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The Cornell veterinarian1982; 72(1); 76-91;

Glucocorticoid-induced inhibition of osteolysis and the development of osteopetrosis, osteonecrosis and osteoporosis.

Abstract: Changes in the developing femoral epiphysis, especially those concerning the osteocytes, were examined in pony foals systemically treated with daily intramuscular injections of either 0.5 or 5.0 mg of dexamethasone per 100 kg bodyweight for either 3, 8 or 11 months. Midsagittal sections of proximal femur from animals treated for 3 months contained significantly more bone tissue subchondrally and epiphyseally than did sections from untreated ponies. Large portions of the bone tissue appeared necrotic, although osteoblasts and patent capillaries were abundant. After 8 months the bone sections revealed marked osteoporosis. Abnormally dense bone was again observed after 11 months. There were significant increases in the severity of these changes in bone from the animals treated with the higher dosage. Calcium kinetics studies revealed an inhibition of calcium deposition (bone formation) in the treated animals after 2 and 7 months. However, calcium removal (bone resorption) was inhibited to a greater extent. Osteopetrosis (radiographic sclerosis) resulted from the initial resorption/formation imbalance, and was accompanied by osteonecrosis and osteocyte death. Continued treatment resulted in osteopenia, caused by the removal of necrotic bone debris and the inhibition of new bone formation. The primary event in the development of glucocorticoid-induced bone disease was shown to be suppression of osteolysis with the development of osteonecrosis.
Publication Date: 1982-01-01 PubMed ID: 7067459
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

This study explores the effects of glucocorticoid treatment on bone health in pony foals. The researchers found that prolonged use of this hormone led to a variety of bone disorders, including increased bone density, necrosis, and osteoporosis due to the suppression of bone breakdown and death of bone cells.

Research Methods

  • The study used pony foals given daily injections of the glucocorticoid dexamethasone. The dosages varied between 0.5 and 5.0 mg per 100 kg body weight, and the treatment periods ranged from 3 to 11 months.
  • The researchers examined midsagittal sections of the foals’ femurs to assess changes in the bone tissue, particularly among the osteocytes, or bone cells.
  • Additional studies were conducted on calcium kinetics to determine the effects of the treatment on bone formation and resorption.

Study Findings

  • After 3 months of treatment, the bone sections from treated animals displayed more subchondral and epiphyseal bone tissue compared to untreated animals.
  • The bone tissue showed signs of necrosis despite the presence of osteoblasts (cells that form new bone) and adequate capillary supply.
  • At the 8-month mark, the bones started showing signs of osteoporosis, while after 11 months, they displayed unusually high density.
  • The severity of these changes was directly proportional to the dosage of the administered dexamethasone.

Implications and Conclusions

  • On monitoring calcium kinetics, the researchers found that bone formation was inhibited in the treated animals after 2 and 7 months. However, the impact on bone resorption was even greater, leading to a disorder called osteopetrosis which is characterised by sclerotic radiographs.
  • Simultaneously, the affected bones experienced osteonecrosis (bone death).
  • Continued glucocorticoid treatment led to osteopenia, a condition of reduced bone density, which was attributed to the removal of necrotic bone debris and inhibited new bone formation.
  • The study conclusively established that the primary outcome of glucocorticoid-induced bone disease is the suppression of bone resorption leading to various bone disorders, with necrosis being a significant factor.

Cite This Article

APA
Glade MJ, Krook L. (1982). Glucocorticoid-induced inhibition of osteolysis and the development of osteopetrosis, osteonecrosis and osteoporosis. Cornell Vet, 72(1), 76-91.

Publication

ISSN: 0010-8901
NlmUniqueID: 0074245
Country: United States
Language: English
Volume: 72
Issue: 1
Pages: 76-91

Researcher Affiliations

Glade, M J
    Krook, L

      MeSH Terms

      • Animals
      • Bone Resorption / veterinary
      • Calcium / metabolism
      • Dexamethasone / adverse effects
      • Epiphyses / drug effects
      • Epiphyses / growth & development
      • Femur / drug effects
      • Femur / growth & development
      • Horse Diseases / chemically induced
      • Horses
      • Osteocytes / drug effects
      • Osteogenesis / drug effects
      • Osteolysis / veterinary
      • Osteonecrosis / chemically induced
      • Osteonecrosis / veterinary
      • Osteopetrosis / chemically induced
      • Osteopetrosis / veterinary
      • Osteoporosis / chemically induced
      • Osteoporosis / veterinary

      Citations

      This article has been cited 2 times.
      1. Mainguy-Seers S, Lavoie JP. Glucocorticoid treatment in horses with asthma: A narrative review.. J Vet Intern Med 2021 Jul;35(4):2045-2057.
        doi: 10.1111/jvim.16189pubmed: 34085342google scholar: lookup
      2. Doige CE, Crowe S, Farrow CS. Asceptic necrosis of bone in a dog.. Can Vet J 1986 Feb;27(2):70-3.
        pubmed: 17422625