痤疮丙酸杆菌致病机制的研究进展

痤疮是由多因素引起的一种慢性炎症性皮肤疾病,现在主流观点认为其发病机制主要包括遗传因素、皮脂分泌过度、毛囊皮脂腺导管角化过度、皮肤炎症反应、痤疮丙酸杆菌致病和雄激素分泌过度等。其中,痤疮丙酸杆菌作为重要的致病因素多年来被广泛关注,随着研究的深入,逐渐发现痤疮丙酸杆菌在痤疮中并非以独立的病因而存在。本文就痤疮丙酸杆菌的致病机制和最新进展做一综述,以期为痤疮的临床治疗及今后的研究方向提供科学思路。     

椎间盘退变机制及动物模型建立的研究进展

椎间盘退变常会引起腰背痛.长期以来人们对椎间盘退变机制进行了大量的探索与研究,目前普遍认为椎间盘退变是一个多因素诱导的(遗传因素、环境因素、年龄因素)、多种因子(生长因子、炎性因子)参与的不可逆的过程,其确切机制尚不明确.模型的建立可与退变机制的研究相互论证,益于对退变机制的探索.     

Toll样受体与痤疮

痤疮是一种累及毛囊皮脂腺的慢性炎症性皮肤病,多发于青春期男女,因此也称为“青春痘”.临床表现为面部粉刺、丘疹、脓疱、结节和囊肿等多种形式损害,严重影响着患者的身心健康.痤疮丙酸杆菌长期以来被认为是痤疮炎症发生的主要原因,但是对痤疮丙酸杆菌引起的炎症机制尚不明了.最近研究证实痤疮丙酸杆菌通过Toll样受体2(Toll-like receptor2,TLR2)依赖途径激活单核细胞,进而释放细胞因子引起炎症[1].     

椎间盘退变模型及其评估指标

腰痛发病率高,严重影响人类健康,椎间盘退变是引起腰痛的重要原因之一.目前椎间盘退变的病因及发病机制尚不清楚,也无有效的治疗方法.因此,建立椎间盘退变模型对于研究其退变机制及治疗方法具有重要意义.笔者对椎间盘退变模型的制备方法及其评估指标进行综述.     

生物力学因素对椎间盘退变的影响及机理

椎间盘退变由多因素引起,现有的研究结果提示其与生物力学、创伤、职业、肥胖、遗传等有关,但确切的发生机制仍不明确。生物力学因素是目前被广大学者所认可的引起椎间盘退变的重要因素。流行病学调查显示,重体力劳动、提重物、长时间驾驶及肥胖等因素是与椎间盘退变     

椎间盘退变病因学研究概况

椎间盘退变是腰背痛的主要原因之一,目前的治疗方法仍不理想,原因在于其病因机制尚未完全阐明.近年研究发现椎间盘退变由多种因素影响所致,椎间盘细胞能合成和分泌一些细胞因子,加重炎症反应并影响椎间盘的物质代谢,促进椎间盘退变;某些具有遗传特性的特异性基因与椎间盘退变相关;椎间盘渗透功能降低会引起椎间盘营养障碍,导致椎间盘退变.     

糖尿病与腰椎间盘退变相关性研究进展

糖尿病和腰椎间盘退变相关疾患是临床常见病多发病,两者的相互关系逐渐引起了脊柱外科医生的兴趣。本文从糖尿病和椎间盘退变的基础及临床多个方面论述两者关系的最新研究进展。椎间盘退变是多因素共同作用导致的结果,糖尿病可能是椎间盘退变相关疾患发病的危险因素之一。基础研究的进展仍未阐明潜在的机制,临床观察的结论也并不统一。正确认识糖尿病和椎间盘退变疾病之间的复杂关系,探讨糖尿病引起或加速椎间盘退变的机制,对椎间盘退变相关疾病的治疗、康复和并发症预防具有重要的临床意义。     

骨质疏松与椎间盘退变相关性的研究进展

骨质疏松症和椎间盘退变性疾病均为骨退行性疾病,临床上两者常可并见于同一病例,二者可能存在相似的发病机制,但骨质疏松和椎间盘退变的内在联系目前没有明确论述。本文就骨质疏松和椎间盘退变两方面的相关性从:骨质疏松对椎间盘营养的影响、炎性因子在椎间盘退变性疾病和骨质疏松症中的作用、雌激素对骨质疏松和椎间盘退变的影响、破骨细胞/破软骨细胞对骨质疏松和椎间盘退变的影响、OPG对骨质疏松和椎间盘的保护作用等几方面做一探讨。最后得出:骨质疏松和椎间盘退变存在一定的相关性和相似的发病机制,骨质疏松这一病理因素可能参与了椎间盘退变的病理进程,从而推测骨质疏松会引起或加速椎间盘的退变。     

肿瘤坏死因子-α在椎间盘细胞凋亡中的作用

<正>椎间盘退变是引起慢性下腰痛的重要原因[1],引起椎间盘退变的具体原因目前还不清楚,但椎间盘细胞,特别是髓核细胞,对维持正常的椎间盘结构与功能具有重要作用[2]。髓核细胞增殖与凋亡平衡的破坏对椎间盘的退变起到了重要作用[3]。近年来,炎性细胞因子在椎间盘退变中作用备受关注[4]。Peng[5]研究发现,由炎症反应所产生的细胞因子对加速椎间盘退变起到了重要作用。但目前导致椎间盘细胞凋亡的原因和机制并不十分明确,肿     

腹主动脉粥样硬化与腰椎间盘退变

椎间盘营养障碍是导致椎间盘退变的主要因素之-,腰椎血供主要源于腹主动脉节段分支,任何影响腹主动脉和其分支循环的因素均会影响腰椎间盘营养供给.流行病学研究证实年龄、吸烟、重负荷体力劳动及肥胖等是动脉粥样硬化与腰椎间盘退变的共同危险因素;解剖学研究也证实腹主动脉粥样硬化可引起腰椎血供减少,腰椎血供又与椎间盘营养供应密切相关.一系列研究表明腹主动脉粥样硬化与腰椎间盘退变确实存在显著相关性,其机制可能是动脉粥样硬化引起腰椎节段动脉狭窄,甚至阻塞,导致椎间盘营养供应不足,进而引起椎间盘退变;也可能通过疼痛敏感结构如神经根、骨或肌肉等产生缺血性疼痛而引起脊柱功能紊乱,改变椎间盘力学环境,进一步加重椎间盘退变.临床上积极地预防和治疗动脉粥样硬化可能是预防和减轻椎间盘退变,降低腰痛发生率的途径之一.     

不同程度椎间盘退变相应椎间孔的影像学变化及其临床意义

目的：从影像学角度研究腰椎间盘不同退变程度时相应椎间孔形态改变的规律,探讨其临床意义。方法：自2006年12月至2008年2月选取37例L4,5椎间盘呈退行性变化的影像学资料（MRI、CT）进行研究,男23例,女14例,年龄28～62岁,平均41.6岁;分别将其矢状位MRIT2WI成像,采用MRI机内Mean/Curve测量软件测量计算L4,5节段退变椎间盘信号强度与相应节段脑脊液平均信号强度比值（RSI）,判断椎间盘退变程度并进行分组。分为3组：轻度退变组11例（A组）,中度退变组13例（B组）,重度退变组13例（C组）。根据CT1.25mm薄层二维旁矢状位重建测量L4,5节段椎间孔的最大高度、最大宽度与面积。分析椎间盘在不同退变程度下相应椎间孔变化规律及可能对神经根状态的影响。结果：①中、轻度退变组椎间孔的最大高度及面积差异均无统计学意义（P〉0.05）,重、中度退变组椎间孔最大高度及面积均有统计学意义（P〈0.05）,重、轻度退变组椎间孔最大高度差异有统计学意义（P〈0.01）;②重、中、轻度退变组椎间孔最大宽度差异均无统计学意义（P〉0.05）。结论：随着腰椎间盘退变程度加重相应椎间孔的高度及面积也逐渐减小,而其对椎间孔宽度影响不大;椎间孔高度及面积变小有可能导致神经根受压。     

转基因修复椎间盘细胞外基质的研究进展

目的综述转基因修复退变椎间盘细胞外基质（extracellular matrix,ECM）的发展及研究进展。方法广泛查阅近年来有关转基因调节椎间盘ECM合成和分解的国内外文献,并进行综述。结果椎间盘正常的形态、功能与ECM的合成、降解密切相关。ECM已经成为转基因修复退变椎间盘的标靶。转基因治疗目前在载体的选择、靶基因的转导、转入基因的调控与安全性等多方面取得明显进展。结论转基因修复退变椎间盘是治疗椎间盘退变性疾病的重点研究方向。     

退变性腰椎侧凸形成和发展的相关因素分析

目的 探讨退变性腰椎侧凸患者椎问盘的不对称指数、腰椎间盘退变程度以及骨密度降低对侧凸角度的影响.方法 采用回顾性研究的方法,选取2002年1月至2010年8月,共96例退变性腰椎侧凸患者为研究对象(侧凸组);2002年1月至2010年8月确诊为腰椎管狭窄症并且资料齐全的患者96例为对照组;两组间性别、年龄、体质量指数匹配.侧凸组:在腰椎正位X线片上测量凸凹侧顶椎间盘及其上下椎间盘的高度和顶椎及其上下椎体的高度,利用Adobe Photoshop 6.0软件,测量MRI图像T2WI顶椎及其上下椎间盘内髓核与脑脊液的相对信号强度.对照组:取2～3、L3-4、L4-5这3个椎间盘为研究对象测定上述指标.应用双能X线吸收法测定两组患者腰椎(L2-4)及股骨颈、股骨粗隆和Ward's三角的T值.结果 侧凸组凸侧椎间盘高度和为(40±7)mm高于凹侧的(28±7)mm(P<0.01),凸侧椎体高度和为(76±12)mm高于凹侧的(72±10)mm(P=0.016):两组之间的椎间盘退变程度差异有统计学差异(P=0.003);两组之间骨密度T值的平均值和骨质疏松的发生率差异有统计学意义(均P<0.01).通过多元线性回归分析结果 显示患者椎间盘的不对称指数、椎间盘的退变程度、骨密度T值影响退变性腰椎侧凸角度.结论 退变性腰椎侧凸常伴有凸凹两侧椎间盘高度以及椎体高度不对称.侧凸角度与椎间盘的不对称指数、椎间盘的退变程度呈正相关,与骨密度值T值呈负相关.

Abstract：

Objectives To investigate the correlation between scoliosis angle and the asymmetric index of degenerative lumbar scoliosis, the degree of intervertebral disc degeneration, decreased bone density. Methods As a retrospectively study, a total of 96 patients with degenerative lumbar scoliosis were retrospectively enrolled from January 2002 to August 2010 as scoliosis group, meanwhile % patients with lumbar spinal stenosis matched in gender, age and body mass index (BMI) were selected as control group.All patients were studied with plain radiographs, MRI and dual energy X-ray absorptiometry at presentation. Radiographic measurements include Cobb angle, the height of the convex and concave side of the apical disc and the contiguous disc superiorly and inferiorly, the height of the convex and concave side of the apical and the contiguous vertebral body superiorly and inferiorly in scoliosis group, the height of L2-3, L3-4, L4-5 discs and the height of L2-4 vertebral body in control group. The average relative signal intensity of lumbar intervertebral disc and cerebrospinal fluid in T2WI sagittal image was measured in apex intervertebral disc and adjacent discs by Adobe Photoshop 6.0 in scoliosis group, which was measured in L2-3, L3-4, L4-5 disc in control group. The bone density of lumbar, femoral neck, trochanter, and Ward's triangle regions were measured with dual-energy X-ray absorptiometry. Results The intervertebral disc height in convex side was greater than the height in the concave side [(40 ± 7) mm vs. (28 ± 7) mm, P < 0. 01] , the vertebral body height in convex side was greater than the height in the concave side [(76 ± 12) mm vs. (72 ± 10) mm, P =0.016] in scoliosis group. There was significant statistically difference in the degenerative degree of intervertebral discs between two groups (P = 0. 003). There was significant statistically difference of the average T-value and the rate of osteoporosis between two groups (P < 0. 01). Multiple linear regression analysis showed that the asymmetric disc index, the degenerative degree of intervertebral disc and osteoporosis were the predominant correlative factors, which affected the development of degenerative lumbar scoliosis. Conclusions Degenerative lumbar scoliosis is always accompanied by the height asymmetry of intervertebral discs and vertebral body from convex and concavity sides. There is positive correlation between the angle of scoliosis and the asymmetric disc index, the degeneration of intervertebral disc, and negative correlation between the angle of scoliosis and the bone density (T-value).     

Infectious damage to the intervertebral disk--before and following discotomy

Bad results after discotomy for treatment of herniated lumbar disc are caused either by postoperative complications or by preoperative diagnostic errors. Very often other degenerative changes of the "Bewegungssegment" are involved and misunderstood. But also septic lesions of the intervertebral disc following pyogenic hematogenous osteomyelitis of the spine are confused with degenerative lesions. They are even treated operatively as a ruptured intervertebral disc. When pyogenic osteomyelitis may no longer by overlooked after discotomy due to her progression, she is misinterpreted as discitis following removal of intervertebral disc. Only 9 of 97 verified patients with vertebral osteomyelitis suffered from true postoperative infection of the intervertebral space after removal of a herniated disc. In 14 patients the signs of hematogenous osteomyelitis of the spine have been missed or have been explained by degenerative changes of the spine. In none of the patients the wrong diagnosis was perioperatively revised. The common confusion of osteomyelitis and degenerative disc changes can be explained by several reasons: the predilection of lumbar spine and the similarity of local signs of both diseases, the unknown or underestimated frequence of radicular lesions in osteomyelitis of the spine and the difficulties to assess osteomyelitis in early stages by X-ray examination and the frequency of accessory degenerative changes. It may be supposed that many of the reported disc space inflammations after diagnostic or therapeutic means have not been caused by these manipulations but have given occasion for them.(ABSTRACT TRUNCATED AT 250 WORDS)     

细胞自噬对腰椎间盘突出后重吸收的意义

细胞自噬作为细胞的一种自我保护性机制,可通过降解自身衰老物质而维持细胞稳定,且可被高度诱导,自噬对细胞的降解能力会随年龄的增加而减弱。腰椎间盘突出后的重吸收现象是临床保守治疗腰椎间盘突出症患者有效的机制之一,退行性病变是腰椎间盘突出的主要原因之一,细胞自噬又广泛参与了腰椎间盘的退行性病变,并延缓了退行性病变的发生,同时细胞自噬可潜在性诱导重吸收现象的发生。细胞自噬的研究对椎间盘退行性病变以及腰椎间盘突出后的重吸收现象意义重大,对临床保守治疗腰椎间盘突出症患者具有指导意义,因此应重视细胞自噬在重吸收现象中的研究。     

uPA、MMP-3在退变椎间盘中的表达及意义

目的探讨尿激酶型纤溶酶原激活剂（uPA）、基质金属蛋白-3（MMP-3）在人类退变椎间盘组织中的表达变化。方法对照组为取自脊柱侧凸患者的正常腰椎间盘组织；实验组为腰椎间盘突出患者的退变椎间盘组织。分别进行免疫组织化学染色，比较2组椎间盘组织中uPA及MMP-3的光密度值。结果uPA和MMP-3在突出椎间盘组织中平均光密度值较正常椎间盘组织中的平均光密度值表达明显升高；相关分析显示突出椎间盘中uPA、MMP-3呈正相关关系。结论uPA和MMP-3均可能参与了人椎间盘组织的退变过程，且MMP-3与uPA在人类退变椎间盘组织中有相同的增高趋势。     

Next-generation sequencing (NGS) to determine microbiome of herniated intervertebral disc

BACKGROUND CONTEXTThere is apparent causality between chronic infection of the intervertebral disc and its degenerative process. Although disc is considered a sterile tissue, collected samples of uninfected patients sent to culture testing resulted positive.PURPOSEThe purpose of this study was to analyze the microbiome of the intervertebral disc by using and validating the next-generation sequencing (NGS) molecular test, controlled with tissue culture and clinical presentation of patients.STUDY DESIGN/SETTINGProspective study of consecutive patients in a hospital.PATIENT SAMPLEPatients with lumbar disc herniation undergoing open microdiscectomy aging 18 to 65 years.OUTCOME MEASURESNGS, tissue cultureMETHODSSubjects undergoing open decompression surgery for lumbar disc herniation were consecutively included and clinically followed for one year. Three samples of the excised herniated disc fragment were sent to tissue culture and another sample of the disc was sent to NGS test for microbiome analysis. Control samples of the ligamentum flavum and deep muscle were collected and sent to culture.RESULTSA total of 17 patients were included. All patients presented negative cultures of the removed disc samples, as well as negative cultures of muscle and yellow ligament. None of the patients evolved to clinical infection one year after surgery, nor presented significant alteration of laboratory markers. NGS mapped a mean of 14,645 (range 6,540 to 27,176) DNA sequences for each disc sample of each patient. There were a total of 45 different bacteria genera remnants with different amount of DNA sequences detected. There was a mean of 8 (range 3-17) different bacterial elements in each sample of intervertebral disc. Three bacteria were present in all disc samples (Herbaspirillum, Ralstonia, and Burkolderia). Although there were a considerable mean number of bacterial sequences mapped in each disc sample, the amount of sequences related to bacteria was low. Cutibacterium acnes elements was not found in any disc microbiome analysis.CONCLUSIONSNGS has been proven to adequately determine bacterial DNA presence within the intervertebral disc. C. acnes was not isolated in culture neither in microbiome analysis of patients with lumbar disc herniation. We cannot confirm disc sterility since, even if it does not cause infection, there is bacterial or remnant DNA in herniated discs.     

uPA、MMP-3在退变椎间盘中的表达及意义

目的探讨尿激酶型纤溶酶原激活剂（uPA）、基质金属蛋白-3（MMP-3）在人类退变椎间盘组织中的表达变化。方法对照组为取自脊柱侧凸患者的正常腰椎间盘组织；实验组为腰椎间盘突出患者的退变椎间盘组织。分别进行免疫组织化学染色，比较2组椎间盘组织中uPA及MMP-3的光密度值。结果uPA和MMP-3在突出椎间盘组织中平均光密度值较正常椎间盘组织中的平均光密度值表达明显升高；相关分析显示突出椎间盘中uPA、MMP-3呈正相关关系。结论uPA和MMP-3均可能参与了人椎间盘组织的退变过程，且MMP-3与uPA在人类退变椎间盘组织中有相同的增高趋势。     

Molecular biology of degenerative disc disease

The intervertebral disc is a complex anatomic and biochemical structure. It is composed primarily of fibrocytes and chondrocytes that are anatomically segregated in an elaborate avascular macromolecular matrix of collagen and proteoglycans. Degenerative processes associated with aging and trauma result in morphological and molecular changes to the disc. Morphological changes are observed as dehydration, fissuring, and tearing of the nucleus, annulus and endplates. On the molecular level, degenerative changes include decreased diffusion, decreased cell viability, decreased proteoglycan synthesis, and alteration in collagen distribution. The role of inflammatory mediators in these processes, and the potential use of growth factors to delay or reverse the degenerative cascade, is poorly understood. However, these areas are under active investigation, the results of which may soon contribute significantly to our understanding of degenerative disc disease.