膝关节骨性关节炎外科手术治疗进展

正膝关节骨性关节炎(knee osteoarthritis,KOA),又称为骨质增生、退行性骨关节疾病,是临床常见的一种以关节软骨退行性改变为核心的,全方位、多层次、不同程度累及骨质、关节囊、滑膜和关节其他结构的慢性、无菌性、退行性炎症,其会侵犯关节,尤其是负重关节,造成膝关节不同程度的疼痛和功能障碍,严重影响患者的生活质量。KOA是一种临床常见的老年性慢性膝关节退行性疾病,老年人群的发病率为80%,是导致老年人下肢活动受限、功能障碍     

几丁聚糖衍生物防治骨性关节病概况

骨性关节病 (骨关节炎 ,增生性、创伤性关节炎等 )是影响中老年人健康的常见疾病 ,如 40岁以上的女性约有 40 %膝关节就出现不同程度的临床症状。骨关节病是人体关节器官退化过程中表现出来的一种病理状态 ,骨关节的软骨基质和滑膜表面受到破坏和流失 ,即引起各种症状。退行性骨关节炎以及各种关节损伤 ,包括关节外伤、手术导致的创伤性骨关节炎 ,是临床常见又尚未能解决的问题。近年来 ,关节软骨保护学说 ,尤其是糖胺类药物作为软骨保护剂应用 ,使骨关节病的研究领域得到开拓 ,对预防骨性关节病的发生或减轻病变程度 ,缓解症状及改善关节功…     

布鲁杆菌性化脓性关节炎1例

布鲁菌病是系统性感染性疾病,临床表现多样,在非流行区易被忽视。本病以骨关节受累常见,关节症状多数为反应性关节炎,以单关节化脓性关节炎为首发表现的病例少见。本文报道1例布鲁杆菌性化脓性单膝关节炎的临床表现和诊疗情况。     

软骨寡聚基质蛋白在关节炎中的作用

研究表明在骨性关节炎和类风湿性关节炎患者血清中软骨寡聚基质蛋白(cartilage oligomeric matrix protein,COMP)可以在出现关节形态学改变以前就在生化代谢方面表现异常,为早期诊断提供了新思路,其可以作为反映早期关节软骨破坏和骨关节疾病急性活动程度的指标。从而能在病变不可逆发展之前及早防治,逆转或延缓病变进展。COMP是关节炎疾病的诊断与判断疾病进展和缓解潜在生物学标志物。本文就软骨寡聚基质蛋白及其在关节炎中的作用作一综述。     

骨关节炎相关细胞因子及蛋白的研究进展

骨关节炎（osteoarthritis,OA）是人体中轴关节及外周运动关节最常见的退行性疾病,该病的临床症状表现为疼痛、关节僵硬和关节活动受限,罹患该病非常痛苦,严重影响生活质量,是成年人疼痛、运动功能障碍和致残的常见原因之一。OA是临床上常见的骨关节疾病,老年人多发,是老年人丧失劳动力的重要原因,对社会经济影响很大。国内外对OA的发病机制做了大量的研究,但其确切的病因及病理机制尚未完全阐明。目前,OA没有特效治愈方法,治疗目标局限于使用止痛药来缓解疼痛,并最终行人工关节置换手术。即使人工关节置换手术成功,人造关节寿命也是有限的,其他严重问题还有植入物的松动和失败等。因此,对该病病因、病理机制的探索成为目前的热点和焦点,也是解决OA这个问题的关键。本文就近年来研究较热门的骨关节炎相关细胞因子及蛋白做一综述。     

蛇药酒治疗强直性脊柱炎38例

强直性脊柱炎（AS）是因骶髂关节周围软组织受损,引起脊柱强直和纤维化形成,是一种由关节慢性炎症为主的不明原因的全身性疾病,又称血清反应阴性关节炎。主要侵犯骶骼关节、髋关节、脊柱,以骶骨关节病变为常见,也有部分病人出现周围关节病变,累及全身结缔组织及内脏,关节活动受限、僵硬,可引起畸形、致残,给患者生活和工作带来很大影响。我们对38例强直性脊柱炎患者采用自制的蛇药酒治疗,疗效显著,现报告如下。     

在加拿大开始销售畸形性关节炎治疗药

美国 Biomatrix 公司(新泽西州 Ridgefield)在加拿大开始销售畸形性关节炎治疗药透明质酸钠衍生物。相同关节疾病有2种,一种是,慢性关节炎,另一种是畸形性关节炎。慢性关节炎是自身免疫疾病,但是畸形性关节炎是由于老化和外伤或关节的驱使使关节的骨骼变形的病。因老化等在关节软骨处发生退化变形,由于关节液的粘性下降而发生。透明质酸钠是这种关节液的主要成分。含于活体内几乎所有结合组织中。关节液防止关节磨损,即起到润滑油的作用。Biomatrix 公司在加拿大及欧洲以重度膝关节变形患者为对象实施临床试验。使用透明质酸钠的小组确认对膝关节的疼痛及可动性有显著效果。据说这种效     

白细胞介素在骨性关节炎中发病机制中的研究现状

骨性关节炎(OA)是临床上常见的关节疾病之一,严重影响患者的关节功能和生活质量,由多种因素相互作用致病,多发于老年人,但是具体的发病原因尚未明确,因此给临床治疗造成障碍。目前研究认为白细胞介素在OA的发生及发展过程中起主要作用,因此可以将白细胞介素作为治疗OA的靶点,为治疗OA提供新思路。本文主要就不同种类白细胞介素在OA的发病机制中的作用进行综述。     

中药熨疗腰椎骨性关节炎的护理

腰椎骨性关节炎(Lumbar osteoarthritls,LOA)是指以腰椎小关节肥大变性等病理改变引起的以腰痛为主要表现的临床病症.临床上又称为腰椎退行性关节病、腰椎增生性关节炎及老年性腰椎关节炎等,其病理特点为关节软骨变性、破坏,软骨下骨硬化,关节边缘和软骨下骨反应性增生,骨赘形成.     

针刀治疗肩周炎研究现状

随着目前人们生活方式的变化,骨关节慢性病易于多发,肩周炎就是其一,中医的理论认为风、寒、湿三种邪气杂至合而痹症,西医认为,人体盂肱关节以外的解剖组织的一系列变化是肩痛及关节活动功能受限的主要原因,肩峰下滑囊无菌性炎症或粘连、变性等被认为是肩关节活动障碍及疼痛症状的原因。目前西医通用疗法口服药物对症抗炎及止痛治疗,效果欠佳,且有明显的复发率。运动系统慢性损伤性疾病为针刀治疗的适应症,包括各种慢性骨关节病,如颈、腰椎相关病、骨性关节炎、肩周炎等,治疗效果明显。     

Hypertrophic differentiation of chondrocytes in osteoarthritis: the developmental aspect of degenerative joint disorders

Osteoarthritis is characterized by a progressive degradation of articular cartilage leading to loss of joint function. The molecular mechanisms regulating pathogenesis and progression of osteoarthritis are poorly understood. Remarkably, some characteristics of this joint disease resemble chondrocyte differentiation processes during skeletal development by endochondral ossification. In healthy articular cartilage, chondrocytes resist proliferation and terminal differentiation. By contrast, chondrocytes in diseased cartilage progressively proliferate and develop hypertrophy. Moreover, vascularization and focal calcification of joint cartilage are initiated. Signaling molecules that regulate chondrocyte activities in both growth cartilage and permanent articular cartilage during osteoarthritis are thus interesting targets for disease-modifying osteoarthritis therapies.     

What can we do about osteoarthritis?

Osteoarthritis is complex in genetics, pathogenesis, monitoring and treatment. Current treatment of osteoarthritis does not influence progression. Much could be gained by more effective 'low-tech-low-cost' treatment. However, many patients have rapidly progressive disease, multiple joint involvement, and severe disease. We need to clarify the genetics of osteoarthritis, identify those at risk for progression and severe disease, and identify molecular processes critical for joint survival and failure. Will saving the cartilage improve patient pain and function? Effective outcome measures are needed to accelerate testing of new treatments. Further improvement is needed in joint implant technology to decrease costs, wear and loosening.     

Aging,osteoarthritis and transforming growth factor-β signaling in cartilage

Osteoarthritis is a common malady of the musculoskeletal system affecting the articular cartilage. The increased frequency of osteoarthritis with aging indicates the complex etiology of this disease, which includes pathophysiology and joint stability including biomechanics. The balance between anabolic morphogens and growth factors and catabolic cytokines is at the crux of the problem of osteoarthritis. One such signal is transforming growth factor-β (TGF-β). The impaired TGF-β signaling has been identified as a culprit in old mice in a recent article in this journal. This commentary places this discovery in the context of anabolic and catabolic signals and articular cartilage homeostasis in the joint.     

Early diagnosis to enable early treatment of pre-osteoarthritis

Osteoarthritis is a prevalent and disabling disease affecting an increasingly large swathe of the world population. While clinical osteoarthritis is a late-stage condition for which disease-modifying opportunities are limited, osteoarthritis typically develops over decades, offering a long window of time to potentially alter its course. The etiology of osteoarthritis is multifactorial, showing strong associations with highly modifiable risk factors of mechanical overload, obesity and joint injury. As such, characterization of pre-osteoarthritic disease states will be critical to support a paradigm shift from palliation of late disease towards prevention, through early diagnosis and early treatment of joint injury and degeneration to reduce osteoarthritis risk. Joint trauma accelerates development of osteoarthritis from a known point in time. Human joint injury cohorts therefore provide a unique opportunity for evaluation of pre-osteoarthritic conditions and potential interventions from the earliest stages of degeneration. This review focuses on recent advances in imaging and biochemical biomarkers suitable for characterization of the pre-osteoarthritic joint as well as implications for development of effective early treatment strategies.     

Hydroxychloroquine is associated with impaired interferon-alpha and tumor necrosis factor-alpha production by plasmacytoid dendritic cells in systemic lupus erythematosus

Osteoarthritis is a prevalent and disabling disease affecting an increasingly large swathe of the world population. While clinical osteoarthritis is a late-stage condition for which disease-modifying opportunities are limited, osteoarthritis typically develops over decades, offering a long window of time to potentially alter its course. The etiology of osteoarthritis is multifactorial, showing strong associations with highly modifiable risk factors of mechanical overload, obesity and joint injury. As such, characterization of pre-osteoarthritic disease states will be critical to support a paradigm shift from palliation of late disease towards prevention, through early diagnosis and early treatment of joint injury and degeneration to reduce osteoarthritis risk. Joint trauma accelerates development of osteoarthritis from a known point in time. Human joint injury cohorts therefore provide a unique opportunity for evaluation of pre-osteoarthritic conditions and potential interventions from the earliest stages of degeneration. This review focuses on recent advances in imaging and biochemical biomarkers suitable for characterization of the pre-osteoarthritic joint as well as implications for development of effective early treatment strategies.     

Molecular mechanisms of cartilage remodelling in osteoarthritis

Osteoarthritis (OA) is a degenerative joint disease that is characterized primarily by progressive breakdown of articular cartilage. The loss of proteoglycans, the mineralization of the extracellular matrix (ECM) and the hypertrophic differentiation of the chondrocytes constitute hallmarks of the disease. The pathogenesis of OA includes several pathways, which in single are very well investigated and partly understood, but in their complex interplay remain mainly unclear. This review summarises recent data on the underlying mechanisms, specifically with respect to cell–matrix interactions and cartilage mineralization. It points out why these findings are of importance for future OA research and for the development of novel therapeutic strategies to treat OA.     

Aging, osteoarthritis and transforming growth factor-beta signaling in cartilage

Osteoarthritis is a common malady of the musculoskeletal system affecting the articular cartilage. The increased frequency of osteoarthritis with aging indicates the complex etiology of this disease, which includes pathophysiology and joint stability including biomechanics. The balance between anabolic morphogens and growth factors and catabolic cytokines is at the crux of the problem of osteoarthritis. One such signal is transforming growth factor-beta (TGF-beta). The impaired TGF-beta signaling has been identified as a culprit in old mice in a recent article in this journal. This commentary places this discovery in the context of anabolic and catabolic signals and articular cartilage homeostasis in the joint.     

Application of <Emphasis Type="Italic">in vivo</Emphasis> micro-computed tomography in the temporal characterisation of subchondral bone architecture in a rat model of low-dose monosodium iodoacetate-induced osteoarthritis

Introduction  

Osteoarthritis (OA) is a complex, multifactorial joint disease affecting both the cartilage and the subchondral bone. Animal models of OA aid in the understanding of the pathogenesis of OA and testing suitable drugs for OA treatment. In this study we characterized the temporal changes in the tibial subchondral bone architecture in a rat model of low-dose monosodium iodoacetate (MIA)-induced OA using in vivo micro-computed tomography (CT).     

Epigenetic Regulation of Chondrocyte Catabolism and Anabolism in Osteoarthritis

Osteoarthritis (OA) is one of the most prevalent forms of joint disorder, associated with a tremendous socioeconomic burden worldwide. Various non-genetic and lifestyle-related factors such as aging and obesity have been recognized as major risk factors for OA, underscoring the potential role for epigenetic regulation in the pathogenesis of the disease. OA-associated epigenetic aberrations have been noted at the level of DNA methylation and histone modification in chondrocytes. These epigenetic regulations are implicated in driving an imbalance between the expression of catabolic and anabolic factors, leading eventually to osteoarthritic cartilage destruction. Cellular senescence and metabolic abnormalities driven by OA-associated risk factors appear to accompany epigenetic drifts in chondrocytes. Notably, molecular events associated with metabolic disorders influence epigenetic regulation in chondrocytes, supporting the notion that OA is a metabolic disease. Here, we review accumulating evidence supporting a role for epigenetics in the regulation of cartilage homeostasis and OA pathogenesis.