Joseph J. Goellner
Research Instructor
Also affiliated: Monsanto (United States) (1994); Howard Hughes Medical Institute (1997); Washington University in St. Louis (1982–1996); Central Arkansas Veterans Healthcare System (2008–2020); Jewish Hospital (1984–1985); Ehime University (1997); Monash Institute of Medical Research (2003); Jewish Hospital (1984)
Faculty Researcher
Internal Med, College of Medicine
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Joseph J. Goellner researches bone remodeling and the impact of pharmacological interventions on skeletal health. His work investigates the mechanisms by which osteocytes regulate bone resorption and the potential for rebound resorption following the discontinuation of treatments like denosumab. Recent publications indicate a focus on how local osteoprotegerin expression by osteoblasts influences bone resorption and how denosumab affects the anabolic response to romosozumab in mouse models. Goellner's research also examines the suppression of bone remodeling by denosumab and its implications for bone health. He has published 28 papers, accumulating over 4,000 citations, with an h-index of 19. His recent work has involved collaborations with researchers at the University of Arkansas for Medical Sciences, including Charles A. O’Brien and Jeff D. Thostenson.
Metrics
- h-index: 19
- Publications: 28
- Citations: 4,059
Selected Publications
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Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice (2025)
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Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation (2023)
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Osteoblasts Suppress Bone Resorption Via Production of Osteoprotegerin (2020)
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A Uromodulin Mutation Drives Autoimmunity and Kidney Mononuclear Phagocyte Endoplasmic Reticulum Stress (2020)
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Local Production of Osteoprotegerin by Osteoblasts Suppresses Bone Resorption (2020)
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Soluble RANKL contributes to osteoclast formation in adult mice but not ovariectomy-induced bone loss (2018)
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Mutant Profilin1 transgenic mice recapitulate cardinal features of motor neuron disease (2016)
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Osteocytes, not Osteoblasts or Lining Cells, are the Main Source of the RANKL Required for Osteoclast Formation in Remodeling Bone (2015)
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A DNA Segment Spanning the Mouse <i>Tnfsf11</i> Transcription Unit and Its Upstream Regulatory Domain Rescues the Pleiotropic Biologic Phenotype of the RANKL Null Mouse (2014)
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Mouse and Human BAC Transgenes Recapitulate Tissue-Specific Expression of the Vitamin D Receptor in Mice and Rescue the VDR-Null Phenotype (2014)
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A Humanized Mouse Model of Hereditary 1,25-Dihydroxyvitamin D–Resistant Rickets Without Alopecia (2014)
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FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice (2010)
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Control of Bone Mass and Remodeling by PTH Receptor Signaling in Osteocytes (2008)
Grants & Funding
As listed on this researcher's institutional profile.
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences Co-Investigator
Collaboration Network
Top Collaborators
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice
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