TRANCE/RANKL knockout mice are protected from bone erosion in a serum transfer model of arthritis.

By A. Pettit, H. Ji, D. Stechow, Ralph Müller, S. Goldring, Yongwon Choi, C. Benoist, E. Gravallese. American Journal of Pathology, 2001

720 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Orthopedics and Sports Medicine

View Paper: https://www.semanticscholar.org/paper/a558443dda25a28612f66612065333d8a65e178d

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In Orthopedics and Sports Medicine

Citations in the corpus

Update on the Pathomechanism, Diagnosis, and Treatment Options for Rheumatoid Arthritis (2020, background): “In line with this, RANK-L knockout mice were protected from serum transfer-induced arthritis [94].”
Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destruction (2006, background): “Based on recent reports using genetically modifi ed mice, the crucial role of osteoclasts in the infl ammatory bone loss has been established (41, 42), but which CD4+ T cells cause the induction of osteoclasts, and by what mechanism, has remained elusive.”
Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems (2007, background): “and the protection of osteoclast-deficient mice from inflammatory bone los”
Cartilage homeostasis in health and rheumatic diseases (2009, result): “Since cartilage destruction is not blocked directly by the inhibition of RANKL, at least in inflammatory models, indirect effects may occur through protection of the bone [195,196], as suggested by recent studies in experimental models [197,198].”
Birth and death of bone cells: basic regulatory mechanisms and implications for the pathogenesis and treatment of osteoporosis. (2000, background): “An explanation for this evidence is now provided by studies demonstrating that bisphosphonates such as etidronate, alendronate, pamidronate, olpadronate, or amino-olpadronate (IG9402, a bisphosphonate that lacks antiresorptive activity), as well as calcitonin have antiapoptotic effects on osteoblast”
Evolving concepts of rheumatoid arthritis (2003, background): “RANKL-knockout mice also have diminished bone erosion in arthritis model”
Dickkopf-1 is a master regulator of joint remodeling (2007, background): “Disruption of osteoclast activity, by genetic deletion or pharmacological blockade of essential differentiation molecules, completely abolishes arthritic bone erosion and preserves the joint architectur”