Administration of anti-receptor activator of nuclear factor-kappa B ligand (RANKL) antibody for the treatment of osteoporosis was associated with amelioration of hepatitis in a female patient with growth hormone deficiency: a case report

Background/Aim: This study aimed to present a rare case of fibrous dysplasia (FD) in a healthy young adult man with a concomitant osteoporotic vertebral compression fracture. FD is a benign lesion of the bone characterized by replacement of the medullary component with fibro-osseous tissue that contains abnormally arranged trabeculae of immature woven bone. Recently it has been reported that several bone tumors including FD express the receptor activator of nuclear factor-kappa B (RANK) and its ligand (RANKL). Therefore, we hypothesized that FD contributed to osteoporosis, linked by the RANK-RANKL pathway of osteoclastogenesis. Case Report: We report the case of a healthy man with monostotic femoral fibrous dysplasia (FD) with concomitant 7th thoracic vertebra compression fracture due to osteoporosis [young adult mean (YAM) was 79% in bone mineral density (BMD)]. After curettage of the FD, artificial bone grafting in the cavity, and administration of alendronate sodium, BMD improved considerably within 9 months. FD is a benign bone condition in which abnormal fibrous tissue replaces normal bone. The axis of the receptor activator of nuclear factor-kappa B (RANK) and its ligand (RANKL) has been implicated in osteoporosis pathogenesis. RANKL immunohistochemical staining was performed, and strong staining of stromal cells was observed compared to other FD cases that showed weak to moderate staining. Conclusion: The presence of FD might have contributed to the low BMD due to the RANK-RANKL axis acting as osteoclastogenesis stimulator.

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QiangGuYin Modulates the OPG/RANKL/RANK Pathway by Increasing Secretin Levels during Treatment of Primary Type I Osteoporosis

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2021/7114139 ◽

2021 ◽

Vol 2021 ◽

pp. 1-11

Author(s):

Xuefei Li ◽

Longkang Cui ◽

Wenhua Chen ◽

Yuan Fang ◽

Gaobo Shen ◽

...

Keyword(s):

Nuclear Factor Kappa B ◽

Underlying Mechanism ◽

Type I ◽

Nuclear Factor ◽

Micro Computed Tomography ◽

Mineral Density ◽

Treatment Of Osteoporosis ◽

Nuclear Factor Kappa ◽

Receptor Activator ◽

Primary Type

QiangGuYin (QGY) is a common Traditional Chinese medicine prescription for the treatment of osteoporosis. Previous clinical studies have found that QGY effectively improves bone mineral density (BMD) in postmenopausal women, but its underlying mechanism remains unclear. The osteoprotegerin (OPG)/receptor activator of nuclear factor kappa B ligand (RANKL)/receptor activator of nuclear factor kappa B (RANK) pathway is a classic pathway involved in osteoporosis. Secretin levels are a serum marker of osteoporosis, but their effect on the OPG/RANKL/RANK pathway has not been reported. Hence, we investigated the relationship between the OPG/RANKL/RANK pathway and secretin and further revealed the mechanism underlying the effect of QGY in the treatment of osteoporosis. Mice were divided into secretin knockdown, secretin overexpression, and corresponding control groups. Micro-computed tomography was used to detect BMD in different groups, and the results show that QGY significantly improved BMD in mice of the secretin knockdown group. To further verify this, the serum levels of OPG, RANKL, RANK, and secretin were measured by enzyme-linked immunosorbent assays, and femur levels of OPG, RANKL, RANK, and secretin were evaluated by real-time quantitative PCR and western blotting. The results show that the expression of OPG was inhibited and that of RANKL and RANK was increased in mice from the secretin knockdown group, whereas the expression of OPG was upregulated and that of RANKL and RANK was downregulated after QGY intervention. Therefore, QGY inhibited bone resorption by promoting the expression of secretin and modulating the OPG/RANKL/RANK pathway. In addition to the effect of QGY, we also revealed the general regulatory effect of secretin on the OPG/RANKL/RANK pathway. We conclude that QGY modulates the OPG/RANKL/RANK pathway by increasing secretin levels during treatment of primary type I osteoporosis. This work provides a theoretical basis for the clinical use of QGY in the treatment of osteoporosis.

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