Experimental studies on osteoporosis.
Abstract: 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.
Publication Date: 1975-01-01 PubMed ID: 1105064
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Summary
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This research article discusses the effects of a diet deficient in calcium and excessive in phosphorus, known as Nutritional Secondary Hyperparathyroidism (NSH), on bone loss in animals and its potential implications for human conditions such as periodontal disease and osteoporosis.
Research Context and Methodology
- The researchers conduct experimental studies on a wide range of domesticated and wild animals to investigate the effects of a diet causing Nutritional Secondary Hyperparathyroidism (NSH).
- The condition of NSH is associated with calcium deficiency and/or excess of phosphorus in the diet, caused by hypocalcemia (low calcium levels in the blood) and/or hyperphosphatemia (high phosphorus levels in the blood). The body tries to normalize these conditions but does so at the expense of progressive bone loss.
Findings and Implications
- The researchers found that the bone loss due to NSH is generalized, affecting different bones in varying degrees. Jaw bones, especially the alveolar bone, are most significantly affected, followed by skull bones, ribs, vertebrae, and long bones.
- Osteocytic osteolysis – the resorption or breakdown of bone tissue caused by activation of osteocytes (bone cells) – is identified as the primary mechanism of this bone loss.
- The early loss of alveolar bone – an event observed in animals with NSH – is believed to be the initial symptom of periodontal disease (a severe gum infection that damages soft tissue).
- They also discovered that the bone loss caused by NSH can be reversed by correcting the levels of dietary calcium and phosphorus, but only if the condition hasn’t progressed to cause a bone disease known as hyperostotic osteodystrophia fibrosa.
Linkage to Human Conditions and Suggestions for Further Research
- The researchers emphasize the relevance of their findings to human conditions like periodontal disease and osteoporosis, mainly due to inadequate dietary consumption of calcium and phosphorus in most Western countries.
- The authors argue that the severity of periodontal disease and osteoporosis in a population can directly correlate with the degree of dietary calcium deficiency and phosphorus excess.
- They indicate periodontal disease as a precursor to spinal osteoporosis and present evidence that the symptoms of these conditions in humans are similar to those of NSH in animals.
- Further, based on their limited experiments, they suggest that adding dietary calcium can have a positive effect on alveolar bone loss, one of the symptoms of periodontal disease.
- Therefore, the authors outline the need for future studies exploring the effects of dietary adjustments on the prevention and treatment of periodontal disease and osteoporosis in humans.
Cite This Article
APA
Krook L, Whalen JP, Lesser GV, Berens DL.
(1975).
Experimental studies on osteoporosis.
Methods Achiev Exp Pathol, 7, 72-108.
Publication
Researcher Affiliations
MeSH Terms
- Adolescent
- Adult
- Alkaline Phosphatase / blood
- Animal Feed / adverse effects
- Animals
- Bone Resorption / etiology
- Bone and Bones / diagnostic imaging
- Bone and Bones / pathology
- Calcium / deficiency
- Calcium, Dietary / therapeutic use
- Carnivora
- Disease Models, Animal
- Dogs
- Female
- Gingivectomy
- Horses
- Humans
- Hyperparathyroidism, Secondary / diagnostic imaging
- Hyperparathyroidism, Secondary / enzymology
- Hyperparathyroidism, Secondary / etiology
- Hyperparathyroidism, Secondary / pathology
- Male
- Middle Aged
- Osteoporosis
- Periodontal Diseases / diagnostic imaging
- Periodontal Diseases / pathology
- Periodontal Diseases / therapy
- Phosphorus
- Radiography
Citations
This article has been cited 2 times.- Sebaoun JD, Kantarci A, Turner JW, Carvalho RS, Van Dyke TE, Ferguson DJ. Modeling of trabecular bone and lamina dura following selective alveolar decortication in rats. J Periodontol 2008 Sep;79(9):1679-88.
- Duriez R, Duriez J. Periosteocyte demineralization in disuse osteoporsis. The effect of calcitonin. Int Orthop 1981;5(4):299-304.
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