survey.Total FM and LM were assessed at birth and 6-7 years of age by dual-energy x-ray absorptiometry (DXA). At 6-7 years, total cross-sectional area (CSA) and trabecular volumetric BMD (vBMD) at the 4% site (metaphysis) of the tibia was assessed using peripheral quantitative computed tomography [pQCT (Stratec XCT-2000)]. Total CSA, cortical CSA, cortical vBMD and strength-strain index (SSI) were measured at the 38% site (diaphysis). FM, LM and bone parameters were adjusted for age and sex and standardised to create within-cohort z-scores. Change in LM (ΔLM) or FM (ΔFM) was represented by change in z-score from birth to 7 years old and conditioned on the birth measurement. Linear regression was used to explore the associations between ΔLM or ΔFM and standardised pQCT outcomes, before and after mutual adjustment and for linear growth. The β-coefficient represents SD change in outcome per unit SD change in predictor.DXA at birth, in addition to both DXA and pQCT scans at 6-7 years, were available for 200 children (48.5% male). ΔLM adjusted for ΔFM was positively associated with tibial total CSA at both the 4% (β=0.57SD/SD, p0.001) and 38% sites (β=0.53SD/SD, p0.001), cortical CSA (β=0.48SD/SD, p0.001) and trabecular vBMD (β=0.30SD/SD, p0.001), but not with cortical vBMD. These relationships persisted after adjustment for linear growth. In contrast, ΔFM adjusted for ΔLM was only associated with 38% total and cortical CSA, which became non-significant after adjustment for linear growth.In this study, gain in childhood LM was positively associated with bone size and trabecular vBMD at 6-7 years of age. In contrast, no relationships between change in FM and bone were observed, suggesting that muscle growth, rather than accrual of fat mass, may be a more important determinant of childhood bone development.

Osteoporosis constitutes a major public health problem through its association with age-related fractures, most notably those of the proximal femur. Substantial geographic variation has been noted in the incidence of hip fracture throughout the world, and estimates of recent incidence trends have varied widely; studies in the published literature have reported an increase, plateau, and decrease, in age-adjusted incidence rates for hip fracture among both men and women. Accurate characterisation of these temporal trends is important in predicting the health care burden attributable to hip fracture in future decades. We therefore conducted a review of studies worldwide, addressing secular trends in the incidence of hip and other fractures. Studies in western populations, whether in North America, Europe or Oceania, have generally reported increases in hip fracture incidence through the second half of the last century, but those continuing to follow trends over the last two decades have found that rates stabilise, with age-adjusted decreases being observed in certain centres. In contrast, some studies suggest that the rate is rising in Asia. This synthesis of temporal trends in the published literature will provide an important resource for preventing fractures; understanding the reasons for the recent declines in rates of hip fracture may help understand ways to reduce rates of hip fracture worldwide.

Background: intrauterine life may be a critical period for the programming of later obesity, but there is conflicting evidence about whether pregnancy weight gain is an important determinant of offspring adiposity. Objective: the purpose of this study was to examine the relation of pregnancy weight gain with neonatal and childhood body composition. Design: the participants (n = 948) were children born to women in the Southampton Women's Survey who had dual-energy X-ray absorptiometry measurements of body composition at birth, 4 y, or 6 y. Pregnancy weight gain was derived from the mothers’ measured weights before pregnancy and at 34 wk gestation and analyzed by using 2009 Institute of Medicine categories (inadequate, adequate, or excessive) and as a continuous measure. Results: almost one-half (49%) of the children were born to women who gained excessive weight in pregnancy. In comparison with children born to women with adequate weight gain, they had a greater fat mass in the neonatal period (SD: 0.17; 95% CI: 0.02, 0.32; P = 0.03), at 4 y (SD: 0.17; 95% CI: 0.00, 0.34; P = 0.05), and at 6 y (SD: 0.30; 95% CI: 0.11, 0.49; P = 0.002). Greater pregnancy weight gain, as a continuous measure, was associated with greater neonatal fat mass (SD: 0.10 per 5-kg weight gain; 95% CI: 0.04, 0.15; P = 0.0004) and was weakly associated with fat mass at 6 y (SD: 0.07 per 5-kg weight gain; 95% CI: 0.00, 0.14; P = 0.05) but not at 4 y (SD: 0.02 per 5-kg weight gain; 95% CI: –0.04, 0.08; P = 0.55). Conclusion: appropriate pregnancy weight gain, as defined by 2009 Institute of Medicine recommendations, is linked to lower levels of adiposity in the offspring

Osteoporosis is a skeletal disorder characterized by low bone mass and micro-architectural deterioration of bone tissue with a consequent increase in bone fragility and susceptibility to fracture. Evidence is now accumulating from human studies that programming of bone growth might be an important contributor to the later risk of osteoporotic fracture. Body weight in infancy is a determinant of adult bone mineral content, as well as of the basal levels of activity of the growth hormone/insulin-like growth factor-1 (GH/IGF-1) and hypothalamo-pituitary-adrenal (HPA) axes, and recent work has suggested a central role for vitamin D. Epidemiological studies have shown that maternal smoking and nutrition during pregnancy influence intrauterine skeletal mineralization. Childhood growth rates have been directly linked to the risk of hip fracture many decades later, and now evidence is emerging from experimental animal studies that support these observational data. Recent studies have also highlighted epigenetic phenomena as potential mechanisms underlying the findings from epidemiological studies.

Osteoporosis is a major cause of morbidity and mortality through its association with age-related fractures. Although most effort in fracture prevention has been directed at retarding the rate of age-related bone loss, and reducing the frequency and severity of trauma among elderly people, evidence is growing that peak bone mass is an important contributor to bone strength during later life. The normal patterns of skeletal growth have been well characterised in cross-sectional and longitudinal studies. It has been confirmed that boys have higher bone mineral content, but not volumetric bone density, than girls. Furthermore, there is a dissociation between the peak velocities for height gain and bone mineral accrual in both genders. Puberty is the period during which volumetric density appears to increase in both axial and appendicular sites. Many factors influence the accumulation of bone mineral during childhood and adolescence, including heredity, gender, diet, physical activity, endocrine status, and sporadic risk factors such as cigarette smoking. In addition to these modifiable factors during childhood, evidence has also accrued that fracture risk might be programmed during intrauterine life. Epidemiological studies have demonstrated a relationship between birthweight, weight in infancy, and adult bone mass. This appears to be mediated through modulation of the set-point for basal activity of pituitary-dependent endocrine systems such as the hypothalamic-pituitary-adrenal (HPA) and growth hormone/insulin-like growth factor-1 (GH/IGF-1) axes. Maternal smoking, diet (particularly vitamin D deficiency) and physical activity also appear to modulate bone mineral acquisition during intrauterine life; furthermore, both low birth size and poor childhood growth, are directly linked to the later risk of hip fracture. The optimisation of maternal nutrition and intrauterine growth should also be included within preventive strategies against osteoporotic fracture, albeit for future generations.

Osteoporosis constitutes a major public health problem through its association with age related fractures. Fracture rates are generally higher in caucasian women than in other populations. Important determinants include estrogen deficiency in women, low body mass index, cigarette smoking, alcohol consumption, poor dietary calcium intake, physical inactivity, certain drugs and illnesses. Thus, modification of physical activity and dietary calcium/vitamin D nutrition should complement high risk approaches. In addition, the recently developed WHO algorithm for evaluation of 10-year absolute risk of fracture provides a means whereby various therapies can be targeted cost-effectively to those at risk. Risk factors, together with bone mineral density (BMD) and biochemical indices of bone turnover, can be utilised to derive absolute risks of fracture and cost-utility thresholds at which treatment is justified. These data will provide the basis for translation into coherent public health strategies aiming to prevent osteoporosis both in individuals and in the general population.

We have previously demonstrated associations between fetal growth in late pregnancy and postnatal bone mass. However, the relationships between the intrauterine and early postnatal skeletal growth trajectory remain unknown. We addressed this in a large population-based mother-offspring cohort study. A total of 628 mother-offspring pairs were recruited from the Southampton Women's Survey. Fetal abdominal circumference was measured at 11, 19 and 34 weeks gestation using high-resolution ultrasound with femur length assessed at 19 and 34 weeks. Bone mineral content was measured postnatally in the offspring using dual-energy X-ray absorptiometry at birth and 4 years; postnatal linear growth was assessed at birth, 6, 12, 24, 36 and 48 months. Late pregnancy abdominal circumference growth (19-34 weeks) was strongly (P < 0.01) related to bone mass at birth, but less robustly associated with bone mass at 4 years. Early pregnancy growth (11-19 weeks) was more strongly related to bone mass at 4 years than at birth. Postnatal relationships between growth and skeletal indices at 4 years were stronger for the first and second postnatal years, than the period aged 2-4 years. The proportion of children changing their place in the distribution of growth velocities progressively reduced with each year of postnatal life. The late intrauterine growth trajectory is a better predictor of skeletal growth and mineralisation at birth, while the early intrauterine growth trajectory is a more powerful determinant of skeletal status at age 4 years. The perturbations in this trajectory which influence childhood bone mass warrant further research.

Osteoporosis-related fractures have a major impact on health at the individual and societal levels, through associated morbidity and increased mortality. Up to 50% of women and 20% of men at age 50 years may have a fragility fracture in their remaining lifetimes. Nutrition is important throughout the life course. Thus, adequate Ca and vitamin D intake has been shown to reduce risk of fracture in old age. Other factors such as protein and vitamin K may also be important, although the evidence here is less strong. In childhood Ca or vitamin D supplementation trials have demonstrated modest short-term increases in bone mass, but the long-term implications have not been established. Over recent years it has become apparent that maternal nutrition may have critical and far-reaching persistent consequences for offspring health. Thus, reduced maternal fat stores and low levels of circulating 25-hydroxyvitamin D in pregnancy are associated with reduced bone mass in the offspring; placental Ca transport may be key to these relationships. Wider maternal dietary patterns have also been shown to predict offspring bone mass. These data suggest that an interventional approach aimed at specific micronutrients, such as vitamin D, should be complemented by general optimisation of the mother's diet and lifestyle in order to maximise intrauterine bone mineral accrual and postnatal skeletal growth and thus reduce the burden of osteoporotic fractures in future generations.

Maternal nutrition is a potentially important determinant of intrauterine skeletal development. Previous studies have examined the effects of individual nutrients, but the pattern of food consumption may be of greater relevance. We therefore examined the relationship between maternal dietary pattern during pregnancy and bone mass of the offspring at 9 yr of age. We studied 198 pregnant women 17-43 yr of age and their offspring at 9 yr of age. Dietary pattern was assessed using principal component analysis from a validated food frequency questionnaire. The offspring underwent measurements of bone mass using DXA at 9 yr of age. A high prudent diet score was characterized by elevated intakes of fruit, vegetables, and wholemeal bread, rice, and pasta and low intakes of processed foods. Higher prudent diet score in late pregnancy was associated with greater (p < 0.001) whole body and lumbar spine BMC and areal BMD in the offspring, after adjustment for sex, socioeconomic status, height, arm circumference, maternal smoking, and vitamin D status. Associations with prudent diet score in early pregnancy were weaker and nonsignificant. We conclude that dietary patterns consistent with current advice for healthy eating during pregnancy are associated with greater bone size and BMD in the offspring at 9 yr of age.

PURPOSE OF REVIEW: Osteoporosis remains a major public health problem through its association with fragility fractures. Recent data suggest that the annual cost in Europe is 13 billion euros, mainly accounted for by hospitalisation after fracture. Understanding the epidemiology of osteoporosis is an essential step in developing strategies to reduce the burden of osteoporotic fracture in the population. RECENT FINDINGS: This article will review recent advances surrounding the epidemiology of osteoporosis, the burden of fracture in children and adults in this country and abroad, morbidity associated with such fractures, associations of disease and medication with fragility fracture, and advances in diagnostic techniques and identification of at-risk groups. SUMMARY: The papers studied highlight the wealth of high-quality research in this field, and they help in the visualisation of strategies to identify individuals at high risk of fragility fracture and to quantify fracture risk by measurement of bone density, bone quality, and risk factor algorithms.

1. This study examines the relative contributions made by inhibition of mast cell degranulation, reduction of mast cell recruitment and maturation, and lowering the responsiveness of the vasculature to histamine, in the inhibition by glucocorticoids of the weal and flare in human skin. 2. One forearm of healthy human volunteers was treated for 24 h (n=6) or daily for 21 days (n=10) with 0.05% clobetasol propionate. The other arm served as control. Weal and flare responses were elicited by intradermal injection of 20 microl of 0.3 mM codeine. The areas of the responses were measured using scanning laser Doppler imaging. Microdialysis was used to assess histamine release. Mast cell numbers and tissue histamine content were assessed in 4-mm punch biopsies. Histamine (20 microl of 1 microM i.d.) was used to assess the status of the vasculature. 3. No significant effects were seen at 24 h. At 21 days, clobetasol reduced the areas of the codeine-induced weal and flare responses by 59 and 58% respectively (both P=0.006). Mast cell numbers were reduced by 47%, (P=0.014) and total tissue histamine content by 52% (P=0.006). Codeine-induced histamine release was reduced by 44% (P=0.022). The weal, but not the flare, induced by histamine was significantly inhibited (P=0.019). Echography revealed a 15% thinning of the skin by clobetasol. 4. These results demonstrate that reduction of the weal and flare responses to codeine following clobetasol treatment, results primarily from reduced mast cell numbers and tissue histamine content rather than inhibition by corticosteroids of mast cell degranulation.

BACKGROUND: We investigated relationships between early growth and proximal femoral geometry at age 6 y in a prospective population-based cohort, the Southampton Women's Survey. METHODS: In 493 mother-offspring pairs, we assessed linear size using high-resolution ultrasound at 11, 19, and 34 wk gestation (femur length) and at birth and 1, 2, 3, 4, and 6 y (crown-heel length/height). SD scores were created and conditional regression modeling generated mutually independent growth variables. Children underwent hip dual-energy X-ray absorptiometry (DXA) at 6 y; hip structure analysis software yielded measures of geometry and strength. RESULTS: There were strong associations between early linear growth and femoral neck section modulus (Z) at 6 y, with the strongest relationships observed for femur growth from 19 to 34 wk gestation (β = 0.26 cm(3)/SD, P < 0.0001), and for height growth from birth to 1 y (β = 0.25 cm(3)/SD, P < 0.0001) and 1 to 2 y (β = 0.33 cm(3)/SD, P < 0.0001), with progressively weaker relationships over years 3 (β = 0.23 cm(3)/SD, P = 0.0002) and 4 (β = 0.10 cm(3)/SD, P = 0.18). CONCLUSION: These results demonstrate that growth before age 3 y predicts proximal femoral geometry at 6 y old. These data suggest critical periods in which there is capacity for long-term influence on the later skeletal growth trajectory.

UNLABELLED: In a free-living cohort of 4-year old children, mean daily time in moderate-vigorous physical activity and daily calcium intake at 3 years, were positively related to hip bone size and density. Relationships between physical activity and bone indices were stronger when calcium intake was above compared with below median (966 mg/day). INTRODUCTION: We examined the cross-sectional relationships between childhood physical activity, dietary calcium intake and bone size and density. METHODS: Children aged 4 years were recruited from the Southampton Women's Survey. They underwent measurement of bone mass by DXA (Hologic Discovery). Physical activity was assessed by accelerometry (Actiheart, Cambridge Neurotechnology Ltd, Cambridge, UK) for seven continuous days. RESULTS: Four hundred twenty-two children (212 boys) participated. In a cross-sectional analysis, after adjusting for gender, daily mean time(minutes per day) spent in moderate to very vigorous activity (MVPA) was positively related to hip BA (R(2) = 3%, p < 0.001), BMC (R(2) = 4%, p < 0.001), aBMD (R (2) = 3%, p = 0.001) and estimated vBMD (R(2) = 2%, p = 0.01), but not height (r (s) = 0.04, p = 0.42) or weight (r(s) = 0.01, p = 0.76). Mean daily calcium intake (assessed at 3 years old) positively predicted bone indices in those with a calcium intake below the median (966 mg/day), but there was a much attenuated relationship in those above this. These associations persisted after inclusion of total energy, protein and phosphorus in multivariate models. The relationships between MVPA and bone indices were stronger in children with calcium intakes above the median. Thus, for aBMD, the variance explained by MVPA when daily calcium intake was below the median was 2% (p = 0.1) and above median was 6% (p = 0.001). CONCLUSIONS: These results support the notion that adequate calcium intake may be required for optimal action of physical activity on bone development and that improving levels of physical activity and calcium intake in childhood may help to optimise accrual of bone mass.

Osteoporosis is a major cause of morbidity and mortality through its association with age-related fractures. Although most effort in fracture prevention has been directed at retarding the rate of age-related bone loss, and reducing the frequency and severity of trauma among elderly people, evidence is growing that peak bone mass is an important contributor to bone strength during later life. The normal patterns of skeletal growth have been well characterised in cross-sectional and longitudinal studies. It has been confirmed that boys have higher bone mineral content, but not volumetric bone density, than girls. Furthermore, there is a dissociation between the peak velocities for height gain and bone mineral accrual in both genders. Puberty is the period during which volumetric density appears to increase in both axial and appendicular sites. Many factors influence the accumulation of bone mineral during childhood and adolescence, including heredity, gender, diet, physical activity, endocrine status, and sporadic risk factors such as cigarette smoking. In addition to these modifiable factors during childhood, evidence has also accrued that fracture risk might be programmed during intrauterine life. Epidemiological studies have demonstrated a relationship between birthweight, weight in infancy, and adult bone mass. This appears to be mediated through modulation of the set-point for basal activity of pituitary-dependent endocrine systems such as the hypothalamic-pituitary-adrenal (HPA) and growth hormone/insulin-like growth factor-1 (GH/IGF-1) axes. Maternal smoking, diet (particularly vitamin D deficiency) and physical activity also appear to modulate bone mineral acquisition during intrauterine life; furthermore, both low birth size and poor childhood growth, are directly linked to the later risk of hip fracture. The optimisation of maternal nutrition and intrauterine growth should also be included within preventive strategies against osteoporotic fracture, albeit for future generations.

Background: Osteoporosis has a huge impact on public health, through the increased morbidity, mortality and economic costs associated with resultant fractures. The goal is to evaluate and identify those that are at risk of osteoporotic fracture in order to start preventative and therapeutic measures to reduce their risk of fracture. Sources of data: This article reviews the data from randomized controlled trials for the current therapeutic agents available in the UK. It also reviews new trial data for promising osteoporosis therapies, in particular Denosumab, a monoclonal antibody against RANK ligand. Areas of agreement: Bisphosphonates are the current recommended first-line treatments for patients with osteoporosis. Areas of controversy/growing points: There are a number of patients where bisphosphonates are contraindicated. Under these circumstances, it is important that clinicians have access to alternative treatments. The long-awaited National Institute for Health and Clinical Excellence (NICE) technology appraisals for both primary and secondary prevention and the clinical guidelines will clarify this. Treatment decisions should be based on risk factors and pharmaceutical intervention given to those with the highest risks. Areas timely for developing research: Future studies are required to look at these agents in combination to see whether anti-fracture efficacy can be improved

Background Rheumatoid arthritis (RA) is a chronic disease that causes significant disability impacts health related quality of life and is a major economic burden. Many studies have shown RA to be associated with absenteeism, job loss, and impairment in work productivity. Biologic therapies have improved the management of RA through marked reductions in the manifestations of RA and improvement of function. Objectives A cross sectional survey was carried out using our biologics database to evaluate the impact of biologics on employment in a cohort of patients with Rheumatoid arthritis. Methods A patient-self-reported questionnaire was developed in conjuction with a patient expert group to assess the work status at the onset of their disease, onset of biological treatment and current work status. Time from diagnosis to first biologic was evaluated, as was smoking status. Patients were also asked about the current impact of RA on their life and how biologic therapy had improved their arthritis. Patients were randomly chosen to receive this questionaire. Results Of the 100 questionnaires distributed, 93 were completed and returned. 27% were male, and 22.5% were current smokers. The mean time from diagnosis to first biologic was 8 years. At diagnosis, 46% were in full-time employment, 26% part-time employment, 15% were retired, and 10% were unable to work due to rheumatoid arthritis or other medical condition. At the start of biologic therapy, 29% were in full time employment, 19% in part time employment, 28% were retired, and 21.5% were unable to work due to RA. At present, 29% remain in full time employment, 23% in part time employment, 31% retired, and only 13% were unable to work due to RA. 53% reported that their arthritis was much better since starting their biologic, and 38% said their arthritis was better. Patients in full time employment had a shorter time before first biologic (mean 6 years), patients unable to work due to their arthritis had a longer time to their first biologic (10.1 years). Conclusions Patients with RA who received biologic therapy remained in full or part time employment and the number of patients unable to work was reduced. Patient satisfaction with their health state also improved with biologic therapy. Earlier biologic therapy improves their ability to retain employment. Disclosure of Interest None declared DOI 10.1136/annrheumdis-2014-eular.1877