Bone remodeling serum markers in children with systemic lupus erythematosus

Abstract

Indroduction SLE is an autoimmune multisystem disease. Glucocorticoid is an irreplaceable medication for SLE. Glucocorticoid and inflammatory mediators impact bone remodeling by OPG/RANKL/RANK signal system, which could lead to osteoporosis. Our aim is to detect the expression of RANKL/OPG in children with SLE, and to preliminarily explore the changes of bone remodeling serum markers in children with SLE. Methods Serum RANKL and OPG of 40 children with SLE and healthy children were detected by ELISA, while 25(OH)VitD3 was detected routinely. Clinical data of children with SLE were recorded, including gender, age, height, weight, BMI, SLEDAI, duration of the disease, cumulative dose of glucocorticoid, and correlation analysis was conducted with RANKL, OPG and 25(OH)VitD3. Results Serum RANKL concentrations in SLE group were significantly higher than health group (9.82 ± 7.20 vs. 6.80 ± 4.35 pg/ml and 0.081 ± 0.072 vs. 0.042 ± 0.034, P < 0.05) respectively, and the concentrations of OPG and 25(OH)VitD3 in serum were significantly lower than health group (156.34 ± 57.33 vs. 189.16 ± 68.70 pg/ml and 43.66 ± 31.27 vs. 59.04 ± 21.56 mmol/L, P < 0.05). Serum RANKL in children with SLE was positively correlated with the duration of SLE, cumulative dose of GC(r = 0.593, 0.727, P < 0.05). And it was negatively correlated with serum OPG and 25(OH)VitD3 (r = -0.601, -0.469, P < 0.05). In addition, serum OPG and 25(OH)VitD3 concentrations were inversely correlated with cumulative dose of GC (r = -0.66, -0.508, P < 0.05). Conclusion Low levels of vitamin D3 and bone metabolic abnormalities still persist in children with SLE even if the disease is in remission, while serum RANKL level was elevated, OPG expression was reduced. In the case of disease remission, GC is involved in the occurrence and development of abnormal bone remodeling through RANKL/OPG.

The Dynamic Role of PD-1, Vitamin D, RANKL, and Sclerostin in Iraqi Patients with Systemic Lupus Erythematosus

“…Because only a tiny amount of serum RANKL may enter the systemic circulation and because some of the serum RANKL concentrations may come from nonskeletal sources, serum RANKL may not accurately reflect its level in the bone microenvironment [50], and this may explain why the current result did not record a significancy in serum level of SLE patients compared to healthy individuals. The current study disagrees with previous studies done by Hao et al, [51] and Ali et al, [52] who showed that RANKL was significantly higher in children with SLE. Another study done by Sandal et al, [53] on children with SLE found that RANKL levels were unrelated to disease activity.…”

Clinical Efficacy and Safety Analysis of Glucocorticoids plus Immunosuppressive Agents for Systemic Lupus Erythematosus and its Influence on N-Glycan

“…The preferred therapeutic agent for SLE is glucocorticoids, which are rapidly and well effective in relieving clinical symptoms. The efficacy of glucocorticoids depends largely on the GRs [25] , which are members of the nuclear hormone receptor superfamily and can alter target genes, thereby modifying the effects of target cells and organs. In clinical treatment, many conditions require high-dose glucocorticoid therapy for effective control of disease progression, especially in critically ill patients, such as severe pneumonia, sepsis and other serious illnesses.…”

Effect of internal heat-type acupuncture on bone remodeling in a glucocorticoid-induced osteoporosis model rabbit by regulating the triplet of OPG-RANKL-RANK

“…Studies have shown that long-term use of glucocorticoids can reduce osteoblast activity and increase osteoclast production, resulting in increased bone resorption, decreased bone formation, and a disruption of the bone remodeling balance, leading to bone loss, which progresses to osteoporosis after a certain degree of bone loss [9,10] . There are also research reports that the triad composed of osteoprotegerin (OPG), receptor activator of nuclear factor-KB (RANK), and receptor activator of nuclear factor-KB ligand (RANKL) is involved in the regulation of bone remodeling and is closely related to GIOP [11] . The current clinical treatment of GIOP mainly focuses on inhibiting bone resorption and promoting bone formation [12] .…”