Odaph, also known as Odontogenesis-associated phosphoprotein, is crucial for enamel formation during amelogenesis [1,2,3,4,5,6]. It is a component of the atypical basal lamina at the interface between maturation ameloblasts and the enamel, and may be involved in pathways related to enamel mineralization and the integrity of the basal lamina [1,5,6]. Understanding its function is important for deciphering the pathophysiology of amelogenesis imperfecta (AI) [1,4]. Genetic models, such as KO mouse models, have been valuable in studying Odaph's function [1,2,3].

In Odaph knockout mice (Odaph -/-), teeth showed severe attrition and reduced enamel mineralization. Ameloblasts shortened rapidly, lost polarity and exhibited pathology from the transition or early-maturation stage. The integrity of the atypical basal lamina was impaired, and the expression of maturation-stage related genes was decreased [1]. Odaph overexpression in ameloblasts (OdaphTg mice) led to thinner enamel, abnormal Tomes' processes, and abnormal enamel mineralization, possibly due to hindrance of Amelx secretion and induction of endoplasmic reticulum stress [2]. In OdaphC41*/C41* mice with Odaph truncation, the secretory stage was normal, but the post-secretory transition failed to generate maturation stage ameloblasts, resulting in cyst formation [3].

In summary, Odaph plays vital roles in amelogenesis, especially in maintaining the integrity of the atypical basal lamina during the maturation stage and influencing enamel mineralization. Studies using Odaph KO mouse models have significantly contributed to understanding the pathophysiology of autosomal recessive hypocalcified AI [1,3,4].

References:

1. Ji, Yikang, Li, Cong, Tian, Yuan, Gao, Yuguang, Zhang, Li. 2021. Maturation stage enamel defects in Odontogenesis-associated phosphoprotein (Odaph) deficient mice. In Developmental dynamics : an official publication of the American Association of Anatomists, 250, 1505-1517. doi:10.1002/dvdy.336. https://pubmed.ncbi.nlm.nih.gov/33772937/

2. Mu, Haiyu, Dong, Zhiheng, Wang, Yumin, Liu, Xiaoying, Gao, Yuguang. 2022. Odontogenesis-Associated Phosphoprotein (ODAPH) Overexpression in Ameloblasts Disrupts Enamel Formation via Inducing Abnormal Mineralization of Enamel in Secretory Stage. In Calcified tissue international, 111, 611-621. doi:10.1007/s00223-022-01023-6. https://pubmed.ncbi.nlm.nih.gov/36163390/

3. Liang, Tian, Hu, Yuanyuan, Kawasaki, Kazuhiko, Simmer, James P, Hu, Jan C-C. 2021. Odontogenesis-associated phosphoprotein truncation blocks ameloblast transition into maturation in OdaphC41*/C41* mice. In Scientific reports, 11, 1132. doi:10.1038/s41598-020-80912-y. https://pubmed.ncbi.nlm.nih.gov/33441959/

4. Wang, Shih-Kai, Lee, Zhe-Hao, Aref, Parissa, Chu, Kuan-Yu. 2023. A novel ODAPH mutation causing amelogenesis imperfecta and its expression in human dental tissues. In Journal of dental sciences, 19, 524-531. doi:10.1016/j.jds.2023.09.020. https://pubmed.ncbi.nlm.nih.gov/38303846/

5. Li, Cong, Gao, Yan, Xu, Zhenzhen, Gao, Yuguang, Zhang, Li. 2021. Expression and localization of amelotin, laminin γ2 and odontogenesis-associated phosphoprotein (ODAPH) on the basal lamina and junctional epithelium. In Journal of molecular histology, 53, 111-118. doi:10.1007/s10735-021-10026-w. https://pubmed.ncbi.nlm.nih.gov/34709488/

6. Tian, Yuan, Mu, Haiyu, Dong, Zhiheng, Gao, Yan, Zhang, Li. 2022. The synergistic effects of TGF-β1 and RUNX2 on enamel mineralization through regulating ODAPH expression during the maturation stage. In Journal of molecular histology, 53, 483-492. doi:10.1007/s10735-022-10060-2. https://pubmed.ncbi.nlm.nih.gov/35165792/