Affiliation:
1. Department of Pediatric Dentistry, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology Peking University Beijing China
2. Department of Oral and Maxillofacial Surgery Peking University School and Hospital of Stomatology Beijing China
3. First Clinical Division Peking University School and Hospital of Stomatology Beijing China
Abstract
AbstractBackground/AimPulp mineralisation is a survival process that may occur in the pulp of immature teeth following trauma. However, the mechanism of this process remains unclear. The aim of this study was to evaluate the histological manifestations of pulp mineralisation after intrusion in immature molars of rats.Materials and MethodsThree‐week‐old male Sprague–Dawley rats were subjected to intrusive luxation of the right maxillary second molar by an impact force from a striking instrument through a metal force transfer rod. The left maxillary second molar of each rat was used as a control. The control and injured maxillae were collected at 3, 7, 10, 14, and 30 days after trauma (n = 15 per time group) and evaluated using haematoxylin and eosin staining and immunohistochemistry. Independent two‐tailed Student's t‐test was used for statistical comparison of the immunoreactive area.ResultsPulp atrophy and mineralisation were observed in 30%–40% of the animals, and no pulp necrosis occurred. Ten days after trauma, pulp mineralisation, with osteoid tissue rather than reparative dentin, formed around the newly vascularised areas in the coronal pulp. CD90‐immunoreactive cells were observed in the sub‐odontoblastic multicellular layer in control molars, whereas the number of these cells was decreased in the traumatised teeth. CD105 localised in cells around the pulp osteoid tissue of the traumatised teeth, whereas in control teeth, it was only expressed in the vascular endothelial cells of capillaries in the odontoblastic or sub‐odontoblastic layers. In specimens with pulp atrophy at 3–10 days after trauma, hypoxia inducible factor expression and CD11b‐immunoreactive inflammatory cells increased.ConclusionsFollowing intrusive luxation of immature teeth without crown fractures in rats, no pulp necrosis occurred. Instead, pulp atrophy and osteogenesis around neovascularisation with activated CD105‐immunoreactive cells were observed in the coronal pulp microenvironment characterised by hypoxia and inflammation.
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2 articles.
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