In vivo (Athens, Greece) · 2025
Analysis of Risedronate Analog on Extraction Socket Healing in Mice.
СтатьяНазвание и аннотация: Перевод в очереди
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Kasagawa Moeka, Mine Yuichi, Sano Mizuho, Kurokui Yukinaga, Ueda Ayano, Kaku Masato, Nikawa Hiroki, Murayama Takeshi
Аннотация
BACKGROUND/AIM: Medication-related osteonecrosis of the jaw (MRONJ) is a severe adverse effect associated with anti-resorptive medications like nitrogen-containing bisphosphonates (N-BPs), particularly zoledronate (ZOL). This study aimed to investigate whether a BP analog with high bone affinity but minimal anti-resorptive activity, NE-58051, could induce MRONJ-like lesions in a mouse model.
MATERIALS AND METHODS: Female C57BL/6J mice (n=6 per group) were administered ZOL (250 μg/kg intravenously, twice weekly) for one or two weeks, or NE-58051 (250 μg/kg intravenously, twice weekly) for two weeks. Two weeks after initiation of study, the bilateral first molars were extracted. Mice were euthanized after a total duration of four weeks. Histological assessments evaluated necrotic bone area and osteoclast activity at extraction sites. Serum tartrate-resistant acid phosphatase isoform 5b (TRAcP-5b) levels were measured.
RESULTS: Mice treated with ZOL for two weeks exhibited significant increases in empty osteocytic lacunae and necrotic bone area compared to the saline group, indicating the development of MRONJ-like lesions. NE-58051-treated mice did not show significant differences in necrotic bone area or osteoclast activity compared to controls. No significant differences were observed in serum TRAcP-5b levels among all groups.
CONCLUSION: High bone affinity without potent inhibition of bone resorption does not induce MRONJ-like lesions in mice. These findings suggest that the potent anti-resorptive activity of N-BPs is a key factor in MRONJ development, highlighting the importance of bone turnover suppression in the pathogenesis of this condition.
MATERIALS AND METHODS: Female C57BL/6J mice (n=6 per group) were administered ZOL (250 μg/kg intravenously, twice weekly) for one or two weeks, or NE-58051 (250 μg/kg intravenously, twice weekly) for two weeks. Two weeks after initiation of study, the bilateral first molars were extracted. Mice were euthanized after a total duration of four weeks. Histological assessments evaluated necrotic bone area and osteoclast activity at extraction sites. Serum tartrate-resistant acid phosphatase isoform 5b (TRAcP-5b) levels were measured.
RESULTS: Mice treated with ZOL for two weeks exhibited significant increases in empty osteocytic lacunae and necrotic bone area compared to the saline group, indicating the development of MRONJ-like lesions. NE-58051-treated mice did not show significant differences in necrotic bone area or osteoclast activity compared to controls. No significant differences were observed in serum TRAcP-5b levels among all groups.
CONCLUSION: High bone affinity without potent inhibition of bone resorption does not induce MRONJ-like lesions in mice. These findings suggest that the potent anti-resorptive activity of N-BPs is a key factor in MRONJ development, highlighting the importance of bone turnover suppression in the pathogenesis of this condition.