Chappard D, Baslé M F, Audran M, Benhamou C L, Rebel A
LHEA-Laboratoire d'Histologie-Embryologie, Faculté de Médecine, Angers; France.
Pathol Res Pract. 1996 Jun;192(6):573-8. doi: 10.1016/S0344-0338(96)80108-7.
In patients with femoral neck fracture, nutritional deficiencies have been shown to be common. A low calcium diet and/or a reduced vitamin D intake have been suspected to cause secondary hyperparathyroidism responsible for increased bone turn over and bone loss. Parathyroid hormone (PTH) levels are increased in these patients, data which are in accordance with the pronounced changes observed on bone biopsies reflecting a true hyperparathyroidism. We have used a cytomorphometrical approach to characterize PTH-induced changes on the osteoclastic population. Osteoclasts were detected histochemically (by tartrate resistant acid phosphatase staining) on bone biopsies from 10 control subjects, 8 patients with primary hyperparathyroidism and 10 patients with a femoral neck fracture of osteoporotic origin. The maximum Feret's diameter of each osteoclast (Oc.Le) was determined with a semiautomatic image analyzer. In all groups, the frequency distribution of Oc.Le appeared positively skewed. In both hip fractured patients and primary hyperparathyroid patients, the mode of the distribution was higher (25-30 microns) than in controls (20-25 microns). When graphically converted on a probability graph, the osteoclastic populations appeared homogeneous and well described by a lognormal distribution in the three groups. However, osteoclasts appeared similarly enlarged in the groups of patients with primary hyperparathyroidism and with femoral neck fracture. PTH has been shown to increase both the recruitment of mononucleated precursors and their fusion into larger osteoclasts than controls. In the present study, a cytomorphometric method appeared able to identify the border line hyperparathyroidism in the hip fractured patients.
在股骨颈骨折患者中,营养缺乏已被证明很常见。低钙饮食和/或维生素D摄入量减少被怀疑会导致继发性甲状旁腺功能亢进,从而导致骨转换增加和骨质流失。这些患者的甲状旁腺激素(PTH)水平升高,这一数据与在骨活检中观察到的明显变化一致,反映了真正的甲状旁腺功能亢进。我们采用细胞形态计量学方法来描述PTH诱导的破骨细胞群体变化。通过组织化学方法(抗酒石酸酸性磷酸酶染色)在10名对照受试者、8名原发性甲状旁腺功能亢进患者和10名骨质疏松性股骨颈骨折患者的骨活检中检测破骨细胞。使用半自动图像分析仪测定每个破骨细胞的最大费雷特直径(Oc.Le)。在所有组中,Oc.Le的频率分布呈正偏态。在髋部骨折患者和原发性甲状旁腺功能亢进患者中,分布模式(25 - 30微米)高于对照组(20 - 25微米)。当在概率图上进行图形转换时,三组中的破骨细胞群体看起来均匀,并且可以用对数正态分布很好地描述。然而,原发性甲状旁腺功能亢进患者组和股骨颈骨折患者组中的破骨细胞似乎同样增大。已证明PTH会增加单核前体细胞的募集及其融合形成比对照组更大的破骨细胞。在本研究中,细胞形态计量学方法似乎能够识别髋部骨折患者中的临界甲状旁腺功能亢进。