Women in rheumatology: major contributions and key discoveries of the twentieth century

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Abstract

In the twentieth century, rheumatology saw an exponential growth. Discoveries in the pathophysiology of rheumatic diseases, progress in research methodology and novel treatments cardinally changed the natural course of rheumatic diseases and revolutionized patient management. Although underrepresented in this field, women have made considerable input in advancing our specialty towards the new era. In this article we acknowledge key scientific discoveries and major contributions made by 18 brilliant women scientists that shaped the field of rheumatology in the twentieth century. We hope that the achievements of these remarkable women will inspire young rheumatologists and researchers.

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Cartilage-specific deletion of mTOR upregulates autophagy and protects mice from osteoarthritis.

Yue Zhang, Faezeh Vasheghani, Ying-Hua Li … (2015)

Mammalian target of rapamycin (mTOR) (a serine/threonine protein kinase) is a major repressor of autophagy, a cell survival mechanism. The specific in vivo mechanism of mTOR signalling in OA pathophysiology is not fully characterised. We determined the expression of mTOR and known autophagy genes in human OA cartilage as well as mouse and dog models of experimental OA. We created cartilage-specific mTOR knockout (KO) mice to determine the specific role of mTOR in OA pathophysiology and autophagy signalling in vivo.

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Bone erosion in rheumatoid arthritis: mechanisms, diagnosis and treatment.

Ellen Gravallese, Georg Schett (2012)

Bone erosion is a central feature of rheumatoid arthritis and is associated with disease severity and poor functional outcome. Erosion of periarticular cortical bone, the typical feature observed on plain radiographs in patients with rheumatoid arthritis, results from excessive local bone resorption and inadequate bone formation. The main triggers of articular bone erosion are synovitis, including the production of proinflammatory cytokines and receptor activator of nuclear factor κB ligand (RANKL), as well as antibodies directed against citrullinated proteins. Indeed, both cytokines and autoantibodies stimulate the differentiation of bone-resorbing osteoclasts, thereby stimulating local bone resorption. Although current antirheumatic therapy inhibits both bone erosion and inflammation, repair of existing bone lesions, albeit physiologically feasible, occurs rarely. Lack of repair is due, at least in part, to active suppression of bone formation by proinflammatory cytokines. This Review summarizes the substantial progress that has been made in understanding the pathophysiology of bone erosions and discusses the improvements in the diagnosis, monitoring and treatment of such lesions.