Recombinant Amelogenin Protein Induces Apical Closure and Pulp Regeneration in Open-apex, Nonvital Permanent Canine Teeth

• Recombinant DNA–expressed purified amelogenin protein was compared with calcium hydroxide.
• Immature apex closure was studied in 24 young mongrel dogs.
• Amelogenin-treated canals revealed apical foramen closure superior to calcium hydroxide.
• Amelogenin-treated canals contained soft tissue organized similarly to authentic pulp tissue.
• Recombinant amelogenin enhanced apex formation in immature teeth with partial soft connective tissue regeneration.

IntroductionRecombinant DNA–produced amelogenin protein was compared with calcium hydroxide in a study of immature apex closure conducted in 24 young mongrel dogs.MethodsRoot 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).ResultsAfter 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.ConclusionsThe 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.