Author
Listed:
- A. Petersen
(Julius Wolff Institute, Charité—Universitätsmedizin Berlin
Berlin-Brandenburg Center for Regenerative Therapies, Charité—Universitätsmedizin Berlin)
- A. Princ
(Julius Wolff Institute, Charité—Universitätsmedizin Berlin)
- G. Korus
(Julius Wolff Institute, Charité—Universitätsmedizin Berlin)
- A. Ellinghaus
(Julius Wolff Institute, Charité—Universitätsmedizin Berlin)
- H. Leemhuis
(Matricel GmbH)
- A. Herrera
(Julius Wolff Institute, Charité—Universitätsmedizin Berlin
Berlin-Brandenburg School for Regenerative Therapies, Charité—Universitätsmedizin Berlin)
- A. Klaumünzer
(Julius Wolff Institute, Charité—Universitätsmedizin Berlin)
- S. Schreivogel
(Julius Wolff Institute, Charité—Universitätsmedizin Berlin
Berlin-Brandenburg School for Regenerative Therapies, Charité—Universitätsmedizin Berlin)
- A. Woloszyk
(Julius Wolff Institute, Charité—Universitätsmedizin Berlin
University of Texas Health Science Center San Antonio)
- K. Schmidt-Bleek
(Julius Wolff Institute, Charité—Universitätsmedizin Berlin
Berlin-Brandenburg Center for Regenerative Therapies, Charité—Universitätsmedizin Berlin)
- S. Geissler
(Julius Wolff Institute, Charité—Universitätsmedizin Berlin
Berlin-Brandenburg Center for Regenerative Therapies, Charité—Universitätsmedizin Berlin)
- I. Heschel
(Matricel GmbH)
- G. N. Duda
(Julius Wolff Institute, Charité—Universitätsmedizin Berlin
Berlin-Brandenburg Center for Regenerative Therapies, Charité—Universitätsmedizin Berlin
Berlin-Brandenburg School for Regenerative Therapies, Charité—Universitätsmedizin Berlin)
Abstract
Biomaterials developed to treat bone defects have classically focused on bone healing via direct, intramembranous ossification. In contrast, most bones in our body develop from a cartilage template via a second pathway called endochondral ossification. The unsolved clinical challenge to regenerate large bone defects has brought endochondral ossification into discussion as an alternative approach for bone healing. However, a biomaterial strategy for the regeneration of large bone defects via endochondral ossification is missing. Here we report on a biomaterial with a channel-like pore architecture to control cell recruitment and tissue patterning in the early phase of healing. In consequence of extracellular matrix alignment, CD146+ progenitor cell accumulation and restrained vascularization, a highly organized endochondral ossification process is induced in rats. Our findings demonstrate that a pure biomaterial approach has the potential to recapitulate a developmental bone growth process for bone healing. This might motivate future strategies for biomaterial-based tissue regeneration.
Suggested Citation
A. Petersen & A. Princ & G. Korus & A. Ellinghaus & H. Leemhuis & A. Herrera & A. Klaumünzer & S. Schreivogel & A. Woloszyk & K. Schmidt-Bleek & S. Geissler & I. Heschel & G. N. Duda, 2018.
"A biomaterial with a channel-like pore architecture induces endochondral healing of bone defects,"
Nature Communications, Nature, vol. 9(1), pages 1-16, December.
Handle:
RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-06504-7
DOI: 10.1038/s41467-018-06504-7
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Cited by:
- M. Gabriele Bixel & Kishor K. Sivaraj & Melanie Timmen & Vishal Mohanakrishnan & Anusha Aravamudhan & Susanne Adams & Bong-Ihn Koh & Hyun-Woo Jeong & Kai Kruse & Richard Stange & Ralf H. Adams, 2024.
"Angiogenesis is uncoupled from osteogenesis during calvarial bone regeneration,"
Nature Communications, Nature, vol. 15(1), pages 1-22, December.
- Wenwen Liu & Han Zhao & Chenguang Zhang & Shiqi Xu & Fengyi Zhang & Ling Wei & Fangyu Zhu & Ying Chen & Yumin Chen & Ying Huang & Mingming Xu & Ying He & Boon Chin Heng & Jinxing Zhang & Yang Shen & X, 2023.
"In situ activation of flexible magnetoelectric membrane enhances bone defect repair,"
Nature Communications, Nature, vol. 14(1), pages 1-14, December.
- Mariya M. Kucherenko & Pengchao Sang & Juquan Yao & Tara Gransar & Saphala Dhital & Jana Grune & Szandor Simmons & Laura Michalick & Dag Wulsten & Mario Thiele & Orr Shomroni & Felix Hennig & Ruhi Yet, 2023.
"Elastin stabilization prevents impaired biomechanics in human pulmonary arteries and pulmonary hypertension in rats with left heart disease,"
Nature Communications, Nature, vol. 14(1), pages 1-23, December.
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