The Effect of Different Vasoconstrictors and Local Anesthetic Solutions on Substance P Expression in Human Dental Pulp

ArticleinJournal of endodontics 35(5):631-3 · June 2009with37 Reads
DOI: 10.1016/j.joen.2008.12.020 · Source: PubMed
Abstract
The purpose of this study was to quantify the effect of the infiltration injection of different vasoconstrictor and anesthetic solutions on substance P (SP) expression in healthy human dental pulp. Thirty pulp samples were obtained from healthy upper premolars in which extraction was indicated for orthodontic reasons and were randomly assigned into three groups of 10 samples each: 2% lidocaine with 1:80,000 epinephrine (Lido group), 3% Prilocaine with 1:200000 felypressin (Prilo group); and 4% Prilocaine without vasoconstrictor (Prilo-no-VC group). All teeth were extracted 10 minutes after anesthetic application. Pulp samples were processed and SP was measured by radioimmunoassay. SP expression for the Lido, Prilo, and Prilo-no-VC groups were 616.49, 663.76, and 760.79 pmol/mg pulp tissue, respectively. Analysis of variance showed statistically significant differences between groups (p = 0.001). Tukey Honestly Significant Difference (HSD) post hoc tests showed significant statistical differences between the Prilo-no-VC group and the Lido group (p < 0.01) and between the Prilo-no-VC group and the Prilo group (p < 0.05). It can be concluded that infiltration injection of local anesthetics with vasoconstrictor attenuate SP expression in human dental pulp.
    • "These data confirm that an induced pulpal lesion seems to be enough to start inflammation in the pulp after 15 minutes, but probably this time is not sufficient for the inflammation process to fully take place and actually no data are present to evaluate exactly the time necessary for the completion of irreversible pulpitis. Moreover, local anaesthetics with vasoconstrictor (4% articaine with 1 : 100.000 epinephrine was used in the present study) seem to attenuate SP expression by the effect of alpha-adrenergic agonists as stated in different studies [19, 20]; actually Caviedes-Bucheli and coworkers [17, 20] used prilocaine without vasoconstrictor and that could also help to explain the difference reported with the data here presented. The presence of increased SP levels may open new directions for treating pulpal inflammation and pain but no studies have yet been performed to evaluate the effect of common used NSAIDs on this parameter and, as far as we know, the present is the first study to address this aspect. "
    [Show abstract] [Hide abstract] ABSTRACT: Objectives. To evaluate substance P (SP) and the effect of ketoprofen administration, a nonsteroidal anti-inflammatory drug (NSAID), on SP in the pulp of upper third molars with experimentally induced pulpal lesion. Materials and Methods. A sample of 20 young systemically healthy adults of both sexes, nonsmokers, with a healthy upper third molar to extract for orthodontic purposes, was selected. Prior to the procedure, an inflammatory process was generated by mechanical exposure of the pulp. After 15 minutes, the pulp was collected using a sterile barbed broach. SP levels were determined by using a commercially available enzyme immunoassay (ELISA) kit. The subjects were randomly divided into two groups: group 1 received a dose of ketoprofen 30 minutes prior to the experimental procedure. The subjects of group 2 did not receive any kind of drug administration. The patients were asked to complete a diary on the postoperative pain. Results. No statistically significant difference could be detected in SP expression between the two groups. In group 1, pain manifestation was significantly delayed in comparison with group 2. Conclusions. Preventive administration of ketoprofen did not significantly affect the pulpal levels of SP but resulted in a significantly postponed manifestation of pain after extraction.
    Full-text · Article · Feb 2016
    • "Substance P values were obtained from healthy premolars in which extraction was indicated for orthodontic reasons. Local anesthetic used in all groups of this study was 4% prilocaine without vasoconstrictor to prevent neuropeptide expression becoming attenuated by vasoconstrictors as previously demonstrated (15). "
    [Show abstract] [Hide abstract] ABSTRACT: Objectives: The purpose of this study was to quantify the effect of glass ionomer and adhesive cements on SP expression in healthy human dental pulp. Study Design: Forty pulp samples were obtained from healthy premolars where extraction was indicated for orthodontic reasons. In thirty of these premolars a Class V cavity preparation was performed and teeth were equally divided in three groups: Experimental Group I: Glass Ionomer cement was placed in the cavity. Experimental Group II: Adhesive Cement was placed in the cavity. Positive control group: Class V cavities only. The remaining ten healthy premolars where extracted without treatment and served as a negative control group. All pulp samples were processed and SP was measured by radioimmunoassay. Results: Greater SP expression was found in the adhesive cement group, followed by the glass ionomer and the positive control groups. The lower SP values were for the negative control group. ANOVA showed statistically significant differences between groups (p<0.0001). Tukey HSD post hoc tests showed statistically significant differences in SP expression between negative control group and the 3 other groups (p<0.01). Differences between the cavity-only group and the two experimental groups were also statistically significant (p<0.05 and p<0.01 respectively). There is also a statistically significant difference between the two experimental groups (p<0.01). Conclusions: These findings suggest that adhesive cements provoke a greater SP expression when compared with glass ionomer. Key words:Glass Ionomer, adhesive cement, Substance P, human dental pulp.
    Full-text · Article · May 2013
    • "SP is abundantly contained in the fibers that innervate the dental pulp and dentin [7]. The production and release of this molecule are highly increased upon noxious, thermal, mechanical, and chemical stimulation of the dental pulp as well as in periodontal ligament [7, 19, 22–24]. The amount of SP released by each sensory fiber is further increased during inflammatory processes, which sustains the vicious circle that underlies inflammation [23, 25]. "
    [Show abstract] [Hide abstract] ABSTRACT: Current evidence supports the central role of neuropeptides in the molecular mechanisms underlying dental pain. In particular, substance P, a neuropeptide produced in neuron cell bodies localised in dorsal root and trigeminal ganglia, contributes to the transmission and maintenance of noxious stimuli and inflammatory processes. The major role of substance P in the onset of dental pain and inflammation is increasingly being recognised. Well-grounded experimental and clinical observations have documented an increase in substance P concentration in patients affected by caries, pulpitis, or granulomas and in those undergoing standard orthodontic or orthodontic/dental care procedures. This paper focuses on the role of substance P in the induction and maintenance of inflammation and dental pain, in order to define future lines of research for the evaluation of therapeutic strategies aimed at modulating the complex effects of this mediator in oral tissues.
    Full-text · Article · Feb 2012
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