D'Amelio Patrizia, Grimaldi Anastasia, Pescarmona Gian Piero, Tamone Cristina, Roato Ilaria, Isaia Giancarlo
Department of Internal Medicine, Center on Experimental Medicine (CeRMS), University of Torino, Turin, Italy.
FASEB J. 2005 Mar;19(3):410-2. doi: 10.1096/fj.04-2214fje. Epub 2004 Dec 20.
Osteoclasts are cells involved in bone reabsorbing and hence in postmenopausal bone loss. There is no evidence of increased in vitro spontaneous osteoclast formation in postmenopausal osteoporosis. The aim of our study was to evaluate spontaneous osteoclastogenesis in osteoporosis. Bone mineral density, markers of bone turnover, and cultures of peripheral blood mononuclear cells (PBMC) on dentine slices with or without the addition of 1,25-OH vitamin D3 ([10(-8) M]) were obtained from 18 osteoporotic women and 15 controls. To verify cytokine production by PBMC cultures, supernatants were collected on days 3 and 6 and tested for TNF-alpha and RANKL. The data obtained were compared between patients and controls by one-way ANOVA and correlated by Pearson's coefficient. We found a significant increase in osteoclast formation and bone reabsorbing activity in patients with respect to controls; in addition, the production of TNF-alpha and RANKL is significantly higher in patients. Furthermore, osteoclast number is inversely correlated with bone mineral density and directly with RANKL in culture supernatants. Our data demonstrated an increased spontaneous osteoclastogenesis in women affected by postmenopausal osteoporosis: this increase may be explained by the higher production of TNF-alpha and RANKL by PBMC cultures of osteoporotic patients.
破骨细胞是参与骨吸收以及绝经后骨质流失的细胞。没有证据表明绝经后骨质疏松症患者体外自发破骨细胞形成增加。我们研究的目的是评估骨质疏松症中的自发破骨细胞生成。从18名骨质疏松症女性和15名对照者中获取骨密度、骨转换标志物,以及在添加或不添加1,25 - 羟基维生素D3([10(-8) M])的牙本质切片上培养的外周血单核细胞(PBMC)。为了验证PBMC培养物产生的细胞因子,在第3天和第6天收集上清液,并检测肿瘤坏死因子 - α(TNF - α)和核因子κB受体活化因子配体(RANKL)。通过单因素方差分析比较患者和对照者获得的数据,并通过皮尔逊系数进行相关性分析。我们发现,与对照组相比,患者的破骨细胞形成和骨吸收活性显著增加;此外,患者体内TNF - α和RANKL的产生明显更高。此外,破骨细胞数量与骨密度呈负相关,与培养上清液中的RANKL呈正相关。我们的数据表明,绝经后骨质疏松症女性的自发破骨细胞生成增加:这种增加可能是由于骨质疏松症患者的PBMC培养物中TNF - α和RANKL产生增加所致。