gms | German Medical Science

German Congress of Orthopedic and Trauma Surgery (DKOU 2017)

24.10. - 27.10.2017, Berlin

Autologous bone marrow aspirate enhanced microfracture counteracts the early loss of subchondral bone in a translational model of osteochondral repair

Meeting Abstract

  • presenting/speaker Liang Gao - Center of Experimental Orthopaedics, Saarland University, Homburg, Germany
  • Kathrin Müller-Brandt - Center of Experimental Orthopaedics, Saarland University, Homburg, Germany
  • Patrick Orth - Center of Experimental Orthopaedics, Saarland University, Homburg, Germany
  • Lars Goebel - Center of Experimental Orthopaedics, Saarland University, Homburg, Germany
  • Magali Cucchiarini - Center of Experimental Orthopaedics, Saarland University, Homburg, Germany
  • Henning Madry - Center of Experimental Orthopaedics, Saarland University, Homburg, Germany

Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2017). Berlin, 24.-27.10.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. DocGR18-519

doi: 10.3205/17dkou533, urn:nbn:de:0183-17dkou5333

Published: October 23, 2017

© 2017 Gao et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.


Outline

Text

Objectives: Microfracture (MFX) is the most clinically used marrow stimulation technique for treatment of symptomatic focal articular cartilage defects. Recent data suggest that enhanced MFX by autologous bone marrow aspirate offers a promising one-step approach to overcome the shortcomings of the standard MFX technique. Here, we investigated the early osteochondral repair of MFX without and with autologous bone marrow aspirate in a large animal model.

Methods: Full-thickness chondral defects were created on the bilateral trochlear facets of both knee joints of 6 adult Göttingen minipigs. Defects were either treated with (1) debridement down to the subchondral bone plate alone, (2) debridement with MFX, or (3) bone marrow aspirate enhanced MFX. At 4 weeks postoperatively, articular cartilage repair was evaluated macroscopically and histologically with the established scoring systems. Type-II collagen content was assessed by immunohistochemistry. Subchondral bone alterations were evaluated by a novel algorithm and micro-CT. The measured and calculated values of bone volume fraction (BV/TV) of the treated subchondral bone were compared among the three groups. Results were analyzed statistically using one-way ANOVA with Tukey's post-hoc test and Mann-Whitney U test.

Results and Conclusion: Macroscopic and histological evaluation of the repair tissue revealed similar quality of the repair tissue following the three treatments. A notably impaired score value of subchondral bone reconstitution was observed after MFX compared with debridement. This adverse effect of MFX was counteracted by additional bone marrow aspirate. Immunoreactivity to type-II collagen was not significantly different among the three groups.

Qualitative evaluation of the subchondral bone with a novel algorithm and micro-CT found no intra-lesional osteophytes and subchondral bone cysts in all groups. Compared with MFX, enhanced MFX yielded more residual MFX holes and less peri-hole bone resorption. In the subchondral bone plate (SBP-defect), compared with MFX and enhanced MFX, debridement alone led to less severe osseous deterioration with the highest cortical thickness (P = 0.006). In the subarticular spongiosa (SAS-defect), enhanced MFX yielded a considerably increased BV/TV (46.07% ± 6.38%) compared with MFX (36.91% ± 3.90%; P = 0.008). Compared with MFX alone, enhanced MFX also led to a significantly lower trabecular separation (P = 0.015).

Comparison between the measured and calculated values of BV/TV of SAS-defect showed that enhanced MFX yielded the significantly highest preservation rate of BV/TV (P = 0.0002).

In summary, microfracture of cartilage defects induced a significant early loss of the underlying subchondral bone. Additional application of bone marrow to the microfractured defects might counteract such early loss of subchondral bone.