Abstract
Reconstruction of articular surfaces destroyed by infection or trauma is hampered by the lack of suitable graft tissues. Perichondrium autotransplants have been used for this purpose. However, the role of the transplanted perichondrium in the healing of resurfaced joints have not been investigated. Perichondrial and periosteal tissues were harvested from rats hemizygous for a ubiquitously expressed enhanced green fluorescent protein (EGFP) transgene and transplanted into full-thickness articular cartilage defects at the trochlear groove of distal femur in wild-type littermates. As an additional control, cartilage defects were left without a transplant (no transplant control). Distal femurs were collected 3, 14, 56, 112 days after surgery. Transplanted cells and their progenies were readily detected in the defects of perichondrium and periosteum transplanted animals but not in defects left without a transplant. Perichondrium transplants expressed SOX9 and with time differentiated into a hyaline cartilage that expanded and filled out the defects with Col2a1-positive chondrocytes and a matrix rich in proteoglycans. Interestingly, at later timepoints the cartilaginous perichondrium transplants were actively remodeled into bone at the transplant-bone interface and at post-surgery day 112 EGFP-positive perichondrium cells at the articular surface were positive for Prg4. In addition, both perichondrium and periosteum transplants contributed cells to the subchondral bone and bone marrow, suggesting differentiation into osteoblast/osteocytes as well as bone marrow cells. In summary, we found that perichondrium transplanted to articular cartilage defects develops into an articular-like, hyaline cartilage that integrates with the subchondral bone, and is maintained for an extended time. The findings indicate that perichondrium is a suitable tissue for repair and engineering of articular cartilage.
Competing Interest Statement
The authors have declared no competing interest.
Footnotes
Grants or fellowships supporting the writing of the paper: The work of D.M. and T.V. was supported by grants from the Uppsala County and D.M. was also supported by Dalarna County Council.
This work was supported by grants from the Swedish Research Council (project K2015–54X-22 736–01–4 & 2015-02227), the Swedish Governmental Agency for Innovation Systems (Vinnova) (2014-01438), Marianne and Marcus Wallenberg Foundation, the Stockholm County Council, Byggmästare Olle Engkvist Stiftelse, the Swedish Society of Medicine, Novo Nordisk Foundation, Erik och Edith Fernström Foundation for Medical Research, HKH Kronprinsessan Lovisas förening för barnasjukvård, Sällskapet Barnavård, Stiftelsen Frimurare Barnhuset i Stockholm, Promobilia, Nyckelfonden, and Karolinska Institutet, Stockholm, Sweden, and Örebro University, Örebro, Sweden.
Disclosure summary: None of the authors have any potential conflict of interests or anything to declare that is directly related to this work. ON has received consulting fees from Kyowa Kirin Inc and speakers’ honoraria from Merck and Pfizer, and research funds to the department of ON from Kyowa Kirin and Novo Nordisk Foundation.
Data availability All data included in this study are available from the corresponding author upon request.