Rheumatoid Arthritis Therapy and Joint-replacement Surgery: Are We Making a Difference?

Goodman, Susan M.

doi:10.3899/jrheum.160043

Cited by 4 publications

(2 citation statements)

References 18 publications

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“…Artificial joint replacement remains one of the most important technological innovations in orthopedics since the 20th century (De-Rong et al, 2017). In recent years, it has become the most effective therapeutic method for endstage osteoarthritis, including advanced osteoarthritis, rheumatoid arthritis and femoral neck fracture in the elderly (Goodman, 2016;Zhang, 2016;Hubley-Kozey and Wilson, 2017). It was estimated that more than 1.5 million joint prostheses have been implanted annually worldwide (Drees et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

MiR‐377 inhibits wear particle‐induced osteolysis via targeting RANKL

Xiaomeng

et al. 2019

Cell Biology International

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Periprosthetic osteolysis caused by wear particles is the main factor that affects the long‐term efficacy of artificial joint replacement, and macrophages play a vital role in the pathogenesis of periprosthetic osteolysis, while the potential mechanism underlying this is still unclear. To investigate the underlying role of miR‐377 in wear particle‐induced osteolysis (PIO), blood samples from patients undergoing arthroplasty were collected for analyzing the correlation between miR‐377 expression and the clinicopathological parameters of PIO. Peripheral blood macrophages were obtained to compare the miR‐377 and receptor activator of NF‐κB ligand (RANKL) expressions. Bone marrow macrophages (BMMs) following titanium (Ti) particle treatment and/or miR‐377 mimic transfection were used. The expressions of RANKL, pro‐inflammatory cytokines interleukin 6 (IL‐6) and tumor necrosis factor‐α (TNF‐α) and the osteoclast‐related molecules tartrate‐resistant acid phosphatase (TRAP) and cathepsin K (CTSK) were determined using real‐time polymerase chain reaction or western blotting or enzyme‐linked immunosorbent assay or TRAP staining, when appropriate. The interaction between miR‐377 and RANKL was assessed by luciferase reporter assay. The in vivo role of miR‐377 in PIO was evaluated using a mouse calvarial osteolysis model. There were significant differences in downregulated miR‐377 expression between the different numbers of particles in the joint prostheses. The Ti particle treatment increased pro‐inflammatory cytokine levels, downregulated RANKL and increased osteoclast activity in BMMs, while miR‐377 overexpression led to the opposite effect. Taken together, miR‐377 downregulated the target gene RANKL, resulting in PIO inhibition. MiR‐377 relieved PIO by negatively regulating RANKL.

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Section: Introductionmentioning

confidence: 99%

MiR‐377 inhibits wear particle‐induced osteolysis via targeting RANKL

Xiaomeng

et al. 2019

Cell Biology International

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“…[2, 4, 5, 13] The prevalence of anemia among RA patients ranges from 33–59%, and anemia has a multifactorial etiology in this population (i.e., direct inflammatory effects, bone marrow suppression secondary to medications, impairment in the synthesis of erythropoietin due to a functional iron deficiency with high iron stores but low availability). [14–16] A low preoperative hemoglobin has been identified to significantly increase the risk of requiring a blood transfusion in patients with RA (odds ratio [OR] 14.4–21.9, p = <. 001).…”

Section: Introductionmentioning

confidence: 99%