Bastos Juliana Vilela, Côrtes Maria Ilma de Souza
Universidade Federal de Minas Gerais - UFMG, School of Dentistry, Department of Restorative Dentistry, Belo Horizonte, MG, Brazil.
Pontifícia Universidade Católica de Minas Gerais - PUC-MG, Department of Dentistry, Belo Horizonte, MG, Brazil.
Braz Oral Res. 2018 Oct 18;32(suppl 1):e75. doi: 10.1590/1807-3107bor-2018.vol32.0075.
Pulp canal obliteration (PCO) is a frequent finding associated with pulpal revascularization after luxation injuries of young permanent teeth. The underlying mechanisms of PCO are still unclear, and no experimental scientific evidence is available, except the results of a single histopathological study. The lack of sound knowledge concerning this process gives rise to controversies, including the most suitable denomination. More than a mere semantic question, the denomination is an important issue, because it reflects the nature of this process, and directly impacts the treatment plan decision. The hypothesis that accelerated dentin deposition is related to the loss of neural control over odontoblastic secretory activity is well accepted, but demands further supportive studies. PCO is seen radiographically as a rapid narrowing of pulp canal space, whereas common clinical features are yellow crown discoloration and a lower or non-response to sensibility tests. Late development of pulp necrosis and periapical disease are rare complications after PCO, rendering prophylactic endodontic intervention useless. Indeed, yellowish or gray crown discoloration may pose a challenge to clinicians, and may demand endodontic intervention to help restore aesthetics. This literature review was conducted to discuss currently available information concerning PCO after traumatic dental injuries (TDI), and was gathered according to three topics: I) physiopathology of PCO after TDI; II) frequency and predictors of pulpal healing induced by PCO; and III) clinical findings related to PCO. Review articles, original studies and case reports were included aiming to support clinical decisions during the follow-up of teeth with PCO, and highlight future research strategies.
牙髓腔闭锁（PCO）是年轻恒牙脱位损伤后牙髓血管再生常见的伴随表现。PCO的潜在机制仍不清楚，除了一项组织病理学研究结果外，尚无实验科学证据。对这一过程缺乏充分的了解引发了诸多争议，包括最合适的命名。这一命名不仅仅是语义问题，而是一个重要问题，因为它反映了这一过程的本质，并直接影响治疗方案的决策。加速牙本质沉积与成牙本质细胞分泌活动神经控制丧失有关的假说已被广泛接受，但仍需进一步的支持性研究。PCO在影像学上表现为牙髓腔空间迅速变窄，而常见的临床特征是牙冠变黄以及对牙髓敏感性测试反应降低或无反应。牙髓坏死和根尖周病的晚期发生是PCO后罕见的并发症，使得预防性牙髓治疗干预并无必要。事实上，牙冠变黄或变灰可能给临床医生带来挑战，可能需要牙髓治疗干预以帮助恢复美观。本综述旨在讨论目前有关牙外伤（TDI）后PCO的可用信息，并根据三个主题进行收集：I）TDI后PCO的病理生理学；II）PCO诱导牙髓愈合的频率和预测因素；III）与PCO相关的临床发现。纳入综述文章、原始研究和病例报告，旨在为PCO患牙随访期间的临床决策提供支持，并突出未来的研究策略。
