Inflammation and Regeneration in the Dentin-Pulp Complex: A Double-edged Sword

Responses of human dental pulp cells after application of a low-concentration bleaching gel to enamel

“…This fact may also be a consequence of the more intense expression of the inflammatory mediators observed for this group. According to Cooper et al, 19 there is a fine balance between inflammatory mediator dosage/contact time and odontoblastic differentiation, as demonstrated by Paula-Silva et al, 12 who applied low-dose TNF-a to HDPCs and observed notable overexpression of DPP, DSP, and DMP-1 after a short treatment time (6 h). Min et al 11 observed increased ALP activity and dentine matrix non-collagenous protein overexpression after 72-hour cultivation of HDPCs with proinflammatory cytokines (IL-1a and TNF-a).…”

“…This specific type of cell death causes intense damage in vivo, since high quantities of intracellular components are released, including lysosomal enzymes, causing damage to the neighbouring cells and triggering an inflammatory tissue reaction. 19,20 Pulpal inflammation associated with local tissue necrosis was previously demonstrated by in vivo studies in which high-concentration H 2 O 2 bleaching gels (35-38%) were applied to rat or human teeth. [20][21][22][23] In the present investigation, the remaining HDPCs showed increased expression of IL-6, TNF-a, COX-2, and IL-1b in comparison to the control group.…”

Expression of high mobility group box 1 in inflamed dental pulp and its chemotactic effect on dental pulp cells

“…The present study showed that bacterial endotoxin LPS from E. coli could induces cytoplasmic expression and up-regulates mRNA level of HMGB1 in cultured DPCs, indicating that DPCs can be a source of HMGB1 in pulpal inflammation. It has been reported that extracellular HMGB1 increases cytokines including TNF-a, IL-1 and IL-6 expression [5] and these cytokines are highly expressed in inflamed pulp tissues [14,23]. It is therefore reasonable to speculate that in inflamed dental pulp, bacterial endotoxins LPS, hypoxia-induced oxidative stress and released cytokines could induce the cytoplasmic expression and release of HMGB1, initiating the immune response.…”

“…Healthy premolars or third molars were collected from orthodontic patients (age [13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29]. In the inflammation group, 15 third molars were collected from patients with symptoms of spontaneous pain or prolonged pain to thermal stimuli and diagnosed as irreversible pulpitis.…”

“…Human dental pulp tissue possesses the ability of resisting and repairing injuries caused by trauma or infection [13,14]. Previous studies have isolated stem cells from human dental pulp and identified the multi-differentiation potentials of these dental pulp stem cells (DPSCs) [15].…”