Chondrocyte death and cartilage degradation after autologous osteochondral transplantation surgery in a rabbit model

Lawrence V. Gulotta, Jonas R. Rudzki, David Kovacevic, Christopher C T Chen, Dejan Milentijevic, Riley J. Williams

Research output: Contribution to journalArticle

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Abstract

Background: Autologous osteochondral transplantation surgery requires an impact force on the graft that may cause chondrocyte death and matrix degradation. This study attempted to determine the degree to which this occurs in a rabbit model shortly after the procedure. Hypothesis: Impaction of a press-fit autologous osteochondral graft in vivo results in chondrocyte necrosis, apoptosis, and matrix degradation at early time points. Study Design: Controlled laboratory study. Methods: Twenty New Zealand White rabbits underwent unilateral osteochondral transplantation (OT) surgeries, and 10, bilateral sham surgeries. Fifteen animals were sacrificed at time zero (10 sham-0 limbs, 10 OT-0 limbs), and 15, 4 days after surgery (10 sham-4 limbs, 10 OT-4 limbs). Chondrocyte viability/necrosis was determined with cell vital staining. Chondrocyte apoptosis was determined by TUNEL, Bcl-2, and M30 assays. Cartilage matrix degradation was determined by routine light and polarized light microscopy and COL2-3/4Cshort immunohistochemistry. Statistical analysis was performed with a 2-way analysis of variance (P <.05). Results: There were significantly fewer viable cells in OT-4 than in sham-4. A similar difference in cell viability was found in OT-0 versus sham-0. There were more TUNEL-positive cells in OT-4 as compared with OT-0, sham-0, and sham-4; however, there was little or no staining of Bcl-2 and M30. Mankin scores were higher in both OT groups versus both sham groups at time zero and day 4. The OT-4 group had positive staining for COL2-3/4Cshort that corresponded with a loss of collagen birefringence at the superficial zone. Conclusion: Osteochondral transplantation procedures performed by tamping a press-fit graft induce chondrocyte necrosis and matrix metalloproteinase-mediated cartilage matrix degradation. However, apoptosis was not found to a major contributor to cell death in this model. Clinical Relevance: Results of osteochondral transplantation procedures may be improved by atraumatic insertion and fixation techniques or by pharmacologic agents that can block these degradative processes.

Original languageEnglish (US)
Pages (from-to)1324-1333
Number of pages10
JournalAmerican Journal of Sports Medicine
Volume37
Issue number7
DOIs
StatePublished - 2009

Fingerprint

Autologous Transplantation
Chondrocytes
Cartilage
Transplantation
Rabbits
Extremities
Necrosis
In Situ Nick-End Labeling
Apoptosis
Staining and Labeling
Transplants
Polarization Microscopy
Birefringence
Matrix Metalloproteinases
Ambulatory Surgical Procedures
Cause of Death
Cell Survival
Analysis of Variance
Cell Death
Collagen

Keywords

  • Apoptosis
  • Cartilage degradation
  • Chondrocyte death
  • Osteochondral transplantation

ASJC Scopus subject areas

  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation
  • Medicine(all)

Cite this

Chondrocyte death and cartilage degradation after autologous osteochondral transplantation surgery in a rabbit model. / Gulotta, Lawrence V.; Rudzki, Jonas R.; Kovacevic, David; Chen, Christopher C T; Milentijevic, Dejan; Williams, Riley J.

In: American Journal of Sports Medicine, Vol. 37, No. 7, 2009, p. 1324-1333.

Research output: Contribution to journalArticle

Gulotta, Lawrence V. ; Rudzki, Jonas R. ; Kovacevic, David ; Chen, Christopher C T ; Milentijevic, Dejan ; Williams, Riley J. / Chondrocyte death and cartilage degradation after autologous osteochondral transplantation surgery in a rabbit model. In: American Journal of Sports Medicine. 2009 ; Vol. 37, No. 7. pp. 1324-1333.
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T1 - Chondrocyte death and cartilage degradation after autologous osteochondral transplantation surgery in a rabbit model

AU - Gulotta, Lawrence V.

AU - Rudzki, Jonas R.

AU - Kovacevic, David

AU - Chen, Christopher C T

AU - Milentijevic, Dejan

AU - Williams, Riley J.

PY - 2009

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N2 - Background: Autologous osteochondral transplantation surgery requires an impact force on the graft that may cause chondrocyte death and matrix degradation. This study attempted to determine the degree to which this occurs in a rabbit model shortly after the procedure. Hypothesis: Impaction of a press-fit autologous osteochondral graft in vivo results in chondrocyte necrosis, apoptosis, and matrix degradation at early time points. Study Design: Controlled laboratory study. Methods: Twenty New Zealand White rabbits underwent unilateral osteochondral transplantation (OT) surgeries, and 10, bilateral sham surgeries. Fifteen animals were sacrificed at time zero (10 sham-0 limbs, 10 OT-0 limbs), and 15, 4 days after surgery (10 sham-4 limbs, 10 OT-4 limbs). Chondrocyte viability/necrosis was determined with cell vital staining. Chondrocyte apoptosis was determined by TUNEL, Bcl-2, and M30 assays. Cartilage matrix degradation was determined by routine light and polarized light microscopy and COL2-3/4Cshort immunohistochemistry. Statistical analysis was performed with a 2-way analysis of variance (P <.05). Results: There were significantly fewer viable cells in OT-4 than in sham-4. A similar difference in cell viability was found in OT-0 versus sham-0. There were more TUNEL-positive cells in OT-4 as compared with OT-0, sham-0, and sham-4; however, there was little or no staining of Bcl-2 and M30. Mankin scores were higher in both OT groups versus both sham groups at time zero and day 4. The OT-4 group had positive staining for COL2-3/4Cshort that corresponded with a loss of collagen birefringence at the superficial zone. Conclusion: Osteochondral transplantation procedures performed by tamping a press-fit graft induce chondrocyte necrosis and matrix metalloproteinase-mediated cartilage matrix degradation. However, apoptosis was not found to a major contributor to cell death in this model. Clinical Relevance: Results of osteochondral transplantation procedures may be improved by atraumatic insertion and fixation techniques or by pharmacologic agents that can block these degradative processes.

AB - Background: Autologous osteochondral transplantation surgery requires an impact force on the graft that may cause chondrocyte death and matrix degradation. This study attempted to determine the degree to which this occurs in a rabbit model shortly after the procedure. Hypothesis: Impaction of a press-fit autologous osteochondral graft in vivo results in chondrocyte necrosis, apoptosis, and matrix degradation at early time points. Study Design: Controlled laboratory study. Methods: Twenty New Zealand White rabbits underwent unilateral osteochondral transplantation (OT) surgeries, and 10, bilateral sham surgeries. Fifteen animals were sacrificed at time zero (10 sham-0 limbs, 10 OT-0 limbs), and 15, 4 days after surgery (10 sham-4 limbs, 10 OT-4 limbs). Chondrocyte viability/necrosis was determined with cell vital staining. Chondrocyte apoptosis was determined by TUNEL, Bcl-2, and M30 assays. Cartilage matrix degradation was determined by routine light and polarized light microscopy and COL2-3/4Cshort immunohistochemistry. Statistical analysis was performed with a 2-way analysis of variance (P <.05). Results: There were significantly fewer viable cells in OT-4 than in sham-4. A similar difference in cell viability was found in OT-0 versus sham-0. There were more TUNEL-positive cells in OT-4 as compared with OT-0, sham-0, and sham-4; however, there was little or no staining of Bcl-2 and M30. Mankin scores were higher in both OT groups versus both sham groups at time zero and day 4. The OT-4 group had positive staining for COL2-3/4Cshort that corresponded with a loss of collagen birefringence at the superficial zone. Conclusion: Osteochondral transplantation procedures performed by tamping a press-fit graft induce chondrocyte necrosis and matrix metalloproteinase-mediated cartilage matrix degradation. However, apoptosis was not found to a major contributor to cell death in this model. Clinical Relevance: Results of osteochondral transplantation procedures may be improved by atraumatic insertion and fixation techniques or by pharmacologic agents that can block these degradative processes.

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