FREE SHIPPING over $40
OVER 9000 FIVE-STAR REVIEWS
5% OFF ALL SUBSCRIPTIONS
100% HAPPINESS GUARANTEE
Analyze Diet
0
Home / Equine Research Bank / Osteoarthritis Cartilage / Physiological death of hypertrophic chondrocytes.
Osteoarthritis and cartilage2006; 15(5); 575-586; doi: 10.1016/j.joca.2006.10.016

Physiological death of hypertrophic chondrocytes.

Abstract: Post-proliferative chondrocytes in growth cartilage are present in two forms, light and dark cells. These cells undergo hypertrophy and die by a mechanism that is morphologically distinct from apoptosis, but has not been characterized. The aims of the current study were to document the ultrastructural appearance of dying hypertrophic chondrocytes, and to establish a culture system in which the mechanism of their death can be examined. Methods: Growth cartilage from fetal and growing postnatal horses was examined by electron microscopy. Chondrocytes were isolated from epiphyseal cartilage from fetal horses and grown in pellet culture, then examined by light and electron microscopy, and quantitative polymerase chain reaction. Results: In tissue specimens, it was observed that dying dark chondrocytes underwent progressive extrusion of cytoplasm into the extracellular space, whereas light chondrocytes appeared to disintegrate within the cellular membrane. Pellets cultured in 0.1% fetal calf serum (FCS) contained dying light and dark chondrocytes similar to those seen in vivo. Transforming growth factor-beta1 or 10% FCS increased the proportion of dark cells and induced cell death. Triiodothyronine increased the differentiation of dark and light cells and induced their death. Dark cells were associated with higher levels of matrix metalloproteinase-13 expression than light cells, and light cells were associated with higher levels of type II collagen expression. Conclusions: Light and dark hypertrophic chondrocytes each undergo a distinctive series of non-apoptotic morphological changes as they die. Pellet culture can be used as a model of the two forms of physiological death of hypertrophic chondrocytes.
Get Full Text
Publication Date: 2006-12-13 PubMed ID: 17174118DOI: 10.1016/j.joca.2006.10.016Google Scholar: Lookup
The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
LinkedInCopy
  • 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.

The research focuses on the unique death mechanism of hypertrophic chondrocytes (a type of cell found in cartilage), which is separate from the commonly-known process of apoptosis. The study aims to understand this process by looking at the ultrastructural changes these cells undergo during their demise and establishing a culture system for further examination.

Methodology

  • The study used growth cartilage samples from both fetal and growing postnatal horses. These samples were studied under electron microscopes.
  • Chondrocytes were extracted from the epiphyseal cartilage of fetal horses and grown in a controlled environment (pellet culture). They were then assessed using light and electron microscopes, and quantitative polymerase chain reaction.

Results

  • The research found that dying dark chondrocytes displayed progressive extrusion of their cytoplasm into the extracellular space. Light chondrocytes, on the other hand, appeared to disintegrate within their cellular membrane.
  • It was observed that culturing pellets in 0.1% fetal calf serum resulted in dying light and dark chondrocytes. These resembled what was visualized in living tissue samples.
  • Adding transforming growth factor-beta1 or increasing fetal calf serum to 10% resulted in an increased proportion of dark cells and led to cell death.
  • The hormone triiodothyronine enhanced the differentiation of both dark and light cells and caused their death.
  • Additionally, the dark cells showed higher expression of matrix metalloproteinase-13 compared to the light cells, which displayed increased type II collagen expression.

Conclusions

  • From the observations, it was concluded that both light and dark hypertrophic chondrocytes undergo unique non-apoptotic morphological changes prior to their death.
  • The study also established that pellet culture could be a viable model for studying the two types of physiological death of hypertrophic chondrocytes.

Cite This Article

APA
Ahmed YA, Tatarczuch L, Pagel CN, Davies HM, Mirams M, Mackie EJ. (2006). Physiological death of hypertrophic chondrocytes. Osteoarthritis Cartilage, 15(5), 575-586. https://doi.org/10.1016/j.joca.2006.10.016

Publication

Osteoarthritis and cartilage
ISSN: 1063-4584
NlmUniqueID: 9305697
Country: England
Language: English
Volume: 15
Issue: 5
Pages: 575-586

Researcher Affiliations

Ahmed, Y A
  • School of Veterinary Science, University of Melbourne, Parkville, Victoria 3010, Australia.
Tatarczuch, L
    Pagel, C N
      Davies, H M S
        Mirams, M
          Mackie, E J

            MeSH Terms

            • Animals
            • Apoptosis
            • Cell Death
            • Chondrocytes / ultrastructure
            • Collagen Type II / metabolism
            • Growth Plate / ultrastructure
            • Horses
            • Matrix Metalloproteinase 13 / metabolism
            • Microscopy, Electron
            • Transforming Growth Factor beta1 / metabolism

            Citations

            This article has been cited 18 times.
            1. Hallett SA, Ono W, Ono N. The hypertrophic chondrocyte: To be or not to be. Histol Histopathol 2021 Oct;36(10):1021-1036.
              doi: 10.14670/HH-18-355pubmed: 34137454google scholar: lookup
            2. Jann J, Gascon S, Roux S, Faucheux N. Influence of the TGF-β Superfamily on Osteoclasts/Osteoblasts Balance in Physiological and Pathological Bone Conditions. Int J Mol Sci 2020 Oct 14;21(20).
              doi: 10.3390/ijms21207597pubmed: 33066607google scholar: lookup
            3. Sheehy EJ, Kelly DJ, O'Brien FJ. Biomaterial-based endochondral bone regeneration: a shift from traditional tissue engineering paradigms to developmentally inspired strategies. Mater Today Bio 2019 Jun;3:100009.
              doi: 10.1016/j.mtbio.2019.100009pubmed: 32159148google scholar: lookup
            4. Olate S, Vásquez B, Sandoval C, Vasconcellos A, Alister JP, Del Sol M. Histological Analysis of Bone Repair in Mandibular Body Osteotomy Using Internal Fixation System in Three Different Gaps without Bone Graft in an Animal Model. Biomed Res Int 2019;2019:8043510.
              doi: 10.1155/2019/8043510pubmed: 31428646google scholar: lookup
            5. Lui JC, Yue S, Lee A, Kikani B, Temnycky A, Barnes KM, Baron J. Persistent Sox9 expression in hypertrophic chondrocytes suppresses transdifferentiation into osteoblasts. Bone 2019 Aug;125:169-177.
              doi: 10.1016/j.bone.2019.05.027pubmed: 31121357google scholar: lookup
            6. Wolff LI, Hartmann C. A Second Career for Chondrocytes-Transformation into Osteoblasts. Curr Osteoporos Rep 2019 Jun;17(3):129-137.
              doi: 10.1007/s11914-019-00511-3pubmed: 30949840google scholar: lookup
            7. Semevolos SA, Duesterdieck-Zellmer KF, Larson M, Kinsley MA. Expression of pro-apoptotic markers is increased along the osteochondral junction in naturally occurring osteochondrosis. Bone Rep 2018 Dec;9:19-26.
              doi: 10.1016/j.bonr.2018.06.003pubmed: 29998174google scholar: lookup
            8. Ayodele BA, Mirams M, Pagel CN, Mackie EJ. The vacuolar H(+) ATPase V(0) subunit d(2) is associated with chondrocyte hypertrophy and supports chondrocyte differentiation. Bone Rep 2017 Dec;7:98-107.
              doi: 10.1016/j.bonr.2017.08.002pubmed: 29062863google scholar: lookup
            9. Santos-Ledo A, Garcia-Macia M, Campbell PD, Gronska M, Marlow FL. Kinesin-1 promotes chondrocyte maintenance during skeletal morphogenesis. PLoS Genet 2017 Jul;13(7):e1006918.
              doi: 10.1371/journal.pgen.1006918pubmed: 28715414google scholar: lookup
            10. Yang C, Chen Y, Li Z, Cao H, Chen K, Lai P, Yan B, Huang B, Tang J, Fan S, Cai D, Jin D, Bai X, Zhou R. Chondrocyte-Specific Knockout of TSC-1 Leads to Congenital Spinal Deformity in Mice. Biomed Res Int 2017;2017:8215805.
              doi: 10.1155/2017/8215805pubmed: 28523278google scholar: lookup
            11. Jiang LB, Liu HX, Zhou YL, Sheng SR, Xu HZ, Xue EX. An ultrastructural study of chondroptosis: programmed cell death in degenerative intervertebral discs in vivo. J Anat 2017 Jul;231(1):129-139.
              doi: 10.1111/joa.12618pubmed: 28436567google scholar: lookup
            12. Samsa WE, Zhou X, Zhou G. Signaling pathways regulating cartilage growth plate formation and activity. Semin Cell Dev Biol 2017 Feb;62:3-15.
              doi: 10.1016/j.semcdb.2016.07.008pubmed: 27418125google scholar: lookup
            13. Haq SH. 5-Aza-2'-deoxycytidine acts as a modulator of chondrocyte hypertrophy and maturation in chick caudal region chondrocytes in culture. Anat Cell Biol 2016 Jun;49(2):107-15.
              doi: 10.5115/acb.2016.49.2.107pubmed: 27382512google scholar: lookup
            14. Millucci L, Giorgetti G, Viti C, Ghezzi L, Gambassi S, Braconi D, Marzocchi B, Paffetti A, Lupetti P, Bernardini G, Orlandini M, Santucci A. Chondroptosis in alkaptonuric cartilage. J Cell Physiol 2015 May;230(5):1148-57.
              doi: 10.1002/jcp.24850pubmed: 25336110google scholar: lookup
            15. Hall-Glenn F, Aivazi A, Akopyan L, Ong JR, Baxter RR, Benya PD, Goldschmeding R, van Nieuwenhoven FA, Hunziker EB, Lyons KM. CCN2/CTGF is required for matrix organization and to protect growth plate chondrocytes from cellular stress. J Cell Commun Signal 2013 Aug;7(3):219-30.
              doi: 10.1007/s12079-013-0201-ypubmed: 23666466google scholar: lookup
            16. Wong DM, Tam V, Lam R, Walsh KA, Tatarczuch L, Pagel CN, Reynolds EC, O'Brien-Simpson NM, Mackie EJ, Pike RN. Protease-activated receptor 2 has pivotal roles in cellular mechanisms involved in experimental periodontitis. Infect Immun 2010 Feb;78(2):629-38.
              doi: 10.1128/IAI.01019-09pubmed: 19933835google scholar: lookup
            17. Zhang P, Han D, Tang T, Zhang X, Dai K. The destruction evaluation in different foot joints: new ideas in collagen-induced arthritis rat model. Rheumatol Int 2009 Apr;29(6):607-13.
              doi: 10.1007/s00296-008-0731-4pubmed: 18982329google scholar: lookup
            18. Huang C, Zeng B, Zhou B, Chen G, Zhang Q, Hou W, Xiao G, Duan L, Hong N, Jin W. Single-cell transcriptomic analysis of chondrocytes in cartilage and pathogenesis of osteoarthritis. Genes Dis 2025 Mar;12(2):101241.
              doi: 10.1016/j.gendis.2024.101241pubmed: 39759119google scholar: lookup
            Subscribe to our newsletter
            Join 99,357 horse owners like you who receive our email updates on horse health and nutrition.