膝内侧稳定结构的解剖特征与软组织平衡的关系

目的:观测国人膝内侧结构解剖学特点,为膝关节置换术中内侧结构软组织平衡的松解策略选择提供形态学依据.方法:80例固定及20例新鲜成人膝关节标本,解剖观察内侧结构的组成及其位置与形态学特点.结果:膝关节内侧面支持结构包括内侧副韧带复合体和半膜肌复合体等结构,可分为3层.内侧副韧带复合体包括内侧副韧带(medial collateral ligament,MCL)深、浅两层,可分为前纵部和后斜部两部分.MCL前纵部以间接止点形式融入胫骨平台关节面下50～60 mm,鹅足深方的胫骨内侧骨面骨膜,长约92mm,中部宽约15mm后斜部纤维以腱板起于股骨内卜髁后侧,下止点弥散;在关节间隙处,后斜部纤维与其深方第3层(内侧关节囊)愈着,被半月板、冠状韧带固定.MCL深层实际上为膝内侧关节囊增厚,自股骨内上髁下半周缘骨面垂直向下走行,连接内侧半月板,止于胫骨平台内侧缘中点关节面下0.8～1.5cm骨面,并与半膜肌腱横臂融合.膝关节后内侧区域为半膜肌腱鞘和半膜肌腱的9处附丽所加强,维持膝关节后内侧角稳定.结论:基于膝关节内侧结构解剖特点,膝关节置换术中软组织平衡可以做到微创化、选择性的松解.尽量保护其结构和功能的完整对术后功能有重要意义.     

个性化喙锁韧带重建导向器的设计及精度评价

目的　设计个性化喙锁韧带重建导向器,并评价其钻孔精度和效率。 方法　使用计算机辅助设计软件设计个性化喙锁韧带重建导向器,并进行3D打印。获取90侧肩关节标本,随机平均分为3组,分别在微创双切口下使用徒手法和C臂导向器、个性化导向器引导法进行锁骨-喙突钻孔。测量手术时间、喙突骨隧道分区和喙突骨隧道至喙突内、外侧缘距离。 结果　徒手组、C臂导向器组、个性化导向器组的手术时间分别为(203±33)、(267±62)、(155±14) s。3组分别有13、28、30个喙突骨隧道位于理想中间区。使用3种方法建立的喙突骨隧道与喙突内、外侧缘距离差分别为(3.7±2.0)、(2.0±0.9)、(0.9±0.5) mm。差异均有统计学意义(P<0.05)。 结论　个性化导向器具有更高的钻孔精度和效率,为微创下辅助锁骨-喙突钻孔提供了新的选择。     

中药双黄补对体外培养人牙周膜细胞增殖活性的影响

背景：目前的研究大多为单味中药或单一中药成分对体外培养人牙周膜细胞的影响,而中药组方提取液对体外培养细胞影响的研究较少。 目的：观察中药双黄补对体外培养的人牙周膜细胞增殖活性的影响。 设计、时间及地点：对比观察实验,于2008-11/2009-02 在河北医科大学第四医院科研中心完成。 材料：人牙周膜细胞组织选自河北医科大学第四医院口腔科要求手术拔除的埋伏多生牙者。黄连、黄芩、骨碎补均购自河北医科大学第四医院中药房。 方法：采用组织块法体外培养人牙周膜细胞。水提醇沉法制备双黄补提取液。以每 1 mL药液含生药 1 g加入体积分数20%的胎牛血清培养液,稀释成质量浓度为10,25,50,100,150,200,250,500,750,1 000 mg/L,分别作用于体外培养的人牙周膜细胞,以不加双黄补提取液的培养细胞为对照。 主要观察指标：采用四甲基偶氮唑蓝法测定培养细胞增殖活性的变化,应用流式细胞术检测100 mg/L的双黄补提取液对牙周膜细胞周期的变化和对成纤维细胞生长因子18水平的影响。 结果：双黄补对人牙周膜细胞的增殖活性的影响存在质量浓度和时间效应,各质量浓度双黄补均能促进体外培养人牙周膜细胞的增殖活性,其中以100 mg/L质量浓度促增殖活性作用最明显(P < 0.01),相同质量浓度不同作用时间对细胞促增殖活性作用也不同,以48 h作用最明显(P < 0.05)。与对照组相比,100 mg/L的双黄补促进牙周膜细胞成纤维细胞生长因子18水平增高,S期和G2M期细胞数目增多,在48 h最明显。 结论：中药双黄补可增强人牙周膜细胞的增殖活性,具有明显的浓度效应和时间效应。     

针刀松解法对第三腰椎横突综合征家兔5-HT和β-EP以及局部组织病理学的影响

目的:观察第三腰椎横突综合征模型兔血清和肌肉组织5-HT、β-EP的含量变化,探讨针刀治疗的作用机制。方法:将30只日本大耳白兔随机分为正常组、模型组、针刀组、电针组和针刀+电针组。造模后28天,腹主动脉取血和左侧第三腰椎横突周围肌肉组织,采用双抗夹心ELISA方法分别检测血清和肌肉组织中5-HT、β-EP含量的变化;HE染色观察局部组织的病理学改变。结果:模型组血清和肌肉组织5-HT、β-EP含量较正常组明显提高;3个治疗组血清和肌肉组织中5-HT以及肌肉组织中β-EP含量较模型组显著降低。模型组局部出现明显炎症反应,3个治疗组,局部炎症反应均有减轻。结论:针刀松解法可通过减轻局部炎症并减少血清和肌肉组织中5-HT和肌肉组织中β-EP的含量,介导外周的镇痛效应。     

Effects of periodontal afferent inputs on corticomotor excitability in humans

Summary The aim of the present study was to determine in humans whether local anaesthesia (LA) or nociceptive stimulation of the periodontal ligaments affects the excitability of the face primary motor cortex (MI) related to the tongue and jaw muscles, as measured by transcranial magnetic stimulation (TMS). Twelve healthy volunteers (11 men, 1 woman, 25·3 ± 4·2 years) participated in two 3‐h sessions separated by 7 days. The LA carbocain or the nociceptive irritant capsaicin was randomly injected into the periodontal ligament of the lower right central incisor. In both sessions, TMS–motor evoked potential (MEP) stimulus–response curves and corticomotor maps were acquired for the tongue and masseter muscles before (baseline) and at 5, 30 and 60 min post‐application of carbocain or capsaicin. Transcranial magnetic stimulation–MEP stimulus–response curves were also acquired at these time points for the first dorsal interosseous (FDI) as an internal control. Burning pain intensity and mechanical sensitivity ratings to a von Frey filament applied to the application site were recorded on an electronic visual analogue scale (VAS). All subjects reported a decreased mechanical sensitivity (anova : P = 0·004) in the LA session and a burning pain sensation (VAS peak pain: 6·4 ± 1·0) in the capsaicin session. No significant changes in cortical excitability of the MI, as reflected by TMS–MEP stimulus–response curves or corticomotor maps for the tongue, masseter or FDI were found between baseline and post‐injection for the LA (anova s: P > 0·22) or capsaicin (anova s: P > 0·16) sessions. These findings suggest that a transient loss or perturbation in periodontal afferent input to the brain from a single incisor is insufficient to cause changes in corticomotor excitability of the face MI, as measured by TMS in humans.     

富血小板血浆对牙周膜成纤维细胞的增殖、迁移和分化的影响

目的: 体外研究不同浓度的富血小板血浆(platelet-rich plasma, PRP)对牙周膜成纤维细胞(periodontal ligament fibroblasts,PDLFs)的增殖、迁移和分化的影响.方法:不同浓度PRP(10, 50, 100, 200, 300, 500 ml/L),加入到原代培养的人PDLFs,培养时间为3、 5、 7 d,MTT法测定细胞增殖效果,transwell系统测定细胞迁移效果,AKP试剂盒测定碱性磷酸酶活性.结果:PRP有明显促进增殖作用,以200 ml/L浓度PRP效果最好,更高浓度促进作用反而减低.细胞迁移效果中,各浓度组均比阴性对照组效果好,尤其是100 ml/L的效果最佳.对于碱性磷酸酶活性,也具有明显的促进作用,以300 ml/L的效果最佳.结论:PRP在一定浓度范围内对人PDLFs功能有明显促进效果,但是在更高浓度下,这种促进效果反而减低.     

Effect of cyclic mechanical loading on osteoclast recruitment in periodontal tissue

Nozaki K, Kaku M, Yamashita Y, Yamauchi M, Miura H. Effect of cyclic mechanical loading on osteoclast recruitment in periodontal tissue. J Periodont Res 2009; doi: 10.1111/j.1600-0765.2008.01193.x. © 2009 The Authors. Journal compilation © 2009 Blackwell Munksgaard
Background and Objective:  It is well accepted that cyclic mechanical loading induces osteoclastogenesis in periodontal tissue, but its molecular mechanisms are not well understood, in part because of a lack of appropriate models. In this study, we investigated a novel device that allows cyclic mechanical loading to be performed in a well-controlled manner. Furthermore, by employing this model, the effect of cyclic loading on osteoclast recruitment in the periodontal tissue was described.
Material and Methods:  By using a newly developed device, the cyclic loading of 20  n (reference loading corresponding to the fracture hardness of dietary pellets) and two excessive loadings (i.e. 30 and 40  n) were applied to maxillary right molars in rats for up to 7 d, and osteoclast recruitment in the periodontal tissue was evaluated by analyzing relevant marker proteins using immunohistochemistry.
Results:  Osteoclastogenesis was induced by day 3 within alveolar bone subjected to a compression force of 30  n . With both 30 and 40  n loadings, cells that were positive to for tartrate-resistant acid phosphate, receptor activator of nuclear factor-κB ligand and osteoprotegerin were significantly increased in the alveolar bone/periodontal ligament in a time-dependent manner.
Conclusion:  A new device was developed that allows various levels of cyclic mechanical loading to be exerted. By using this device in rats, early events of osteoclast recruitment in the periodontal tissues were observed with excessive loadings in a time-dependent manner, indicating the usefulness of this model.     

Localization of SOST/sclerostin in cementocytes in vivo and in mineralizing periodontal ligament cells in vitro

Jäger A, Götz W, Lossdörfer S, Rath‐Deschner B. Localization of SOST/sclerostin in cementocytes in vivo and in mineralizing periodontal ligament cells in vitro. J Periodont Res 2009; doi: 10.1111/j.1600‐0765.2009.01227.x. © 2009 John Wiley & Sons A/S Background and Objective: Cementum and bone are rather similar hard tissues, and osteocytes and cementocytes, together with their canalicular network, share many morphological and cell biological characteristics. However, there is no clear evidence that cementocytes have a function in tissue homeostasis of cementum comparable to that of osteocytes in bone. Recent studies have established an important role for the secreted glycoprotein sclerostin, the product of the SOST gene, as an osteocyte‐derived signal to control bone remodelling. In this study, we investigated the expression of sclerostin in cementocytes in vivo as well as the expression of SOST and sclerostin in periodontal ligament cell cultures following induction of mineralization. Material and Method: Immunolocalization of sclerostin was performed in decalcified histological sections of mouse and human teeth and alveolar bone. Additionally, periodontal ligament cells from human donors were cultured in osteogenic conditions, namely in the presence of dexamethasone, ascorbic acid and β‐glycerophosphate, for up to 3 wk. The induction of calcified nodules was visualized by von Kossa stain. SOST mRNA was detected by real‐time PCR, and the presence of sclerostin was verified using immunohistochemistry and western blots. Results: Expression of sclerostin was demonstrated in osteocytes of mouse and human alveolar bone. Distinct immunolocalization in the cementocytes was shown. In periodontal ligament cultures, following mineralization treatment, increasing levels of SOST mRNA as well as of sclerostin protein could be verified. Conclusion: The identification of SOST/sclerostin in cementocytes and mineralizing periodontal ligament cells adds to our understanding of the biology of the periodontium, but the functional meaning of these findings can only be unravelled after additional in vitro and in vivo studies.     

Heme oxygenase‐1 protects human periodontal ligament cells against substance P‐induced RANKL expression

Lee H‐J, Jeong G‐S, Pi S‐H, Lee S‐I, Bae W‐J, Kim S‐J, Lee S‐K, Kim E‐C. Heme oxygenase‐1 protects human periodontal ligament cells against substance P‐induced RANKL expression. J Periodont Res 2010; 45: 367–374. © 2010 John Wiley & Sons A/S Background and Objective: Although substance P (SP) stimulates bone resorption activity and this is reported to be correlated with the degree of periodontal inflammation, it is unclear how human periodontal ligament cells regulate neuropeptide‐induced osteoclastogenesis or the possible involvement of heme oxygenase‐1 (HO‐1) might be. This study examines how SP affects osteoprotegerin (OPG) and RANKL expression via HO‐1. Material and Methods: Using immortalized human periodontal ligament cells, the effects of SP on the expression of HO‐1, RANKL and OPG mRNA and proteins were determined by RT‐PCR and western blotting, respectively. Various concentrations of SP (10^?7, 10^?8, 10^?9 and 10^?10 m ) were added to the medium, and the cells were treated for 0, 0.25, 0.5, 1, 2 and 3 d. Results: Substance P upregulated RANKL and HO‐1 and downregulated OPG mRNA and protein expression in periodontal ligament cells, in a concentration‐ and time‐dependent manner. A HO‐1 inducer inhibited both the upregulation of RANKL expression and downregulation of OPG expression by SP in periodontal ligament cells. By contrast, treatment with a HO‐1 inhibitor or HO‐1 small interferring RNA (siRNA) enhanced SP‐stimulated RANKL expression. Inhibitors of ERK and p38 MAP kinases, phosphoinositide 3‐kinase and nuclear factor‐κB blocked the effects of SP on RANKL expression in periodontal ligament cells. Conclusion: These results suggest that SP stimulates osteoclastic differentiation by increasing the expression of RANKL vs. OPG via the HO‐1 pathway in periodontal ligament cells. The HO‐1 pathway may be an effective therapeutic target for inhibiting chronic periodontitis involving alveolar bone resorption.