10.2.8 - Histological and Inflammatory Cytokine Analysis of OLT After Failed Microfracture, a Comparison to Fresh Allograft Controls
- R. Danilkowicz (Durham, US)
- R. Danilkowicz (Durham, US)
- N. Allen (Durham, US)
- N. Grimm (Boise, US)
- D. Nettles (Durham, US)
- J. Nunley (Durham, US)
- M. Easley (Durham, US)
- S. Adams (Morrisville, US)
Abstract
Purpose
The purpose of this study is to characterize the structural and biochemical makeup of failed microfracture lesions in an effort to identify potential reasons for continued pain and poor OLT healing after microfracture as well as identify potential avenues for future research and early intervention.
Methods and Materials
Eight specimens were analyzed from symptomatic OLTs after microfracture who later underwent fresh osteochondral allograft transplantation. For each patient, the failed microfracture specimen and a portion of the fresh allograft replacement tissue were collected. The allograft served as a control. Histology of the failed microfracture and the allograft replacement were scored using the Osteoarthritis Research Society International (OARSI) system. Surface roughness was also compared. In addition, tissue culture supernatants were analyzed for sixteen secreted cytokines and matrix metalloproteinases (MMPs) responsible for inflammation, pain, cartilage damage, and chondrocyte death.
Results
The OARSI grade, stage, and total score as well as surface smoothness were significantly lower in the failed microfracture sample, indicating better cartilage and bone morphology for the allografts compared to the failed microfracture lesions. Analyzed cytokines and MMPs were significantly elevated in the microfracture tissue culture supernatants when compared to fresh osteochondral tissue supernatants.
Conclusion
The current study is the first to provide histologic and secretomic evidence demonstrating insufficiencies of osteochondral tissue after failed microfracture. These data demonstrate a significantly rougher cartilage surface, cartilage and subchondral bone histology that more closely resembles osteoarthritis, and elevated inflammatory cytokines and matrix metalloproteinases responsible for pain, inflammation, cartilage damage, and chondrocyte death when compared to fresh osteochondral allografts used as controls.