Neurochemical Properties of Dental Primary Afferent Neurons

Vang, Hue; Chung, Grace H.; Kim, Hyun Yeong; Park, Seok-Beom; Jung, Sung Jun; Kim, Joong-Soo; Oh, Seunghee

doi:10.5607/en.2012.21.2.68

Cited by 12 publications

(13 citation statements)

References 29 publications

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“…The optimal goal of regenerative endodontics is to regenerate the pulp tissue. The present study showed no pulp regeneration as revealed by absence of immuno-reactivity to nestin, which detects the neuronal derivatives of the neural crest that comprises the dental pulp [ 19 , 20 ]. Treatment modalities will change in teeth with regenerated roots and regenerated pulps as compared to teeth with regenerated roots and no regenerated pulps.…”

Section: Discussionmentioning

confidence: 90%

Characterization of the apical bridge barrier formed following amelogenin apexification

Mounir¹,

Farsi²,

Alhazzazi³

et al. 2018

BMC Oral Health

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BackgroundRecombinant amelogenin protein (RAP) is reported to induce complete root apex formation in dog model when used as apexification therapy. It also induces pulp regeneration in 85% of the treated group. Thus, the aim of this study was to investigate the nature of the remaining regenerated calcified tissues of the RAP group that showed no pulp regeneration compared to the calcium hydroxide treated group (CH).MethodsA total of 240 dogs’ open apex root canals were used, after establishment of canals contamination. Canals were cleaned, irrigated, and filled with RAP as an apexification material and compared with CH. Treated teeth were assessed by H&E, trichrome staining, and/or immunohistochemistry technique, at 1, 3, and 6 months.ResultsA time-dependent increase in the calcified tissue barrier was observed in the apex of the RAP-treated group compared to the CH-treated group. The newly formed dentin in this RAP group was mainly tubular dentin and was functionally attached to the bone by periodontal ligament, while the CH group showed dentin-associated mineralized tissue (DAMT) associated with the newly formed apical barrier.ConclusionsOut results suggest that RAP can be used as novel apexification material, resulting in a thickening and strengthening of the canal walls, and achieving apical closure.

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Section: Discussionmentioning

confidence: 90%

Characterization of the apical bridge barrier formed following amelogenin apexification

Mounir¹,

Farsi²,

Alhazzazi³

et al. 2018

BMC Oral Health

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“…In this study, peripherin immunoreactivity was identified in the soft connective tissue within the pulp chamber and canals. Peripherin is highly enriched in neuronal derivatives of the neural crest, the embryological tissue from which the dental ectomesenchyme derives (65), and plays a role in neurite elongation during development and axonal regeneration cells (66). Lastly, we showed Wnt1a immunoreactivity is present throughout the restored soft connective tissue found within the pulp chambers, suggesting that Wnt activation is locally available and thus may exercise a role in promoting regeneration.…”

Section: Discussionmentioning

confidence: 99%

Recombinant Amelogenin Protein Induces Apical Closure and Pulp Regeneration in Open-apex, Nonvital Permanent Canine Teeth

Mounir

Matar

Lei

et al. 2016

Journal of Endodontics

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Introduction Recombinant DNA produced amelogenin protein was compared to calcium hydroxide in a study of immature apex closure conducted in 24 young mongrel dogs. Methods Root canals of maxillary and mandibular right premolars (n = 240) were instrumented and left open for 14 days. Canals were cleansed, irrigated and split equally for treatment with recombinant mouse amelogenin (n = 120) or calcium hydroxide (n = 120). Results After 1, 3, and 6 months, the animals were sacrificed and the treated teeth recovered for histological assessment and immunodetection of protein markers associated with odontogenic cells. After 1 month, amelogenin-treated canals revealed calcified tissue formed at the apical foramen and a pulp chamber containing soft connective tissue and hard tissue; amelogenin-treated canals assessed after 3 and 6 month intervals further included apical tissue functionally attached to bone by a periodontal ligament. In contrast, calcified apical tissue was poorly formed in the calcium hydroxide group and soft connective tissue within the pulp chamber was not observed. Conclusions The findings from this experimental strategy suggest recombinant amelogenin protein can signal cells to enhance apex formation in non-vital immature teeth and promote soft connective tissue regeneration.

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“…Some 5-HT3-receptor-positive fibers contained neurofilaments (Fig. 6F), a neurochemical marker of myelinated A-fibers (Bae et al, 2015;Vang et al, 2012), whereas others did not (not shown). Taken together, these results suggested a major role of 5-HT3 receptors in activation of the trigeminal nerve terminals by 5-HT.…”

Section: Receptor Mediating the Peripheral 5-ht Effectmentioning

confidence: 94%

Serotonergic mechanisms of trigeminal meningeal nociception: Implications for migraine pain

et al. 2017

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Serotonergic mechanisms play a central role in migraine pathology. However, the region-specific effects of serotonin (5-HT) mediated via multiple types of receptors in the nociceptive system are poorly understood. Using extracellular and patch-clamp recordings, we studied the action of 5-HT on the excitability of peripheral and central terminals of trigeminal afferents. 5-HT evoked long-lasting TTX-sensitive firing in the peripheral terminals of meningeal afferents, the origin site of migraine pain. Cluster analysis revealed that in majority of nociceptive fibers 5-HT induced either transient or persistent spiking activity with prevailing delta and theta rhythms. The 5-HT3-receptor antagonist MDL-72222 or 5-HT1B/D-receptor antagonist GR127935 largely reduced, but their combination completely prevented the excitatory pro-nociceptive action of 5-HT. The 5-HT3 agonist mCPBG activated spikes in MDL-72222-dependent manner but the 5HT-1 receptor agonist sumatriptan did not affect the nociceptive firing. 5-HT also triggered peripheral CGRP release in meninges, which was blocked by MDL-72222.5-HT evoked fast membrane currents and Ca transients in a fraction of trigeminal neurons. Immunohistochemistry showed expression of 5-HT3A receptors in fibers innervating meninges. Endogenous release of 5-HT from degranulated mast cells increased nociceptive firing. Low pH but not histamine strongly activated firing. 5-HT reduced monosynaptic inputs from trigeminal Aδ- and C-afferents to the upper cervical lamina I neurons and this effect was blocked by MDL-72222. Consistent with central inhibitory effect, 5-HT reduced CGRP release in the brainstem slices. In conclusion, 5-HT evokes powerful pro-nociceptive peripheral and anti-nociceptive central effects in trigeminal system transmitting migraine pain.

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Neurochemical Properties of Dental Primary Afferent Neurons

Cited by 12 publications

References 29 publications

Characterization of the apical bridge barrier formed following amelogenin apexification

Characterization of the apical bridge barrier formed following amelogenin apexification

Recombinant Amelogenin Protein Induces Apical Closure and Pulp Regeneration in Open-apex, Nonvital Permanent Canine Teeth

Serotonergic mechanisms of trigeminal meningeal nociception: Implications for migraine pain

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