1 Retrograde labeling of
pulpal afferents demonstrated that a low proportion of p
2 Given that the majority of
pulpal afferents express ASIC3 and TRPA1, our results ra
3 erents demonstrated that a low proportion of
pulpal afferents was co-localized with GFP.
4 Although TRPV1 is expressed in
pulpal afferents, it is not known whether the applicatio
5 ducers could underlie mechanotransduction in
pulpal afferents, we used a single-cell PCR approach to
6 PCR approach to screen retrogradely labeled
pulpal afferents.
7 Therefore,
pulpal and periapical pathosis were independent of the p
8 ultrasonic scalers which may cause injury to
pulpal and periodontal tissues.
9 seline to a level reported as deleterious to
pulpal and periodontal tissues.
10 on of soft-tissue anesthesia exceeds that of
pulpal anesthesia.
11 ent fibers participates in the regulation of
pulpal blood flow (PBF) via opposing effects.
12 the sympatho-adrenomedullary system regulate
pulpal blood flow (PBF), in part, by the inhibition of v
13 Of 93 units isolated, 14 produced changes in
pulpal blood flow when stimulated electrically at 1 or 1
14 single units produced detectable changes in
pulpal blood flow.
15 ant mice did not have unusual wear and their
pulpal CGRP immunoreactivity remained normal, but their
16 onded dentin and does not cause irreversible
pulpal damage to vital teeth when the air pressure emplo
17 tructural, spatial, and transport aspects of
pulpal development and maintenance.
18 rst molars of both strains were subjected to
pulpal exposure and infection with a mixture of four ana
19 st be utilized for deep caries removal where
pulpal exposure is a concern.
20 Pulpal fibroblasts express nerve growth factor (NGF) and
21 s may be involved in immune responses during
pulpal infection through activating NF-kappaB.
22 cesses and disseminated infections following
pulpal infection, whereas immunocompetent control mice d
23 bone destruction occurs as a consequence of
pulpal infection.
24 tionally more important in the regulation of
pulpal inflammation and healing than in the processing a
25 s of the pulpal innate immunity-can regulate
pulpal inflammation and repair, the authors investigated
26 Chronic
pulpal inflammation under caries appears to be elicited
27 ing a mechanism whereby PAR-2 could modulate
pulpal inflammation.
28 ammatory activity plays an important role in
pulpal inflammation.
29 in pulpal neurons from rats with and without
pulpal inflammation.
30 Therefore, nitric oxide may mediate the
pulpal inflammatory response through its effects on the
31 Pulpal injury and inflammation were reduced by DEX treat
32 ce macrophages-essential cell players of the
pulpal innate immunity-can regulate pulpal inflammation
33 t tooth structure would be abnormal and that
pulpal innervation would be greatly reduced because it c
34 is was associated with anatomical changes in
pulpal innervation.
35 The prognosis was further compromised by the
pulpal involvement.
36 oth structure associated with a restoration;
pulpal involvement; or retained roots.
37 proaches in endodontic regeneration based on
pulpal mesenchymal stem cells (MSCs) have demonstrated p
38 uding aging-associated phenotypic changes in
pulpal MSCs, availability of tissue sources, and safety
39 Pulpal necrosis was induced in foxhounds along with surg
40 that NTPDase2 was predominantly expressed in
pulpal nerve bundles, Raschkow's nerve plexus, and in th
41 Dental
pulpal nerve fibers express ionotropic adenosine triphos
42 Single
pulpal nerve fibres were electrically stimulated at just
43 zed decrease in CGRP and SP neuropeptides in
pulpal nerves but not in periodontal ligament; (2) it re
44 tion; and (4) it does not block sprouting of
pulpal nerves towards fibrous dentin.
45 macNOS, nor nNOS reactivity was observed in
pulpal nerves.
46 ls (TREK1, TREK2) and TRAAK were screened in
pulpal neurons from rats with and without pulpal inflamm
47 t in approximately 67%, 64%, 14%, and 10% of
pulpal neurons, respectively.
48 The selective loss of
pulpal neuropeptides CGRP and SP during dexamethasone tr
49 Following tooth injury, there is increased
pulpal NGF, sprouting of sensory nerve endings, and incr
50 A large proportion of
pulpal nociceptors are known to contain neuropeptides su
51 Since mechanical irritation of
pulpal nociceptors is critical for evoking tooth pain un
52 and infection with a mixture of four common
pulpal pathogens, including Prevotella intermedia, Fusob
53 ave a major impact on the initial lesion and
pulpal pathology.
54 c neurotransmission inhibits exocytosis from
pulpal peptidergic afferent fibers.
55 imens were bonded based on whether simulated
pulpal pressure (SPP) or thermomechanical cycling was im
56 he dental pulp may result in increased intra-
pulpal pressure, and contribute to pain and irreversible
57 surrounded by sound dentin, with or without
pulpal pressure.
58 Although
pulpal regeneration requires the cell-based approach, se
59 The
pulpal response to orthodontic force is thought to invol
60 d be used to investigate the early stages of
pulpal responses.
61 Pulpal revascularization is commonly used in the dental
62 UVECs as a promising new clinically relevant
pulpal revascularization treatment to regenerate human d
63 NTPDase2 was expressed in
pulpal Schwann cells, with processes accompanying the ne
64 tion of vasoactive neuropeptide release from
pulpal sensory neurons.
65 This is formed on the
pulpal surface of existing dentine and rethickens the de
66 sory nerve fibers express p75 and trk A, and
pulpal sympathetic fibers lack p75.
67 tly tested the hypothesis that activation of
pulpal sympathetic terminals inhibits exocytosis of immu
68 The
pulpal tissue was collected from partially erupted bovin