Association between oral malodor and adult periodontitis: a review

BACKGROUND: Bad breath has a significant impact on our daily social life to those who suffer from it. The majority of bad breath originates within the oral cavity. However, it is also possible that it can come from other sources such as gastric-intestine imbalance. The term "oral malodor" is used to describe a foul or offensive odor emanating from the oral cavity, in which proteolysis, metabolic products of the desquamating cell, and bacterial putrefaction are involved. Recent evidence has demonstrated a link between oral malodor and adult periodontitis. The process of developing bad breath is similar to that noted in the progression of gingivitis/periodontitis. Oral malodor is mainly attributed to volatile sulfur compounds (VSC) such as hydrogen sulfide, methyl mercaptan and dimethyl sulfide. The primary causative microbes are gram-negative, anaerobic bacteria that are similar to the bacteria causing periodontitis. These bacteria produce the VSC by metabolizing different cells/tissues (i.e., epithelial cells, leukocytes, etc.) located in saliva, dental plaque, and gingival crevicular fluid. Tongue surface is composed of blood components, nutrients, large amounts of desquamated epithelial cells and bacteria, suggesting that it has the proteolytic and putrefactive capacity to produce VSC. One of the challenges in dealing with oral malodor is to identify a reliable test for detecting bad breath. AIMS: The purposes of this review article were: (1) to correlate the relationship between oral malodor and adult periodontitis; (2) to analyze current malodor tests and discuss available treatment regimens.     

The involvement of bradykinin in adrenaline-induced pulmonary edema in rats

We investigated the effect of endogenous bradykinin on adrenaline-induced pulmonary edema (PE) by blocking bradykinin receptors. In preliminary experiments, a bolus injection of adrenaline (ADR; 10 microg/kg) solution (10 microg/ml) was determined to be an edematogenic dose for inducing PE. The lung body weight index (LBI) and incidence of PE (IPE) were determined. The IPE and LBI of the group pretreated with Des-Arg9-[Leu8]-Bradykinin (DA-BK, 50 microg/kg, 50 microg/ml) increased significantly compared with those of the control group (p<0.05). On the other hand, there were no remarkable changes in IPE and LBI in the groups pretreated with Hoe140 (D-Arginyl-[Hyp3, Thi5, D-Tic7, Oic8]-Bradykinin (100 microg/kg, 100 microg/ml), captopril (20 mg/kg, 20 mg/ml) or L-NAME (1 mg/kg, 1 mg/ml). Moreover, the IPE and LBI of the group co-treated with L-NAME and DA-BK decreased compared with the DA-BK group (p<0.05). Thus, bradykinin aggravates adrenaline-induced PE through activation of the B2 receptor by the kallikreins as a result of the ADR administration, although the precise mechanism is not known.     

不同排牙方法对全口义齿咀嚼效能的影响

目的:探讨不同排牙法的全口义齿咀嚼效能的异同。方法:采用上颌排牙法、下颌排牙法和综合排牙法为10名无牙颌患者分别制作3副全口义齿。戴用3个月后,通过吸光度法测定咀嚼效率,比较不同排牙法的全口义齿咀嚼效能的异同,并与有牙颌进行对比。结果:在单侧咀嚼和双侧咀嚼2种咀嚼方式下,全口义齿患者的咀嚼次数和咀嚼效能均少于有牙颌组,本实验3组全口义齿在3个月后均发挥了良好的咀嚼效能。下颌排牙法和综合排牙法全口义齿的咀嚼次数和咀嚼效能无统计学差异,但均好于上颌排牙法全口义齿。结论:下颌排牙法和综合排牙法的全口义齿排列的人工牙能够减少在咀嚼过程中不利于全口义齿稳定因素的影响,提高咀嚼效能。     

Consensus conference on immediate loading: the single tooth and partial edentulous areas

PURPOSE: A consensus conference was held to determine what the parameters should be for the immediate functional loading of the single-tooth implant restoration and short-span fixed implant-supported bridgework. MATERIALS: Forty-one clinicians and researchers presented cases and situations relating to the topic. A panel then distilled questions that were presented to the audience (430) at large. Answers were gleaned to formulate a consensus. RESULTS: Ten distinct answers evolved that constituted the essence of guidelines for clinicians to be aware of when undertaking immediate loading. These guidelines are contained within the body of the text. CONCLUSIONS: Extreme caution and adherence to a universal generic protocol are suggested for clinicians who are involved with single-tooth and short-span multiple-teeth implant replacements as related to immediate loading as defined within this text.     

游离血管化髂骨瓣：26例回顾分析

该文对应用游离髂骨瓣修复颌骨缺损的病例进行回顾研究，并分析手术并发症。作者共用26块髂骨肌瓣、1块髂骨肌皮瓣修复18例下颌骨和8例上颌骨缺损。1例因微血管再灌注问题而导致手术失败：3例术后行组织瓣抢救，其中2例吻合口血栓形成，重新吻合血管后抢救成功；10例术后出现股外侧皮神经支配区皮肤麻木，3例并发切口疝，1例供区创口裂开，2例并发口鼻瘘，1例颈部创口感染，     

云南省双江县布朗族头面部器官微机测量研究

目的 对云南省双江县邦丙乡布朗族头面部器官进行全面系统地测量研究。方法 采用自行研制的头面部摄相—计算机测量系统，对正常布朗族成人155人进行了头面部器官全面系统的测量，其中男性96人，女性59人。结果 得出了布朗族成年男女两性头面部器官41个项目测量值和17个头面部指数资料。结论 该研究委仅对临床医学和美学研究有重要意义，而且对人类学、民族学和工业等相关学科也有重要的参考价值。     

Induction of dental pulp fibroblast matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 gene expression by interleukin-1alpha and tumor necrosis factor-alpha through a prostaglandin-dependent pathway

Matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) are involved in the degradation of extracellular matrix in many inflammatory diseases. Little is known regarding the expression of these mediators in dental pulp fibroblasts. The effects of proinflammatory cytokines (interleukin (IL)-1alpha and tumor necrosis factor-alpha (TNF-alpha)) and prostaglandin E2 (PGE2) on pulp fibroblast MMP-1 and TIMP-1 gene expression were investigated. Northern hybridization showed that IL-1alpha and TNF-alpha induced significant MMP-1 gene expression, with only little effect on TIMP-1 gene. Exogenous PGE2, however, upregulated TIMP-1 mRNA synthesis but not MMP-1. Concomitant addition of IL-1alpha and PGE2 or TNF-alpha and PGE2 suppressed MMP-1 mRNA production, compared with the groups treated with IL-1alpha or TNF-alpha alone. In contrast, PGE2 enhanced the upregulatory effects of TIMP-1 mRNA by IL-1alpha or TNF-alpha. Furthermore, cytokine stimulation of MMP-1 and TIMP-1 gene expressions can be enhanced or blocked by indomethacin, respectively, and reversed by exogenous PGE2. These results suggested that cytokine-stimulated MMP-1 and TIMP-1 gene expression in dental pulp fibroblasts was mediated, at least in part, by a prostaglandin-dependent pathway. The differential regulation of IL-1alpha or TNF-alpha-induced MMP-1 and TIMP-1 mRNA synthesis, as well as the direct upregulation of TIMP-1 gene expression by PGE2, also implied that prostaglandin may serve as a protective mechanism from excessive tissue breakdown during pulpitis.