It is often presumed that apical periodontitis follows total pulp necrosis, and consequently root canal treatment is commonly performed. Periapical lesion development is usually caused by bacteria and its byproduct which irritate pulp, develop pulpitis, and result in necrosis through an irreversible process. Afterwards, apical periodontitis occurs. This phenomenon is observed as an apical radiolucency in radiographic view. However, this unusual case presents a spontaneous healing of periapical lesion, which has developed without pulp necrosis in a vital tooth, through conservative treatment.

The purpose of this study was to evaluate the pulp tissue reaction to direct pulp capping of mechanically exposed beagle dogs'pulp with several capping materials. A total of 36 teeth of 2 healthy beagle dongs were used. The mechanically exposed pulps were capped with one of the followings: (1) Mineral Trioxide Aggregate (MTA: ProRoot® MTA, Dentsply, Tulsa, USA), (2) Clearfil SE Bond (Dentin adhesive system: Kuraray, Osaka, Japan), (3) Ultra-Blend (Photo-polymerized Calcium hydroxide: Ultradent, South Jordan, USA), (4) Dycal (Quick setting Calcium hydroxide: LD Caulk Co., Milford, USA) at 7, 30, and 90 days before sacrificing. The cavities were restored with Z350 flowable composite resin (3M ESPE, St. Paul. MN, USA). After the beagle dogs were sacrificed, the extracted teeth were fixed, decalcified, prepared for histological examination and stained with HE stain. The pulpal tissue responses to direct pulp capping materials were assessed.

In MTA, calcium hydroxide, and photo-polymerized calcium hydroxide groups, initial mild inflammatory cell infiltration, newly formed odontoblast-like cell layer and hard tissue bridge formation were observed. Compared with dentin adhesive system, these materials were biocompatible and good for pulp tissue regeneration.

In dentin adhesive system group, severe inflammatory cell infiltration, pulp tissue degeneration and pulp tissue necrosis were observed. It seemed evident that application of dentin adhesive system in direct pulp capping of beagle dog teeth cannot lead to acceptable repair of the pulp tissue with dentine bridge formation.

Dental pulp is a loose, mesenchymal tissue almost entirely enclosed in the dentin. It consists of cells, ground substance, and neural and vascular supplies. Damage to the dental pulp by mechanical, chemical, thermal, and microbial irritants can provoke various types of inflammatory response. Pulpal inflammation leads to the tissue degradation, which is mediated in part by Matrix metalloproteinase leads to accelerate extracellular matrix degradation with pathological pathway. We have now investigated the induction of MMPs and inflammatory cytokines by Lipopolysaccharide (LPS) control of inflammatory mediators by peroxisome proliferator-activated receptors (PPARs).

Human dental pulp cells exposed to various concentrations of LPS (1-10 µg/ml) revealed elevated levels of MMP-2 and MMP-9 at 24 hrs of culture. LPS also stimulated the production of ICAM-1, VCAM-1, IL-1β, and TNF-α. Adenovirus PPARγ (Ad/PPARγ) and PPARγ agonist rosiglitazone reduced the synthesis of MMPs, adhesion molecules and pro-inflammatory cytokines. The inhibitory effect of Ad/PPARγ was higher than that of PPARγ agonist.

These result offer new insights in regard to the anti-inflammatory potential of PPARγ in human dental pulp cell.

The purpose of this clinical study is to assess whether calcium hydroxide as an intracanal medication affects post-treatment pain in teeth especially odontogenic pain which comes from inflammation of the pulp and periradicular tissues when compared with no intracanal medication.

From 213 patients who has been treated 237 root canals due to significant pain (moderate-to-severe), we recorded their age, sex, treated tooth, degree of pain, pre-operative states of the tooth. We classified patients into 2 test group; Group 1 (not gain intracanal Ca(OH)₂), Group 2 (gain intracanal Ca(OH)₂). Through the survey from the patients, we let them write down the occurrence and degree of post-treatment pain in 4hours, 2days, 7days after treatment as none, mild, moderate or severe. The followings were evaluated; the overall incidence of flare-ups, the overall incidence of post-treatment pain in each group at each time period, the incidence of post-treatment pain in each group at each time period as related to pre-operative states of the teeth. These were compared statistically with Chi-square analysis (p < 0.05).

Under the condition of this investigation, no difference was observed in the incidence of post-treatment pain between the two groups. Therefore, Ca(OH)₂ as intracanal medication had no effect on preventing or decreasing the post-treatment pain.

The aims of the study were to evaluate the effect of epinephrine-containing local anesthetics on pulpal blood flow (PBF) and to investigate its effect on cavity preparation-induced PBF change. PBF was recorded using a laser Doppler flowmeter (Perimed Co., Sweden) from canines of nine cats under general anesthesia before and after injection of local anesthetics and after cavity preparation. 2% lidocaine hydrochloride with 1 : 100,000 epinephrine was administered by local infiltration given apical to the mandibular canine at the vestibular area and the same volume of isotonic saline was injected on the contralateral tooth as a control. A round carbide bur was operated at slow speed with isotonic saline flushing to grind spherical cavities with increasing depth through the enamel and into the dentin on both teeth. The obtained data was analyzed with paired t-test.

Cavity preparation caused significant increase of PBF (n = 9, p < 0.05). Local infiltration of lidocaine with epinephrine resulted in decreases of PBF (n = 9, p < 0.05), whereas there was no significant change of PBF with the physiologic saline as a control. Cavity preparation on tooth anesthetized with lidocaine with epinephrine caused significantly less increase of PBF than in control tooth (p < 0.05).

Therefore, the result of the present study demonstrates that local infiltration of 2% lidocaine with 1 : 100,000 epinephrine effectively reduces PBF increase caused by cavity preparation.

The induction of the IL-8 and MCP-1 by the stimulation of Substance P and TNF-α (IL-8 agonist) and the specificity for SP using Spantide (SP antagonist) in the dental pulp tissues was measured quantitatively. In addition, the secretion of the IL-8 in the human dental pulp tissue 36 hrs after the stimulation of SP was observed after the stimulation of SP qualitatively.

According to this study, the results were as follows:

1. There was the significant IL-8 induction at 36 h after SP (10^-4M) stimulation of the pulp tissue comparing with the unstimulated dental pulp tissues (p < 0.05). IL-8 immunostaining was weakly detected along the periphery of the pulp tissue after Mock stimulation and IL-8 immunostaining was detected around the fibroblast in the pulp tissue 36h After SP (10^-4M) stimulation,

2. The secretion of MCP-1 from the dental pulp tissues comparing with Mock stimulation was induced at 36 hrs after TNF-α (40 ng/ml) stimulation, but no induction with SP(10^-4M). TNF-α (40 ng/ml) did not induce the IL-8 secretion from the pulp tissue, weak IL-8 immunostaining was detected along the periphery of the pulp tissue.

3. Spantide (10^-5M) inhibited IL-8 induction from the pulp tissues 36 h after SP (10^-4M) stimulation.

These results suggest that SP significantly induces IL-8 recruiting neutrophils in localized human dental pulp tissue. MCP-1 appears to be less involved in the early establishment of pulpal inflammation in response to irritation such as mechanical insult of dentin. SP may have positive relation with the inflammation of the human dental pulp tissues.

The purpose of this study was to investigate the function of calcitonin gene-related peptide (CGRP) in regulatory mechanism of pulpal microcirculation with the aim of elucidating neurogenic inflammation.

Experiments were performed on twelve cats under general anesthesia. CGRP was administered through the femoral vein to see the systemic influence and through the external carotid artery to see the local effect. Sympathetic nerve to the dental pulp was stimulated electrically and pulpal blood flow (PBF) was measured with a laser Doppler flowmeter on the canine teeth to the drug administration. The paired variables of control and experimental data were compared by paired t-test and differences with p < 0.05 were considered statistically significant.

Systemic administration of CGRP (0.3 μg/kg) exerted decreases in systemic blood pressure and caused changes in PBF with an initial increase followed by decrease and a more marked second increase and decrease.

Close intra-arterial (i.a.) injection of CGRP (0.03 μ/kg) resulted in slight PBF increase. The effect of CGRP resulted in no significant increase in PBF in the presence of CGRP_8-37.

The electrical stimulation of the sympathetic nerve alone resulted in PBF decreases. The i.a. administration of CGRP following the electrical stimulation of the sympathetic nerve compensated the decreased PBF. Therefore, CGRP effectively blocked the sympathetic nerve stimulation-induced PBF decrease.

Results of the present study have provided evidences that even though the local vasodilatory function of CGRP are weak, CGRP is effectively involved in blocking the vasoconstriction caused by sympathetic nerve stimulation in the feline dental pulp.

The purpose of this study was to investigate the influence of NK1 receptor antagonists on the pulpal blood flow (PBF) when applied iontophoretically through the dentinal cavity of the teeth in order to understand whether iontophoretically applied NK1 receptor antagonists can control the pulpal inflammation.

Eleven cats were anesthetized with alpha-chloralose and urethane, and substance P (SP) was administered to the dental pulp through the catheterized lingual artery in doses that caused PBF change without the influence of systemic blood pressure. NK1 receptor antagonists were applied iontophoretically to the prepared dentinal cavity of ipsilateral canine teeth of the drug administration, and PBF was monitored. Data were analyzed statistically with paired t-test.

PBF increase after iontophoretic application of the NK1 receptor antagonists followed by the intra-arterial administration of SP was significantly less than PBF increase after iontophoretic application of the 0.9% saline followed by the intra-arterial administration of SP as a control (p < 0.05).

Iontophoretic application of the NK1 receptor antagonists (0.2~3.4 mM) following the intra-arterial administration of SP resulted in less increase of PBF than the iontophoretic application of the 0.9% saline following the intra-arterial administration of SP as a control (p < 0.05).

Therefore, the results of the present study provide evidences that the iontophoretic application is an effective method to deliver drugs to the dental pulp, and that iontophoretically applied NK1 receptor antagonists block SP-induced vasodilation effectively. The above results show the possibility that the iontophoretical application of NK1 receptor antagonists can control the neurogenic inflammation in the dental pulp.