Journal of Oral Biosciences最新文献

{"title":"Y-27632 enables long-term expansion of mouse submandibular gland epithelial cells via inactivation of TGF-β1/CTGF/p38 and ROCK2/JNK signaling pathway","authors":"Kichul Kim ,&nbsp;Naeun Oh ,&nbsp;Hyewon Kim ,&nbsp;Sangho Roh","doi":"10.1016/j.job.2024.08.005","DOIUrl":"10.1016/j.job.2024.08.005","url":null,"abstract":"<div><h3>Objectives</h3><div>This study aimed to investigate the effects of Y-27632 on the long-term maintainence of mouse submandibular epithelial cells (SG-Epis) <em>in vitro</em> and to elucidate the underlying mechanisms.</div></div><div><h3>Methods</h3><div>The role of the Rho-associated kinase (ROCK) inhibitor Y-27632 in maintaining SG-Epis and its underlying mechanisms were evaluated by examining the <em>in vitro</em> expansion of mouse SG-Epis. Changes in key cellular characteristics, such as proliferation, long-term expansion, and mRNA and protein expression, were assessed in the presence or absence of Y-27632.</div></div><div><h3>Results</h3><div>Treatment with Y-27632 significantly enhanced the proliferative potential of SG-Epis, preserving Krt8 and Krt14 expression over 17 passages. In the absence of Y-27632, SG-Epis lost their epithelial morphology. However, Y-27632 treatment maintained the epithelial morphology and downregulated mRNA levels of <em>Tgf-β1</em>, <em>Ctgf</em>, and <em>Rock2</em>. Treatment with TGF-β1 indicated that TGF-β/CTGF/p38 signaling is responsible for the maintenance of SG-Epis, while RNA interference studies revealed that ROCK2/c-Jun N-terminal kinase (JNK) signaling is also crucial for SG-Epis proliferation and maintenance.</div></div><div><h3>Conclusions</h3><div>The TGF-β1/CTGF/p38 and ROCK2/JNK signaling pathways are responsible for SG-Epis proliferation, and Y-27632 treatment effectively inactivates these pathways, enabling long-term <em>in vitro</em> maintenance of SG-Epis. The culture method utilizing Y-27632 provides an effective approach for the <em>in vitro</em> expansion of SG-Epis.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 4","pages":"Pages 98-106"},"PeriodicalIF":2.6,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142120851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of fimbriae variations in Porphyromonas gulae biofilm formation","authors":"Sho Yoshida ,&nbsp;Hiroaki Inaba ,&nbsp;Ryota Nomura ,&nbsp;Kazuhiko Nakano ,&nbsp;Michiyo Matsumoto-Nakano","doi":"10.1016/j.job.2024.08.003","DOIUrl":"10.1016/j.job.2024.08.003","url":null,"abstract":"<div><h3>Objectives</h3><div><em>Porphyromonas gulae</em> is a major causative agent of periodontal disease in companion animals that possesses various virulence factors, including fimbriae, lipopolysaccharides, and proteases. <em>P. gulae</em> fimbriae are classified into three genotypes (A, B, and C) based on their nucleotide sequences. Type C fimbrial isolates have been reported to be more virulent than other <em>fimA</em> types, suggesting that different <em>fimA</em> types may aid in the regulation of periodontal pathogenesis. Detailed findings regarding the ability of <em>P. gulae</em> to form biofilms have yet to be reported. Here, we investigated the contributions of fimbrial genotypes in <em>P. gulae</em> biofilm formation.</div></div><div><h3>Methods</h3><div><em>P. gulae</em> and <em>P. gingivalis</em> biofilms were generated on plates and analyzed using confocal laser microscopy. Additionally, the biofilms formed were assessed by staining with crystal violet. Furthermore, the physical strength of <em>P. gulae</em> biofilms was examined by ultrasonication.</div></div><div><h3>Results</h3><div>Biofilms formed by <em>P. gulae</em> type C were denser than those formed by types A and B. Moreover, the amount of biofilm formed by type C strains was significantly greater than that formed by type A and B strains, which was similar to the biofilms formed by <em>P. gingivalis</em> with type II fimbriae. Additionally, the physical strength of the type C biofilm was significantly greater than that of the other strains.</div></div><div><h3>Conclusions</h3><div>These results suggest that FimA variation may coordinate for biofilm formation. This is the first report on the observation and characterization of <em>P. gulae</em> biofilm formation.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 4","pages":"Pages 28-33"},"PeriodicalIF":2.6,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142113246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Invasion of human dental pulp fibroblasts by Porphyromonas gingivalis leads to autophagy via the phosphoinositide 3-kinase/Akt/mammalian target of rapamycin signaling pathway","authors":"Ying Feng ,&nbsp;Mingxiang Liu ,&nbsp;Yi Liu ,&nbsp;Hong Li","doi":"10.1016/j.job.2024.08.004","DOIUrl":"10.1016/j.job.2024.08.004","url":null,"abstract":"<div><h3>Objectives</h3><div><em>Porphyromonas gingivalis</em> is a pathogenic bacterium that causes periodontitis and dental pulp infection. Autophagy is a potential mechanism involved in inflammatory disease. This study established an in vitro model of <em>P. gingivalis</em> intracellular infection in human dental pulp fibroblasts (HDPFs) to investigate the effects of live <em>P. gingivalis</em> on HDPFs.</div></div><div><h3>Methods</h3><div>Morphological and quantification techniques such as fluorescence microscopy, transmission electron microscopy (TEM), indirect immunofluorescence analysis, enzyme-linked immunosorbent assay (ELISA), real-time polymerase chain reaction (PCR), and western blotting were used in this study.</div></div><div><h3>Results</h3><div>After cell invasion, <em>P. gingivalis</em> is mainly localized in the cytoplasm and lysosomes. Additionally, <em>P. gingivalis</em> activates autophagy in HDPFs by upregulating the expression of autophagy-related gene Beclin-1, activate autophagy-related gene12 (ATG12), and microtubule-associated protein light chain 3 (LC3). Furthermore, the invasion of <em>P. gingivalis</em> leads to increased phosphorylation of PI3K, Akt, and mTOR with the addition of rapamycin, whereas the addition of wortmannin decreased phosphorylation. This invasion of <em>P. gingivalis</em>, also causes an inflammatory response, leading to the upregulation of IL-1β, IL-6, and TNF-α. Rapamycin helps decrease levels of pro-inflammatory cytokines, but the addition of wortmannin increases them. These results show that the invasion of <em>P. gingivalis</em> can cause excessive inflammation and promote the autophagy of HDPFs, which is regulated by PI3K/Akt/mTOR.</div></div><div><h3>Conclusions</h3><div><em>P. gingivalis</em> escapes the immune system by inducing autophagy in the host cells, causing excessive inflammation. <em>P. gingivalis</em> regulates autophagy in HDPFs through the phosphoinositide 3-kinase/Akt/mammalian target of rapamycin pathway.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 4","pages":"Pages 10-18"},"PeriodicalIF":2.6,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142047327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PLAG1 overexpression in salivary gland duct-acinar units results in epithelial tumors with acinar-like features: Tumorization of luminal stem/progenitor cells may result in the development of salivary gland tumors consisting of only luminal cells","authors":"Yunosuke Ikeda ,&nbsp;Rika Yasuhara ,&nbsp;Junichi Tanaka ,&nbsp;Hiroko Ida-Yonemochi ,&nbsp;Haruhiko Akiyama ,&nbsp;Keishi Otsu ,&nbsp;Ikuya Miyamoto ,&nbsp;Hidemitsu Harada ,&nbsp;Hiroyuki Yamada ,&nbsp;Toshiyuki Fukada ,&nbsp;Tarou Irié","doi":"10.1016/j.job.2024.08.002","DOIUrl":"10.1016/j.job.2024.08.002","url":null,"abstract":"<div><h3>Objectives</h3><div>Details about salivary gland tumor histogenesis remain unknown. Here, we established a newly generated murine salivary gland tumor model that could overexpress pleomorphic adenoma gene 1 (PLAG1) and attempted to clarify the events that occur during the early phase of salivary gland tumor histogenesis.</div></div><div><h3>Methods</h3><div>Salivary gland tumors were generated using murine models (Sox9IRES-CreERT2; ROSA26-PLAG1). Lineage tracing of Sox9-expressing cells was performed using Sox9IRES-CreERT2; ROSA26-tdTomato mice, which were generated by crossing Sox9^CreERT2/- and ROSA26-tdTomato mice (expressing the tdTomato fluorescent protein). Organ-cultured embryonic salivary glands from the murine model were morphologically analyzed, and mRNA sequencing was conducted two days after tumor induction for gene enrichment and functional annotation analysis.</div></div><div><h3>Results</h3><div>Salivary gland tumors exhibited epithelial features with acinar-like structures because of gene rearrangements in the luminal cells. Structural disturbances in the duct-acinar unit of the salivary gland were observed and cancer-related pathways were enriched among the differentially upregulated genes in the early phase of tumor induction in an organ-cultured embryonic salivary gland tumor model.</div></div><div><h3>Conclusions</h3><div>The newly generated murine salivary gland tumor model may show that the tumorization of luminal stem/progenitor cells can result in the development of salivary gland tumors comprising only luminal cells.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 4","pages":"Pages 88-97"},"PeriodicalIF":2.6,"publicationDate":"2024-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142005506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-Streptococcus mutans and anti-inflammatory effects of ginsenoside Compound K and enzyme-treated red ginseng extract (BTEX-K)","authors":"Jin-Hwan Oh ,&nbsp;SangJoon Mo ,&nbsp;Le Thi Nhu Ngoc ,&nbsp;Jonghyuk Lee ,&nbsp;Moon-Young Kim ,&nbsp;Hae-Seo Park ,&nbsp;Jin-Hee Kim ,&nbsp;Yu-Jin Ha ,&nbsp;Lee Sung ,&nbsp;Young-Chul Lee ,&nbsp;Youl Hour","doi":"10.1016/j.job.2024.08.001","DOIUrl":"10.1016/j.job.2024.08.001","url":null,"abstract":"<div><h3>Objectives</h3><div>Dental caries, or tooth decay, is an oral health issue worldwide. Oral healthcare researchers are considering how to develop safe and effective preventive measures and treatments for dental caries. This study evaluated the potential applications of Compound K and BTEX-K, a Compound K–rich red ginseng extract, for the prevention and treatment of dental caries. Moreover, this study briefly confirmed its inhibitory effect on inflammation, an important factor in dental health.</div></div><div><h3>Methods</h3><div>The amount of organic acids produced by bacteria in biofilm was determined using in vitro and in vivo assays. The ability of these extracts to promote tooth remineralization and microhardness was evaluated using an in vivo mouse assay. We evaluated their anti-inflammatory potential by inhibiting proinflammatory cytokine expression and lipopolysaccharide-induced nitrous oxide production in cell lines.</div></div><div><h3>Results</h3><div>Compound K (10–20 μg/mL) and BTEX-K (50–100 μg/mL) effectively inhibited the growth of <em>Streptococcus mutans</em> bacteria, demonstrating significant antibacterial properties. They can potentially prevent biofilm formation by reducing lactic acid production in the teeth. These compounds showed a strong ability to promote tooth remineralization and improve the microhardness of acid-producing bacteria. They also possess potent anti-inflammatory properties that downregulate proinflammatory cytokine (interleukin-6, interleukin-1β, inducible nitric oxide synthase) expression, suppress nuclear factor-kappa B transcription factor activation (∼1.6 times), and reduce nitrous oxide production in lipopolysaccharide-induced RAW264.7 cells.</div></div><div><h3>Conclusions</h3><div>Compounds K and BTEX-K may provide a novel approach to dental caries prevention as well as inflammation prevention and treatment.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 4","pages":"Pages 19-27"},"PeriodicalIF":2.6,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141917734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular microbiological profiling of bottled unsweetened tea beverages: A screening experiment","authors":"Nagara Kaku ,&nbsp;Miho Kawachi ,&nbsp;Anna Wakui ,&nbsp;Misato Miyazawa ,&nbsp;Manami Imai ,&nbsp;Nanase Takahashi ,&nbsp;Aya Sato ,&nbsp;Takashi Abe ,&nbsp;Haruna Sato ,&nbsp;Yuki Kato ,&nbsp;Rika Okabe ,&nbsp;Yuka Naruse ,&nbsp;Nao Sato ,&nbsp;Nanami Asano ,&nbsp;Momoko Morohashi ,&nbsp;Hiroto Sano ,&nbsp;Jumpei Washio ,&nbsp;Yuki Abiko ,&nbsp;Kaori Tanaka ,&nbsp;Nobuhiro Takahashi ,&nbsp;Takuichi Sato","doi":"10.1016/j.job.2024.07.006","DOIUrl":"10.1016/j.job.2024.07.006","url":null,"abstract":"<div><p>To explore the potential storage and safety of drinking leftover bottled tea beverages from various manufacturers after direct drinking from bottles, we conducted a screening experiment on the growth of salivary bacteria in plastic bottles of tea. The diluted saliva samples from 10 participants were inoculated into the test bottled beverages, which resulted in bacteria, particularly former members of the genus <em>Lactobacillus</em>, growing in some green tea beverages with a neutral pH. In contrast, tea beverages with less bacterial growth contained <em>Streptococcus</em> spp., and the leftovers may be safe to store and drink again.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 3","pages":"Pages 628-632"},"PeriodicalIF":2.6,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141789435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic effects of mesenchymal stem cells derived from bone marrow and adipose tissue in a rat model of temporomandibular osteoarthritis","authors":"Saba Khazeni ,&nbsp;Mohammadali Ghavimi ,&nbsp;Mehran Mesgari-Abbasi ,&nbsp;Leila Roshangar ,&nbsp;Sara Abedi ,&nbsp;Tannaz Pourlak","doi":"10.1016/j.job.2024.07.007","DOIUrl":"10.1016/j.job.2024.07.007","url":null,"abstract":"<div><h3>Objectives</h3><div>To examine the potential of intra-articular administration of mesenchymal stem cells (MSCs) derived from bone marrow or adipose tissue to mitigate synovial inflammation in a rat model of temporomandibular joint (TMJ) osteoarthritis (OA).</div></div><div><h3>Methods</h3><div>In this experimental study, 40 rats were divided into 4 groups: (1) Control group; (2) Untreated TMJ-OA group; (3) TMJ-OA group treated with bone marrow-derived MSCs; (4) TMJ-OA group treated with adipose tissue-derived MSCs. The TMJ-OA model was established by inducing synovial inflammation through the intra-articular administration of complete Freund's adjuvant (CFA). After 8 weeks of TMJ-OA establishment, the animals were sacrificed and each mandibular condyle was extracted for histological evaluation.</div></div><div><h3>Results</h3><div>The untreated TMJ-OA group had significantly higher synovial inflammation, as indicated microscopically by higher grades of synovial membrane hyperplasia and adhesion, vascular vasodilation, and fibrin deposition than the control group (p &lt; 0.001). Both TMJ-OA groups treated with MSCs had lower grades of synovial inflammation and less severe synovitis than the untreated TMJ-OA group (p &lt; 0.001). The TMJ-OA group treated with adipose tissue-derived MSCs showed lower grades of synovial membrane hyperplasia and higher grades of fibrin deposition than the that treated with bone marrow-derived MSCs (p &lt; 0.001). Other indicators of synovial inflammation and synovitis severity were comparable between the two treatment groups.</div></div><div><h3>Conclusions</h3><div>Administration of CFA to the TMJ-OA rat model augmented synovial inflammation. Intra-articular administration of MSCs derived from either bone marrow or adipose tissue attenuated the microscopic manifestations of this inflammation, indicating the therapeutic potential of this treatment for TMJ-OA.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 4","pages":"Pages 107-115"},"PeriodicalIF":2.6,"publicationDate":"2024-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141767628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cytoarchitecture and intercellular interactions in the trigeminal ganglion: Associations with neuropathic pain in the orofacial region","authors":"Tetsuya Goto,&nbsp;Eriko Kuramoto,&nbsp;Haruki Iwai,&nbsp;Atsushi Yamanaka","doi":"10.1016/j.job.2024.07.003","DOIUrl":"10.1016/j.job.2024.07.003","url":null,"abstract":"<div><h3>Background</h3><p>Disorders of the trigeminal nerve, a sensory nerve of the orofacial region, often lead to complications in dental practice, including neuropathic pain, allodynia, and ectopic pain. Management of these complications requires an understanding of the cytoarchitecture of the trigeminal ganglion, where the cell bodies of the trigeminal nerve are located, and the mechanisms of cell-cell interactions.</p></div><div><h3>Highlights</h3><p>In the trigeminal ganglion, ganglion, satellite, Schwann, and immune cells coexist and interact. Cell-cell interactions are complex and occur through direct contact via gap junctions or through mediators such as adenosine triphosphate, nitric oxide, peptides, and cytokines. Interactions between the nervous and immune systems within the trigeminal ganglion may have neuroprotective effects during nerve injury or may exacerbate inflammation and produce chronic pain. Under pathological conditions of the trigeminal nerve, cell-cell interactions can cause allodynia and ectopic pain. Although cell-cell interactions that occur via mediators can act at some distance, they are more effective when the cells are close together. Therefore, information on the three-dimensional topography of trigeminal ganglion cells is essential for understanding the pathophysiology of ectopic pain.</p></div><div><h3>Conclusions</h3><p>A three-dimensional map of the somatotopic localization of trigeminal ganglion neurons revealed that ganglion cells innervating distant orofacial regions are often apposed to each other, interacting with and potentially contributing to ectopic pain. Elucidation of the complex network of mediators and their receptors responsible for intercellular communication within the trigeminal ganglion is essential for understanding ectopic pain.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 3","pages":"Pages 485-490"},"PeriodicalIF":2.6,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1349007924001518/pdfft?md5=03deb21023fdafb0f2ce165d9d73cd9f&pid=1-s2.0-S1349007924001518-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141735264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-neuronal cells act as crucial players in neuropathic orofacial pain","authors":"Koichi Iwata,&nbsp;Yoshinori Hayashi,&nbsp;Suzuro Hitomi,&nbsp;Yoshiyuki Tsuboi,&nbsp;Masamichi Shinoda","doi":"10.1016/j.job.2024.07.005","DOIUrl":"10.1016/j.job.2024.07.005","url":null,"abstract":"<div><h3>Background</h3><p><span>Following peripheral nerve damage, various non-neuronal cells are activated, triggering accumulation in the peripheral and </span>central nervous systems<span>, and communicate with neurons. Evidence suggest that neuronal and non-neuronal cell communication is a critical mechanism of neuropathic pain<span>; however, its detailed mechanisms in contributing to neuropathic orofacial pain development remain unclear.</span></span></p></div><div><h3>Highlight</h3><p><span><span><span>Neuronal and non-neuronal cell communication in the trigeminal ganglion (TG) is believed to cause neuronal </span>hyperactivation following </span>trigeminal nerve damage, resulting in neuropathic orofacial pain. Trigeminal nerve damage activates and accumulates non-neuronal cells, such as satellite cells and macrophages in the TG and </span>microglia<span><span>, astrocytes, and oligodendrocytes<span> in the trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1–C2). These non-neuronal cells release various molecules, contributing to the hyperactivation of TG, Vc, and C1–C2 nociceptive neurons. These hyperactive nociceptive neurons release molecules that enhance non-neuronal </span></span>cell activation. This neuron and non-neuronal cell crosstalk causes hyperactivation of nociceptive neurons in the TG, Vc, and C1–C2. Here, we addressed previous and recent data on the contribution of neuronal and non-neuronal cell communication and its involvement in neuropathic orofacial pain development.</span></p></div><div><h3>Conclusion</h3><p>Previous and recent data suggest that neuronal and non-neuronal cell communication in the TG, Vc, and C1–C2 is a key mechanism that causes neuropathic orofacial pain associated with trigeminal nerve damage.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 3","pages":"Pages 491-495"},"PeriodicalIF":2.6,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141735265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Platelet-rich fibrin as an adjunct to scaling and root planing in treatment of shallow periodontal pockets: A randomized clinical trial","authors":"","doi":"10.1016/j.job.2024.07.002","DOIUrl":"10.1016/j.job.2024.07.002","url":null,"abstract":"<div><h3>Objectives</h3><p>To evaluate the efficacy of platelet-rich fibrin (PRF) as an adjunct to scaling and root planing<span> (ScRp) for healing shallow periodontal pockets.</span></p></div><div><h3>Methods</h3><p>Twelve patients with periodontitis<span><span><span> were enrolled in this split-mouth, randomized clinical trial<span><span><span>. A total of 24 shallow periodontal pockets (4–6 mm) were treated by either ScRp alone (control) or PRF (test). </span>Clinical attachment loss (CAL), probing pocket depth (PPD), </span>bleeding on probing (BOP), and </span></span>plaque index (PLI), as well as platelet-derived growth factor-BB (PDGF-BB) by enzyme-linked immunosorbent assay (ELISA) in </span>gingival crevicular fluid (GCF) were measured at baseline and at 1- and 3-month follow-up visits.</span></p></div><div><h3>Results</h3><p>At 1- and 3-month follow-up visits, greater CAL gains (2.6 ± 0.25 mm and 3.26 ± 0.31 mm, respectively) and PPD reductions (2.58 ± 0.38 and 3.31 ± 0.39 mm, respectively) were observed in the test group compared to those in controls (CAL gain of 1.01 ± 0.49 mm and 1.43 ± 0.48 mm; PPD reduction of 1.1 ± 0.55 and 1.37 ± 0.49 mm, respectively). In addition, the increase in PDGF-BB in GCF in the test group (724.5 ± 186.09 pg/μl and 1957.5 ± 472.9 pg/μl) was significantly greater than that in controls (109.3 ± 24.07 and 614.64 ± 209.3 pg/μl) at 1- and 3-month follow-up visits, respectively.</p></div><div><h3>Conclusions</h3><p>The noninvasive use of PRF as an adjunct to ScRp successfully improved clinical periodontal parameters and might contribute to increased PDGF-BB in GCF.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 3","pages":"Pages 612-618"},"PeriodicalIF":2.6,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141601885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}