Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK

Vienna, Austria

Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK

Vienna, Austria

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Al Kaissi A.,Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK | Al Kaissi A.,Orthopaedic Hospital of Speising | Ganger R.,Orthopaedic Hospital of Speising | Kenis V.,systemIC | And 3 more authors.
International Journal of Medical Sciences | Year: 2013

To further investigate the underlying pathology of axial and appendicular skeletal abnormalities such as painful spine stiffness, gait abnormalities, early onset osteoarthritis and patellar instability in patients with Stickler syndrome type I. Radiographic and tomographic analyses were organized. Methods: From a series of Stickler syndrome patients followed from early life to late childhood. Ten patients (6 boys and four girls of different ethnic origins were consistent with the diagnosis of Stickler syndrome type I).Phenotypic characterization was the baseline tool applied for all patients and genotypic correlation was performed on four families Results: A constellation of axial abnormalities namely; anterolateral ossification of the anterior longitudinal spinal ligament with subsequent fusion of two cervical vertebrae, early onset Forestier disease (progressive spinal hyperostosis with subsequent vertebral fusion on top of bridging osteophytes and "Bamboo-like spine" resembling ankylosing spondylitis) and severe premature spine degeneration were evident. Appendicular abnormalities in connection with generalized epiphyseal dysplasia were the underlying aetiology in patients with Intoeing gait and femoral anteversion, early onset severe osteoarthritis of the weight bearing joint. Remarkable trochleo-patellar dysplasia secondary to severe osteoarthritis causing effectively the development of patellar instability was additional pathology. Mutation of COL2A1 has been confirmed as the causative gene for Stickler syndrome type I Conclusion: We concluded that conventional radiographs and the molecular determination of a COL2A1 in patients with (Stickler syndrome type I) are insufficient tools to explain the reasons behind the tremendous magnitude of axial and appendicular skeletal abnormalities. We were able to modify the criteria of the clinical phenotype as designated by Rose et al in accordance with the novel axial and appendicular criteria as emerged from within our current study. © Ivyspring International Publisher.


Hofstetter B.,Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK | Gamsjaeger S.,Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK | Varga F.,Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK | Dobnig H.,Medical University of Graz | And 5 more authors.
Osteoporosis International | Year: 2014

Summary: The results of the present study, involving analysis of biopsies from patients who received teriparatide for 2 years and were previously either treatment-naïve or on long-term alendronate therapy, suggest that prior alendronate use does not blunt the favorable effects of teriparatide on bone quality.Introduction: Examine the effect of 2 years of teriparatide (TPTD) treatment on mineral and organic matrix properties of the newest formed bone in patients who were previously treatment-naïve (TN) or on long-term alendronate (ALN) therapy.Methods: Raman and Fourier transform infrared microspectroscopic analyses were used to determine the mineral/matrix (M/M) ratio, the relative proteoglycan (PG) content, and the mineral maturity/crystallinity (MMC; determined by three methods: carbonate content, full width at half height of the v1PO4 band [FWHH], and wavelength at maxima of the v1PO4 band), as well as collagen maturity (ratio of pyridinoline/divalent cross-links), in paired iliac crest biopsies at trabecular, endosteal, and osteonal surfaces of newly formed bone in postmenopausal osteoporotic women who were previously either TN (n = 16) or receiving long-term ALN treatment (n = 24).Results: Trabecular M/M ratio increased and matrix content decreased significantly in the ALN pretreated group. Collagen maturity decreased in both patient groups. Endosteal M/M ratio increased significantly in the TN group. Trabecular M/M ratio was higher at endpoint in the ALN pretreated group than in the TN group. Overall, no changes from baseline were observed in PG content, except that PG content was higher in the ALN pretreated group than in the TN group at endosteal surfaces at endpoint. The ability of TPTD treatment to reduce MMC in both patient groups and at the different bone surfaces depended on the measurement tool (relative carbonate content or wavelength at maxima of the v1PO4 band). None of the changes in MMC were different between the two patient groups.Conclusions: The results suggest some favorable impact of TPTD on bone mineral and organic matrix properties of in situ forming bone in terms of increased initial mineralization and decreased MMC and collagen maturity. Moreover, prior long-term ALN administration may have only limited influence on these properties in bone newly formed after 2 years of TPTD treatment. © 2014, International Osteoporosis Foundation and National Osteoporosis Foundation.


Rintelen B.,Lower Austrian State Hospital Stockerau | Rintelen B.,Karl Landsteiner Institute for Clinical Rheumatology | Zwerina J.,Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK | Herold M.,Innsbruck Medical University | And 9 more authors.
BMC Musculoskeletal Disorders | Year: 2016

Background: The purpose of the present study was to check the validity of data collected in BIOREG, the Austrian register for biological treatment in rheumatology, and to elucidate eventual differences with respect to disease activity (DA) in patients with rheumatoid arthritis (RA) on established biological DMARDs (bDMARDs) before inclusion into the register (EST) and beginners at the time point of inclusion (NEW) after 1 year of treatment. Methods: RA patients with a complete follow-up of 1 year in BIOREG were divided into EST and NEW and compared with respect to DA, remission rates, concomitant synthetic DMARDs (csDMARDs) and glucocorticoid therapy (GC) at baseline and after 1-year follow-up. Safety concerns are listed. Descriptive statistics are applied. Results: For 346 RA patients (284 EST, 62 NEW) out of 970 RA patients included into BIOREG, a full data set for a 1-year follow-up was available. No differences in DA were observed after 1 year as expressed by DAS28 or RADAI-5, and small differences as expressed by remission rates according to DAS28, RADAI-5 or Boolean criteria (namely approximately 1/2, 1/3 to 1/4 and 1/4 to 1/5 of the patients respectively). Sixty-four adverse events (AEs) were noted in 56 (20 %) of EST and 20 in 19 (31 %) of NEW patients. Malignancy occurred in four patients. After 1 year, 48 % of EST patients but only 16 % of NEW patients were on bDMARD monotherapy. Conclusion: Regarding DA, the date collected in BIOREG appeared to be valid. After 1 year of bDMARD therapy, all patients, whether EST or NEW, achieved a similar level of DA. AEs occurred more frequently during the early phase of bDMARD treatment. Austrian rheumatologists initiate bDMARD therapy in patients with lower disease levels than in other European countries, leading to high remission rates. © 2016 The Author(s).


Bidan C.M.,Max Planck Institute of Colloids and Interfaces | Kommareddy K.P.,Max Planck Institute of Colloids and Interfaces | Rumpler M.,Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK | Kollmannsberger P.,ETH Zurich | And 2 more authors.
Advanced Healthcare Materials | Year: 2013

Scaffolds for tissue engineering are usually designed to support cell viability with large adhesion surfaces and high permeability to nutrients and oxygen. Recent experiments support the idea that, in addition to surface roughness, elasticity and chemistry, the macroscopic geometry of the substrate also contributes to control the kinetics of tissue deposition. In this study, a previously proposed model for the behavior of osteoblasts on curved surfaces is used to predict the growth of bone matrix tissue in pores of different shapes. These predictions are compared to in vitro experiments with MC3T3-E1 pre-osteoblast cells cultivated in two-millimeter thick hydroxyapatite plates containing prismatic pores with square- or cross-shaped sections. The amount and shape of the tissue formed in the pores measured by phase contrast microscopy confirms the predictions of the model. In cross-shaped pores, the initial overall tissue deposition is twice as fast as in square-shaped pores. These results suggest that the optimization of pore shapes may improve the speed of ingrowth of bone tissue into porous scaffolds. Bone tissue growth depends on the local curvature of the substrate. A simple mathematical model predicts the observations of in vitro tissue growth inside convex and non-convex pores. Experiments show that tissue growth rates can be doubled by changing the geometry of a prismatic pore from square to cross-like. Methods based on these observations are proposed to optimize the design of porous scaffolds. © 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.


Zwerina K.,Friedrich - Alexander - University, Erlangen - Nuremberg | Koenders M.,Radboud University Nijmegen | Hueber A.,Friedrich - Alexander - University, Erlangen - Nuremberg | Hueber A.,University of Glasgow | And 10 more authors.
European Journal of Immunology | Year: 2012

Tumour necrosis factor alpha (TNF-α) is a major inducer for inflammation and bone loss. Here, we investigated whether interleukin (IL)-17 plays a role in TNF-α-mediated inflammation and bone resorption. Human TNF-α transgenic (hTNFtg) mice were treated with a neutralizing anti-IL-17A antibody and assessed for inflammation, cartilage and bone damage. T-cell transcription factors and lymphokine patterns were measured in the LNs. IL-17A inhibition in the absence of IL-1 was also evaluated by treating hTNFtg/IL-1 -/- mice with an IL-17A neutralizing antibody. IL-17A neutralization had only minor effects on TNF-α-induced inflammation but effectively reduced local and systemic bone loss by blocking osteoclast differentiation in vivo. Effects were based on a shift to bone-protective T-cell responses such as enhanced Th2 differentiation, IL-4 and IL-12 expression and Treg cell numbers. Whereas inflammation in hTNFtg/IL-1 -/- mice was highly sensitive to IL-17A blockade, no shift in the T-cell lineages and no additional benefit on bone mass were observed in response to IL-17A neutralization. We thus conclude that IL-17A is a key mediator of TNF-α-induced bone loss by closely interacting with IL-1 in blocking bone protective T-cell responses. © 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.


Timmen M.,University Hospital Muenster | Hidding H.,University Hospital Muenster | Wieskotter B.,University Hospital Muenster | Baum W.,Friedrich - Alexander - University, Erlangen - Nuremberg | And 5 more authors.
BMC Musculoskeletal Disorders | Year: 2014

Background: The overexpression of tumor necrosis factor (TNF)-α leads to systemic as well as local loss of bone and cartilage and is also an important regulator during fracture healing. In this study, we investigate how TNF-α inhibition using a targeted monoclonal antibody affects fracture healing in a TNF-α driven animal model of human rheumatoid arthritis (RA) and elucidate the question whether enduring the anti TNF-α therapy after trauma is beneficial or not. Methods. A standardized femur fracture was applied to wild type and human TNF-α transgenic mice (hTNFtg mice), which develop an RA-like chronic polyarthritis. hTNFtg animals were treated with anti-TNF antibody (Infliximab) during the fracture repair. Untreated animals served as controls. Fracture healing was evaluated after 14 and 28 days of treatment by clinical assessment, biomechanical testing and histomorphometry. Results: High levels of TNF-α influence fracture healing negatively, lead to reduced cartilage and more soft tissue in the callus as well as decreased biomechanical bone stability. Blocking TNF-α in hTNFtg mice lead to similar biomechanical and histomorphometrical properties as in wild type. Conclusions: High levels of TNF-α during chronic inflammation have a negative impact on fracture healing. Our data suggest that TNF-α inhibition by an anti-TNF antibody does not interfere with fracture healing. © 2014 Timmen et al.; licensee BioMed Central Ltd.


Gamsjaeger S.,Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK | Buchinger B.,Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK | Zoehrer R.,Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK | Phipps R.,Procter and Gamble | And 3 more authors.
Bone | Year: 2011

In the present work we examined the effect of teriparatide administration following bisphosphonate treatment on bone compositional properties by Raman and Fourier Transform Infrared Imaging (FTIR) microspectroscopic analysis. Thirty two paired iliac crest biopsies (before and after 1. year teriparatide) from sixteen osteoporotic women previously treated with either Alendronate (ALN) or Risedronate (RIS) and subsequently treated 12. months with teriparatide (TPTD) were analyzed at anatomical areas of similar tissue age in bone forming areas (within the fluorescent double labels). The outcomes that were monitored and reported were mineral to matrix ratio (corresponding to ash weight), mineral maturity (indicative of the mineral crystallite chemistry and stoichiometry, and having a direct bearing on crystallite shape and size), relative proteoglycan content (regulating mineralization commencement), and the ratio of two of the major enzymatic collagen cross-links (pyridinoline/divalent). Significant differences in mineral/matrix, mineral maturity/crystallinity, and collagen cross-link ratio bone quality indices after TPTD treatment were observed, indicating a specific response of these patients to TPTD treatment. Moreover differences between ALN and RIS treated patients at baseline in the collagen cross-link ratio were observed. Since tissue areas of similar tissue age were analyzed, these differences may not be attributed to differences in bone turnover. © 2011 Elsevier Inc.


PubMed | Ludwig Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK
Type: Journal Article | Journal: European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society | Year: 2011

The aim of the article is fourfold; firstly, to detect the aetiology of torticollis in patients with Mllerian duct/renal aplasia-cervicothoracic somite dysplasia syndrome; secondly, spine pathology in Mllerian duct/renal aplasia-cervicothoracic somite dysplasia syndrome varies considerably from one patient to another and there are remarkable differences in severity and localization; thirdly, mismanagement of congenital spine pathology is a frequent cause of morbid/fatal outcome; and fourthly, the application of prophylactic surgical treatment to balance the growth of the spine at an early stage is mandatory. Reformatted CT scans helped in exploring the craniocervical and the entire spine in these patients. The reason behind torticollis ranged between aplasia of the posterior arch of the atlas, assimilation of the atlas and extensive fusion of the lower cervical vertebrae (bilateral failure of segmentation) in four patients; in one patient, in addition to the hypoplastic posterior arch of the atlas, we observed ossification of the anterior and the posterior longitudinal spinal ligaments giving rise to a block vertebrae-like suggestive of early senile ankylosing vertebral hyperostosis (Forestier disease). Scoliosis at different spine levels was attributable to variable spine defects. Pelvic ultrasound showed the classical renal agenesis in four patients; whereas in one patient, the MRI showed pelvic cake kidney (renal fused ectopia) associated with ovarian, uterine and vaginal abnormalities. This is the first exploratory study on the craniocervical and the entire spine in a group of patients with MURCS association.

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