Detail

Keywords

Arthritis, Experimental; Bone Diseases; Inflammation

Research interests

 My major research interest focuses on the identification of pathophysiological mechanisms involved in inflammatory and degenerative bone as well as cartilage damage like in patients suffering from rheumatoid arthritis or osteoarthritis.  The contributing role of various inflammatory cells, cytokines or other mediators on joint and bone pathobiology are elucidated by the use of genetically modified mice or administration of therapeutic compounds in experimental models of muskuloskeletal disorders. For translational aspects, studies are also evaluated using human synovial tissue, joint or blood-derived cells from patients with musculoskeletal diseases.

Techniques, methods & infrastructure

Experimental models of musculoskeletal disorders (human tumor necrosis factor transgenic mice, collagen-induced arthritis, serum transfer arthritis, ovarectomy-induced osteoporosis, age-related disorders,…), in vivo assessment of clinical signs and gait analysis, in vivo imaging, organ preparation, blood collection,  ex vivo µCT bone analysis of structural bone damage and systemic bone mass, histology (conventional stainings, immunohistochemistry), quantification of regions and cells of interest on histological sections (Osteomeasure software), in vitro primary cell cultures and differentiation assays (bone resorbing osteoclasts, bone forming osteoblasts, synovial fibroblast,…), bone resorption assays,  standard molecular biology  assays for transcriptomic and proteomic studies; signaling transduction pathways (MAPKinases, JAK/STAT, Syk,…).

Selected publications

1. Hayer, S. et al. (2021) ‘“SMASH” recommendations for standardised microscopic arthritis scoring of histological sections from inflammatory arthritis animal models’, Annals of the Rheumatic Diseases, 80(6), pp. 714–726. Available at: http://dx.doi.org/10.1136/annrheumdis-2020-219247.
2. Hayer, S. et al. (2019) ‘Multimodal [ 18 F]FDG PET/CT Is a Direct Readout for Inflammatory Bone Repair: A Longitudinal Study in TNFα Transgenic Mice’, Journal of Bone and Mineral Research, 34(9), pp. 1632–1645. Available at: http://dx.doi.org/10.1002/jbmr.3748.
3. Hayer, S. et al. (2016) ‘Preservation of cartilage and bone architecture is the most important aspect for maintaining functionality in longstanding experimental arthritis’, Disease Models & Mechanisms [Preprint]. Available at: http://dx.doi.org/10.1242/dmm.025460.
4. Hayer, S. et al. (2010) ‘Interleukin 6 is not a crucial regulator in an animal model of tumour necrosis factor-mediated bilateral sacroiliitis’, Annals of the Rheumatic Diseases, 69(7), pp. 1403–1406. Available at: http://dx.doi.org/10.1136/ard.2010.129148.
5. Hayer, S. et al. (2009) ‘PI3Kγ regulates cartilage damage in chronic inflammatory arthritis’, The FASEB Journal, 23(12), pp. 4288–4298. Available at: http://dx.doi.org/10.1096/fj.09-135160.