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Occurrence and Histopathologic Features of Odontoclastic Resorption on the Internal Dentin Wall after Replantation of Rat Molars.

吸收 臼齿 牙髓(牙) 牙本质 牙科 牙再植 再植 人口 医学 化学 病理 解剖 牙根吸收 环境卫生
作者
Yoshihito Shimazu,Hisao Yagishita,Shunichiro Sato,Chihiro Kondo,Ichiroh Katsuumi,Takaaki Aoba
出处
期刊:Oral Medicine & Pathology [The Japanese Society for Oral Pathology]
卷期号:6 (2): 59-64
标识
DOI:10.3353/omp.6.59
摘要

The etiology, pathogenesis and prognosis of internal root resorption in human dentition remain to be better understood. The present study aimed to gain better insight into the pathways by which multinucleated odontoclasts are recruited and activated on the dentin wall, giving rise to resorption lacunae in the disrupted pulp environment after tooth replantation. The upper first molars were luxated and then repositioned in the original socket. Post-treatment events were monitored over 28 days, and tissue specimens were prepared at time intervals. Histologic examination of the mesial and disto-palatal roots of the replanted first molars verified the occurrence of resorption lacunae accompanying TRAP-positive multinuclear cells on the internal dentin wall around day 7 after tooth replantation. Ninety-nine resorption lacunae were detected for the histologically examined 46 roots. These lacunae were classified into A and B types, which appeared to correspond to surface and inflammatory types of external root resorption, respectively. Key events leading to the establishment of odontoclastic resorption of the pulp-side dentin wall were the replacement of the innate pulp tissue with the ingrowth of granulation tissues and the assembly of a new cell population comprising macrophages and fibroblastic stromal cells. The overall results support the hypothesis that the innate pulp of rat molars possesses in potency inhibitory functions against undesirable resorption activities, but after impairment of the innate pulp environment after tooth replantation, a new paradigm of cell-matrices and cell-cell interactions may act cooperatively to induce clastic activities on the internal predentin/dentin wall.

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