Cartilage in normal and osteoarthritis conditions

The preservation of articular cartilage depends on keeping the cartilage architecture intact. Cartilage strength and function depend on both the properties of the tissue and on their structural parameters. The main structural macromolecules are collagen and proteoglycans (aggrecan). During life, cartilage matrix turnover is mediated by a multitude of complex autocrine and paracrine anabolic and catabolic factors. These act on the chondrocytes and can lead to repair, remodeling or catabolic processes like those that occur in osteoarthritis. Osteoarthritis is characterized by degradation and loss of articular cartilage, subchondral bone remodeling, and, at the clinical stage of the disease, inflammation of the synovial membrane. The alterations in osteoarthritic cartilage are numerous and involve morphologic and metabolic changes in chondrocytes, as well as biochemical and structural alterations in the extracellular matrix macromolecules.     

Histone Deacetylases in Cartilage Homeostasis and Osteoarthritis

The involvement of the epigenome in complex diseases is becoming increasingly clear and more feasible to study due to new genomic and computational technologies. Moreover, therapies altering the activities of proteins that modify and interpret the epigenome are available to treat cancers and neurological disorders. Many additional uses have been proposed for these drugs based on promising preclinical results, including in arthritis models. Understanding the effects of epigenomic drugs on the skeleton is of interest because of its importance in maintaining overall health and fitness. In this review, we summarize ongoing advancements in how one class of epigenetic modifiers, histone deacetylases (Hdacs), controls normal cartilage development and homeostasis, as well as recent work aimed at understanding the alterations in the expression and activities of these enzymes in osteoarthritis (OA). We also review recent studies utilizing Hdac inhibitors and discuss the potential therapeutic benefits and limitations of these drugs for preventing cartilage destruction in OA.     

Abnormal Collagen Fibrillogenesis in Epiphyseal Cartilage of CMD (Cartilage Matrix Deficiency) Mouse

Light and electron microscopic observations on the structure of epiphyseal cartilages in the cmd/cmd mice, which had genetically failed to synthesize cartilage-characteristic proteoglycan but were normal in type II collagen synthesis, showed apparent abnormalities of collagen fibrils: e.g. increase in the diameter, appearance of periodic banding patterns and bundle-formation of collagen fibrils. These findings suggest that cartilage-characteristic proteoglycan normally limits the lateral growth of collagen fibrils and affects collagen fibrillogenesis in vivo.     

Cartilage destruction in experimentally induced osteoarthritis

Section of the anterior cruciate ligament in the knee joint of mature dogs resulted in a progressive fibrillation of both tibial and femoral condylar cartilages. Reduced tissue microhardness and increased water content preceded fibrillation while fixed charge density remained unchanged. A different histological pattern of initial fibrillation was found, however, in femoral and tibial cartilages which exhibited tangential cleft and vertical splits, respectively. Tangential fibrillation alone was associated with necrosis of superficial cells. This suggests that the mechanism of early osteoarthritic cartilage destruction varies in different articular surfaces.     

Cartilage Collagen Analysis in the Chondrodystrophies

A simple and reproducible method for analyzing small samples of cartilage collagens was developed. Following extraction with guanidine HCl, the cartilage specimens were digested directly with CNBr and the resultant peptides separated by gel-permeation high-performance liquid chromatography. Resting cartilage collagen CNBr peptide maps differed from normal in two inherited chondrodystrophies, achondrogenesis II and spondyloepiphyseal dysplasia congenita.     

Cartilage matrix in hereditary pyrophosphate arthropathy

Morphological and biochemical studies of articular cartilage were performed in 6 members of 3 families with hereditary pyrophosphate arthropathy. Evidence of metabolic disturbance of cartilage matrix was obtained from light and electron microscopic findings and by the content and composition of glycosaminoglycans.     

Decellularized Avian Cartilage,a Promising Alternative for Human Cartilage Tissue Regeneration

Articular cartilage defects, and subsequent degeneration, are prevalent and account for the poor quality of life of most elderly persons; they are also one of the main predisposing factors to osteoarthritis. Articular cartilage is an avascular tissue and, thus, has limited capacity for healing and self-repair. Damage to the articular cartilage by trauma or pathological causes is irreversible. Many approaches to repair cartilage have been attempted with some potential; however, there is no consensus on any ideal therapy. Tissue engineering holds promise as an approach to regenerate damaged cartilage. Since cell adhesion is a critical step in tissue engineering, providing a 3D microenvironment that recapitulates the cartilage tissue is vital to inducing cartilage regeneration. Decellularized materials have emerged as promising scaffolds for tissue engineering, since this procedure produces scaffolds from native tissues that possess structural and chemical natures that are mimetic of the extracellular matrix (ECM) of the native tissue. In this work, we present, for the first time, a study of decellularized scaffolds, produced from avian articular cartilage (extracted from Gallus Gallus domesticus), reseeded with human chondrocytes, and we demonstrate for the first time that human chondrocytes survived, proliferated and interacted with the scaffolds. Morphological studies of the decellularized scaffolds revealed an interconnected, porous architecture, ideal for cell growth. Mechanical characterization showed that the decellularized scaffolds registered stiffness comparable to the native cartilage tissues. Cell growth inhibition and immunocytochemical analyses showed that the decellularized scaffolds are suitable for cartilage regeneration.     

氟中毒对软骨的损伤及其机理

地方性氟中毒是一种全身性慢性疾病 ,由于长期摄入过量氟引起 ,主要侵害牙齿和骨骼 ,表现为氟斑牙和氟骨症。氟骨症的临床症状有腰部及四肢关节疼痛、活动受限、骨骼变形以致瘫痪 ,严重地危害着病区人群的健康。氟中毒对骨骼、牙齿损伤的研究很多 ,但对软骨损伤的报道较少。本文就氟中毒对软骨的损伤及其发生机理进行综述。1　氟中毒对软骨的损伤1.1　氟中毒对软骨细胞的损害 :氟中毒可引起软骨细胞坏死和成熟障碍。1981年 Rean报道饮含氟化钠 ( Na F) 12 0 mg/ L水 4 w的大鼠股骨骺板软骨细胞增多。 1991年李广生等发现 ,摄入过量氟的大…