The role of inflammation modulation in dental pulp regeneration

Zaky, Samer H.; Shehabeldin, Mostafa; Ray, Herbert L.; Sfeir, Charles

doi:10.22203/ecm.v041a13

Cited by 33 publications

(20 citation statements)

References 73 publications

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“…However, experimental results were not always reproducible, and none of these biomarkers has yet become a reference (Brizuela et al, 2020; Hirsch et al, 2017; Rechenberg et al, 2016; Zanini et al, 2017). Levels of IL‐8 in the pulp blood, as well as IL‐6/IL‐10 and IL‐8/IL‐10 ratios, were also proposed, but their quantification implies pulp opening, which could increase pulp inflammation and impair tissue healing (Colombo et al, 2020; Elsalhy et al, 2013; Zaky et al, 2021). MMP‐9 was measured in the dentine fluid without access to the pulp, but results were not reproducible owing to the very low amount of molecule collected (Rechenberg & Zehnder, 2014).…”

Section: Reviewmentioning

confidence: 99%

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

et al. 2022

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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.

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Section: Reviewmentioning

confidence: 99%

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

et al. 2022

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“…When the inflammatory phenomenon persists, the neutrophils recruit monocytes at the site of injury, which differentiate into macrophages; once recruited, and differentiated, the macrophages acquire a pro-inflammatory phenotype, M1 macrophages [28], induced by exposure to pro-inflammatory cytokines, such as IL-1α and IFN-γ [29]. M1 macrophages mediate phagocytosis of bacteria, and cellular debris (efferocytosis) derived from the localized inflammatory process [30].…”

Section: Biogenesis Of Micrornasmentioning

confidence: 99%

“…M1 macrophages mediate phagocytosis of bacteria, and cellular debris (efferocytosis) derived from the localized inflammatory process [30]. As pulp inflammation progresses, the synthesis of IL-10 and IL-4 induces polarization of macrophages from an M1 to M2 phenotype [29]. M2 macrophages exert immunomodulatory functions, through the release of anti-inflammatory cytokines, such as TGF-1β and IL-10, which signal tissue remodeling and repair [30,31], leading to the resolution of pulp inflammation.…”

Section: Biogenesis Of Micrornasmentioning

confidence: 99%

The Role of microRNAs in Pulp Inflammation

Muñoz‐Carrillo

Vázquez-Alcaraz

Vargas-Barbosa

et al. 2021

Cells

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The dental pulp can be affected by thermal, physical, chemical, and bacterial phenomena that stimulate the inflammatory response. The pulp tissue produces an immunological, cellular, and vascular reaction in an attempt to defend itself and resolve the affected tissue. The expression of different microRNAs during pulp inflammation has been previously documented. MicroRNAs (miRNAs) are endogenous small molecules involved in the transcription of genes that regulate the immune system and the inflammatory response. They are present in cellular and physiological functions, as well as in the pathogenesis of human diseases, becoming potential biomarkers for diagnosis, prognosis, monitoring, and safety. Previous studies have evidenced the different roles played by miRNAs in proinflammatory, anti-inflammatory, and immunological phenomena in the dental pulp, highlighting specific key functions of pulp pathology. This systematized review aims to provide an understanding of the role of the different microRNAs detected in the pulp and their effects on the expression of the different target genes that are involved during pulp inflammation.

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“…Therefore, mild and slow inflammatory stimulation is conducive to the repair/regeneration of dental pulp, whilst high‐intensity inflammatory stimulation can directly destroy the repair/regeneration potential of the dental pulp, and eventually lead to pulp necrosis (Bjørndal, 2008). DPSCs display strong regenerative potential in a controlled inflammatory microenvironment (Fawzy El‐Sayed et al, 2019; Zaky et al, 2021). These indicate that inflammation is a double‐edged sword for pulp repair/regeneration, being either an important contributing factor or a destructive factor.…”

Section: Introductionmentioning

confidence: 99%

Effects of BMAL1 on dentinogenic differentiation of dental pulp stem cells via PI3K/Akt/mTOR pathway

Zhao

Chen

et al. 2022

Int Endodontic J

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Aim: This study aimed to investigate the effect of the circadian clock gene Bmal1 on dentinogenic differentiation of dental pulp stem cells (DPSCs) under inflammatory conditions.Methodology: Dental pulp stem cells were isolated from the pulp tissue of the healthy donor and were then stimulated with different concentrations of lipopolysaccharide (LPS) to mimic inflammatory conditions. Real-time polymerase chain reaction was used to detect the gene expression of circadian clock genes Bmal1, Clock, Per1, Per2, Cry1, and Cry2. Western blot (WB) was applied to analyse the protein expression of circadian clock proteins (BMAL1, CLOCK) and dentinogenic differentiation-related proteins (DSPP, DMP1). In addition, the apoptosis and osteogenic differentiation of DPSCs were also analysed in the presence of different concentrations of LPS. Results:The expression of circadian clock genes of DPSCs significantly changed in an inflammatory environment. WB analysis shows that BMAL1 is relevant to the dentinogenic differentiation of DPSCs. In low concentrations of LPS-mimicked inflammatory conditions, the expression of BMAL1 increased and promoted the dentinogenic differentiation of DPSCs. However, under high concentrations of LPSmimicked inflammatory conditions, the expression of BMAL1 decreased and inhibited the dentinogenic differentiation of DPSCs. Moreover, the effects of BMAL1 on dentinogenic differentiation of DPSCs may be through PI3K/Akt/mTOR pathway. Conclusions:This study showed that the circadian clock gene Bmal1 affected dentinogenic differentiation of DPSCs, providing a new insight for clinical stem cell-based restorative dentinogenesis therapies.

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The role of inflammation modulation in dental pulp regeneration

Cited by 33 publications

References 73 publications

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

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

The Role of microRNAs in Pulp Inflammation

Effects of BMAL1 on dentinogenic differentiation of dental pulp stem cells via PI3K/Akt/mTOR pathway

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