Searchable abstracts of presentations at key conferences on calcified tissues

ba0001pp434 | Osteoporosis: treatment | ECTS2013

Bone histology and histomorphometry: effects of 5 years of denosumab in the FREEDOM Extension

Brown Jacques P , Wagman Rachel , Dempster David W , Kendler David , Miller Paul , Bolognese Michael , Valter Ivo , Beck Jensen Jens-Erik , Zerbini Cristiano , Zanchetta Jose R , Daizadeh Nadia , Reid Ian

DMAb increases BMD and reduces bone resorption and risk of vertebral, nonvertebral and hip fractures in women with PMO. Transiliac crest bone biopsies in 47 subjects treated with DMAb for 1–3 years showed reduced bone turnover vs 45 Pbo-treated subjects, which reversed on treatment cessation. Since bone turnover reduction is sustained and fracture incidence low over 6 years’ DMAb treatment, we evaluated DMAb’s effects on tissue-level remodelling in the FREEDOM E...

ba0003pp357 | Osteoporosis: treatment | ECTS2014

In postmenopausal women previously treated with an oral bisphosphonate and at higher risk of fracture, denosumab significantly increases bone mineral density compared with ibandronate and risedronate

Brown Jacques P , Bolognese Michael A , Ho Pei-Ran , Roux Christian , Bone Henry G , Bonnick Sydney L , van den Bergh Joop , Ferreira Irene , Ghelani Prayashi , Dakin Paula , Wagman Rachel B , Recknor Christopher

Low bone mineral density (BMD) is an important and modifiable risk factor for fracture in postmenopausal women with osteoporosis. Denosumab (DMAb) shows a stronger relationship between BMD increases and antifracture efficacy than oral bisphosphonate (BP) therapies. Subjects who remain at higher risk of fracture despite current BP therapy need treatment. In two studies, DMAb significantly increased BMD and decreased bone turnover markers vs a BP (ibandronate (IBN) or risedronat...

ba0003w5.3 | The interactive extracellular matrix | ECTS2014

Skeletal genetic diseases involving matrix proteins

Briggs Michael

Skeletal diseases are a large and diverse group of rare monogenic phenotypes and there are more than 450 unique and well-characterised chondrodysplasia phenotypes that range in severity from relatively mild to severe and lethal forms. Studying these genetically tractable chondrodysplasia phenotypes provides insight into disease pathways that may be relevant to the more common and polygenic forms of OA.Pseudoachondroplasia (PSACH) and multiple epiphyseal ...

ba0005ht5 | (1) | ECTS2016

Superior Gains in Bone Mineral Density (BMD) and Estimated Strength at the Hip for Romosozumab Compared With Teriparatide (TPTD) in Women With Postmenopausal Osteoporosis Transitioning From Bisphosphonate Therapy: Results of the Phase 3 Open-label STRUCTURE Study

Langdahl B , Libanati C , Crittenden D B , Bolognese M A , Brown J P , Daizadeh N S , Dokoupilova E , Engelke K , Finkelstein J S , Genant H K , Goemaere S , Hyldstrup L , Jodar-Gimeno E , Keaveny T M , Kendler D , Lakatos P , Maddox J , Malouf J , Massari F E , Molina J F

STRUCTURE was a phase 3, open-label study evaluating the effect of romosozumab or TPTD for 12 months in women with postmenopausal osteoporosis transitioning from bisphosphonate therapy (NCT01796301). This study enrolled women with postmenopausal osteoporosis who had taken an oral bisphosphonate for ≥3 years prior to screening and alendronate in the year prior to screening; had a BMD T-score ≤−2.5 at the total hip (TH), lumbar spine (LS), or femoral neck (FN);...

ba0004is18 | (1) (1) | ICCBH2015

Management of sclerosing bone disease

Whyte Michael P

Many disorders cause osteosclerosis, and many exclusively affect adults. Pediatricians are likely to encounter those that are Mendelian diseases, with most still classified as ‘dysplasias’ although now understood at the gene level. Thus, there is promise for defining their molecular and biochemical pathogeneses, and for developing targeted medical treatments. Sclerosing bone dysplasias too have become the ‘turf’ of the metabolic bone disease specialist. How...

ba0004is18biog | (1) (1) | ICCBH2015

Management of sclerosing bone disease

Whyte Michael P

Biographical DetailsMichael P Whyte is Professor of Medicine, Pediatrics, and Genetics at the Washington University School of Medicine, a staff member of Barnes-Jewish Hospital and St. Louis Children’s Hospital, and Medical-Scientific Director at the Center for Metabolic Bone Disease and Molecular Research, Shriners Hospital for Children in St. Louis, Missouri, USA.<p class="abst...

ba0004oc8 | (1) | ICCBH2015

Combination sclerostin antibody and zoledronic acid treatment outperforms either treatment alone in a mouse model of osteogenesis imperfecta

Munns Craig , Peacock Lauren , Mikulec Kathy , Kneissel Michaela , Kramer Ina , Cheng Tegan , Schindeler Aaron , Little David

Introduction: Bisphosphonate treatment in children with osteogenesis imperfecta reduces bone catabolism and relies on modelling to form new bone. An anabolic treatment, anti-sclerostin antibody (Anti-SOST Ab), is being investigated in clinical trials. We hypothesized that combined treatment may produce superior outcomes in OI.Methods: Female Col1a2 G610C mice and their wild type littermates (WT) were treated from week 5 to week 9 of life with either sali...

ba0002p163 | (1) | ICCBH2013

Phenotype–genotype correlation and role of ancillary investigations in atypical and rare forms of osteogenesis imperfecta

Balasubramanian Meena , Parker Michael , Bishop Nicholas J

Background: Osteogenesis imperfecta (OI) is a heterogeneous group of inherited disorders of bone formation, resulting in low bone mass and an increased propensity to fracture. It is a variable condition with a range of clinical severity. About 90% of patients with a clinical diagnosis of OI have a mutation in the COL1A1 or COL1A2 genes, which shows an autosomal dominant pattern (AD) of inheritance. Other genes are associated with the autosomal recessive (AR) ...