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Right arrow Trachea and bronchi

J Thorac Cardiovasc Surg 2004;127:329-334
© 2004 The American Association for Thoracic Surgery


General thoracic surgery

Slow release of bone morphogenetic protein 2 from a gelatin sponge to promote regeneration of tracheal cartilage in a canine model

Taku Okamoto, MDa, Yasumichi Yamamoto, MDa, Masashi Gotoh, MDa, Cheng-Long Huang, MDa, Tatsuo Nakamura, MDb, Yasuhiko Shimizu, MDb, Yasuhiko Tabata, PhDb, Hiroyasu Yokomise, MDa,*

a Second Department of Surgery, Kagawa Medical University, Kagawa, Japan
b Institute for Frontier Medical Sciences, Kyoto University, Kyoto, Japan

Received for publication May 28, 2003; revisions received August 11, 2003; accepted for publication August 19, 2003.

* Address for correspondence: Hiroyasu Yokomise, MD, Second Department of Surgery, Kagawa Medical University, 1750-1, Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan
yokomise{at}kms.ac.jp

OBJECTIVES: We investigated whether bone morphogenetic protein 2, released slowly from a gelatin sponge, could induce cartilage regeneration in a canine model of tracheomalacia and evaluated the long-term results.

METHODS: A 1 x 5-cm gap was made in the anterior cervical trachea by removing 5-cm long strips of 10 sequential cartilagines. In the control group (n = 5), the gaps were left untreated. In the gelatin sponge group (n = 5), a gelatin sponge soaked in a buffer solution was implanted in each defect. In the bone morphogenetic protein group (n = 5), a gelatin sponge soaked in a buffer solution containing 12 µg bone morphogenetic protein 2 was implanted in each defect.

RESULTS: Tracheomalacia was observed in the control and gelatin sponge groups but not in the bone morphogenetic protein group. No regenerated cartilage was detected in the control or gelatin sponge groups, even 6 months after surgery. In contrast, regenerated cartilage, which had developed from the host perichondrium, was observed around the stumps of the resected cartilagines in the bone morphogenetic protein group. This regenerated cartilage maintained the integrity of the internal lumen for longer than 6 months. A compressive fracture test revealed that the tracheal cartilage in the bone morphogenetic protein group was significantly more stable than that in the gelatin sponge and control groups (P = .0015 and P = .0001, respectively).

CONCLUSIONS: In this canine model of tracheomalacia, cartilage regeneration was induced around the stumps of tracheal cartilagines by bone morphogenetic protein 2 released slowly from a gelatin sponge. This regenerated cartilage was not reabsorbed for longer than 6 months and was strong enough to maintain the integrity of the internal lumen of the trachea.





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