RANKL、MMP-9和MMP-2在成釉细胞瘤中的表达及意义

目的：探讨RANKL、MMP-9和MMP-2与成釉细胞瘤骨吸收机制之间的关系。方法：应用免疫组化、荧光定量RT—PCR及Western印迹方法，分别在不同分子水平检测RANKL、MMP-2和MMP-9在成釉细胞瘤中的表达，所有实验数据均经SPSS11．0统计软件包进行分析处理，组间比较采用t检验。结果：在所有成釉细胞瘤标本中，3种方法均可检测到RANKL、MMP-2和MMP-9的表达。其中，RANKL各型成釉细胞瘤中均呈恒定的高表达，而荧光定量RT—PCR检测结果显示，MMP-2在基底细胞型成釉细胞瘤中的表达水平显著高于其他两型（P〈0．05）。结论：MMP-2、MMP-9及RANKL可能共同参与成釉细胞瘤引起的骨质吸收过程。与MMP-9相比，MMP-2可能与成釉细胞瘤的侵袭性更为相关。     

平阳霉素对颊囊癌金黄地鼠肺毒性的实验研究

目的 探讨平阳霉素对颊囊癌金黄地鼠肺组织的毒副作用。立法 将75只金黄地鼠用5％DM—BA涂擦颊囊诱发颊囊癌后分别用0．2mg/kg、0．4mg/kg和0．5mg／kg三种剂量的平阳霉素行腹腔注射；对照组每日灌服消炎痛拮抗。结果 随平阳霉素用量的增加，金黄地鼠肺炎样变及肺纤维化呈上升趋势；消炎痛具有良好的拮抗作用，可对抗平阳霉素的肺毒性。结论 平阳霉素用量较大时(超过0．4mg/kg)可出现肺炎样变及肺纤维化，如果同时使用消炎痛，则可有效地抑制肺纤维化的发生。     

上中切牙短根畸形患者骨性错[牙合]和轴倾度的临床分析

目的探讨昆明市人群中非综合征型短根畸形(short root anomaly,SRA)的患病率及与骨性错[牙合]和上中切牙轴倾度分布的关系,为SRA患者的正畸临床诊疗提供一定参考。方法回顾性分析2011年1月~2019年7月笔者所在医院收治患者CBCT数据库并随机抽样选取1000例,诊断出SRA患者27例(SRA组);对照组,为非SRA患者中随机选取的100例患者,根据其临床资料以及头影测量数据,将骨性错[牙合]分为I类骨性错,Ⅱ类骨性错[牙合],Ⅲ类骨性错[牙合]3个亚组,将中切牙轴倾度分为唇倾型、腭倾型和正常唇倾度型3个亚组,分析SRA组和对照组的性别、骨性错[牙合]以及上中切牙轴倾度分布情况。结果本研究所选人群中SRA的患病率为2.7%,女性的SRA患病率为3.67%(21/572),高于男性患病率1.4%(6/428),SRA患病率的性别差异具有统计学意义(χ^2=4.562,P=0.033)。SRA患者与对照组骨性错[牙合]构成比差异具有统计学意义(χ^2=8.710,P=0.013)。SRA患者骨性错以Ⅲ类骨性错[牙合]为主。SRA患者与对照组上中切牙轴倾度型构成比不同,差异具有统计学意义(χ^2=16.75,P<0.001)。SRA患者上中切牙轴倾度以腭倾型为主。结论SRA与Ⅲ类骨性错[牙合]及前牙腭倾型轴倾度有关,正畸治疗前需对此类患者的冠根比和根形进行评估。     

Do buffered local anesthetics provide more successful anesthesia than nonbuffered solutions in patients with pulpally involved teeth requiring dental therapy?: A systematic review

Background

The authors conducted a systematic review that addresses the following population, intervention, comparison, outcome question: “In adults requiring dental therapy with pulpally involved teeth, what is the comparative efficacy of buffered local anesthetics (LAs) compared with that of nonbuffered LAs in achieving anesthetic success?”

Laminin-5 gamma2-chain and collagenase-2 (MMP-8) in human peri-implant sulcular fluid

Laminin-5 (LN-5) is an important epithelial cell-derived structural and adhesive component in hemidesmosomes and basement membranes (BM). In peri-implant tissue, gingival BM underlies the junctional epithelium (JE) and reflects the peri-implant health. Matrix metalloproteinase-8 (MMP-8 or collagenase-2) is one of the key mediators of periodontal tissue destruction. Western immunoblotting with image analysis was used to quantitate the molecular forms of LN-5 gamma2-chain and MMP-8 in peri-implant sulcular fluid (PISF) from healthy and diseased implants. These observations were related to the recorded gingival (GI) and bone resorption (BR) indices of the studied sites. Altogether, 72 PISF samples from osseointegrated dental implants were examined. Significantly elevated levels of fragmented LN-5 gamma2-chain species (45 and 70 kDa) and MMP-8 immunoreactivities were observed in diseased PISF in relation to healthy PISF. The elevated levels of both LN-5 gamma2-chain 45 and 70 kDa fragments and MMP-8 in diseased PISF from peri-mucositis (BR = 0) and peri-implantitis (BR >/= 1) lesions strongly correlated with elevated GI. Low levels - almost comparable to those seen in healthy control PISF - were seen in PISF from peri-implantitis lesions (BR >/= 1) with no GI. Activation of 75 kDa neutrophil (PMN)-type proMMP-8 to 10 kDa lower-molecular-size active forms was especially detected in PISF from peri-implantitis with elevated GI. These cross-sectional findings indicate that elevated MMP-8 and LN-5 gamma2-chain fragment levels in PISF can reflect the active phase of the inflammatory peri-implant disease. Longitudinal studies are required to assess their use, either alone or in combination as molecular biochemical PISF markers, to predict the risk of progression of peri-implantitis, as well as to monitor the impact of treatment of the disease.     

Human T‐cell responses to oral streptococci in human PBMC‐NOD/SCID mice

We investigated cellular and humoral immune responses to oral biofilm bacteria, including Streptococcus mutans, Streptococcus anginosus, Streptococcus sobrinus, and Streptococcus sanguinis, in NOD/SCID mice immunized with human peripheral blood mononuclear cells (hu‐PBMC‐NOD/SCID mice) to explore the pathogenicity of each of those organisms in dental and oral inflammatory diseases. hu‐PBMC‐NOD/SCID mice were immunized by intraperitoneal injections with the whole cells of the streptococci once a week for 3 weeks. FACS analyses were used to determine the percentages of various hu‐T cell types, as well as intracellular cytokine production of interleukin‐4 and interferon‐γ. Serum IgG and IgM antibody levels in response to the streptococci were also determined by enzyme‐linked immunosorbent assay. S. anginosus induced a significant amount of the proinflammatory cytokine interferon‐γ in CD4⁺ and CD8⁺ T cells in comparison with the other streptococci. However, there was no significant differences between the streptococci in interleukin‐4 production by CD4⁺ and CD8⁺ T cells after inoculation. Further, S. mutans significantly induced human anti‐S. mutans IgG, IgG₁, IgG₂, and IgM antibodies in comparison with the other organisms. In conclusion, S. anginosus up‐regulated Th1 and Tc1 cells, and S. mutans led to increasing levels of their antibodies, which was associated with the induction of Th2 cells. These results may contribute to a better understanding of human lymphocyte interactions to biofilm bacteria, along with their impact on dental and mucosal inflammatory diseases, as well as endocarditis.     

Stretching stimulates fibulin-5 expression and controls microfibril bundles in human periodontal ligament cells

Background and Objective:  The elastic fiber system comprises oxytalan, elaunin and elastic fibers, differing in their relative microfibril and elastin contents. Human periodontal ligaments contain oxytalan fibers (pure microfibrils). Periodontal ligaments are continuously exposed to various functional forces, such as tooth movement and occlusal loading. We have reported that bundles of microfibrils coalesce in response to mechanical strain in cultured periodontal ligament fibroblasts, as assessed in terms of their positivity for fibrillin-1 (the major component of microfibrils). However, the mechanism of microfibril coalescence is unclear. We hypothesized that the fibrillin-1-binding molecule, fibulin-5, contributes to oxytalan fiber formation under mechanical strain.
Material and Methods:  We subjected periodontal ligament fibroblasts to stretching in order to examine the effects of fibulin-5 on the formation of oxytalan fibers in cell/matrix layers. We transfected periodontal ligament cells with small interference RNA for fibulin-5, then examined oxytalan fibers using immunofluorescence and electron microscopy.
Results:  Immunofluorescence showed that fibrillin-1-positive microfibrils coalesced as a result of stretching, compared with cells that were not subjected to stretching. Fibulin-5 colocalized on fibrillin-1-positive microfibrils. Stretching increased fibulin-5 gene expression and protein deposition. Immunofluorescence and immunogold electron microscopy analysis revealed that fibulin-5 suppression inhibited the coalescence of microfibrils under stretching conditions.
Conclusion:  These results suggest that fibulin-5 up-regulated in response to tension strain may control the formation of microfibril bundles in periodontal ligament.     

Involvement of angiotensin II type 1 receptors in interleukin-1β-induced interleukin-6 production in human gingival fibroblasts

The renin-angiotensin system is thought to be involved in inflammatory processes such as periodontitis. However, its precise role is still unclear. Therefore, in the present study the expression of the angiotensin II type 1 receptor (AT1R) was investigated in inflamed human gingival tissue, and the possible involvement of the AT1R in interleukin-1β (IL-1β)-induced interleukin-6 (IL-6) production by cultured human gingival fibroblasts (HGFs) was also studied. Immunohistochemical staining revealed that inflammatory cells and fibroblast-like cells were positive for the AT1R. However, in healthy gingival tissue, AT1R staining was very weak. The levels of AT1R mRNA and AT1R protein increased in HGFs after stimulation with IL-1β. The levels of IL-1β-induced IL6 mRNA and IL-6 protein were significantly reduced in AT1R gene-silenced HGFs compared with control HGFs. The data suggest that the AT1R may be involved in the regulation of gingival inflammation by modulating IL-1β-induced IL-6 production in HGFs.