Equine dyschondroplasia (osteochondrosis)–histological findings and type VI collagen localization.
Abstract: This study describes (1) the histological appearance of dyschondroplasia, the primary lesion of osteochondrosis, in articular cartilage of the horse and (2) the localization of type VI collagen which is an important constituent of the extracellular matrix (ECM). Dyschondroplastic cartilage was identified on the basis of the presence of cartilage cores (i.e., cartilage extending into the subchondral bone) and confirmed with subsequent histological examination. Full-thickness cartilage samples from 57 horses were collected and paraffin embedded. Histological examination was used to examine the normal architecture of equine growth cartilage and to determine the presence of various pathological changes in dyschondroplastic lesions. Immunolocalization was used to identify type VI collagen in normal and dyschondroplastic lesions. The abnormalities observed in the dyschondroplastic cartilage fell into two groups. In Group A (n = 18) the lesions were associated with a disruption in the normal sequential transition of the chondrocytes through proliferation and maturation resulting in an accumulation of large numbers of small, rounded chondrocytes. A decrease in type VI collagen immunoreactivity compared with normal animals was detected except around chondrocyte clusters. Group B lesions (n = 9) were characterized by an alteration in the staining pattern of the mineralized cartilage and underlying bone. In these lesions type VI collagen immunoreactivity was increased. In both groups the presence of retained blood vessels, chondrocyte clusters, chondronecrosis and fissure formation was detected. These two histologically-distinct groups suggest that equine dyschondroplasia may be comprised of different pathological entities and that it is associated with alterations in the pattern of distribution of an ECM protein.
Publication Date: 1997-07-01 PubMed ID: 9265853DOI: 10.1016/s1090-0233(05)80008-5Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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The research is a deep study of dyschondroplasia in horses, an underlying cause of osteochondrosis, examining the abnormalities and how they relate with type VI collagen, a key constituent of the extracellular matrix, in the cartilage.
Study Methodology
- The researchers identified dyschondroplastic cartilage based on the presence of cartilage cores extending into the subchondral bone and confirmed the findings via histological examination.
- The research involved full-thickness cartilage samples collected from 57 horses which were paraffin-embedded.
- They employed histological examination to observe the regular construct of equine growth cartilage and identify various pathological alterations in dyschondroplastic lesions.
- Immunolocalization was also used to determine type VI collagen in such lesions and normal conditions.
Key Findings
- Aberrations noticed in dyschondroplastic cartilage were placed into two groups.
- Group A include lesions connected with disrupted sequences of chondrocyte proliferation and maturation, leading to an increase of small and rounded chondrocytes.
- Group B comprise of lesions characterized by changes in staining patterns of the mineralized cartilage and underlying bone.
- In Group A, there was lesser type VI collagen immunoreactivity compared to normal conditions, except around chondrocyte clusters.
- In Group B, the type VI collagen immunoreactivity exhibited an increase.
- Preserved blood vessels, chondrocyte clusters, chondronecrosis, and fissure formation were spotted in both groups.
Study Conclusions
- The detection of two histologically-distinct groups implies that equine dyschondroplasia might be composed of different pathological entities.
- The conditions are associated with alterations in the pattern of distribution of an ECM protein.
In this way, the research sheds new light on our understanding of equine dyschondroplasia, highlighting the role of type VI collagen and suggesting the presence of multiple pathological entities within this condition. It thus opens the door towards more targeted research to identify specific treatment options for each of these entities.
Cite This Article
APA
Henson FM, Davies ME, Jeffcott LB.
(1997).
Equine dyschondroplasia (osteochondrosis)–histological findings and type VI collagen localization.
Vet J, 154(1), 53-62.
https://doi.org/10.1016/s1090-0233(05)80008-5 Publication
Researcher Affiliations
- Department of Clinical Veterinary Medicine, University of Cambridge, UK.
MeSH Terms
- Animals
- Cartilage, Articular / chemistry
- Cartilage, Articular / pathology
- Cartilage, Articular / physiopathology
- Cell Division / physiology
- Collagen / analysis
- Extracellular Matrix / chemistry
- Extracellular Matrix / pathology
- Female
- Horse Diseases / pathology
- Horses
- Immunohistochemistry
- Male
- Osteochondrodysplasias / pathology
- Osteochondrodysplasias / veterinary
Citations
This article has been cited 7 times.- Meng X, Grad S, Wen C, Lai Y, Alini M, Qin L, Wang X. An impaired healing model of osteochondral defect in papain-induced arthritis. J Orthop Translat 2021 Jan;26:101-110.
- McGivney BA, Han H, Corduff LR, Katz LM, Tozaki T, MacHugh DE, Hill EW. Genomic inbreeding trends, influential sire lines and selection in the global Thoroughbred horse population. Sci Rep 2020 Jan 16;10(1):466.
- Chiaradia E, Pepe M, Orvietani PL, Renzone G, Magini A, Sforna M, Emiliani C, Di Meo A, Scaloni A. Proteome Alterations in Equine Osteochondrotic Chondrocytes. Int J Mol Sci 2019 Dec 7;20(24).
- Bourebaba L, Röcken M, Marycz K. Osteochondritis dissecans (OCD) in Horses - Molecular Background of its Pathogenesis and Perspectives for Progenitor Stem Cell Therapy. Stem Cell Rev Rep 2019 Jun;15(3):374-390.
- Getgood A, Henson F, Skelton C, Brooks R, Guehring H, Fortier LA, Rushton N. Osteochondral tissue engineering using a biphasic collagen/GAG scaffold containing rhFGF18 or BMP-7 in an ovine model. J Exp Orthop 2014 Dec;1(1):13.
- Desjardin C, Riviere J, Vaiman A, Morgenthaler C, Diribarne M, Zivy M, Robert C, Le Moyec L, Wimel L, Lepage O, Jacques C, Cribiu E, Schibler L. Omics technologies provide new insights into the molecular physiopathology of equine osteochondrosis. BMC Genomics 2014 Oct 31;15(1):947.
- Desjardin C, Vaiman A, Mata X, Legendre R, Laubier J, Kennedy SP, Laloe D, Barrey E, Jacques C, Cribiu EP, Schibler L. Next-generation sequencing identifies equine cartilage and subchondral bone miRNAs and suggests their involvement in osteochondrosis physiopathology. BMC Genomics 2014 Sep 17;15(1):798.
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