Pulp canal obliteration after traumatic injuries in permanent teeth - scientific fact or fiction?

Abstract: 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.

Etiologic role of root canal infection in apical periodontitis and its relationship with clinical symptomatology

Abstract: Evidence shows the polymicrobial etiology of endodontic infections, in which bacteria and their products are the main agents for the development, progression, and dissemination of apical periodontitis. Microbial factors in necrotic root canals (e.g., endotoxin) may spread into apical tissue, evoking and supporting a chronic inflammatory load. Thus, apical periodontitis is the result of the complex interplay between microbial factors and host defense against invasion of periradicular tissues. This review of the literature aims to discuss the complex network between endodontic infectious content and host immune response in apical periodontitis. A better understanding of the relationship of microbial factors with clinical symptomatology is important to establish appropriate therapeutic procedures for a more predictable outcome of endodontic treatment.

Bases morfofisiopatológicas de la respuesta inflamatoria aguda pulpar / Morphophysiopathological bases of pulpar acute inflammatory response

Teniendo en cuenta el desconocimiento existente sobre las bases morfofisiopatológicas que caracterizan la respuesta inflamatoria aguda pulpar; conocimiento este que resulta imprescindible para tomar decisiones según se trate de enfermedades pulpares reversibles o irreversibles, tratables o intratables, tejidos para el recubrimiento y su conservación o pulpas que deben ser extraídas, se decidió describir las mencionadas bases en el presente artículo, con la finalidad de que se reflexione acerca de ello y se debatan los aspectos de mayor interés en relación con el tema.

Given the lack of knowledge on morphophysiopathological bases characterizing pulpar acute inflammatory response, which becomes essential knowledge to make decisions depending on reversible or irreversible and treatable or untreatable pulpar diseases, tissues for covering and preservation or pulps to be extracted, it was decided to describe the bases mentioned in this article in order to reflect on this and to discuss the aspects of greatest significance in relation to the topic.