壮骨关节丸致肝脏损害8例报告

笔者从１９９０年６月～１９９５年１１月,对骨与关节退行性病变３９例患者,临床治疗均使用壮骨关节丸其中８例致肝脏损害。现报告如下。临床资料１一般情况：本组８例中男３例,女５例;年龄４１～７８岁。职业：干部７例,工人１例;腰椎骨关节退行性变４例,膝部骨...     

椎间盘退变模型的建立及其历史和现状

腰腿痛是影响人类健康的常见病和多发病。研究表明约２３％的腰腿痛患者其病因与椎间盘的退行性改变有关［１］。但椎间盘退变的确切病因及病理生理机制目前仍不十分清楚。为深入探讨椎间盘退变的病理过程,有必要建立类似人类椎间盘退变的动物实验模型,对椎间盘退变的诱发因素,早期发生的形态学、生物化学及其它方面的变化进行较为详尽的研究。 一、动物模型的要求及动物选择 建立的动物模型要求与人类的椎间盘退变具有相似性和可比拟性。应包括以下几个方面：（１）能再现椎间盘退行性病变的客观规律;（２）模型重复性好;（３）所选动…     

微创技术干预成年人不同类型脊柱侧凸的疗效分析

目的比较微创技术治疗成年人退行性与非退行性脊柱侧凸病人的效果评价及相关预后。方法脊柱侧凸病人83例,其中退行性病变41例,非退行性病变42例。均采用微创手术治疗。对比成年人退行性与非退行性脊柱侧凸治疗中使用微创技术的效果。结果退行性病变组术后侧凸Cobb角变化量为(50.45±3.98)度,非退行性变组为(55.77±4.03)度;术后半年随访侧凸Cobb角变化两组分别为(52.41±4.09)度和(58.98±4.12)度,两组比较差异有统计学意义(P0.05)。半年后随访结果提示,退行性病变组和非退行性病变组的迟发感染率、术后背痛的发生率无明显差异。结论微创手术治疗退行性成人脊柱侧凸和非退行性脊柱侧凸,术后即时以及短期侧凸Cobb角变化量在退行性病变的减低量均低于非退行性变组,其他疗效及预后无明显差别。     

股骨干骺端髓内血运阻断诱发兔膝关节骨性关节炎模型

目的：髓腔内血供阻断可能诱发邻近软骨退变，利用此方法可制作骨性关节炎的动物模型。方法：以髓腔内髓质刮除、骨蜡填充的方法，将20只成年大耳白兔的股骨远端干骺端髓内血供阻断。在术后8、16周时进行关节软骨的组织切片和透射电镜观察。结果：在术后8周时，关节软骨无显著性改变。在16周时关节软骨出现显著的退行性变。结论：实验证实，采用干骺端髓内血供阻断是获得满意的骨关节炎动物实验模型的好方法，并为骨关节炎的研究提供了一种新的动物模型。     

局部松解对膝关节退行性变模型滑液中IL-1β、IL-6及TNF-α变化的影响

膝关节退行性变引起的老年性膝痛是临床上常见的病症。为寻求更好的治疗方法,本文通过膝周软组织松解疗法,观察实验性膝关节退变动物模型治疗前、后关节液中IL1β、IL6及TNFα水平变化,探讨松解膝周软组织对膝关节退行性变的影响。1材料与方法1.1实验动物采用10～14个月龄,体质     

骨质疏松症与骨关节炎的相关性研究进展

骨质疏松症(Osteoporosis,OP)是以单位体积内骨量低于正常、骨强度降低而脆性增加为特征的退行性骨骼疾病,主要表现为骨质有机成分生成不足、继发钙盐减少及骨组织的结构破坏,多发于绝经后妇女和老年人。骨关节炎(osteoarthritis,OA)是一种常见的慢性退行性关节炎,其主要病变为关节软骨的退变和继发性骨质增生,多见于中老年人和肥胖者。OP和OA都是与人体衰老密切联系的退行性疾病,其发生率随年龄增长而逐渐上升。国外30多年前就开始注意两者之间的关系[1],发现OP和OA很少同时存在,一些流行病学调查发现OA患者发生股骨颈骨折的机会较少…     

膝关节常见病变的影像学诊断(二)

一、膝关节退行性病变的影像表现 1．临床特点：退行性骨关节炎（degenerative osteoarthritis）是骨关节非炎症性退行性的常见疾病，可分为原发性和继发性两大类。膝关节是最常受累的部位，发病多在50岁以上，是关节软骨退行性改变引起的慢性骨关节病，包括软骨、半月板、骨质、韧带及滑膜等病理改变。病变以关节软骨损伤和骨质增生为特点。膝关节在受到长期大量摩擦后，     

血管病理与骨关节炎发病关系的研究进展

有大量证据显示,血管病理学在大多数关节疾病特别是在关节炎中发挥着重要作用。其主要发病机制包括静脉血栓导致长骨末端软骨下骨的小血管间歇性血流供应不足,由此造成软骨下骨血流量减少,组织间液也相应减少,软骨下骨缺血使关节软骨处的营养和气体交换受到限制,这是引起软骨退行性变的一个主要诱发因素。其次,软骨下骨缺血引起局部骨细胞凋亡,促使骨破骨性吸收,进而导致骨质对外层软骨的支撑作用减弱。深刻理解诱发骨关节炎的早期病因对于制定有效治疗的措施阻止关节炎的发病进程具有重要意义。     

老年腰椎退行性病变椎弓根螺钉融合术后周围节段退变预测模型构建

目的 探讨老年腰椎退行性病变椎弓根螺钉融合术后周围节段退变危险因素并构建预测模型,旨在为早期识别周围节段退变高危人群及预后预测提供更多参考。方法 回顾性纳入2017年1月至2022年1月于本院行椎弓根螺钉融合术治疗老年腰椎退行性病变患者共80例,根据术后12个月是否发生周围节段退变分为退变组（21例）和未退变组（59例）;采用单因素和多因素法评估老年腰椎退行性病变椎弓根螺钉融合术后周围节段退变独立危险因素,同时基于上述独立危险因素构建偏回归系数模型方程式,分析该模型用于年腰椎退行性病变椎弓根螺钉融合术后周围节段退变风险预测临床效能。结果 单因素和多因素分析结果显示,年龄增加、体质量指数增加、存在失用性骨质疏松及存在融合不良均是老年腰椎退行性病变椎弓根螺钉融合术后周围节段退变独立危险因素（P<0.05）;基于多因素分析所证实老年腰椎退行性病变椎弓根螺钉融合术后周围节段退变独立危险因素,构建自变量偏回归系数模型方程式;ROC曲线分析结果显示,上述临床模型用于老年腰椎退行性病变椎弓根螺钉融合术后周围节段退变风险预测曲线下面积为0.90(95%CI:0.85～0.98),最佳cut-of...     

膝骨性关节炎关节镜清理术治疗进展

膝骨关节炎(knee osteoarthritis,KOA)是老年性的膝关节慢性退行性病变,是引起老年人下肢功能障碍、活动受限的主要原因,是基本病变为关节软骨退变,继而新骨增生的一种慢性、进行性关节病。患者多为中老年人,随着社会人口老龄化,发病率逐年上升。本文对膝关节镜治疗膝骨关节炎的进展综述如下。1历史背景自从1960年Wantanabe和Takeda将第一台实用关节镜用于临床以来,关节镜治疗膝退行性关节炎再次引起人们的重视,已成为膝关节疾病诊断和治疗的重要方法之一。1972年,Jackson对200例膝关节疼痛患者,采用关节镜观察关节内部的病理变化,并行镜下摘除游离体,切除损伤半月板,临床症状有所好转。1981年,Sprague[1]采用关节镜清理术治疗膝退行性关节炎,采用切除损伤半月板、滑膜、骨赘,刨削软骨面等方法治疗69膝,结果优良率为74%。近年来,由于微骨折技术简便易行、并发症少及其使用成本较低,常被用作首选治疗方案。2手术方法2.1关节镜冲洗术老年性膝骨关节炎病变常累及关节软骨、软骨下骨和滑膜。软骨表面软化、脱落、溃疡,形成关节内游离体。滑膜充血、炎症细胞浸润,后期滑膜呈绒毛样增生,包埋破碎软骨...     

An overview of underlying causes and animal models for the study of age‐related degenerative disorders of the spine and synovial joints

As human lifespan increases so does the incidence of age‐associated degenerative joint diseases, resulting in significant negative socioeconomic consequences. Osteoarthritis (OA) and intervertebral disc degeneration (IDD) are the most common underlying causes of joint‐related chronic disability and debilitating pain in the elderly. Current treatment methods are generally not effective and involve either symptomatic relief with non‐steroidal anti‐inflammatory drugs and physical therapy or surgery when conservative treatments fail. The limitation in treatment options is due to our incomplete knowledge of the molecular mechanism of degeneration of articular cartilage and disc tissue. Basic understanding of the age‐related changes in joint tissue is thus needed to combat the adverse effects of aging on joint health. Aging is caused at least in part by time‐dependent accumulation of damaged organelles and macromolecules, leading to cell death and senescence and the eventual loss of multipotent stem cells and tissue regenerative capacity. Studies over the past decades have uncovered a number of important molecular and cellular changes in joint tissues with age. However, the precise causes of damage, cellular targets of damage, and cellular responses to damage remain poorly understood. The objectives of this review are to provide an overview of the current knowledge about the sources of endogenous and exogenous damaging agents and how they contribute to age‐dependent degenerative joint disease, and highlight animal models of accelerated aging that could potentially be useful for identifying causes of and therapies for degenerative joint diseases. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31: 831–837, 2013     

骨关节炎病因及小鼠模型相关研究进展

骨关节炎是最常见的退行性关节病变,常见于老年人.骨关节炎的特征性改变是关节软骨进行性退变、软骨细胞凋亡、软骨下骨重建、炎症、滑膜炎和骨赘形成,引起受累关节疼痛、活动受限并最终导致关节功能障碍.骨关节炎的病因主要包括年龄、肥胖、关节损伤、炎性因子和遗传因素等.伴随着社会人口老龄化进程的加速,骨关节炎发病率逐年升高,并成为严重的社会医学问题.由于其病因复杂多样,目前没有确切的结论,故缺乏有效的治疗手段.本文对骨性关节炎病因及用于骨关节炎病因研究的小鼠模型进展进行综述,对骨关节炎的病理机制进行阐述,以期为骨关节炎的治疗带来新思路.     

膝骨性关节炎合并骨质疏松症调节机制的研究进展

膝骨性关节炎和骨质疏松症都是与年龄增长相关的骨与关节退行性疾病,两者在发病机制、病理变化、调节机制、临床治疗等方面存在着诸多的共同点,在膝骨关节炎和骨质疏松症的进程中通过复杂的调节机制维持骨代谢平衡、减轻炎症、保护关节软骨、稳定膝关节,进而延缓膝关节的退变;虽然两者间复杂的调节机制已有研究,但是仍然不完善。本研究从炎症、生物力学、激素与骨代谢、遗传、蛋白等方面对膝骨性关节炎并骨质疏松症的调节机制进行了综述,以期为临床防治该病提供新的思路和理论依据。     

Degenerative joint disease: An example of calcium paradox

Osteoporosis and degenerative arthropathy such as osteoarthritis and spondylosis deformans represent the two most common diseases seen in later life, sharing some common clinical features such as pain, deformity, and restriction of motion. Augmented bone resorption, possibly mediated by cytokines such as interleukin 1, and favorable therapeutic response to estrogen also characterize both diseases. Both osteoarthritis of the knee and osteoporosis occur frequently in postmenopausal women, whereas spondylosis deformans mainly affects men who experienced a heavy labor load, and women are less susceptible unless they worked as hard as men at some time in their lives. Degeneration of the cartilage with decrease of water content, increase of calcium content, hardening, and subsequent wear and loss would lead to narrowing of the joint space and direct contact of bones, resulting in excessive reactive bone formation such as osteophytes. Because increased physical load on the cartilage and bone would intensify such response, excessive weight and physical exercise always remain important risk factors for degenerative joint disease. The metabolic state precipitating cartilage degeneration, however, may be even more important as the background. Calcium is confined to bone so long as adequate calcium intake is maintained and the hormonal environment remains intact. When calcium deficiency and secondary hyperparathyroidism occur in old age, calcium comes out of bone and starts to accumulate in soft tissues such as blood vessels, brain, and intracellular compartments, where little calcium should be present under normal physiological circumstances. Cartilage should also be devoid of calcium in health, but calcium may accumulate when bone loss occurs in response to estrogen deficiency, calcium deficiency, and secondary hyperparathyroidism. Calcium overabundance prompted by calcium deficiency is known as the calcium paradox. Degenerative joint disease should be included in the group of diseases based on calcium deficiency and calcium paradox, such as hypertension, arteriosclerosis, Alzheimer's disease and other degenerative diseases of the nervous system, diabetes mellitus, and malignancy. Calcium deficiency is thus responsible for both osteoporosis and degenerative joint disease. Received: April 9, 1998     

肌少-骨质疏松症动物模型及评价方法研究进展

随着社会人口老龄化程度的日益加剧，肌少-骨质疏松症这类肌骨协同退变疾病的发病率逐渐增高，严重影响了老年人的身体健康，给社会医疗带来巨大负担。为了深入研究肌少-骨质疏松症的病理机制并研制有效的临床药物，构建切实有效的肌少-骨质疏松症实验动物模型至关重要。笔者综述了5种肌少-骨质疏松症模型的研究进展，即衰老肌少-骨质疏松症模型、去势肌少-骨质疏松症模型、化学诱导肌少-骨质疏松症模型、废用肌少-骨质疏松症模型以及基因肌少-骨质疏松症模型。深入探究了不同模型的研究进展、特点及应用范围，并简述了模型的评价方法，为后期肌少-骨质疏松症病理机制及临床药物的研究提供合理的动物模型。     

不同腰椎融合术式治疗腰椎退行性疾病的研究进展

腰椎退行性疾病是由椎间盘退变、椎间小关节增生紊乱、腰椎韧带松弛以及肌肉劳损等原因相互作用引起的以腰椎自然退化为特征的临床常见病.近年来随着生活水平的提高,老龄化进程的加剧,腰椎退行性疾病在临床上的发病率也越来越高,给众多老年人的生活质量和身体健康带来严重的影响.腰椎融合手术是治疗腰椎退行性疾病的重要手段,临床上腰椎融合...     

Hip endoprostheses in Paget's disease

When the region around the hip joint is affected by Paget's disease it takes up to 10 years for degenerative joint disease requiring treatment to develop. Medium-term follow-up examination of 27 hip replacements in patients with Paget's disease revealed generally good results, though the rate of loosening, with 30%, was clearly elevated compared with that observed in a control group of patients not suffering from Paget's disease. The reduced bone stability and the increased bleeding tendency can cause complications even during the operation when Paget's disease is present. Since most of the patients affected are elderly prosthetic hip joint replacement is practically always indicated.     

抗肝纤维化药物研究进展

HF是各种慢性肝病的共同病理学基础,也是肝硬化的必经阶段。积极的抗HF治疗可以控制多种肝组织疾病,尤其是肝硬化的病理进程。靶点明确、疗效显著的抗HF药物是治疗的首选。本研究从HF药物作用靶点、药物研究的体内外模型及药物研究3个方面展开阐述抗HF药物的最新研究进展。     

80岁以上高龄老年骨质疏松症的规范诊治和注意事项

骨质疏松症（OP）是一种以骨量低下、骨微结构破坏,导致骨脆性增加、易发生骨折为特征的全身性疾病。近年来,随着人口老龄化社会的到来,高龄老年OP患者越来越多。高龄老年OP的发生与高龄老人体内性激素（包括雌激素和雄激素）水平下降、营养物质摄入减少、活动量下降、某些疾病等因素有关。高龄老年OP患者不仅脆性骨折的发生率高,而且骨折后容易致残、致死。高龄老年OP诊治的基本内容包括普查和健康教育、选择合适的抗OP药物、及时调整治疗方案等。骨转换标志物（BTMs）的检测是高龄老年OP患者选择抗OP药物的重要依据,一般来说,对BTMs较高的高龄骨量减少和OP患者,应选择使用抗骨吸收药物,如双膦酸盐类和选择性雌激素受体调节剂等,而对BTMs较低的高龄OP患者,应选择使用促骨形成药物（如重组人甲状旁腺激素1-34）。要注意根据高龄老年OP患者骨密度和BTMs的变化,及时调整治疗方案,避免长期使用双膦酸盐类药物。