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The Cornell veterinarian1983; 73(2); 170-192;

Morphologic and biochemical changes in cartilage of foals treated with dexamethasone.

Abstract: Epiphyseal and articular cartilages were examined in pony foals treated with intramuscular injections of either 0.5 mg dexamethasone per 100 kg bodyweight daily for 3, 8 or 11 months, or 5.0 mg per 100 kg for 11 months, and in horse foals treated with 5.0 mg per 100 kg for 20 weeks. The proximal femoral growth plates exhibited increased spatial separation between chondrocyte columns, narrowed zones of disorganized columnar and hypertrophic cartilage, abnormal penetration of hypertrophic cartilage by metaphyseal capillaries, retained cartilage in the spongiosa, distal terminal plate formation, transverse trabeculation, chondronecrosis and metaphyseal osteochondrosis dissecans. Destructive articular lesions were observed after 3 months of treatment with 0.5 mg per 100 kg bodyweight. Joint damage originated either at the joint surface or deep within the cartilage. Signs of surface deterioration included edema, fibrillation, enlargement of lacunae, pitting, shredding and erosions of cartilage. Inactivity of articular cartilage growth centers was common, with failure of epiphyseal capillaries to penetrate the lacunae in the calcified cartilage. Chondronecrosis adjacent to the calcification front was accompanied by cartilage ulceration and fracture. Intracartilaginous cysts and subchondral chondroid cysts were also observed. Healing responses included reparative chondrogenesis (focal cartilage hyperplasia), formation of fibrous or fibrocartilaginous "scars," subchondral osteopetrosis and epiphyseal marrow petrosis. Lactate dehydrogenase specific activities per chondrocyte, 35S uptake per cell and glycosaminoglycan contents of articular cartilages were all reduced 55% by 3 months of treatment. This inhibition of articular chondrocyte metabolism initiated cartilage degeneration. Surface destruction and osteochondrosis dissecans followed continued mechanical stress of compromised cartilage.
Publication Date: 1983-04-01 PubMed ID: 6839784
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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This research article focuses on morphologic and biochemical changes observed in the cartilage of pony foals that have been treated with dexamethasone, a type of steroid drug. The primary findings highlight the adverse impacts of administered dexamethasone on articular and epiphyseal cartilages and the resulting initiation of cartilage degeneration.

Methodology and Treatment regimens

  • Pony foals were administered intramuscular injections of 0.5 mg dexamethasone per 100 kg of body weight daily for 3, 8 or 11 months. Some were given 5.0 mg per 100 kg for 11 months.
  • Horse foals were treated with 5.0 mg dexamethasone per 100 kg for 20 weeks. This group of foals was made a part of the study to gauge the effects of the drug over different durations and dosages in different types of foals.
  • The researchers then examined the epiphyseal and articular cartilages of the treated animals.

Changes in Cartilage Morphology and Biochemistry

  • Proximal femoral growth plates in the foals revealed increased distances between chondrocyte columns and narrow zones of disorganized columnar and hypertrophic cartilage.
  • Other observed abnormalities included abnormal penetration of hypertrophic cartilage by metaphyseal capillaries and retention of cartilage in the spongiosa.
  • Destructive articular lesions were observed after three months of dexamethasone treatment at the lower dosage level of 0.5 mg/100 kg. The joint damage originated either at the joint surface or deep within the cartilage.
  • Signs of the surface damage included edema, fibrillation, enlargement of lacunae, pitting, shredding, and erosions of cartilage.
  • There was a common inactivity in the growth centres of the articular cartilage, where epiphyseal capillaries failed to penetrate the lacunae in the calcified cartilage.
  • Chondronecrosis adjacent to the calcification front was accompanied by cartilage ulceration and fracture.
  • Intracartilaginous cysts and subchondral chondroid cysts were also observed.
  • The healing responses brought about reparative chondrogenesis (focal cartilage hyperplasia), formation of fibrous or fibrocartilaginous “scars”, subchondral osteopetrosis, and epiphyseal marrow petrosis.

Biochemical Changes in Cartilage

  • The authors showcase that lactate dehydrogenase specific activities per chondrocyte, 35S uptake per cell, and glycosaminoglycan contents of articular cartilages were all reduced by approximately 55% after 3 months of dexamethasone treatment.
  • This inhibition of articular chondrocyte metabolism resulted in the initiation of cartilage degeneration, the onset of destructive surface alterations, and osteochondrosis dissecans (a joint condition in which bone underneath the cartilage of a joint dies due to lack of blood flow).

The study overall provides critical insights into how the use of dexamethasone in young ponies and horses can lead to significant morphologic and biochemical alterations in the animals’ cartilage, initiating degenerative processes.

Cite This Article

APA
Glade MJ, Krook L, Schryver HF, Hintz HF. (1983). Morphologic and biochemical changes in cartilage of foals treated with dexamethasone. Cornell Vet, 73(2), 170-192.

Publication

ISSN: 0010-8901
NlmUniqueID: 0074245
Country: United States
Language: English
Volume: 73
Issue: 2
Pages: 170-192

Researcher Affiliations

Glade, M J
    Krook, L
      Schryver, H F
        Hintz, H F

          MeSH Terms

          • Animals
          • Bone Development / drug effects
          • Bone and Bones / pathology
          • Cartilage / drug effects
          • Cartilage / pathology
          • Cartilage Diseases / pathology
          • Cartilage Diseases / veterinary
          • Cartilage, Articular / drug effects
          • Cartilage, Articular / pathology
          • Dexamethasone / pharmacology
          • Horse Diseases / pathology
          • Horses
          • Joint Diseases / pathology
          • Joint Diseases / veterinary
          • Osteochondritis / pathology
          • Osteochondritis / veterinary

          Citations

          This article has been cited 4 times.
          1. Black RM, Wang Y, Struglics A, Lorenzo P, Chubinskaya S, Grodzinsky AJ, Önnerfjord P. Proteomic Clustering Reveals the Kinetics of Disease Biomarkers in Bovine and Human Models of Post-Traumatic Osteoarthritis. Osteoarthr Cartil Open 2021 Dec;3(4).
            doi: 10.1016/j.ocarto.2021.100191pubmed: 36313736google scholar: lookup
          2. Chen L, Ni Z, Huang J, Zhang R, Zhang J, Zhang B, Kuang L, Sun X, Zhang D, Su N, Qi H, Yang J, Jin M, Luo F, Chen H, Zhou S, Du X, Ouyang J, Wang Z, Xie Y, Tan Q, Chen L. Long term usage of dexamethasone accelerating accelerates the initiation of osteoarthritis via enhancing chondrocyte apoptosis and the extracellular matrix calcification and apoptosis of chondrocytes. Int J Biol Sci 2021;17(15):4140-4153.
            doi: 10.7150/ijbs.64152pubmed: 34803488google scholar: lookup
          3. Suhovskih AV, Molodykh OP, Ushakov VS, Politko MO, Sokolov DK, Koldysheva EV, Grigorieva EV. Long-Term Exposure to Temozolomide Affects Locomotor Activity and Cartilage Structure of Elderly Experimental Rats. Biomedicines 2020 Nov 26;8(12).
            doi: 10.3390/biomedicines8120541pubmed: 33255948google scholar: lookup
          4. Black R, Grodzinsky AJ. Dexamethasone: chondroprotective corticosteroid or catabolic killer?. Eur Cell Mater 2019 Nov 22;38:246-263.
            doi: 10.22203/eCM.v038a17pubmed: 31755076google scholar: lookup