Disease relevance of Pulpitis

• METHODS: Forty-eight primary molars with deep occlusal caries, but without preoperative signs and symptoms of irreversible pulpitis, received indirect pulp treatment and were restored with a composite resin (Z100) [1].
• These findings suggest that Gram-positive bacteria, such as L. casei, from carious lesions, might be involved in developing pulpitis through the stimulation of IL-6 production [2].

High impact information on Pulpitis

• Histological examination of LPS-treated teeth revealed features of an acute pulpitis [3].
• A higher prevalence of IFN-gamma (67%) than IL-4 (19%) or IL-10 (29%) was obtained in shallow caries, suggesting a type 1 cytokine mechanism in early pulpitis where S. mutans predominates [4].
• We investigated whether vascular endothelial growth factor (VEGF) production by human pulp cells (HPC) is regulated by lipopolysaccharide (LPS) in relation to the pathogenesis of pulpitis [5].
• Effect of NOS Inhibitor on Cytokine and COX2 Expression in Rat Pulpitis [6].
• Nitric oxide synthase (NOS) plays a significant role in the pathogenesis of pulpitis [7].

Chemical compound and disease context of Pulpitis

• In the Formalin-induced pulpitis of rats and the electrically stimulated pulps of dogs, a bradykininlike substance developed by the pulps and released into a saline pool on the exposed pulps disappeared after a local application of Apernyl solution [8].
• Pulpitis of the fingers from a shoe glue containing 1,2-benzisothiazolin-3-one (BIT) [9].
• Re: The use of an intra-oral injection of ketorolac in the treatment of irreversible pulpitis [10].
• Anesthetic efficacy of the supplemental intraosseous injection of 2% lidocaine with 1:100,000 epinephrine in irreversible pulpitis [11].
• We concluded that, for posterior teeth diagnosed with irreversible pulpitis, the supplemental intraosseous injection of 2% lidocaine (1:100,000 epinephrine) was successful when conventional techniques failed [11].

Anatomical context of Pulpitis

• E. vivo gene transfer of BMP-7 may be an effective method for inducing dentin regeneration in teeth with reversible pulpitis [12].
• 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 [13].
• In the mature tooth, HGF expression by fibroblasts is enhanced in pulpitis and mediated through the induction of prostaglandin (PG) E(2); it is induced not only by inflammatory cytokines, but also by components of oral bacteria [14].
• Sixty-four emergency patients diagnosed with irreversible pulpitis of a mandibular posterior tooth randomly received, in a blinded manner, 2.8 ml of 2% lidocaine with 1:100,000 epinephrine using either a conventional inferior alveolar nerve block or a bidirectional-needle-rotational technique using the Wand II injection system [15].
• T lymphocyte subpopulations and interleukin-2, interferon-gamma, and interleukin-4 in rat pulpitis experimentally induced by specific bacteria [16].

Gene context of Pulpitis

• The concentration of MMP-3 in acute pulpitis was significantly higher than the control and chronic pulpitis groups (p < 0.05) [17].
• Because excessive levels of IL-6 and prostaglandins have been connected with the pathogenesis of several inflammatory diseases, our results suggest the involvement of HDP fibroblasts in the development of pulpitis via producing IL-6 and COX-2 [18].
• However, vascular TRPV1 expression does appear to be positively correlated with dental pain, thus providing new insights into symptomatic pulpitis [19].
• AIM: To use radioreceptor analysis for comparing calcitonin gene-related peptide (CGRP) receptor expression in human pulp tissue samples collected from teeth having a clinical diagnosis of acute irreversible pulpitis, healthy pulps and teeth with induced inflammation [20].
• CONCLUSIONS: TNF-alpha may be an objective marker for determining extent of pulpal inflammation associated with irreversible pulpitis [21].

Analytical, diagnostic and therapeutic context of Pulpitis

• Inflammation was induced by drilling tooth cusps to create pulpal exposures; the induced pulpitis and subsequent periapical lesions were studied 1-35 days later using standard CGRP immunohistochemistry and the avidin-biotin peroxidase method [22].
• We determined in vivo pulpal levels of immunoreactive substance P in human teeth with a diagnosis of normal pulp or irreversible pulpitis using CMA/20 microdialysis probes inserted into vital pulps of 24 teeth from 21 patients [23].
• METHODS: The PICOT statement was: (P) In human carious primary molars with reversible coronal pulpitis, (I) does a pulpotomy performed with ferric sulfate, (C) compared with formocresol, (O) result in dinical/radiographic success, (T) in time periods up to exfoliation [24]?

References