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Clinical orthopaedics and related research2003; (407); 215-227; doi: 10.1097/00003086-200302000-00031

Early events in cartilage repair after subchondral bone microfracture.

Abstract: The current study investigated healing of large full-thickness articular cartilage defects during the first 8 weeks with and without penetration of the subchondral bone using microfracture in an established equine model of cartilage healing. Chondral defects in the weightbearing portion of the medial femoral condyle were made bilaterally; one defect in each horse was microfractured whereas the contralateral leg served as the control. The expression of cartilage extracellular matrix components (Types I and II collagen and aggrecan) was evaluated using histologic techniques, reverse transcription coupled polymerase chain reaction, in situ hybridization, and immunohistochemistry. This study confirms an increase in Type II collagen mRNA expression in repair tissue as early as 6 weeks after microfracture. Although other matrix mRNA and protein levels changed in concentration and tissue location over the course of the study, no significant differences were seen in microfractured defects. Although the microfracture techniques appear to improve clinical functionality, volume of repair tissue, and augment Type II collagen content, aggrecan content is less than ideal. Therefore, methods to enhance key matrix components such as aggrecan after microfracture may additionally improve repair tissue observed after the procedure.
Publication Date: 2003-02-05 PubMed ID: 12567150DOI: 10.1097/00003086-200302000-00031Google Scholar: Lookup
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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.

The research investigated the healing process of large full-thickness cartilage defects with and without subchondral bone penetration using microfracture within an 8-week period. Observations reveal increased expression of Type II collagen and changes in other matrix components’ concentration and location, with microfracture techniques improving clinical functionality, repair tissue volume and Type II collagen content.

Investigation Method

  • The study utilized an established equine model for cartilage healing to observe the recovery of large full-thickness chondral (cartilage) defects.
  • In each horse, a chondral defect was created in the weight-bearing portion of the medial femoral condyle (part of the knee joint) on both legs.
  • One defect in each horse was treated with microfracture (a surgical technique where small holes are drilled into the bone to stimulate healing), while the other defect served as a control for comparison purposes.

Data Collection & Evaluation

  • The research team evaluated the expression of cartilage extracellular matrix components, specifically Types I and II collagen and a protein called ‘aggrecan’, important in the cartilage structure.
  • The evaluation methods involved histologic techniques, reverse transcription polymerase chain reaction (a method to convert RNA to DNA for analysis), in situ hybridization (the use of a labeled complementary DNA strand to locate a specific DNA sequence in a tissue), and immunohistochemistry (a method to visualize specific antigens in tissues).

Findings & Implications

  • The study confirmed an increase in Type II collagen mRNA expression in the repair tissue as early as six weeks after undergoing microfracture.
  • Changes were also observed in the concentration and tissue location of other matrix mRNA and protein levels, but significant differences were not detected in defects treated with microfracture.
  • The microfracture technique appeared to improve clinical functionality, augment the volume of repair tissue, and increase the content of Type II collagen.
  • Nonetheless, the content of aggrecan in the tissue healed by microfracture was found to be less than optimal.
  • The researchers suggest that methods which further enhance key matrix components such as aggrecan following microfracture might improve the quality of repair tissue after this procedure.

Cite This Article

APA
Frisbie DD, Oxford JT, Southwood L, Trotter GW, Rodkey WG, Steadman JR, Goodnight JL, McIlwraith CW. (2003). Early events in cartilage repair after subchondral bone microfracture. Clin Orthop Relat Res(407), 215-227. https://doi.org/10.1097/00003086-200302000-00031

Publication

ISSN: 0009-921X
NlmUniqueID: 0075674
Country: United States
Language: English
Issue: 407
Pages: 215-227

Researcher Affiliations

Frisbie, David D
  • Orthopaedic Research Center, Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO, USA. dfrisbie@lamar.colostate.edu
Oxford, Julia T
    Southwood, Louise
      Trotter, Gayle W
        Rodkey, William G
          Steadman, J Richard
            Goodnight, Jennifer L
              McIlwraith, C Wayne

                MeSH Terms

                • Aggrecans
                • Animals
                • Cartilage, Articular / injuries
                • Cartilage, Articular / pathology
                • Cartilage, Articular / physiopathology
                • Collagen Type I / analysis
                • Collagen Type I / genetics
                • Collagen Type II / analysis
                • Collagen Type II / genetics
                • Disease Models, Animal
                • Extracellular Matrix Proteins
                • Hip Fractures / pathology
                • Hip Fractures / physiopathology
                • Hip Fractures / surgery
                • Horses
                • In Situ Hybridization
                • Lectins, C-Type
                • Proteoglycans / analysis
                • Proteoglycans / genetics
                • RNA, Messenger / analysis
                • RNA, Messenger / genetics
                • Reverse Transcriptase Polymerase Chain Reaction
                • Time Factors
                • Wound Healing / physiology

                Grant Funding

                • R01 AR047985-02 / NIAMS NIH HHS
                • R01 AR047985-03 / NIAMS NIH HHS
                • K02 AR048672-01 / NIAMS NIH HHS
                • R01 AR047985-04 / NIAMS NIH HHS
                • P20 RR016454-096114 / NCRR NIH HHS
                • R01 AR047985-05 / NIAMS NIH HHS
                • P20 RR016454-086155 / NCRR NIH HHS
                • K02 AR048672-05 / NIAMS NIH HHS
                • K02 AR048672-02 / NIAMS NIH HHS
                • R01 AR047985-01 / NIAMS NIH HHS
                • K02 AR048672-04 / NIAMS NIH HHS
                • K02 AR048672-03 / NIAMS NIH HHS

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