“…0.05). Such an increase was noted when irreversible pulpitis was diagnosed 17,26 after 10 minutes of induced pulp inflammation 27 and after orthodontic stimulation. 29 When considered together, it must be remembered that both are known to be collocated within the same sensory nonmyelinated fiber, a fact corroborated by evidence that demonstrated that an increased density of both nerve-containing fibers is found in the dental pulp of mechanically stressed teeth.…”
Section: Discussionmentioning
confidence: 93%
“…The increase of SP coincided with reports of a higher expression in symptomatic cases of irreversible pulpitis 17,21,26 and cases in which inflammation was induced, such as deep restorative cavities, the use of certain whitening systems, and the placement of adhesives for cervical preparations. 27 Specifically, a greater immunoreactive presence of SP on cats' teeth was reported when orthodontic movement was applied. 28 CGRP expression levels were also higher but were not significantly different (P .…”
Objective: To determine the levels of two sensory neuropeptides (substance P [SP] and calcitonin gene-related peptide [CGRP]) and two endogenous opioids (methionine-enkephalin [Met-Enk] and bendorphin [b-End]) in dental pulp tissue samples subjected to controlled orthodontic intrusive forces. Materials and Methods: Sixteen healthy premolars were selected from eight patients who were undergoing extraction for orthodontic purposes. Eight were randomly used as controls, and the other eight were assigned to an experimental group (controlled orthodontic intrusive forces applied for 24 hours). After this period, teeth were extracted, and pulp samples were obtained. All samples were processed to quantify the expression levels of SP, CGRP, Met-Enk, and b-End using commercial radioimmunoassay kits. Results: All samples exhibited basal levels of both neuropeptides and endogenous opioids. After 24 hours of the intrusive stimulus, all patients reported a tolerable discomfort localized at the involved premolar. Only SP was significantly increased (P , .05). For the other molecules, no statistically significant differences were observed (P . .05); however, they expressed important increasing trends. Conclusions: The expression levels of SP and CGRP in dental pulp samples from the experimental group support the positive correlation between the symptomatic clinical scenario and increased expression levels of neuropeptides, clarifying the role of neurogenic inflammation in early injury response. (Angle Orthod. 2014;84:521-526.)
“…0.05). Such an increase was noted when irreversible pulpitis was diagnosed 17,26 after 10 minutes of induced pulp inflammation 27 and after orthodontic stimulation. 29 When considered together, it must be remembered that both are known to be collocated within the same sensory nonmyelinated fiber, a fact corroborated by evidence that demonstrated that an increased density of both nerve-containing fibers is found in the dental pulp of mechanically stressed teeth.…”
Section: Discussionmentioning
confidence: 93%
“…The increase of SP coincided with reports of a higher expression in symptomatic cases of irreversible pulpitis 17,21,26 and cases in which inflammation was induced, such as deep restorative cavities, the use of certain whitening systems, and the placement of adhesives for cervical preparations. 27 Specifically, a greater immunoreactive presence of SP on cats' teeth was reported when orthodontic movement was applied. 28 CGRP expression levels were also higher but were not significantly different (P .…”
Objective: To determine the levels of two sensory neuropeptides (substance P [SP] and calcitonin gene-related peptide [CGRP]) and two endogenous opioids (methionine-enkephalin [Met-Enk] and bendorphin [b-End]) in dental pulp tissue samples subjected to controlled orthodontic intrusive forces. Materials and Methods: Sixteen healthy premolars were selected from eight patients who were undergoing extraction for orthodontic purposes. Eight were randomly used as controls, and the other eight were assigned to an experimental group (controlled orthodontic intrusive forces applied for 24 hours). After this period, teeth were extracted, and pulp samples were obtained. All samples were processed to quantify the expression levels of SP, CGRP, Met-Enk, and b-End using commercial radioimmunoassay kits. Results: All samples exhibited basal levels of both neuropeptides and endogenous opioids. After 24 hours of the intrusive stimulus, all patients reported a tolerable discomfort localized at the involved premolar. Only SP was significantly increased (P , .05). For the other molecules, no statistically significant differences were observed (P . .05); however, they expressed important increasing trends. Conclusions: The expression levels of SP and CGRP in dental pulp samples from the experimental group support the positive correlation between the symptomatic clinical scenario and increased expression levels of neuropeptides, clarifying the role of neurogenic inflammation in early injury response. (Angle Orthod. 2014;84:521-526.)
“…74,75 Indeed, the role of several neuropeptides in pulpal disease pathogenesis is now well recognised and studies have thus far examined the roles of a range of these molecules within the pulp including calcitonin (CT), calcitonin gene-related peptide (CGRP), neuropeptide Y (NPY), substance P (SP) and vasoactive intestinal polypeptide (VIP) elsewhere. 76 Whilst the release of these molecules within the pulp is also involved in the development of dental pain, several of these molecules have also been shown to be able to stimulate regenerative dentinogenic events. Indeed SP, CGRP, VIP and NPY may represent novel regulators of pulpal angiogenic events whilst CGRP and CT stimulated osteodentin deposition in ferret canines.…”
“…Substance P (SP) is capable of triggering vasodilation, plasma extravasation, immune system activation, chemotaxis, and recruitment and/or regulation of inflammatory cells such as macrophages, mast cells, and lymphocytes (7). Finally, the release of inflammatory mediators in the tissue generates vascular stasis in the affected area (3,8).…”
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