Risk Factors for Tooth Loss in Patients with ≥25 Remaining Teeth Undergoing Mid-Long-Term Maintenance : A Retrospective Study

Tooth loss represents a diffused pathologic condition affecting the worldwide population. Risk factors have been identified in both general features (smoking, diabetes, economic status) and local tooth-related factors (caries, periodontitis). In this retrospective study, we examined the data of 366 patients with a large number of remaining teeth (≥25) undergoing maintenance therapy in order to identify specific risk factors for tooth loss. The number of remaining teeth, number of non-vital teeth, and number of occlusal units were investigated for their correlation with tooth loss. The mean follow-up of patients was 9.2 years (range 5 to 14). Statistically significant risk factors for tooth loss were identified as number of remaining teeth at baseline (p = 0.05), number of occlusal units (p = 0.03), and number of non-vital teeth in posterior regions (p < 0.001). Multiple logistic regression showed that the number of occlusal units and number of non-vital teeth in the posterior regions were significantly associated with a greater risk of tooth loss (odds ratio 1.88 and 3.17, respectively). These results confirm that not only the number of remaining teeth, but also their vital or non-vital status and the distribution between the anterior and posterior regions influence the long-term survival

中長期的なメンテナンスを受けている患者の歯の喪失の危険因子 : 後ろ向き研究

In this retrospective study, we identified risk factors for tooth loss in patients undergoing mid–long-term maintenance therapy. We surveyed 674 maintenance patients for ≥5 years after active treatment who visited a dental clinic between January 2015 and December 2016. Of these, 265 were men (mean age 54.6 ± 8.0 years old) and 409 were women (mean age 54.0 ± 7.9 years old). Study variables included patient compliance, sex, number of teeth lost, cause of tooth loss (dental caries, periodontal disease, root fracture, others, vital or non-vital teeth), age at start of maintenance, number of remaining teeth at start of maintenance, smoking, use of salivary secretion inhibitors, presence of diabetes mellitus, condition of periodontal bone loss, and use of a removable denture. Most lost teeth were non-vital teeth (91.7% of all cases) and the most common cause of tooth loss was tooth fracture (62.1% of all cases). A statistically significant risk factors for tooth loss was number of remaining teeth at the start of maintenance (p = 0.003)

骨－歯根膜線維の複合組織形成による三次元的な歯周組織再生技術の開発

Periodontal tissue is a distinctive tissue structure composed three-dimensionally of cementum, periodontal ligament (PDL) and alveolar bone. Severe periodontal diseases cause fundamental problems for oral function and general health, and conventional dental treatments are insufficient for healing to healthy periodontal tissue. Cell sheet technology has been used in many tissue regenerations, including periodontal tissue, to transplant appropriate stem/progenitor cells for tissue regeneration of a target site as a uniform tissue. However, it is still difficult to construct a three-dimensional structure of complex tissue composed of multiple types of cells, and the transplantation of a single cell sheet cannot sufficiently regenerate a large-scale tissue injury. Here, we fabricated a three-dimensional complex cell sheet composed of a bone-ligament structure by layering PDL cells and osteoblast-like cells on a temperature responsive culture dish. Following ectopic and orthotopic transplantation, only the complex cell sheet group was demonstrated to anatomically regenerate the bone-ligament structure along with the functional connection of PDL-like fibers to the tooth root and alveolar bone. This study represents successful three-dimensional tissue regeneration of a large-scale tissue injury using a bioengineered tissue designed to simulate the anatomical structure

神経障害性疼痛における三叉神経筋内のIL-10とCXCL2

Many trigeminal neuropathic pain patients suffer severe chronic pain. The neuropathic pain might be related with cross-excitation of the neighboring neurons and satellite glial cell (SGCs) in the sensory ganglia and increasing the pain signals from the peripheral tissue to the central nervous system. We induced trigeminal neuropathic pain by infraorbital nerve constriction injury (IONC) in Sprague-Dawley rats. We tested cytokine (CXCL2 and IL-10) levels in trigeminal ganglia (TGs) after trigeminal neuropathic pain induction, and the effect of direct injection of the anti-CXCL2 and recombinant IL-10 into TG. We found that IONC induced pain behavior. Additionally, IONC induced satellite glial cell activation in TG and cytokine levels of TGs were changed after IONC. CXCL2 levels increased on day 1 of neuropathic pain induction and decreased gradually, with IL-10 levels showing the opposite trend. Recombinant IL-10 or anti-CXCL2 injection into TG decreased pain behavior. Our results show that IL-10 or anti-CXCL2 are therapy options for neuropathic pain

Dentin-pulp regeneration by 3D layered cell sheet

The dentin-pulp complex is a unique structure in teeth that contains both hard and soft tissues. Generally, deep caries and trauma cause damage to the dentin-pulp complex, and if left untreated, this damage will progress to irreversible pulpitis. The aim of this study was to fabricate a layered cell sheet composed of rat dental pulp (DP) cells and odontogenic differentiation of pulp (OD) cells and to investigate the ability to regenerate the dentin-pulp complex in a scaffold tooth. We fabricated two single cell sheets composed of DP cells (DP cell sheet) or OD cells (OD cell sheet) and a layered cell sheet made by layering both cells. The characteristics of the fabricated cell sheets were analyzed using light microscopy, scanning electron microscopy (SEM), hematoxylin-eosin (HE) staining, and immunohistochemistry (IHC). Furthermore, the cell sheets were transplanted into the subrenal capsule of immunocompromised mice for 8 weeks. Following this, the regenerative capacity to form dentin-like tissue was evaluated using micro-computed tomography (Micro-CT), HE staining, and IHC. The findings of SEM and IHC confirmed that layered cell sheets fabricated by stacking OD cells and DP cells maintained their cytological characteristics. Micro-CT of layered cell sheet transplants revealed a mineralized capping of the access cavity in the crown area, similar to that of natural dentin. In contrast, the OD cell sheet group demonstrated the formation of irregular fragments of mineralized tissue in the pulp cavity, and the DP cell sheet did not develop any hard tissue. Moreover, bone volume/tissue volume (BV/TV) showed a significant increase in hard tissue formation in the layered cell sheet group compared to that in the single cell sheet group (p<0.05). HE staining also showed a combination of soft and hard tissue formation in the layered cell sheet group. Furthermore, IHC confirmed that the dentin-like tissue generated from the layered cell sheet expressed characteristic markers of dentin but not bone equivalent to that of a natural tooth. In conclusion, this study demonstrates the feasibility of regenerating dentin-pulp complex using a bioengineered tissue designed to simulate the anatomical structure

Effect of Short-term TNF-α-stimulation of MC3T3-E1

Tumor necrosis factor-alpha (TNF-α) is an inflammatory cytokine known to cause bone resorption, swelling and edema during tissue organization. Conversely, TNF-α has also been shown to participate in tissue regeneration during the wound healing process. We have previously investigated the effects of TNF-α on human dental pulp cell differentiation. Dental pulp cells are composed of different cell types including primary odontoblasts and fibroblasts. We determined that the ratio of stem cells within the pulp cell population was increased following short-term stimulation with TNF-α. The aim of this study therefore was to investigate the effect of short-term stimulation with TNF-α on osteoblast-like MC3T3-E1 cell growth and differentiation. MC3T3-E1 cells were cultured in standard growth medium and on reaching sub-confluence were exposed to recombinant TNF-α (10 and 100 ng/ml) for 2 days prior to assessing their cell proliferation and differentiation properties in comparison to non-stimulated MC3T3-E1 cells (control). Although no significant differences in cell proliferation were observed between the TNF-α-stimulated and control groups, cell differentiation was delayed in the TNF-α-stimulated groups. In summary, short-term stimulation of cultured MC3T3-E1 cells with TNF-α had only minimal effect on their growth and differentiation

Thin-film and single-crystal transistors based on a trifluoromethyl-substituted alternating (thiophene/phenylene)-co-oligomer

We demonstrated the performance of thin-film transistors (TFTs) and single-crystal field-effect transistors (FETs) based on a trifluoromethyl-substituted alternating (thiophene/phenylene)-co-oligomer (AC5-CF3), 1,4-bis(5'-(4 ''-trifluoromethylphenyl)thiophene-2'-yl) benzene. An FET with a fine AC5-CF3 single-crystal demonstrated field-effect mobility as high as 3.1 cm(2) V-1 s(-1). This value implies that AC5-CF3 must be a useful n-type organic semiconducting material. The performance of AC5-CF3 TFTs depended on the substrate temperatures at which AC5-CF3 thin films were deposited. From the viewpoint of mobility, threshold voltage and sub-threshold slope, we obtained the highest performance at the substrate temperature of 100 degrees C. This was because a higher substrate temperature for deposition enlarged the size of grains in AC-CF3 thin films and improved the characteristics of grain boundaries. However, 120 degrees C depositions of AC5-CF3 induced deep valley-like cracks in the thin films, probably because of the difference between the coefficients of thermal expansion for AC5-CF3 thin films and silicon wafer substrates, resulting in effects such as worsening mobility. AC5-CF3 TFTs prepared at 100 degrees C deposition showed no channel length dependence of the field-effect mobility, and their average field-effect mobility was 0.55 +/- 0.05 cm(2) V-1 s(-1).ArticleOrganic Electronics. 11(9):1549-1554 (2010)journal articl

CGRPは三叉神経節衛星グリア細胞からのサイトカイン遊離と口腔顔面侵害性疼痛を誘発する

Neuron-glia interactions contribute to pain initiation and sustainment. Intra-ganglionic (IG) secretion of calcitonin gene-related peptide (CGRP) in the trigeminal ganglion (TG) modulates pain transmission through neuron-glia signaling, contributing to various orofacial pain conditions. The present study aimed to investigate the role of satellite glial cells (SGC) in TG in causing cytokine-related orofacial nociception in response to IG administration of CGRP. For that purpose, CGRP alone (10 μL of 10-5 M), Minocycline (5 μL containing 10 μg) followed by CGRP with one hour gap (Min + CGRP) were administered directly inside the TG in independent experiments. Rats were evaluated for thermal hyperalgesia at 6 and 24 h post-injection using an operant orofacial pain assessment device (OPAD) at three temperatures (37, 45 and 10 ℃). Quantitative real-time PCR was performed to evaluate the mRNA expression of IL-1β, IL-6, TNF-α, IL-1 receptor antagonist (IL-1RA), sodium channel 1.7 (NaV 1.7, for assessment of neuronal activation) and glial fibrillary acidic protein (GFAP, a marker of glial activation). The cytokines released in culture media from purified glial cells were evaluated using antibody cytokine array. IG CGRP caused heat hyperalgesia between 6–24 h (paired-t test, p < 0.05). Between 1 to 6 h the mRNA and protein expressions of GFAP was increased in parallel with an increase in the mRNA expression of pro-inflammatory cytokines IL-1β and anti-inflammatory cytokine IL-1RA and NaV1.7 (one-way ANOVA followed by Dunnett’s post hoc test, p < 0.05). To investigate whether glial inhibition is useful to prevent nociception symptoms, Minocycline (glial inhibitor) was administered IG 1 h before CGRP injection. Minocycline reversed CGRP-induced thermal nociception, glial activity, and down-regulated IL-1β and IL-6 cytokines significantly at 6 h (t-test, p < 0.05). Purified glial cells in culture showed an increase in release of 20 cytokines after stimulation with CGRP. Our findings demonstrate that SGCs in the sensory ganglia contribute to the occurrence of pain via cytokine expression and that glial inhibition can effectively control the development of nociception

Macrophage centripetal migration drives spontaneous healing process after spinal cord injury.

Traumatic spinal cord injury (SCI) brings numerous inflammatory cells, including macrophages, from the circulating blood to lesions, but pathophysiological impact resulting from spatiotemporal dynamics of macrophages is unknown. Here, we show that macrophages centripetally migrate toward the lesion epicenter after infiltrating into the wide range of spinal cord, depending on the gradient of chemoattractant C5a. However, macrophages lacking interferon regulatory factor 8 (IRF8) cannot migrate toward the epicenter and remain widely scattered in the injured cord with profound axonal loss and little remyelination, resulting in a poor functional outcome after SCI. Time-lapse imaging and P2X/YRs blockade revealed that macrophage migration via IRF8 was caused by purinergic receptors involved in the C5a-directed migration. Conversely, pharmacological promotion of IRF8 activation facilitated macrophage centripetal movement, thereby improving the SCI recovery. Our findings reveal the importance of macrophage centripetal migration via IRF8, providing a novel therapeutic target for central nervous system injury