A critical analysis of research methods and experimental models to study pulpitis

Abstract

Pulpitis is the inflammatory response of the dental pulp to a tooth insult, whether it is microbial, chemical, or physical in origin. It is traditionally referred to as reversible or irreversible, a classification for therapeutic purposes that determines the capability of the pulp to heal. Recently, new knowledge about dental pulp physiopathology led to orientate therapeutics towards more frequent preservation of pulp vitality. However, full adoption of these vital pulp therapies by dental practitioners will be achieved only following better understanding of cell and tissue mechanisms involved in pulpitis. The current narrative review aimed to discuss the contribution of the most significant experimental models developed to study pulpitis. Traditionally, in vitro two (2D)‐ or three (3D)‐dimensional cell cultures or in vivo animal models were used to analyse the pulp response to pulpitis inducers at cell, tissue or organ level. In vitro, 2D cell cultures were mainly used to decipher the specific roles of key actors of pulp inflammation such as bacterial by‐products, pro‐inflammatory cytokines, odontoblasts or pulp stem cells. However, these simple models did not reproduce the 3D organisation of the pulp tissue and, with rare exceptions, did not consider interactions between resident cell types. In vitro, tissue/organ‐based models were developed to better reflect the complexity of the pulp structure. Their major disadvantage is that they did not allow the analysis of blood supply and innervation participation. On the contrary, in vivo models have allowed researchers to identify key immune, vascular and nervous actors of pulpitis and to understand their function and interplay in the inflamed pulp. However, inflammation was mainly induced by iatrogenic dentine drilling associated with simple pulp exposure to the oral environment or stimulation by individual bacterial by‐products for short periods. Clearly, these models did not reflect the long and progressive development of dental caries. Lastly, the substantial diversity of the existing models makes experimental data extrapolation to the clinical situation complicated. Therefore, improvement in the design and standardisation of future models, for example by using novel molecular biomarkers, databased models and artificial intelligence, will be an essential step in building an incremental knowledge of pulpitis in the future.

Effectiveness of diagnosing pulpitis: A systematic review

“…Thus, all teeth included in this review were either scheduled for root canal treatment or extraction after conclusion of the diagnostic tests. Included studies were limited to permanent teeth and studies evaluating pulp vitality after any kind of dental trauma were excluded, as a temporary loss of sensitivity can occur following dental trauma (Richert et al, 2022) (Table S3). The characteristics of the included studies are summarized in Table 1.…”

“…In contrast, for severe pulpitis, full pulpotomy is indicated, or in case of persisting pulp haemorrhage, vital extirpation (Wolters et al, 2017). Thus, the suggested new classification may lead to more frequent preservation of pulp vitality as it seems to be of benefit in cases in which vital pulp treatment (VPT) is considered to be a treatment option (Richert et al, 2022).…”

Where Is the Artificial Intelligence Applied in Dentistry? Systematic Review and Literature Analysis

“…The pandemic situation may have forced an accelerated utilization of the smart technologies that are often combined with tele-health solutions [ 7 , 60 ]. Current high-quality publications regarding AI utilization in the category of Dentistry, Oral Surgery & Medicine registered by Web of Science—Core Collection include 24 review articles in the year 2021 and 5 review articles published in the year 2022 [ 60 , 191 , 192 , 193 ]. Of these, only one paper covered the whole dental field.…”

Approaches to vital pulp therapies

“…If the infection is not controlled, the more intense immune and inflammatory response develops, and it can result in necrosis of the pulpal tissue [25]. The mechanism of necrotic tissue formation is generally considered to happen as a result of a decrease in oxygen, nutrient supply, capacity of lymphatic drainage, and wound debridement by local immune cells in dental pulp [26]. Pattern‐recognition receptors of these cells as well as pulp fibroblasts, leucocytes and pulpal stem cells recognise the PAMPs as a threat and evoke host cell to response.…”