Eriksen Erik Fink
University Department of Endocrinology, Aarhus Amtssygehus, Denmark.
J Bone Miner Res. 2002 Nov;17 Suppl 2:N95-7.
The chronic excessive hypersecretion of parathyroid hormone (PTH) in primary hyperparathyroidism (PHPT) has significant impact on bone remodeling. Bone turnover increases by about 50%, leading to increased resorption at the endosteal envelope, increased cortical porosity, and thinning of cortical bone. In cancellous bone a different response is seen. Despite stimulation of bone resorption and formation at the tissue level, osteoclastic resorption and osteoblastic bone formation at individual bone multicellular units (BMUs) are reduced. This causes reduced erosion depth, reduced bone formation rate, and decreased thickness of bone structural units (BSUs), and bone balance at individual BMUs is preserved and may even improve. Thus, PHPT causes cortical bone loss. At the same time, however, cancellous bone structure remains unchanged or even improved, which may offset cortical bone loss. This probably explains the preservation of bone mass demonstrated in long-term follow-up studies of patients with mild PHPT (S-Ca2+ < 2.80 mM). In severe cases of PHPT (S-Ca2+ > 3.00 mM), the negative effects on cortical bone may override the positive impact on cancellous bone, and lead to bone loss and increased risk of fracture.
原发性甲状旁腺功能亢进症（PHPT）中甲状旁腺激素（PTH）的慢性过度分泌对骨重塑有重大影响。骨转换增加约50%，导致骨内膜表面吸收增加、皮质骨孔隙率增加和皮质骨变薄。在松质骨中则观察到不同的反应。尽管在组织水平上骨吸收和形成受到刺激，但单个骨多细胞单位（BMU）处的破骨细胞吸收和成骨细胞骨形成减少。这导致侵蚀深度减小、骨形成率降低以及骨结构单位（BSU）厚度减小，并且单个BMU处的骨平衡得以维持甚至可能改善。因此，PHPT导致皮质骨丢失。然而，与此同时，松质骨结构保持不变甚至有所改善，这可能抵消皮质骨丢失。这可能解释了轻度PHPT患者（血清总钙[S-Ca2+]<2.80 mM）长期随访研究中所显示的骨量维持现象。在严重的PHPT病例（S-Ca2+>3.00 mM）中，对皮质骨的负面影响可能超过对松质骨的积极影响，并导致骨丢失和骨折风险增加。
