The effects of thermal and electrical injury on pulpal histamine levels

DelBalso, Angelo M.; Nishimura, Roger S.; Setterstrom, Jean A.

doi:10.1016/0030-4220(76)90259-0

Cited by 23 publications

(8 citation statements)

References 9 publications

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“…Histamine is an inflammatory mediator that is expressed in inflamed pulp tissue Antila, 1969, 1970;DelBalso et al, 1976). Thus, it may regulate TLR-induced pulp fibroblast activation during pulpal inflammation.…”

Section: Resultsmentioning

confidence: 99%

Synergy of TLR2 and H1R on Cox-2 Activation in Pulpal Cells

et al. 2009

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Although pulp fibroblasts are a major cell type in dental pulp, their roles in microbial recognition and pulpal inflammation are not well-understood. Considering the pivotal role of Toll-like receptors (TLRs) in the recognition of micro-organisms, we hypothesized that TLRs on pulp fibroblasts may induce inflammatory signals in dental pulp. In human pulp fibroblasts, TLR2, 3, 4, and 5 were constitutively expressed. Stimulation of TLR2 and 3 induced the expression of pro-inflammatory genes such as CXCL10, CCL5, and/or Cox-2 in pulp fibroblasts. Interestingly, histamine synergistically activated TLR2-mediated Cox-2 expression and PGE(2) production. The synergistic effect of histamine is mediated by histamine receptor-1 (H1R). Studies on the intra-cellular signaling pathways revealed that p38 activation is required for the synergistic activation of Cox-2 by TLR2 and histamine. Analysis of these data suggests that TLR2 on pulp fibroblasts, in concert with H1R, can induce an inflammatory response during microbial infection in dental pulp.

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Section: Resultsmentioning

confidence: 99%

Synergy of TLR2 and H1R on Cox-2 Activation in Pulpal Cells

et al. 2009

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“…A fourfold increase can be found in pulp histamine levels within 30 minutes of thermal injury, suggesting that histamine may play a role in the initial stages of pulp inflammation. 132 Platelets aggregated in the vessels release serotonin, which along with the other inflammatory mediators induce a state of hyperalgesia in the pulp nociceptors. Plasma or tissue kallikreins contact kinogens leading to the production of bradykinin and other kinins to produce many signs and symptoms of inflammation.…”

Section: Inflammationmentioning

confidence: 99%

An overview of the dental pulp: its functions and responses to injury

Yu¹,

Abbott²

2007

Australian Dental Journal

230

158

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The dental pulp is a unique tissue and its importance in the long-term prognosis of the tooth is often ignored by clinicians. It is unique in that it resides in a rigid chamber which provides strong mechanical support and protection from the microbial rich oral environment. If this rigid shell loses its structural integrity, the pulp is under the threat of the adverse stimuli from the mouth, such as caries, cracks, fractures and open restoration margins, all of which provide pathways for micro-organisms and their toxins to enter the pulp. The pulp initially responds to irritation by becoming inflamed and, if left untreated, this will progress to pulp necrosis and infection. The inflammation will also spread to the surrounding alveolar bone and cause periapical pathosis. The magnitude of pulp-related problems should not be underestimated since their most serious consequence is oral sepsis, which can be life threatening, and hence correct diagnosis and management are essential. Clinicians must have a thorough understanding of the physiological and pathological features of the dental pulp as well as the biological consequences of treatment interventions.

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“…In pulpal inflammation, immune responses are induced against bacteria, their components and the other irritants which invade dental pulp. Recent studies have revealed the presence of immunocompetent cells in inflamed dental pulp, a situation that could produce a variety of chemical mediators in the course of pulpitis (9–14). These mediators would then modify the development and progression of pulpal inflammation.…”

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confidence: 99%

Effects of an inducible nitric oxide synthase inhibitor on experimentally induced rat pulpitis

Kawanishi¹,

Kawashima²,

Suzuki³

et al. 2004

European J Oral Sciences

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Nitric oxide (NO) is a biological effector molecule involved in a large variety of reactions and, as synthesized by inducible nitric oxide synthase (iNOS), has many important roles in inflammatory conditions. This study aimed to evaluate the anti-inflammatory effects of an iNOS-specific inhibitor, N-(3-(aminomethyl)benzyl)acetamidine (1400W), on experimentally induced rat pulpitis in the upper incisors of 6-wk-old male Wistar rats. 1400W (1 mg kg(-1)), the non-specific NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 50 mg kg(-1)), or sterile saline (control) were administered before the application of lipopolysaccharide (LPS). Rats were killed 3, 6, 9, 12, 24, 48, and 72 h after LPS application, and immunocompetent cells were detected immunohistochemically. The numbers of granulocytes infiltrating into the pulp were significantly depressed in the 1400W group compared with the saline and L-NAME groups. The kinetics of the macrophages and Ia(+) cells in the 1400W group were similar to those in the L-NAME group, while the maximum numbers in both groups were significantly reduced compared with those in the saline group. These results suggest that NO may be responsible for the infiltration of immunocompetent cells in the progress of pulpitis, and that 1400W is a promising candidate for controlling pulpal inflammatory reactions.

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The effects of thermal and electrical injury on pulpal histamine levels

Cited by 23 publications

References 9 publications

Synergy of TLR2 and H1R on Cox-2 Activation in Pulpal Cells

Synergy of TLR2 and H1R on Cox-2 Activation in Pulpal Cells

An overview of the dental pulp: its functions and responses to injury

Effects of an inducible nitric oxide synthase inhibitor on experimentally induced rat pulpitis

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