Maha M F Mounir1, Moustafa A Matar2, Yaping Lei3, Malcolm L Snead4. 1. Faculty of Dentistry, King Abdulaziz University (KAU), Jamaa District, Jeddah, Kingdom of Saudi Arabia; Faculty of Dentistry, Alexandria University, Alexandria, Egypt. 2. Faculty of Dentistry, Pharos University, Alexandria, Egypt. 3. Center for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry of USC, The University of Southern California, Los Angeles, California. 4. Center for Craniofacial Molecular Biology, Herman Ostrow School of Dentistry of USC, The University of Southern California, Los Angeles, California. Electronic address: mlsnead@usc.edu.
Abstract
INTRODUCTION: Recombinant DNA-produced amelogenin protein was compared with calcium hydroxide in a study of immature apex closure conducted in 24 young mongrel dogs. METHODS: Root canals of maxillary and mandibular right premolars (n = 240) were instrumented and left open for 14 days. Canals were cleansed, irrigated, and split equally for treatment with recombinant mouse amelogenin (n = 120) or calcium hydroxide (n = 120). RESULTS: After 1, 3, and 6 months, the animals were sacrificed and the treated teeth recovered for histologic assessment and immunodetection of protein markers associated with odontogenic cells. After 1 month, amelogenin-treated canals revealed calcified tissue formed at the apical foramen and a pulp chamber containing soft connective tissue and hard tissue; amelogenin-treated canals assessed after 3- and 6-month intervals further included apical tissue functionally attached to bone by a periodontal ligament. In contrast, calcified apical tissue was poorly formed in the calcium hydroxide group, and soft connective tissue within the pulp chamber was not observed. CONCLUSIONS: The findings from this experimental strategy suggest recombinant amelogenin protein can signal cells to enhance apex formation in nonvital immature teeth and promote soft connective tissue regeneration.
INTRODUCTION: Recombinant DNA-produced amelogenin protein was compared with calcium hydroxide in a study of immature apex closure conducted in 24 young mongrel dogs. METHODS: Root canals of maxillary and mandibular right premolars (n = 240) were instrumented and left open for 14 days. Canals were cleansed, irrigated, and split equally for treatment with recombinant mouseamelogenin (n = 120) or calcium hydroxide (n = 120). RESULTS: After 1, 3, and 6 months, the animals were sacrificed and the treated teeth recovered for histologic assessment and immunodetection of protein markers associated with odontogenic cells. After 1 month, amelogenin-treated canals revealed calcified tissue formed at the apical foramen and a pulp chamber containing soft connective tissue and hard tissue; amelogenin-treated canals assessed after 3- and 6-month intervals further included apical tissue functionally attached to bone by a periodontal ligament. In contrast, calcified apical tissue was poorly formed in the calcium hydroxide group, and soft connective tissue within the pulp chamber was not observed. CONCLUSIONS: The findings from this experimental strategy suggest recombinant amelogenin protein can signal cells to enhance apex formation in nonvital immature teeth and promote soft connective tissue regeneration.
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