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Nature Reviews. Rheumatology Jan 2015Chondral and osteochondral lesions due to injury or other pathology commonly result in the development of osteoarthritis, eventually leading to progressive total joint... (Review)
Review
Chondral and osteochondral lesions due to injury or other pathology commonly result in the development of osteoarthritis, eventually leading to progressive total joint destruction. Although current progress suggests that biologic agents can delay the advancement of deterioration, such drugs are incapable of promoting tissue restoration. The limited ability of articular cartilage to regenerate renders joint arthroplasty an unavoidable surgical intervention. This Review describes current, widely used clinical repair techniques for resurfacing articular cartilage defects; short-term and long-term clinical outcomes of these techniques are discussed. Also reviewed is a developmental pipeline of acellular and cellular regenerative products and techniques that could revolutionize joint care over the next decade by promoting the development of functional articular cartilage. Acellular products typically consist of collagen or hyaluronic-acid-based materials, whereas cellular techniques use either primary cells or stem cells, with or without scaffolds. Central to these efforts is the prominent role that tissue engineering has in translating biological technology into clinical products; therefore, concomitant regulatory processes are also discussed.
Topics: Biocompatible Materials; Biological Factors; Cartilage, Articular; Chondrocytes; Humans; Knee Injuries; Knee Joint; Mesenchymal Stem Cell Transplantation; Osteoarthritis; Prospective Studies; Randomized Controlled Trials as Topic; Regeneration; Tissue Engineering; Tissue Scaffolds; Wound Healing
PubMed: 25247412
DOI: 10.1038/nrrheum.2014.157 -
Clinics in Sports Medicine Jul 2017The most challenging aspects in treating articular cartilage injury include identifying the cellular and molecular mechanism(s) that lead to matrix changes and the... (Review)
Review
The most challenging aspects in treating articular cartilage injury include identifying the cellular and molecular mechanism(s) that lead to matrix changes and the differentiation and dedifferentiation behavior of chondrocytes, and understanding how they affect the structural integrity of the articular cartilage and tissue remodeling. Several treatment strategies have been proposed. A better understanding of the signaling pathways and growth and transcription factors for genes responsible for chondrogenesis is an important component in the development of new therapies to prevent cartilage degeneration or promote repair to replicate the physiologic and functional properties of the original cartilage.
Topics: Cartilage, Articular; Cell Differentiation; Chondrocytes; Chondrogenesis; Cytokines; Extracellular Matrix; Humans
PubMed: 28577703
DOI: 10.1016/j.csm.2017.02.001 -
Cell and Tissue Research Oct 2017The degradation of cartilage in the human body is impacted by aging, disease, genetic predisposition and continued insults resulting from daily activity. The burden of... (Review)
Review
The degradation of cartilage in the human body is impacted by aging, disease, genetic predisposition and continued insults resulting from daily activity. The burden of cartilage defects (osteoarthritis, rheumatoid arthritis, intervertebral disc damage, knee replacement surgeries, etc.) is daunting in light of substantial economic and social stresses. This review strives to broaden the scope of regenerative medicine and tissue engineering approaches used for cartilage repair by comparing and contrasting the anatomical and functional nature of the meniscus, articular cartilage (AC) and nucleus pulposus (NP). Many review papers have provided detailed evaluations of these cartilages and cartilage-like tissues individually but none have comprehensively examined the parallels and inconsistencies in signaling, genetic expression and extracellular matrix composition between tissues. For the first time, this review outlines the importance of understanding these three tissues as unique entities, providing a comparative analysis of anatomy, ultrastructure, biochemistry and function for each tissue. This novel approach highlights the similarities and differences between tissues, progressing research toward an understanding of what defines each tissue as distinctive. The goal of this paper is to provide researchers with the fundamental knowledge to correctly engineer the meniscus, AC and NP without inadvertently developing the wrong tissue function or biochemistry.
Topics: Animals; Biomechanical Phenomena; Cartilage, Articular; Collagen; Humans; Meniscus; Nucleus Pulposus; Regeneration; Tissue Engineering
PubMed: 28413859
DOI: 10.1007/s00441-017-2613-0 -
The Journal of Orthopaedic and Sports... Feb 2018The Orthopaedic Section of the American Physical Therapy Association (APTA) has an ongoing effort to create evidence-based practice guidelines for orthopaedic physical...
The Orthopaedic Section of the American Physical Therapy Association (APTA) has an ongoing effort to create evidence-based practice guidelines for orthopaedic physical therapy management of patients with musculoskeletal impairments described in the World Health Organization's International Classification of Functioning, Disability, and Health (ICF). The purpose of these revised clinical practice guidelines is to review recent peer-reviewed literature and make recommendations related to meniscus and articular cartilage lesions. J Orthop Sports Phys Ther. 2018;48(2):A1-A50. doi:10.2519/jospt.2018.0301.
Topics: Arthralgia; Cartilage, Articular; Humans; Knee Injuries; Mobility Limitation; Physical Therapy Modalities; Tibial Meniscus Injuries
PubMed: 29385940
DOI: 10.2519/jospt.2018.0301 -
Osteoarthritis and Cartilage Mar 2022Osteoarthritis (OA) is a multifactorial arthritic disease of weight-bearing joints concomitant with chronic and intolerable pain, loss of locomotion and impaired quality... (Review)
Review
Osteoarthritis (OA) is a multifactorial arthritic disease of weight-bearing joints concomitant with chronic and intolerable pain, loss of locomotion and impaired quality of life in the elderly population. Although the prevalence of OA increases with age, its specific mechanisms have not been elucidated and effective therapeutic disease-modifying drugs have not been developed. As essential organelles in chondrocytes, mitochondria supply energy and play vital roles in cellular metabolism, proliferation and apoptosis. Mitochondrial quality control (MQC) is the key mechanism to coordinate various mitochondrial biofunctions, primarily through mitochondrial biogenesis, dynamics, autophagy and the newly discovered mitocytosis. An increasing number of studies have revealed that a loss of MQC homeostasis contributes to the cartilage damage during the occurrence and development of OA. Several master MQC-associated signaling pathways and regulators exert chondroprotective roles in OA, while cartilage damage-related molecular mechanisms have been partially identified. In this review, we summarized known mechanisms mediated by dysregulated MQC in the pathogenesis of OA and latent bioactive ingredients and drugs for the prevention and treatment of OA through the maintenance of MQC.
Topics: Autophagy; Cartilage, Articular; Chondrocytes; Down-Regulation; Humans; Mitochondria; Osteoarthritis; Oxidative Stress; Reactive Oxygen Species; Up-Regulation
PubMed: 34715366
DOI: 10.1016/j.joca.2021.10.009 -
Sports Medicine and Arthroscopy Review Jun 2016
Topics: Cartilage Diseases; Cartilage, Articular; Humans
PubMed: 27135284
DOI: 10.1097/JSA.0000000000000114 -
Cartilage Dec 2021Since the first introduction of the MOCART (Magnetic Resonance Observation of Cartilage Repair Tissue) score, significant progress has been made with regard to surgical...
OBJECTIVE
Since the first introduction of the MOCART (Magnetic Resonance Observation of Cartilage Repair Tissue) score, significant progress has been made with regard to surgical treatment options for cartilage defects, as well as magnetic resonance imaging (MRI) of such defects. Thus, the aim of this study was to introduce the MOCART 2.0 knee score - an incremental update on the original MOCART score - that incorporates this progression.
MATERIALS AND METHODS
The volume of cartilage defect filling is now assessed in 25% increments, with hypertrophic filling of up to 150% receiving the same scoring as complete repair. Integration now assesses only the integration to neighboring native cartilage, and the severity of surface irregularities is assessed in reference to cartilage repair length rather than depth. The signal intensity of the repair tissue differentiates normal signal, minor abnormal, or severely abnormal signal alterations. The assessment of the variables "subchondral lamina," "adhesions," and "synovitis" was removed and the points were reallocated to the new variable "bony defect or bony overgrowth." The variable "subchondral bone" was renamed to "subchondral changes" and assesses minor and severe edema-like marrow signal, as well as subchondral cysts or osteonecrosis-like signal. Overall, a MOCART 2.0 knee score ranging from 0 to 100 points may be reached. Four independent readers (two expert readers and two radiology residents with limited experience) assessed the 3 T MRI examinations of 24 patients, who had undergone cartilage repair of a femoral cartilage defect using the new MOCART 2.0 knee score. One of the expert readers and both inexperienced readers performed two readings, separated by a four-week interval. For the inexperienced readers, the first reading was based on the evaluation sheet only. For the second reading, a newly introduced atlas was used as an additional reference. Intrarater and interrater reliability was assessed using intraclass correlation coefficients (ICCs) and weighted kappa statistics. ICCs were interpreted according to Koo and Li; weighted kappa statistics were interpreted according to the criteria of Landis and Koch.
RESULTS
The overall intrarater (ICC = 0.88, < 0.001) as well as the interrater (ICC = 0.84, < 0.001) reliability of the expert readers was almost perfect. Based on the evaluation sheet of the MOCART 2.0 knee score, the overall interrater reliability of the inexperienced readers was poor (ICC = 0.34, < 0.019) and improved to moderate (ICC = 0.59, = 0.001) with the use of the atlas.
CONCLUSIONS
The MOCART 2.0 knee score was updated to account for changes in the past decade and demonstrates almost perfect interrater and intrarater reliability in expert readers. In inexperienced readers, use of the atlas may improve interrater reliability and, thus, increase the comparability of results across studies.
Topics: Cartilage, Articular; Humans; Magnetic Resonance Imaging; Magnetic Resonance Spectroscopy; Reproducibility of Results; Transplantation, Autologous
PubMed: 31422674
DOI: 10.1177/1947603519865308 -
Joint Bone Spine Mar 2016Degradation of the articular cartilage is at the centre of the pathogenesis of osteoarthritis (OA), for which age is the major risk factor. Maintaining the chondrocytes... (Review)
Review
Degradation of the articular cartilage is at the centre of the pathogenesis of osteoarthritis (OA), for which age is the major risk factor. Maintaining the chondrocytes in a healthy condition appears to be an important factor for preservation of the entire cartilage and preventing its degeneration. Autophagy, which is an essential cellular homeostatic mechanism for the removal of dysfunctional cellular organelles and macromolecules, is increased by catabolic and nutritional stresses. Autophagy is increased in OA chondrocytes and cartilage, particularly during the initial degenerative phase, to regulate changes in OA-like gene expression through modulation of apoptosis and reactive oxygen species (ROS). In this way, autophagy acts as an adaptive response to protect chondrocytes from various environmental changes, while with gradual cartilage degradation, decreased autophagy is linked with cell death. Rapamycin, which is a specific inhibitor of the mTOR signaling pathway, enhances expression of autophagy regulators and prevents chondrocyte death. In the future, pharmacological activation of autophagy may be an effective therapeutic approach for OA.
Topics: Autophagy; Cartilage, Articular; Chondrocytes; Humans; Immunosuppressive Agents; Inflammation; Osteoarthritis; Sirolimus
PubMed: 26453105
DOI: 10.1016/j.jbspin.2015.06.009 -
Clinics in Sports Medicine Jul 2017Osteochondral autologous transplantation (OAT) is a treatment strategy for small and medium sized focal articular cartilage defects in the knee. This article reviews the... (Review)
Review
Osteochondral autologous transplantation (OAT) is a treatment strategy for small and medium sized focal articular cartilage defects in the knee. This article reviews the indications, surgical techniques, outcomes, and limitations of OAT for the management of symptomatic chondral and osteochondral lesions in the knee joint.
Topics: Arthroplasty; Bone Transplantation; Cartilage; Cartilage Diseases; Cartilage, Articular; Contraindications; Humans; Knee Joint; Osteoarthritis, Knee; Tissue and Organ Harvesting; Transplantation, Autologous
PubMed: 28577708
DOI: 10.1016/j.csm.2017.02.006 -
Clinics in Sports Medicine Jul 2017Articular cartilage damage remains a significant cause for early osteoarthritis in adolescents and young adults. After chondroplasty alone, the mainstay procedure for... (Review)
Review
Articular cartilage damage remains a significant cause for early osteoarthritis in adolescents and young adults. After chondroplasty alone, the mainstay procedure for cartilage injuries is microfracture. Although in small lesions this may be successful long-term, positive results of treating larger lesions this way are less certain. This inconsistency in outcomes has led to augmentation of these defects with scaffolding for autograft regeneration or for allograft cartilage to fill the defect with a hyaline cartilage. This discussion includes current techniques for the addition of scaffolding to the microfracture defect for larger lesions, the rationale, and preliminary results.
Topics: Arthroplasty, Subchondral; Bone Transplantation; Cartilage; Cartilage Diseases; Cartilage, Articular; Humans; Tissue Scaffolds; Transplantation, Autologous
PubMed: 28577709
DOI: 10.1016/j.csm.2017.02.012