RANKL: A therapeutic target for bone destruction in rheumatoid arthritis

@article{Tanaka2018RANKLAT,
  title={RANKL: A therapeutic target for bone destruction in rheumatoid arthritis},
  author={Sakae Tanaka and Yoshiya Tanaka and Naoki Ishiguro and Hisashi Yamanaka and Tsutomu Takeuchi},
  journal={Modern Rheumatology},
  year={2018},
  volume={28},
  pages={16 - 9}
}
Abstract Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by progressive joint destruction. Recent studies have indicated the critical involvement of osteoclasts in bone destruction in RA. The osteoclast differentiation factor receptor activator of NF-κB ligand (RANKL), which belongs to the tumor necrosis factor superfamily, plays a critical role in osteoclast differentiation and bone destruction in RA. Denosumab, an antibody against human RANKL, efficiently suppressed… 
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RANKL as a therapeutic target of rheumatoid arthritis
TLDR
Denosumab, a specific antibody to human RANKL, efficiently suppressed the progression of bone destruction in patients with RA in a randomized controlled study and is considered a putative therapeutic option for RA.
Emerging anti-osteoclast therapy for rheumatoid arthritis.
  • Sakae Tanaka
  • Biology, Medicine
    Journal of orthopaedic science : official journal of the Japanese Orthopaedic Association
  • 2018
RANKL is a therapeutic target of bone destruction in rheumatoid arthritis
TLDR
Denosumab efficiently suppressed the progression of bone erosion in patients with RA by suppressing osteoclast differentiation and activation in several clinical studies, although it had no effect on inflammation or cartilage destruction.
Pathogenesis and Function of Interleukin-35 in Rheumatoid Arthritis
TLDR
It is suggested that IL-35 played an important role in the pathogenesis of RA, and can be used as a potential target for the future treatment of RA.
Suppression of hematopoietic cell kinase ameliorates the bone destruction associated with inflammation
TLDR
The results demonstrate that the administration of A-419259 is effective for the inhibition of osteoclast differentiation induced by TNF-α in the presence of RANKL, and an inhibitor of Hck may be useful as a potent anti-osteoclastogenic agent for the treatment of inflammatory bone destruction.
An overview of the NF-kB mechanism of pathophysiology in rheumatoid arthritis, investigation of the NF-kB ligand RANKL and related nutritional interventions.
Identifying the preferable rheumatoid arthritis subgroups for intervention with the anti-RANKL antibody denosumab to reduce progression of joint destruction
TLDR
Denosumab broadly reduced the progression of joint destruction in RA patients with risk factors for radiographic damage such as especially anti- CCP antibody positivity and was particularly effective in patients who were anti-CCP antibody positive.
Predictors of new bone erosion in rheumatoid arthritis patients receiving conventional synthetic disease-modifying antirheumatic drugs: Analysis of data from the DRIVE and DESIRABLE studies
TLDR
In RA patients treated with csDMARDs, new bone erosion predictors were seropositivity, elevated inflammatory markers, and baseline ES ≥3.
CD109 regulates the inflammatory response and is required for the pathogenesis of rheumatoid arthritis
TLDR
This study uncovers an antiarthritic role for CD109 and suggests that CD109 inhibition might serve as a promising novel therapeutic strategy for RA.
Understanding the Role of Interleukin-6 (IL-6) in the Joint and Beyond: A Comprehensive Review of IL-6 Inhibition for the Management of Rheumatoid Arthritis
  • E. Favalli
  • Medicine, Biology
    Rheumatology and Therapy
  • 2020
TLDR
The role of IL-6 in the pathogenesis of RA, its comorbidities, and extra-articular systemic manifestations are described, and the effects of the IL- 6 receptor inhibitors sarilumab and tocilizumab on clinical endpoints of RA are examined.
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RANKL is a therapeutic target of bone destruction in rheumatoid arthritis
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Denosumab efficiently suppressed the progression of bone erosion in patients with RA by suppressing osteoclast differentiation and activation in several clinical studies, although it had no effect on inflammation or cartilage destruction.
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