Abstract
The role of inflammatory mediators in dental pulp is unique. The local environment of pulp responds to any changes in the physiology that are highly fundamental, like odontoblast cell differentiation and other secretory activity. The aim of this review is to assess the role of cathelicidins based on their capacity to heal wounds, their immunomodulatory potential, and their ability to stimulate cytokine production and stimulate immune-inflammatory response in pulp and periapex. Accessible electronic databases were searched to find studies reporting the role of cathelicidins in pulpal inflammation and regeneration published between September 2010 and September 2020. The search was performed using the following databases: Medline, Scopus, Web of Science, SciELO and PubMed. The electronic search was performed using the combination of keywords “cathelicidins” and “dental pulp inflammation”. On the basis of previous studies, it can be inferred that LL-37 plays an important role in odontoblastic cell differentiation and stimulation of antimicrobial peptides. Furthermore, based on these outcomes, it can be concluded that LL-37 plays an important role in reparative dentin formation and provides signaling for defense by activating the innate immune system.
Highlights
The dental pulp undergoes various stages of repair and regeneration throughout its functioning as a result of microbial activity and other insults
REVIEW this review aims to assess the role of cathelicidin (LL-37) peptides in dental pulp, 3 of 12
37 was done by ELISA and in normal pulp stimulate LL-37 expression in innate immunity
Summary
The dental pulp undergoes various stages of repair and regeneration throughout its functioning as a result of microbial activity and other insults. The histology of reversibly injured dental pulp shows an absence of bacteria and localized coagulation necrosis, while in inflamed pulp, it exhibits the infiltration of inflammatory cells such as neutrophils, suggesting chemotaxis [2,4]. These inflammatory cells release lysosomal enzymes that cause tissue destruction, leading to permanent, irreversible damage, or necrosis [5], requiring endodontic treatment with/without placement of intracanal medicaments to achieve complete disinfection and the prevention of postendodontic pain [6,7]. This increased patrolling by memory T-lymphocytes and macrophage-derived cytokines IL-1, IL-6, and TNF-α, as well as upregulation of the adherence molecules intercellular adhesion molecule
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
