Krook L, Whalen J P, Lesser G V, Berens D L
Methods Achiev Exp Pathol. 1975;7:72-108.
Nutritional secondary hyperparathyroidism (NSH) defines a spontaneous and experimental disease in most domesticated and in some wild animals, caused by dietary calcium deficiency and/or phosphorus excess. Calcium deficiency results directly in hypocalcemia, and phosphorus excess induces hyperphosphatemia which causes hypocalcemia. Secondary hyperparathyroidism thus results and the plasma parameters return to normal and are maintained but only at the expense of progressive bone loss. The bone loss is generalized but the bones are not uniformly affected. The hierarchy of bone loss is, in decreasing order, the jaw bones, especially the alveolar bone, other skull bones, ribs, vertebrae and, finally, long bones. Osteocytic osteolysis is the main mechanism of resorption and application of this concept is a condition sine qua non in the interpretation of the histologic lesions. The early loss of alveolar bone constitutes the initial event in periodontal disease in animals. The osseous lesions in animal NSH are reversible by correction of dietary calcium and phosphorus levels, provided a hyperostotic osteodystrophia fibrosa has not yet developed. The applicability of animal NSH as a model for human osteopenic conditions, including periodontal disease and spinal osteoporosis, is supported by the very inadequate calcium and phosphorus nutrition in most Western countries. The diet is deficient in calcium and excessive in phosphorus; both conditions induce NSH in animals. The degree of dietary calcium deficiency, as influenced by geographic, economic, and social factors, is positively correlated to the degree of periodontal disease and osteoporosis in the population. Evidence is presented to show that the radiographic and histologic manifestations of human periodontal disease and osteoporosis are the same as those of animal NSH. Periodontal disease is therefore considered a fore-runner to the clinically more important spinal osteoporosis. Limited experiments in human periodontal disease indicate that added dietary calcium can positively influence the alveolar bone loss.
营养性继发性甲状旁腺功能亢进（NSH）是一种在大多数家养动物和一些野生动物中自然发生及可通过实验诱导的疾病，由饮食中钙缺乏和/或磷过量引起。钙缺乏直接导致低钙血症，而磷过量会引发高磷血症，进而导致低钙血症。由此引发继发性甲状旁腺功能亢进，血浆参数虽可恢复正常并维持，但这是以渐进性骨质流失为代价的。骨质流失是全身性的，但骨骼各部位受影响程度并不一致。骨质流失程度由高到低依次为颌骨，尤其是牙槽骨、其他颅骨、肋骨、椎骨，最后是长骨。骨细胞性骨溶解是主要的吸收机制，运用这一概念是解释组织学病变的必要条件。牙槽骨的早期流失是动物牙周病的起始事件。如果尚未发展为骨质增生性纤维性骨营养不良，通过纠正饮食中钙和磷的水平，动物NSH的骨病变是可逆的。大多数西方国家钙和磷营养严重不足，这支持了将动物NSH作为人类骨质减少病症（包括牙周病和脊柱骨质疏松症）模型的适用性。饮食中钙缺乏而磷过量，这两种情况均可在动物中诱发NSH。受地理、经济和社会因素影响，饮食中钙缺乏的程度与人群中牙周病和骨质疏松症的程度呈正相关。有证据表明，人类牙周病和骨质疏松症的影像学和组织学表现与动物NSH相同。因此，牙周病被认为是临床上更重要的脊柱骨质疏松症的先兆。在人类牙周病方面的有限实验表明，增加饮食中的钙可对牙槽骨流失产生积极影响。
