首页 > 最新文献

Journal of dental research最新文献

英文 中文
Cannabidiol for Toothache: Ups, Downs, and Regulatory Considerations. 治疗牙痛的大麻二酚:起伏与监管考虑。
Pub Date : 2024-03-01 Epub Date: 2024-02-12 DOI: 10.1177/00220345231223691
K N Theken, E V Hersh
{"title":"Cannabidiol for Toothache: Ups, Downs, and Regulatory Considerations.","authors":"K N Theken, E V Hersh","doi":"10.1177/00220345231223691","DOIUrl":"10.1177/00220345231223691","url":null,"abstract":"","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10900851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139725481","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}
引用次数: 0
Cannabidiol as an Alternative Analgesic for Acute Dental Pain. 大麻二酚作为急性牙痛的替代镇痛药。
Pub Date : 2024-03-01 Epub Date: 2023-11-01 DOI: 10.1177/00220345231200814
V Chrepa, S Villasenor, A Mauney, G Kotsakis, L Macpherson

Odontogenic pain can be debilitating, and nonopioid analgesic options are limited. This randomized placebo-controlled clinical trial aimed to assess the effectiveness and safety of cannabidiol (CBD) as an analgesic for patients with emergency acute dental pain. Sixty-one patients with moderate to severe toothache were randomized into 3 groups: CBD10 (CBD 10 mg/kg), CBD20 (CBD 20 mg/kg), and placebo. We administered a single dose of respective oral solution and monitored the subjects for 3 h. The primary outcome measure was the numerical pain differences using a visual analog scale (VAS) from baseline within and among the groups. Secondary outcome measures included ordinal pain intensity differences, the onset of significant pain relief, maximum pain relief, changes in bite force within and among the groups, psychoactive effects, mood changes, and other adverse events. Both CBD groups resulted in significant VAS pain reduction compared to their baseline and the placebo group, with a maximum median VAS pain reduction of 73% from baseline pain at the 180-min time point (P < 0.05). CBD20 experienced a faster onset of significant pain relief than CBD10 (15 versus 30 min after drug administration), and both groups reached maximum pain relief at 180-min. Number needed to treat was 3.1 for CBD10 and 2.4 for CBD20. Intragroup comparisons showed a significant increase in bite forces in both CBD groups (P < 0.05) but not in the placebo group (P > 0.05). CBD20 resulted in a significant difference in mean percent bite force change in the 90- and 180-min time points compared to the placebo group (P < 0.05). Compared to placebo, sedation, diarrhea, and abdominal pain were significantly associated with the CBD groups (P < 0.05). There were no other significant psychoactive or mood change effects. This randomized trial provides the first clinical evidence that oral CBD can be an effective and safe analgesic for dental pain.

牙源性疼痛可能会使人衰弱,非鸦片类镇痛的选择有限。这项随机安慰剂对照临床试验旨在评估大麻二酚(CBD)作为紧急急性牙痛患者止痛药的有效性和安全性。61名中度至重度牙痛患者被随机分为3组:CBD10(CBD 10 mg/kg)、CBD20(CBD 20 mg/kg)和安慰剂。我们分别给予单剂量口服溶液,并对受试者进行3小时的监测。主要的结果测量是使用视觉模拟量表(VAS)从基线开始测量各组内部和组之间的疼痛数值差异。次要结果测量包括顺序疼痛强度差异、显著疼痛缓解的开始、最大疼痛缓解、组内和组间咬合力的变化、精神活性影响、情绪变化和其他不良事件。与基线和安慰剂组相比,两个CBD组的VAS疼痛显著减轻,在180分钟的时间点,VAS疼痛的最大中位数从基线疼痛减轻了73%(P<0.05)。CBD20的显著疼痛缓解速度比CBD10更快(给药后15分钟和30分钟),两组在180分钟时都达到了最大疼痛缓解。CBD10和CBD20需要治疗的数量分别为3.1和2.4。组内比较显示,两个CBD组的咬合力显著增加(P<0.05),但安慰剂组没有(P>0.05)。与安慰剂组相比,CBD20导致90和180分钟时间点的平均咬合力变化百分比显著差异(P<0.05),腹痛与CBD组显著相关(P<0.05)。没有其他显著的精神活动或情绪变化影响。这项随机试验首次提供了临床证据,证明口服CBD是一种有效、安全的牙痛镇痛药。
{"title":"Cannabidiol as an Alternative Analgesic for Acute Dental Pain.","authors":"V Chrepa, S Villasenor, A Mauney, G Kotsakis, L Macpherson","doi":"10.1177/00220345231200814","DOIUrl":"10.1177/00220345231200814","url":null,"abstract":"<p><p>Odontogenic pain can be debilitating, and nonopioid analgesic options are limited. This randomized placebo-controlled clinical trial aimed to assess the effectiveness and safety of cannabidiol (CBD) as an analgesic for patients with emergency acute dental pain. Sixty-one patients with moderate to severe toothache were randomized into 3 groups: CBD10 (CBD 10 mg/kg), CBD20 (CBD 20 mg/kg), and placebo. We administered a single dose of respective oral solution and monitored the subjects for 3 h. The primary outcome measure was the numerical pain differences using a visual analog scale (VAS) from baseline within and among the groups. Secondary outcome measures included ordinal pain intensity differences, the onset of significant pain relief, maximum pain relief, changes in bite force within and among the groups, psychoactive effects, mood changes, and other adverse events. Both CBD groups resulted in significant VAS pain reduction compared to their baseline and the placebo group, with a maximum median VAS pain reduction of 73% from baseline pain at the 180-min time point (<i>P</i> < 0.05). CBD20 experienced a faster onset of significant pain relief than CBD10 (15 versus 30 min after drug administration), and both groups reached maximum pain relief at 180-min. Number needed to treat was 3.1 for CBD10 and 2.4 for CBD20. Intragroup comparisons showed a significant increase in bite forces in both CBD groups (<i>P</i> < 0.05) but not in the placebo group (<i>P</i> > 0.05). CBD20 resulted in a significant difference in mean percent bite force change in the 90- and 180-min time points compared to the placebo group (<i>P</i> < 0.05). Compared to placebo, sedation, diarrhea, and abdominal pain were significantly associated with the CBD groups (<i>P</i> < 0.05). There were no other significant psychoactive or mood change effects. This randomized trial provides the first clinical evidence that oral CBD can be an effective and safe analgesic for dental pain.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10900863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71430538","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}
引用次数: 0
Impact of Periodontitis on the Leakage of Oral Bacteria to the Gut. 牙周炎对口腔细菌渗入肠道的影响
Pub Date : 2024-03-01 Epub Date: 2024-01-09 DOI: 10.1177/00220345231221709
E Buetas, M Jordán-López, A López-Roldán, A Mira, M Carda-Diéguez

Colorectal cancer (CRC) and periodontitis have recently been related due to the higher incidence of CRC in periodontal patients and the involvement of periodontal pathogens in carcinogenesis, suggesting that leakage from the oral cavity to the gut occurs. However, the magnitude of this pass-through in healthy individuals is controversial, and the effect that periodontitis could play in it is understudied. To evaluate the rate of bacterial leakage from the oral cavity to the gut, we analyzed the microbial composition of saliva, subgingival plaque, and fecal samples in healthy individuals without gastrointestinal disorders, including 20 periodontitis patients and 20 oral healthy controls, using PacBio full-length 16S rRNA gene sequencing. As expected, we observed a higher abundance of periodontal pathogens in the subgingival plaque and saliva of periodontal patients. In contrast, no significant differences were found between the fecal samples of both groups, implying that gut samples from periodontal patients were not enriched in periodontal pathogens. Fusobacterium nucleatum, a biomarker of CRC, was not found in the fecal samples of any participant. Our study does show a small leakage of some oral bacteria (mainly streptococci) to the gut, regardless of periodontal health status. Future studies should test whether other host factors and/or the preexistence of a gut disorder must be present in addition to periodontitis to promote the colonization of the gut by oral pathogens. The absence of periodontal pathogens in feces supports the idea that these bacteria could be used as biomarkers of intestinal disorders, including CRC.

最近,大肠癌(CRC)和牙周炎被联系起来,因为牙周病患者的大肠癌发病率较高,而且牙周病原体也参与了致癌过程。然而,健康人的这种渗透程度还存在争议,牙周炎在其中可能发挥的作用也未得到充分研究。为了评估细菌从口腔渗漏到肠道的速度,我们使用 PacBio 全长 16S rRNA 基因测序分析了没有胃肠道疾病的健康人(包括 20 名牙周炎患者和 20 名口腔健康对照组)唾液、龈下牙菌斑和粪便样本中的微生物组成。不出所料,我们在牙周炎患者的龈下牙菌斑和唾液中观察到了更多的牙周病原体。相比之下,两组患者的粪便样本没有发现明显差异,这意味着牙周病患者的肠道样本中并没有富集牙周病原体。在所有参与者的粪便样本中都没有发现作为 CRC 生物标志物的核酸镰刀菌。我们的研究确实表明,无论牙周健康状况如何,一些口腔细菌(主要是链球菌)会少量渗入肠道。未来的研究应该检验,除了牙周炎之外,是否还必须存在其他宿主因素和/或预先存在肠道疾病,才能促进口腔病原体在肠道的定植。粪便中没有牙周病原体支持了这样一种观点,即这些细菌可用作肠道疾病(包括 CRC)的生物标志物。
{"title":"Impact of Periodontitis on the Leakage of Oral Bacteria to the Gut.","authors":"E Buetas, M Jordán-López, A López-Roldán, A Mira, M Carda-Diéguez","doi":"10.1177/00220345231221709","DOIUrl":"10.1177/00220345231221709","url":null,"abstract":"<p><p>Colorectal cancer (CRC) and periodontitis have recently been related due to the higher incidence of CRC in periodontal patients and the involvement of periodontal pathogens in carcinogenesis, suggesting that leakage from the oral cavity to the gut occurs. However, the magnitude of this pass-through in healthy individuals is controversial, and the effect that periodontitis could play in it is understudied. To evaluate the rate of bacterial leakage from the oral cavity to the gut, we analyzed the microbial composition of saliva, subgingival plaque, and fecal samples in healthy individuals without gastrointestinal disorders, including 20 periodontitis patients and 20 oral healthy controls, using PacBio full-length 16S rRNA gene sequencing. As expected, we observed a higher abundance of periodontal pathogens in the subgingival plaque and saliva of periodontal patients. In contrast, no significant differences were found between the fecal samples of both groups, implying that gut samples from periodontal patients were not enriched in periodontal pathogens. <i>Fusobacterium nucleatum</i>, a biomarker of CRC, was not found in the fecal samples of any participant. Our study does show a small leakage of some oral bacteria (mainly streptococci) to the gut, regardless of periodontal health status. Future studies should test whether other host factors and/or the preexistence of a gut disorder must be present in addition to periodontitis to promote the colonization of the gut by oral pathogens. The absence of periodontal pathogens in feces supports the idea that these bacteria could be used as biomarkers of intestinal disorders, including CRC.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139405728","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}
引用次数: 0
Lacticaseibacillus rhamnosus GG Improves Periodontal Bone Repair via Gut-Blood Axis in Hyperlipidemia. 鼠李糖乳杆菌 GG 通过肠道-血液轴改善高脂血症患者的牙周骨修复
Pub Date : 2024-03-01 Epub Date: 2024-01-10 DOI: 10.1177/00220345231217402
Y Huang, R Ge, J Qian, J Lu, D Qiao, R Chen, H Jiang, D Cui, T Zhang, N Wang, S He, M Wang, F Yan

Periodontal bone regeneration remains a clinical challenge, and hyperlipidemia can aggravate alveolar bone resorption. Probiotics have recently been reported to improve bone mass. We aimed to determine the role of Lacticaseibacillus rhamnosus GG (LGG) in periodontal bone regeneration improvement within the context of periodontitis with hyperlipidemia. A Sprague Dawley rat model for periodontitis, hyperlipidemia, and periodontal fenestration defect was constructed (n = 36) and administered LGG gavage for 6 wk (the rats were subsequently sacrificed). Fecal microbiota from donor rats 3 wk after LGG gavage was transplanted into recipient rats to evaluate the role of LGG-modulated gut microbiota in periodontal bone regeneration. Regenerated bone mass was detected using micro-computerized tomography and hematoxylin and eosin stain. Gut microbiota was analyzed using 16S ribosomal RNA sequencing. Serum metabolites were detected by liquid chromatography-mass spectrometry (6 wk after LGG gavage). The pro-osteogenic effects of screened serum metabolite were verified in vitro on bone marrow mesenchymal stem cells (BMMSCs). We found that the bone mineral density, bone volume (BV), trabecular bone volume fraction (BV/TV), and trabecular thickness of the regenerated periodontal bone increased after LGG gavage (P < 0.05) but had little effect on oral flora. After LGG gavage, Staphylococcus, Corynebacterium, and Collinsella in the gut of donors were significantly changed, and these differences were maintained in recipients, who also showed increased trabecular thickness of the regenerated periodontal bone (P < 0.05). These key genera were correlated with BV/TV and BV (P < 0.05). In addition, LGG gavage significantly regulated bone-related blood metabolites, of which selenomethionine promoted BMMSC osteogenesis. Notably, selenomethionine was associated with key gut genera (P < 0.05). Collectively, LGG improved periodontal bone regeneration in the context of periodontitis with hyperlipidemia by modulating gut microbiota and increasing pro-osteogenic metabolites in the blood. These results reveal new insights into the use of probiotics to promote periodontal bone regeneration via the gut-blood-bone axis.

牙周骨再生仍是一项临床挑战,而高脂血症会加剧牙槽骨吸收。最近有报道称益生菌可改善骨量。我们旨在确定鼠李糖乳杆菌 GG(LGG)在牙周炎合并高脂血症的情况下对改善牙周骨再生的作用。构建了一个具有牙周炎、高脂血症和牙周瘘管缺损的 Sprague Dawley 大鼠模型(n = 36),给大鼠灌胃 LGG 6 周(随后大鼠被处死)。将供体大鼠灌胃 LGG 3 周后的粪便微生物群移植到受体大鼠体内,以评估 LGG 调节的肠道微生物群在牙周骨再生中的作用。使用微型计算机断层扫描和苏木精及伊红染色检测再生骨量。使用 16S 核糖体 RNA 测序分析肠道微生物群。采用液相色谱-质谱法检测血清代谢物(灌胃 LGG 6 周后)。筛选出的血清代谢物对骨髓间充质干细胞(BMMSCs)的促成骨作用在体外得到了验证。我们发现,灌胃 LGG 后,再生牙周骨的骨矿密度、骨量(BV)、骨小梁体积分数(BV/TV)和骨小梁厚度均有所增加(P < 0.05),但对口腔菌群的影响很小。灌胃 LGG 后,供体肠道中的葡萄球菌、棒状杆菌和柯林斯菌发生了显著变化,这些差异在受体中保持不变,受体再生牙周骨小梁厚度也有所增加(P < 0.05)。这些关键菌属与 BV/TV 和 BV 相关(P < 0.05)。此外,灌胃 LGG 能显著调节骨相关血液代谢物,其中硒蛋氨酸能促进 BMMSC 骨生成。值得注意的是,硒蛋氨酸与主要肠道菌属有关(P < 0.05)。总之,在牙周炎合并高脂血症的情况下,LGG通过调节肠道微生物群和增加血液中的促骨生成代谢物改善了牙周骨再生。这些结果揭示了使用益生菌通过肠道-血液-骨骼轴促进牙周骨骼再生的新见解。
{"title":"Lacticaseibacillus rhamnosus GG Improves Periodontal Bone Repair via Gut-Blood Axis in Hyperlipidemia.","authors":"Y Huang, R Ge, J Qian, J Lu, D Qiao, R Chen, H Jiang, D Cui, T Zhang, N Wang, S He, M Wang, F Yan","doi":"10.1177/00220345231217402","DOIUrl":"10.1177/00220345231217402","url":null,"abstract":"<p><p>Periodontal bone regeneration remains a clinical challenge, and hyperlipidemia can aggravate alveolar bone resorption. Probiotics have recently been reported to improve bone mass. We aimed to determine the role of <i>Lacticaseibacillus rhamnosus</i> GG (LGG) in periodontal bone regeneration improvement within the context of periodontitis with hyperlipidemia. A Sprague Dawley rat model for periodontitis, hyperlipidemia, and periodontal fenestration defect was constructed (<i>n</i> = 36) and administered LGG gavage for 6 wk (the rats were subsequently sacrificed). Fecal microbiota from donor rats 3 wk after LGG gavage was transplanted into recipient rats to evaluate the role of LGG-modulated gut microbiota in periodontal bone regeneration. Regenerated bone mass was detected using micro-computerized tomography and hematoxylin and eosin stain. Gut microbiota was analyzed using 16S ribosomal RNA sequencing. Serum metabolites were detected by liquid chromatography-mass spectrometry (6 wk after LGG gavage). The pro-osteogenic effects of screened serum metabolite were verified in vitro on bone marrow mesenchymal stem cells (BMMSCs). We found that the bone mineral density, bone volume (BV), trabecular bone volume fraction (BV/TV), and trabecular thickness of the regenerated periodontal bone increased after LGG gavage (<i>P</i> < 0.05) but had little effect on oral flora. After LGG gavage, <i>Staphylococcus</i>, <i>Corynebacterium</i>, and <i>Collinsella</i> in the gut of donors were significantly changed, and these differences were maintained in recipients, who also showed increased trabecular thickness of the regenerated periodontal bone (<i>P</i> < 0.05). These key genera were correlated with BV/TV and BV (<i>P</i> < 0.05). In addition, LGG gavage significantly regulated bone-related blood metabolites, of which selenomethionine promoted BMMSC osteogenesis. Notably, selenomethionine was associated with key gut genera (<i>P</i> < 0.05). Collectively, LGG improved periodontal bone regeneration in the context of periodontitis with hyperlipidemia by modulating gut microbiota and increasing pro-osteogenic metabolites in the blood. These results reveal new insights into the use of probiotics to promote periodontal bone regeneration via the gut-blood-bone axis.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139405729","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}
引用次数: 0
Sjögren's Disease and Oral Health: A Genetic Instrumental Variable Analysis. 斯约格伦病与口腔健康:遗传工具变量分析》。
Pub Date : 2024-03-01 Epub Date: 2024-01-29 DOI: 10.1177/00220345231218903
S L Reckelkamm, Z Alayash, B Holtfreter, M Nolde, S E Baumeister

Epidemiological studies have consistently shown that Sjögren's disease (SjD) increases the risk of dental caries. Despite similar evidence indicating an elevated risk of periodontitis, SjD remains a disputed risk factor for this disease. The risk of bias in observational research is a major impediment to confirming this link. Within an instrumental variable framework, genetic variants associated with a risk factor can be used to proxy its effect on an outcome while avoiding common sources of observational study bias. In this study, we leveraged an instrumental variable approach to investigate whether SjD affects the risk of caries and periodontitis. A total of 57 genetic variants strongly associated with SjD were identified from a genome-wide association study of 2,247 European descent cases and 332,115 controls. We tested for associations of these genetic instruments with caries (measured as the number of decayed, missing, and filled surfaces in 26,792 individuals) and periodontitis (17,353 clinical periodontitis cases and 28,210 European controls). Several sensitivity analyses were used to further validate the primary inverse variance weighted (IVW) estimate. IVW analysis revealed an adverse effect of SjD on caries (β = 0.039, P = 6.3e-16) and periodontitis (odds ratio = 1.033, P = 2.3e-05). Sensitivity analyses, conducted to assess the robustness to potential violations of instrumental variable assumptions, further support these findings. Our results showed that SjD has a detrimental effect on caries and also suggest that SjD promotes periodontitis.

流行病学研究一致表明,斯约格伦病(SjD)会增加龋齿的风险。尽管有类似的证据表明牙周炎的风险升高,但 SjD 仍然是一个有争议的风险因素。观察性研究中的偏倚风险是证实这种联系的主要障碍。在工具变量框架内,与风险因素相关的遗传变异可用于替代风险因素对结果的影响,同时避免观察性研究中常见的偏倚来源。在本研究中,我们利用工具变量方法研究了 SjD 是否会影响龋齿和牙周炎的风险。在对 2,247 例欧洲血统病例和 332,115 例对照进行的全基因组关联研究中,共发现了 57 个与 SjD 密切相关的遗传变异。我们检测了这些基因工具与龋齿(以 26,792 人的蛀蚀、缺失和填充表面的数量来衡量)和牙周炎(17,353 例临床牙周炎病例和 28,210 例欧洲对照)之间的关联。为了进一步验证主要的逆方差加权(IVW)估计值,我们进行了多项敏感性分析。IVW 分析显示,SjD 对龋齿(β = 0.039,P = 6.3e-16)和牙周炎(几率比 = 1.033,P = 2.3e-05)有不利影响。为评估可能违反工具变量假设的稳健性而进行的敏感性分析进一步支持了这些发现。我们的研究结果表明,SjD 对龋病有不利影响,同时也表明 SjD 会促进牙周炎。
{"title":"Sjögren's Disease and Oral Health: A Genetic Instrumental Variable Analysis.","authors":"S L Reckelkamm, Z Alayash, B Holtfreter, M Nolde, S E Baumeister","doi":"10.1177/00220345231218903","DOIUrl":"10.1177/00220345231218903","url":null,"abstract":"<p><p>Epidemiological studies have consistently shown that Sjögren's disease (SjD) increases the risk of dental caries. Despite similar evidence indicating an elevated risk of periodontitis, SjD remains a disputed risk factor for this disease. The risk of bias in observational research is a major impediment to confirming this link. Within an instrumental variable framework, genetic variants associated with a risk factor can be used to proxy its effect on an outcome while avoiding common sources of observational study bias. In this study, we leveraged an instrumental variable approach to investigate whether SjD affects the risk of caries and periodontitis. A total of 57 genetic variants strongly associated with SjD were identified from a genome-wide association study of 2,247 European descent cases and 332,115 controls. We tested for associations of these genetic instruments with caries (measured as the number of decayed, missing, and filled surfaces in 26,792 individuals) and periodontitis (17,353 clinical periodontitis cases and 28,210 European controls). Several sensitivity analyses were used to further validate the primary inverse variance weighted (IVW) estimate. IVW analysis revealed an adverse effect of SjD on caries (β = 0.039, <i>P</i> = 6.3e-16) and periodontitis (odds ratio = 1.033, <i>P</i> = 2.3e-05). Sensitivity analyses, conducted to assess the robustness to potential violations of instrumental variable assumptions, further support these findings. Our results showed that SjD has a detrimental effect on caries and also suggest that SjD promotes periodontitis.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10900855/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139572356","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}
引用次数: 0
Pth1r in Neural Crest Cells Regulates Nasal Cartilage Differentiation. 神经顶细胞中的 Pth1r 调控鼻软骨分化
Pub Date : 2024-03-01 Epub Date: 2024-01-17 DOI: 10.1177/00220345231221954
K Amano, D Okuzaki, Y Kitaoka, S Kato, M Fujiwara, S Tanaka, S Iida

Neural crest cells (NCC) arise from the dorsal margin of the neural plate border and comprise a unique cell population that migrates to and creates the craniofacial region. Although factors including Shh, Fgf8, and bone morphogenetic proteins have been shown to regulate these biological events, the role of parathyroid hormone 1 receptor (Pth1r) has been less studied. We generated an NCC-specific mouse model for Pth1r and researched gene expression, function, and interaction focusing on nasal cartilage framework and midfacial development. Wnt1-Cre;Pth1rfl/fl;Tomatofl/+ mice had perinatal lethality, but we observed short snout and jaws, tongue protrusion, reduced NCC-derived cranial length, increased mineralization in nasal septum and hyoid bones, and less bone mineralization at interfrontal suture in mutants at E18.5. Importantly, the mutant nasal septum and turbinate cartilage histologically revealed gradual, premature accelerated hypertrophic differentiation. We then studied the underlying molecular mechanisms by performing RNA seq analysis and unexpectedly found that expression of Ihh and related signaling molecules was enhanced in mutant nasomaxillary tissues. To see if Pth1r and Ihh signaling are associated, we generated a Wnt1-Cre; Ihhfl/fl;Pth1rfl/fl;Tomatofl/+ (DKO) mouse and compared the phenotypes to those of each single knockout mouse: Wnt1-Cre; Ihhfl/fl;Pth1rfl/+;Tomatofl/+ (Ihh-CKO) and Wnt1-Cre;Ihhfl/+;Pth1rfl/fl;Tomatofl/+ (Pth1r-CKO). Ihh-CKO mice displayed a milder effect. Of note, the excessive hypertrophic conversion of the nasal cartilage framework observed in Pth1r-CKO was somewhat rescued DKO embryos. Further, a half cAMP responsive element and the 4 similar sequences containing 2 mismatches were identified from the promoter to the first intron in Ihh gene. Gli1-CreERT2;Pth1rfl/fl;Tomatofl/+, a Pth1r-deficient model targeted in hedgehog responsive cells, demonstrated the enlarged hypertrophic layer and significantly more Tomato-positive chondrocytes accumulated in the nasal septum and ethmoidal endochondral ossification. Collectively, the data suggest a relevant Pth1r/Ihh interaction. Our findings obtained from novel mouse models for Pth1r signaling illuminate previously unknown aspects in craniofacial biology and development.

神经嵴细胞(NCC)产生于神经板边缘的背缘,是迁移到并形成颅面区域的独特细胞群。虽然包括Shh、Fgf8和骨形态发生蛋白在内的因子已被证明能调节这些生物事件,但对甲状旁腺激素1受体(Pth1r)的作用研究较少。我们建立了一个 Pth1r 的 NCC 特异性小鼠模型,并重点研究了鼻软骨框架和中面部发育的基因表达、功能和相互作用。Wnt1-Cre;Pth1rfl/fl;Tomatofl/+小鼠围产期死亡,但我们观察到突变体在E18.5时鼻和下颌短小、舌前突、NCC衍生颅骨长度减少、鼻中隔和舌骨矿化增加以及额间缝骨矿化减少。重要的是,突变体的鼻中隔和鼻甲软骨在组织学上显示出逐渐、过早的加速肥大分化。随后,我们通过 RNA seq 分析研究了潜在的分子机制,意外地发现突变体鼻颌组织中 Ihh 和相关信号分子的表达增强。为了弄清 Pth1r 和 Ihh 信号是否相关,我们生成了 Wnt1-Cre; Ihhfl/fl;Pth1rfl/fl;Tomatofl/+ (DKO) 小鼠,并将其表型与每种单一基因敲除小鼠的表型进行了比较:Wnt1-Cre;Ihhfl/fl;Pth1rfl/+;Tomatofl/+(Ihh-CKO)和Wnt1-Cre;Ihhfl/+;Pth1rfl/fl;Tomatofl/+(Pth1r-CKO)。Ihh-CKO 小鼠的影响较轻。值得注意的是,在 Pth1r-CKO 中观察到的鼻软骨框架过度肥大转化在一定程度上得到了 DKO 胚胎的缓解。此外,还发现了 Ihh 基因从启动子到第一个内含子的半 cAMP 反应元件和含有 2 个错配的 4 个类似序列。Gli1-CreERT2;Pth1rfl/fl;Tomatofl/+是一种针对刺猬反应细胞的Pth1r缺陷模型,它表现出肥厚层增大,鼻中隔和乙状结肠内软骨骨化中积累的Tomato阳性软骨细胞明显增多。总之,这些数据表明了 Pth1r/Ihh 的相关相互作用。我们从 Pth1r 信号传导的新型小鼠模型中获得的发现阐明了颅面生物学和发育过程中以前未知的方面。
{"title":"Pth1r in Neural Crest Cells Regulates Nasal Cartilage Differentiation.","authors":"K Amano, D Okuzaki, Y Kitaoka, S Kato, M Fujiwara, S Tanaka, S Iida","doi":"10.1177/00220345231221954","DOIUrl":"10.1177/00220345231221954","url":null,"abstract":"<p><p>Neural crest cells (NCC) arise from the dorsal margin of the neural plate border and comprise a unique cell population that migrates to and creates the craniofacial region. Although factors including Shh, Fgf8, and bone morphogenetic proteins have been shown to regulate these biological events, the role of parathyroid hormone 1 receptor (Pth1r) has been less studied. We generated an NCC-specific mouse model for <i>Pth1r</i> and researched gene expression, function, and interaction focusing on nasal cartilage framework and midfacial development. <i>Wnt1-Cre;Pth1r</i><sup><i>fl</i>/<i>fl</i></sup>;<i>Tomato</i><sup><i>fl</i>/+</sup> mice had perinatal lethality, but we observed short snout and jaws, tongue protrusion, reduced NCC-derived cranial length, increased mineralization in nasal septum and hyoid bones, and less bone mineralization at interfrontal suture in mutants at E18.5. Importantly, the mutant nasal septum and turbinate cartilage histologically revealed gradual, premature accelerated hypertrophic differentiation. We then studied the underlying molecular mechanisms by performing RNA seq analysis and unexpectedly found that expression of Ihh and related signaling molecules was enhanced in mutant nasomaxillary tissues. To see if Pth1r and Ihh signaling are associated, we generated a <i>Wnt1-Cre;</i> <b><i>Ihh</i></b><sup><i>fl</i>/<i>fl</i></sup>;<b><i>Pth1r</i></b><sup><i>fl</i>/<i>fl</i></sup>;<i>Tomato</i><sup><i>fl</i>/+</sup> (DKO) mouse and compared the phenotypes to those of each single knockout mouse: <i>Wnt1-Cre;</i> <b><i>Ihh</i></b><sup><i>fl</i>/<i>fl</i></sup>;<i>Pth1r</i><sup><i>fl</i>/+</sup>;<i>Tomato</i><sup><i>fl</i>/+</sup> (Ihh-CKO) and <i>Wnt1-Cre;Ihh</i><sup><i>fl</i>/+</sup>;<b><i>Pth1r</i></b><sup><i>fl</i>/<i>fl</i></sup>;<i>Tomato</i><sup><i>fl</i>/+</sup> (Pth1r-CKO). Ihh-CKO mice displayed a milder effect. Of note, the excessive hypertrophic conversion of the nasal cartilage framework observed in Pth1r-CKO was somewhat rescued DKO embryos. Further, a half cAMP responsive element and the 4 similar sequences containing 2 mismatches were identified from the promoter to the first intron in Ihh gene. <i>Gli1-Cre</i><sup><i>ERT2</i></sup>;<i>Pth1r</i><sup><i>fl</i>/<i>fl</i></sup>;<i>Tomato</i><sup><i>fl</i>/+</sup>, a Pth1r-deficient model targeted in hedgehog responsive cells, demonstrated the enlarged hypertrophic layer and significantly more Tomato-positive chondrocytes accumulated in the nasal septum and ethmoidal endochondral ossification. Collectively, the data suggest a relevant Pth1r/Ihh interaction. Our findings obtained from novel mouse models for Pth1r signaling illuminate previously unknown aspects in craniofacial biology and development.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139486736","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}
引用次数: 0
Murine IRF8 Mutation Offers New Insight into Osteoclast and Root Resorption. 小鼠 IRF8 基因突变为了解破骨细胞和牙根吸收提供了新视角
Pub Date : 2024-03-01 Epub Date: 2024-02-12 DOI: 10.1177/00220345231222173
A Das, S K Yesupatham, D Allison, H Tanwar, J Gnanasekaran, B Kear, X Wang, S Wang, C Zachariadou, Y Abbasi, M K Chung, K Ozato, C Liu, B L Foster, V Thumbigere-Math

Interferon regulatory factor 8 (IRF8), a transcription factor expressed in immune cells, functions as a negative regulator of osteoclasts and helps maintain dental and skeletal homeostasis. Previously, we reported that a novel mutation in the IRF8 gene increases susceptibility to multiple idiopathic cervical root resorption (MICRR), a form of tooth root resorption mediated by increased osteoclast activity. The IRF8 G388S variant in the highly conserved C-terminal motif is predicted to alter the protein structure, likely impairing IRF8 function. To investigate the molecular basis of MICRR and IRF8 function in osteoclastogenesis, we generated Irf8 knock-in (KI) mice using CRISPR/Cas9 technique modeling the human IRF8G388S mutation. The heterozygous (Het) and homozygous (Homo) Irf8 KI mice showed no gross morphological defects, and the development of hematopoietic cells was unaffected and similar to wild-type (WT) mice. The Irf8 KI Het and Homo mice showed no difference in macrophage gene signatures important for antimicrobial defenses and inflammatory cytokine production. Consistent with the phenotype observed in MICRR patients, Irf8 KI Het and Homo mice demonstrated significantly increased osteoclast formation and resorption activity in vivo and in vitro when compared to WT mice. The oral ligature-inserted Het and Homo mice displayed significantly increased root resorption and osteoclast-mediated alveolar bone loss compared to WT mice. The increased osteoclastogenesis noted in KI mice is due to the inability of IRF8G388S mutation to inhibit NFATc1-dependent transcriptional activation and downstream osteoclast specific transcripts, as well as its impact on autophagy-related pathways of osteoclast differentiation. This translational study delineates the IRF8 domain important for osteoclast function and provides novel insights into the IRF8 mutation associated with MICRR. IRF8G388S mutation mainly affects osteoclastogenesis while sparing immune cell development and function. These insights extend beyond oral health and significantly advance our understanding of skeletal disorders mediated by increased osteoclast activity and IRF8's role in osteoclastogenesis.

干扰素调节因子 8(IRF8)是一种在免疫细胞中表达的转录因子,它是破骨细胞的负调控因子,有助于维持牙齿和骨骼的平衡。此前,我们曾报道 IRF8 基因中的一种新型突变增加了对多发性特发性颈牙根吸收(MICRR)的易感性,MICRR 是一种由破骨细胞活性增加介导的牙根吸收形式。据预测,IRF8 G388S 变异位于高度保守的 C 端基序,会改变蛋白质结构,很可能会损害 IRF8 的功能。为了研究MICRR和IRF8在破骨细胞生成过程中功能的分子基础,我们利用CRISPR/Cas9技术模拟人类IRF8G388S突变产生了Irf8基因敲入(KI)小鼠。杂合子(Het)和同源杂合子(Homo)Irf8 KI小鼠没有明显的形态学缺陷,造血细胞的发育也不受影响,与野生型(WT)小鼠相似。Irf8 KI Het小鼠和Homo小鼠的巨噬细胞基因特征在抗微生物防御和炎症细胞因子产生方面没有差异。与在 MICRR 患者身上观察到的表型一致,与 WT 小鼠相比,Irf8 KI Het 和 Homo 小鼠体内和体外的破骨细胞形成和吸收活性显著增加。与 WT 小鼠相比,口腔结扎插入的 Het 和 Homo 小鼠显示出明显增加的牙根吸收和破骨细胞介导的牙槽骨损失。KI 小鼠的破骨细胞生成增加是由于 IRF8G388S 突变无法抑制 NFATc1 依赖性转录激活和下游破骨细胞特异性转录物,以及对破骨细胞分化自噬相关途径的影响。这项转化研究描述了对破骨细胞功能非常重要的IRF8结构域,并对与MICRR相关的IRF8突变提供了新的见解。IRF8G388S突变主要影响破骨细胞的生成,而不影响免疫细胞的发育和功能。这些见解超越了口腔健康的范畴,极大地推动了我们对破骨细胞活性增强介导的骨骼疾病以及 IRF8 在破骨细胞生成中的作用的认识。
{"title":"Murine IRF8 Mutation Offers New Insight into Osteoclast and Root Resorption.","authors":"A Das, S K Yesupatham, D Allison, H Tanwar, J Gnanasekaran, B Kear, X Wang, S Wang, C Zachariadou, Y Abbasi, M K Chung, K Ozato, C Liu, B L Foster, V Thumbigere-Math","doi":"10.1177/00220345231222173","DOIUrl":"10.1177/00220345231222173","url":null,"abstract":"<p><p>Interferon regulatory factor 8 (IRF8), a transcription factor expressed in immune cells, functions as a negative regulator of osteoclasts and helps maintain dental and skeletal homeostasis. Previously, we reported that a novel mutation in the <i>IRF8</i> gene increases susceptibility to multiple idiopathic cervical root resorption (MICRR), a form of tooth root resorption mediated by increased osteoclast activity. The IRF8 G388S variant in the highly conserved C-terminal motif is predicted to alter the protein structure, likely impairing IRF8 function. To investigate the molecular basis of MICRR and IRF8 function in osteoclastogenesis, we generated <i>Irf8</i> knock-in (<i>KI</i>) mice using CRISPR/Cas9 technique modeling the human <i>IRF8</i><sup><i>G388S</i></sup> mutation. The heterozygous (Het) and homozygous (Homo) <i>Irf8 KI</i> mice showed no gross morphological defects, and the development of hematopoietic cells was unaffected and similar to wild-type (WT) mice. The <i>Irf8 KI</i> Het and Homo mice showed no difference in macrophage gene signatures important for antimicrobial defenses and inflammatory cytokine production. Consistent with the phenotype observed in MICRR patients, <i>Irf8 KI</i> Het and Homo mice demonstrated significantly increased osteoclast formation and resorption activity in vivo and in vitro when compared to WT mice. The oral ligature-inserted Het and Homo mice displayed significantly increased root resorption and osteoclast-mediated alveolar bone loss compared to WT mice. The increased osteoclastogenesis noted in <i>KI</i> mice is due to the inability of <i>IRF8</i><sup><i>G388S</i></sup> mutation to inhibit NFATc1-dependent transcriptional activation and downstream osteoclast specific transcripts, as well as its impact on autophagy-related pathways of osteoclast differentiation. This translational study delineates the IRF8 domain important for osteoclast function and provides novel insights into the <i>IRF8</i> mutation associated with MICRR. <i>IRF8</i><sup><i>G388S</i></sup> mutation mainly affects osteoclastogenesis while sparing immune cell development and function. These insights extend beyond oral health and significantly advance our understanding of skeletal disorders mediated by increased osteoclast activity and IRF8's role in osteoclastogenesis.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10985390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139725482","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}
引用次数: 0
Polymicrobial Infection Induces Adipose Tissue Dysfunction via Gingival Extracellular Vesicles. 多微生物感染通过牙龈细胞外小泡诱发脂肪组织功能障碍
Pub Date : 2024-02-01 Epub Date: 2023-12-14 DOI: 10.1177/00220345231211210
Y Liu, B Cui, P Zhang, S Xiao, D Duan, Y Ding

Recent studies have indicated that periodontitis promotes metabolic dysregulation and insulin resistance by affecting the function of white adipose tissue (WAT). However, the mechanisms linking periodontitis to adipose tissue dysfunction still need to be explored. Extracellular vesicles (EVs) deliver messages to distal sites and regulate their function. Also, recent studies have shown that periodontitis changes the composition of EVs in body fluids and that EVs might be one of the mechanisms underlying the relationship between periodontitis and insulin resistance. Herein, we explored the impact of polymicrobial oral infection with periodontal pathogens on the function of WAT and the role of gingival EVs (gEVs) in the process. Mice were subjected to oral inoculation with 109 Porphyromonas gingivalis and 108 Fusobacterium nucleatum every other day for 14 wk. This prolonged bacterial infection induced WAT dysfunction, characterized by reduced levels of AKT phosphorylation, adiponectin, leptin, and genes associated with adipogenesis and lipogenesis. We successfully isolated gEVs with satisfactory yield and purity. The RNA sequencing results showed that the differentially expressed microRNAs in the gEVs of mice with polymicrobial oral infection were involved in insulin signaling and adipose tissue function. Notably, our in vitro experiments and RNA sequencing results revealed the functional similarities between gEVs and plasma-derived EVs. Furthermore, intraperitoneal injection with gEVs derived from mice with oral infection induced the dysfunction of WAT in healthy mice. Overall, our findings provide evidence for the influence of polymicrobial oral infection on WAT function and propose gEVs as a novel pathway through which periodontal infection may exert its effects on WAT.

最近的研究表明,牙周炎会影响白色脂肪组织(WAT)的功能,从而导致代谢失调和胰岛素抵抗。然而,牙周炎与脂肪组织功能障碍之间的关联机制仍有待探索。细胞外囊泡(EVs)向远端部位传递信息并调节其功能。最近的研究还表明,牙周炎会改变体液中EVs的组成,EVs可能是牙周炎与胰岛素抵抗之间关系的机制之一。在此,我们探讨了牙周病原体多微生物口腔感染对WAT功能的影响以及牙龈EVs(gEVs)在这一过程中的作用。每隔一天给小鼠口腔接种 109 株牙龈卟啉单胞菌和 108 株核分枝杆菌,持续 14 周。这种长期的细菌感染会诱发小鼠脂肪腺功能障碍,其特征是 AKT 磷酸化、脂肪连素、瘦素以及与脂肪生成和脂肪生成相关的基因水平降低。我们成功分离出了产量和纯度均令人满意的 gEVs。RNA 测序结果显示,多微生物口腔感染小鼠 gEVs 中表达不同的 microRNAs 参与了胰岛素信号转导和脂肪组织功能。值得注意的是,我们的体外实验和 RNA 测序结果揭示了 gEVs 与血浆衍生 EVs 在功能上的相似性。此外,腹腔注射来自口腔感染小鼠的 gEVs 会诱发健康小鼠 WAT 的功能障碍。总之,我们的研究结果为多微生物口腔感染对WAT功能的影响提供了证据,并提出gEVs是牙周感染对WAT产生影响的一种新途径。
{"title":"Polymicrobial Infection Induces Adipose Tissue Dysfunction via Gingival Extracellular Vesicles.","authors":"Y Liu, B Cui, P Zhang, S Xiao, D Duan, Y Ding","doi":"10.1177/00220345231211210","DOIUrl":"10.1177/00220345231211210","url":null,"abstract":"<p><p>Recent studies have indicated that periodontitis promotes metabolic dysregulation and insulin resistance by affecting the function of white adipose tissue (WAT). However, the mechanisms linking periodontitis to adipose tissue dysfunction still need to be explored. Extracellular vesicles (EVs) deliver messages to distal sites and regulate their function. Also, recent studies have shown that periodontitis changes the composition of EVs in body fluids and that EVs might be one of the mechanisms underlying the relationship between periodontitis and insulin resistance. Herein, we explored the impact of polymicrobial oral infection with periodontal pathogens on the function of WAT and the role of gingival EVs (gEVs) in the process. Mice were subjected to oral inoculation with 10<sup>9</sup> <i>Porphyromonas gingivalis</i> and 10<sup>8</sup> <i>Fusobacterium nucleatum</i> every other day for 14 wk. This prolonged bacterial infection induced WAT dysfunction, characterized by reduced levels of AKT phosphorylation, adiponectin, leptin, and genes associated with adipogenesis and lipogenesis. We successfully isolated gEVs with satisfactory yield and purity. The RNA sequencing results showed that the differentially expressed microRNAs in the gEVs of mice with polymicrobial oral infection were involved in insulin signaling and adipose tissue function. Notably, our in vitro experiments and RNA sequencing results revealed the functional similarities between gEVs and plasma-derived EVs. Furthermore, intraperitoneal injection with gEVs derived from mice with oral infection induced the dysfunction of WAT in healthy mice. Overall, our findings provide evidence for the influence of polymicrobial oral infection on WAT function and propose gEVs as a novel pathway through which periodontal infection may exert its effects on WAT.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138815319","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}
引用次数: 0
The Use of Dynamic Navigation Systems as a Component of Digital Dentistry. 使用动态导航系统作为数字牙科的组成部分。
Pub Date : 2024-02-01 Epub Date: 2023-12-15 DOI: 10.1177/00220345231212811
W L Tang, X Y Chao, Z Ye, M W Liu, H Jiang

The development of dynamic navigation system (DNS) has facilitated the development of modern digital medicine. In the field of dentistry, the cutting-edge technology is garnering widespread recognition. Based on the principles of 3-dimensional visualization, virtual design, and precise motion tracking, DNS is mainly composed of a computer, a tracking system, specialized tracer instruments, and navigation software. DNS employs a workflow that begins with preoperative data acquisition and imaging data reconstruction, followed by surgical instrument calibration and spatial registration, culminating in real-time guided operations. Currently, the system has been applied in a broad spectrum of dental procedures, encompassing dental implants, oral and maxillofacial surgery (such as tooth extraction, the treatment of maxillofacial fractures, tumors, and foreign bodies, orthognathic surgery, and temporomandibular joint ankylosis surgery), intraosseous anesthesia, and endodontic treatment (including root canal therapy and endodontic surgery). These applications benefit from its enhancements in direct visualization, treatment precision, efficiency, safety, and procedural adaptability. However, the adoption of DNS is not without substantial upfront costs, required comprehensive training, additional preparatory time, and increased radiation exposure. Despite challenges, the ongoing advancements in DNS are poised to broaden its utility and substantially strengthen digital dentistry.

动态导航系统(DNS)的开发促进了现代数字医学的发展。在口腔医学领域,这项尖端技术得到了广泛认可。基于三维可视化、虚拟设计和精确运动追踪的原理,DNS 主要由计算机、追踪系统、专用追踪器械和导航软件组成。DNS 采用的工作流程是,首先进行术前数据采集和成像数据重建,然后进行手术器械校准和空间配准,最后进行实时引导手术。目前,该系统已广泛应用于牙科手术,包括牙科种植、口腔和颌面外科手术(如拔牙、颌面部骨折、肿瘤和异物治疗、正颌手术和颞下颌关节强直手术)、骨内麻醉和牙髓治疗(包括根管治疗和牙髓手术)。这些应用得益于 DNS 在直接可视化、治疗精确性、效率、安全性和程序适应性方面的改进。然而,采用 DNS 需要大量的前期费用、所需的全面培训、额外的准备时间以及更多的辐射暴露。尽管存在挑战,但 DNS 的不断进步有望扩大其用途,并大大加强数字化牙科。
{"title":"The Use of Dynamic Navigation Systems as a Component of Digital Dentistry.","authors":"W L Tang, X Y Chao, Z Ye, M W Liu, H Jiang","doi":"10.1177/00220345231212811","DOIUrl":"10.1177/00220345231212811","url":null,"abstract":"<p><p>The development of dynamic navigation system (DNS) has facilitated the development of modern digital medicine. In the field of dentistry, the cutting-edge technology is garnering widespread recognition. Based on the principles of 3-dimensional visualization, virtual design, and precise motion tracking, DNS is mainly composed of a computer, a tracking system, specialized tracer instruments, and navigation software. DNS employs a workflow that begins with preoperative data acquisition and imaging data reconstruction, followed by surgical instrument calibration and spatial registration, culminating in real-time guided operations. Currently, the system has been applied in a broad spectrum of dental procedures, encompassing dental implants, oral and maxillofacial surgery (such as tooth extraction, the treatment of maxillofacial fractures, tumors, and foreign bodies, orthognathic surgery, and temporomandibular joint ankylosis surgery), intraosseous anesthesia, and endodontic treatment (including root canal therapy and endodontic surgery). These applications benefit from its enhancements in direct visualization, treatment precision, efficiency, safety, and procedural adaptability. However, the adoption of DNS is not without substantial upfront costs, required comprehensive training, additional preparatory time, and increased radiation exposure. Despite challenges, the ongoing advancements in DNS are poised to broaden its utility and substantially strengthen digital dentistry.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138815322","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}
引用次数: 0
Copy Number Alterations Predict Development of OSCC from Oral Leukoplakia. 拷贝数畸变可预测口腔白斑病发展成 OSCC
Pub Date : 2024-02-01 Epub Date: 2024-01-12 DOI: 10.1177/00220345231217160
X Cai, J Zhang, L Li, L Liu, M Tang, X Zhou, C Peng, X Li, X Chen, M Xu, H Zhang, J Wang, Y Huang, T Li

Oral leukoplakia (OLK) is a common type of potentially malignant disorder. Early identification of the malignancy potential leads to a better management of OLK and prediction of development of oral squamous cell carcinoma (OSCC). However, there has been no effective biomarker to assess the risk of malignancy in OLK. Genomic copy number alteration (CNA) is a complex chromosomal structural variation in the genome and has been identified as a potential biomarker in multiple cancers. This study aimed to develop a predictive model for the malignant transformation risk of OLK by copy number analysis. A total of 431 OLK samples with long-term follow-up (median follow-up of 67 mo) from multiple academic centers were analyzed for CNAs. CNA events increased with the severity of hyperplasia, mild dysplasia, moderate dysplasia, and severe dysplasia. More CNA events were present in patients with OLK who later developed OSCC than in those with OLK who did not. By multivariate Cox regression analysis, the OLK of the CNA scorehigh group showed an increased risk of malignant transformation than the CNA scorelow group (P < 0.001). A CNA score model was developed to accurately predict the prognosis (area under the receiver operating characteristic curve [AUC] = 0.879; 95% confidence interval [CI], 0.799-0.959) and was validated using data from 2 external centers (AUC = 0.836, 95% CI, 0.683-0.989; AUC = 0.876, 95% CI, 0.682-1.000), and all of them showed better prediction performances than histopathological grade in assessing the transformation risk of OLK. Furthermore, we performed CNA models among 4 subgroups of OLK with hyperplasia, mild dysplasia, moderate dysplasia, and severe dysplasia and found that CNA score can accurately predict malignant transformation of different subgroups. CNA score may be a useful biomarker to predict malignant transformation of OLK. Subtyping of OLK by the CNA score could contribute to better management of OLK and predicting development of OSCC.

口腔白斑病(OLK)是一种常见的潜在恶性疾病。早期识别恶性肿瘤的可能性有助于更好地治疗口腔白斑病和预测口腔鳞状细胞癌(OSCC)的发展。然而,目前还没有有效的生物标志物来评估 OLK 的恶性风险。基因组拷贝数改变(CNA)是基因组中一种复杂的染色体结构变异,已被确定为多种癌症的潜在生物标志物。本研究旨在通过拷贝数分析建立OLK恶性转化风险预测模型。研究人员对来自多个学术中心、长期随访(中位随访时间为67个月)的431份OLK样本进行了CNA分析。CNA事件随着增生、轻度发育不良、中度发育不良和重度发育不良的严重程度而增加。在后来发展为 OSCC 的 OLK 患者中,出现 CNA 事件的人数多于未发展为 OSCC 的 OLK 患者。通过多变量 Cox 回归分析,CNA 评分高组的 OLK 比 CNA 评分低组的 OLK 恶性转化风险更高(P < 0.001)。我们建立了一个能准确预测预后的CNA评分模型(接收者操作特征曲线下面积[AUC]=0.879;95%置信区间[CI],0.799-0.959),并用2个外部中心的数据进行了验证(AUC=0.836,95% CI,0.683-0.989;AUC=0.876,95% CI,0.682-1.000),在评估OLK的转化风险方面,它们都比组织病理学分级显示出更好的预测性能。此外,我们还在OLK增生、轻度发育不良、中度发育不良和重度发育不良四个亚组中建立了CNA模型,发现CNA评分能准确预测不同亚组的恶性转化。CNA评分可能是预测OLK恶性转化的有用生物标志物。通过CNA评分对OLK进行亚型分类有助于更好地管理OLK和预测OSCC的发展。
{"title":"Copy Number Alterations Predict Development of OSCC from Oral Leukoplakia.","authors":"X Cai, J Zhang, L Li, L Liu, M Tang, X Zhou, C Peng, X Li, X Chen, M Xu, H Zhang, J Wang, Y Huang, T Li","doi":"10.1177/00220345231217160","DOIUrl":"10.1177/00220345231217160","url":null,"abstract":"<p><p>Oral leukoplakia (OLK) is a common type of potentially malignant disorder. Early identification of the malignancy potential leads to a better management of OLK and prediction of development of oral squamous cell carcinoma (OSCC). However, there has been no effective biomarker to assess the risk of malignancy in OLK. Genomic copy number alteration (CNA) is a complex chromosomal structural variation in the genome and has been identified as a potential biomarker in multiple cancers. This study aimed to develop a predictive model for the malignant transformation risk of OLK by copy number analysis. A total of 431 OLK samples with long-term follow-up (median follow-up of 67 mo) from multiple academic centers were analyzed for CNAs. CNA events increased with the severity of hyperplasia, mild dysplasia, moderate dysplasia, and severe dysplasia. More CNA events were present in patients with OLK who later developed OSCC than in those with OLK who did not. By multivariate Cox regression analysis, the OLK of the CNA score<sup>high</sup> group showed an increased risk of malignant transformation than the CNA score<sup>low</sup> group (<i>P</i> < 0.001). A CNA score model was developed to accurately predict the prognosis (area under the receiver operating characteristic curve [AUC] = 0.879; 95% confidence interval [CI], 0.799-0.959) and was validated using data from 2 external centers (AUC = 0.836, 95% CI, 0.683-0.989; AUC = 0.876, 95% CI, 0.682-1.000), and all of them showed better prediction performances than histopathological grade in assessing the transformation risk of OLK. Furthermore, we performed CNA models among 4 subgroups of OLK with hyperplasia, mild dysplasia, moderate dysplasia, and severe dysplasia and found that CNA score can accurately predict malignant transformation of different subgroups. CNA score may be a useful biomarker to predict malignant transformation of OLK. Subtyping of OLK by the CNA score could contribute to better management of OLK and predicting development of OSCC.</p>","PeriodicalId":94075,"journal":{"name":"Journal of dental research","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139467594","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}
引用次数: 0
期刊
Journal of dental research
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1