Changes of human menisci in osteoarthritic knee joints

Katsuragawa, Yozo; Saitoh, Kiyoshi; Tanaka, Nobuhiro; Wake, Masahiro; Ikeda, Yasuko; Furukawa, Hiroshi; Tohma, Shigeto; Sawabe, Motoji; Ishiyama, Miyako; Yagishita, Saburou; Suzuki, Ryuji; Mitomi, Hiroyuki; Fukui, Naoshi

doi:10.1016/j.joca.2010.05.017

Cited by 53 publications

(45 citation statements)

References 43 publications

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“…The increased Safranin O staining with meniscus aging could represent a shift from a fibroblastic to chondrocytic phenotype during early degeneration and warrants further investigation. Our results along with biochemical data published by Herwig and Adams [15, 57] as well as gene expression studies [59] provide evidence for an accumulation of water-binding proteoglycans in aging and degenerating human menisci and these changes suggest an attempt at adaption or regeneration of the menisci [56, 58]. …”

Section: Discussionsupporting

confidence: 76%

Macroscopic and histopathologic analysis of human knee menisci in aging and osteoarthritis

Pauli

Grogan

Patil

et al. 2011

Osteoarthritis and Cartilage

318

306

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Objective Meniscus lesions following trauma or associated with osteoarthritis (OA) have been described, yet meniscus aging has not been systematically analyzed. The objectives of this study were to (i) establish standardized protocols for representative macroscopic and microscopic analysis, (ii) improve existing scoring systems, and (iii) apply these techniques to a large number of human menisci. Design Medial and lateral menisci from 107 human knees were obtained and cut in two different planes (triangle/crossection and transverse/horizontal) in three separate locations (mid portion, anterior and posterior horns). All sections included vascular and avascular regions and were graded for i) surface integrity, ii) cellularity, iii) matrix/fiber organization and collagen alignment, and iv) Safranin-O staining intensity. The cartilage in all knee compartments was also scored. Results The new macroscopic and microscopic grading systems showed high inter-reader and intra-reader intraclass correlation coefficients. The major age-related changes in menisci in joints with no or minimal OA included increased Safranin-O staining intensity, decreased cell density, the appearance of acellular zones, and evidence of mucoid degeneration with some loss of collagen fiber organization. The earliest meniscus changes occurred predominantly along the inner rim. Menisci from OA joints showed severe fibrocartilaginous separation of the matrix, extensive fraying, tears and calcification. Abnormal cell arrangements included decreased cellularity, diffuse hypercellularity along with cellular hypertrophy and abnormal cell clusters. In general, the anterior horns of both medial and lateral menisci were less affected by age and OA. Conclusions New standardized protocols and new validated grading systems allowed us to conduct a more systematic evaluation of changes in aging and OA menisci at a macroscopic and microscopic level. Several meniscus abnormalities appear to be specific to aging in the absence of significant OA. With aging the meniscal surface can be intact but abnormal matrix organization and cellularity was observed within the meniscal substance. The increased Safranin-O staining appears to represent a shift from fibroblastic to chondrocytic phenotype during aging and early degeneration.

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Section: Discussionsupporting

confidence: 76%

Macroscopic and histopathologic analysis of human knee menisci in aging and osteoarthritis

Pauli

Grogan

Patil

et al. 2011

Osteoarthritis and Cartilage

318

306

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“…The pathologic changes in the menisci in both aging and OA have similarities to changes noted in the articular cartilage, including matrix disruption, fibrillation, cell clusters, calcification and cell death (47, 48). There is significant correlation between gross morphologic changes of OA in the knee cartilage and those in the menisci from the same joints (48).…”

Section: Meniscus and Ligamentsmentioning

confidence: 91%

Osteoarthritis: A disease of the joint as an organ

Loeser¹,

Goldring²,

Scanzello³

et al. 2012

Arthritis & Rheumatism

2,379

1,949

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“…ACLT also resulted in GAG loss in the patellar cartilage that did not improve with Dex or Av-Dex treatment. Similar to articular cartilage, mechanical injuries can also alter the meniscus biomechanical properties, cause disorganisation of collagen network, tissue calcification and concomitant changes in GAG and collagen content (Katsuragawa et al , 2010; Kwok et al , 2014; Pauli et al , 2011; Sun et al , 2012). It was found that the changes in meniscus mechanical properties accompanied changes in the articular cartilage post ACLT; a significant loss (by almost a factor of two) of equilibrium and dynamic compressive stiffness in meniscus from the ACLT knee was observed at week 9, which is consistent with previous studies (Levillain et al , 2015).…”

Section: Discussionmentioning

confidence: 99%

Sustained intra-cartilage delivery of low dose dexamethasone using a cationic carrier for treatment of post traumatic osteoarthritis

Bajpayee¹,

Vega²,

Scheu³

et al. 2017

eCM

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Disease-modifying osteoarthritis drugs (DMOADs) should reach their intra-tissue target sites at optimal doses for clinical efficacy. The dense, negatively charged matrix of cartilage poses a major hindrance to the transport of potential therapeutics. In this work, electrostatic interactions were utilised to overcome this challenge and enable higher uptake, full-thickness penetration and enhanced retention of dexamethasone (Dex) inside rabbit cartilage. This was accomplished by using the positively charged glycoprotein avidin as nanocarrier, conjugated to Dex by releasable linkers. Therapeutic effects of a single intra-articular injection of low dose avidin-Dex (0.5 mg Dex) were evaluated in rabbits 3 weeks after anterior cruciate ligament transection (ACLT). Immunostaining confirmed that avidin penetrated the full cartilage thickness and was retained for at least 3 weeks. Avidin-Dex suppressed injury-induced joint swelling and catabolic gene expression to a greater extent than free Dex. It also significantly improved the histological score of cell infiltration and morphogenesis within the periarticular synovium. Micro-computed tomography confirmed the reduced incidence and volume of osteophytes following avidin-Dex treatment. However, neither treatment restored the loss of cartilage stiffness following ACLT, suggesting the need for a combinational therapy with a pro-anabolic factor for enhancing matrix biosynthesis. The avidin dose used caused significant glycosaminoglycan (GAG) loss, suggesting the use of higher Dex : avidin ratios in future formulations, such that the delivered avidin dose could be much less than that shown to affect GAGs. This charge-based delivery system converted cartilage into a drug depot that could also be employed for delivery to nearby synovium, menisci and ligaments, enabling clinical translation of a variety of DMOADs.

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Changes of human menisci in osteoarthritic knee joints

Abstract: Although the expression of major matrix components was markedly enhanced, matrix synthesis was enhanced only modestly, and the changes of matrix in human OA menisci were rather modest in the non-degenerated areas.

Cited by 53 publications

References 43 publications

Macroscopic and histopathologic analysis of human knee menisci in aging and osteoarthritis

Macroscopic and histopathologic analysis of human knee menisci in aging and osteoarthritis

Osteoarthritis: A disease of the joint as an organ

Sustained intra-cartilage delivery of low dose dexamethasone using a cationic carrier for treatment of post traumatic osteoarthritis

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