-
Frontiers in Medicine 2023Knee osteoarthritis (KOA) is a degenerative disease with synovial inflammation, articular surface cartilage degeneration, meniscus degeneration, ligament and muscle... (Review)
Review
Knee osteoarthritis (KOA) is a degenerative disease with synovial inflammation, articular surface cartilage degeneration, meniscus degeneration, ligament and muscle changes, subchondral bone changes, and osteophyte formation around the joint as the main pathological changes. Osteoporosis (OP) is a disease characterized by low bone mass and deterioration of the microstructure of bone tissue. KOA and OP are both geriatric diseases, and the incidence of KOA combined with OP is high, but there is a lack of specific drugs, and the major treatments are limited to drug therapy. Most traditional Chinese medicine (TCM) treatments use plant-based natural products, and they help patients obtain good clinical benefits and at the same time provide researchers with ideas to study the mechanism of disease occurrence and the relationship between the two diseases. This article summarizes the research progress of TCM monomers and TCM compounds that are frequently used to treat KOA combined with OP to provide ideas for future clinical treatments and related basic research.
PubMed: 37841009
DOI: 10.3389/fmed.2023.1254086 -
Journal of Orthopaedic Surgery and... Aug 2023The onset of OA is affected by a variety of factors, which eventually lead to the loss of cartilage in the joints, the formation of osteophytes, the loss of normal knee... (Meta-Analysis)
Meta-Analysis
PURPOSE
The onset of OA is affected by a variety of factors, which eventually lead to the loss of cartilage in the joints, the formation of osteophytes, the loss of normal knee mobility, and pain and discomfort, which seriously affects the quality of life. HUC-MSCs can promote cartilage production and have been widely used in research in the past decade. This article systematically summarizes that it is well used in basic research and clinical studies to promote inflammatory chondrogenesis in the treatment of OA. Provide a theoretical basis for clinical treatment.
PATIENTS AND METHODS
This study collected CNKI, Wanfang, PubMed, and articles related to the treatment of OA with HUC-MSCs since their publication, excluding non-basic and clinical studies such as reviews and meta-analysis. A total of 31 basic experimental studies and 12 clinical studies were included. Systematically analyze the effects of HUC-MSCs on inhibiting inflammatory factors, promoting chondrocyte production, and current clinical treatment.
RESULTS
HUC-MSCs can reduce inflammatory factors such as MMP-13, ADAMTS-5, IL-1β, IL-1, IL-6, TNF-α, induced conversion from M1 to M2 in OA to protect cartilage damage and reduce OA inflammation. Synthesize ColII, SOX9, and aggrecan at the same time to promote cartilage synthesis.
CONCLUSION
HUC-MSCs not only have typical stem cell biological characteristics, but also have rich sources and convenient material extraction. Compared with stem cells from other sources, HUC-MSCs have stronger proliferation, differentiation, and immune regulation abilities. Furthermore, there are no ethical issues associated with their use.
SAFETY
Primarily attributed to pain, the majority of individuals experience recovery within 24 h following injection. HUC-MSCs possess the ability to alleviate pain, enhance knee joint function, and potentially postpone the need for surgical intervention in both non-surgical and other cases, making them highly deserving of clinical promotion and application.
Topics: Humans; Osteoarthritis, Knee; Chondrogenesis; Quality of Life; Knee Joint; Mesenchymal Stem Cells; Umbilical Cord
PubMed: 37644595
DOI: 10.1186/s13018-023-04131-7 -
Biomaterials and Biosystems Mar 2024Osteoarthritis (OA) is a chronic musculoskeletal disorder characterized by an imbalance between (synthesis) and catabolism (degradation) in altered homeostasis of... (Review)
Review
Osteoarthritis (OA) is a chronic musculoskeletal disorder characterized by an imbalance between (synthesis) and catabolism (degradation) in altered homeostasis of articular cartilage mediated primarily by the innate immune system. OA degenerates the joints resulting in synovial hyperplasia, degradation of articular cartilage with damage of the structural and functional integrity of the cartilage extracellular matrix, subchondral sclerosis, osteophyte formation, and is characterized by chronic pain, stiffness, and loss of function. Inflammation triggered by factors like biomechanical stress is involved in the development of osteoarthritis. In OA apart from catabolic effects, anti-inflammatory anabolic processes also occur continually. There is also an underlying chronic inflammation present, not only in cartilage tissue but also within the synovium, which perpetuates tissue destruction of the OA joint. The consideration of inflammation in OA considers synovitis and/or other cellular and molecular events in the synovium during the progression of OA. In this review, we have presented the progression of joint degradation that results in OA. The critical role of inflammation in the pathogenesis of OA is discussed in detail along with the dysregulation within the cytokine networks composed of inflammatory and anti-inflammatory cytokines that drive catabolic pathways, inhibit matrix synthesis, and promote cellular apoptosis. OA pathogenesis, fluctuation of synovitis, and its clinical impact on disease progression are presented here along with the role of synovial macrophages in promoting inflammatory and destructive responses in OA. The role of interplay between different cytokines, structure, and function of their receptors in the inter-cellular signaling pathway is further explored. The effect of cytokines in the increased synthesis and release of matrix-decomposing proteolytic enzymes, such as matrix metalloproteinase (MMPs) and a disintegrin-like and metalloproteinase with thrombospondin motif (ADAMTS), is elaborated emphasizing the potential impact of MMPs on the chondrocytes, synovial cells, articular and periarticular tissues, and other immune system cells migrating to the site of inflammation. We also shed light on the pathogenesis of OA via oxidative damage particularly due to nitric oxide (NO) via its angiogenic response to inflammation. We concluded by presenting the current knowledge about the tissue inhibitors of metalloproteinases (TIMPs). Synthetic MMP inhibitors include zinc binding group (ZBG), non-ZBG, and mechanism-based inhibitors, all of which have the potential to be therapeutically beneficial in the treatment of osteoarthritis. Improving our understanding of the signaling pathways and molecular mechanisms that regulate the MMP gene expression, may open up new avenues for the creation of therapies that can stop the joint damage associated with OA.
PubMed: 38440290
DOI: 10.1016/j.bbiosy.2024.100090 -
Research (Washington, D.C.) 2024Subcellular mitochondria serve as sensors for energy metabolism and redox balance, and the dynamic regulation of functional and dysfunctional mitochondria plays a...
Subcellular mitochondria serve as sensors for energy metabolism and redox balance, and the dynamic regulation of functional and dysfunctional mitochondria plays a crucial role in determining cells' fate. Selective removal of dysfunctional mitochondria at the subcellular level can provide chondrocytes with energy to prevent degeneration, thereby treating osteoarthritis. Herein, to achieve an ideal subcellular therapy, cartilage affinity peptide (WYRGRL)-decorated liposomes loaded with mitophagy activator (urolithin A) were integrated into hyaluronic acid methacrylate hydrogel microspheres through microfluidic technology, named HM@WY-Lip/UA, that could efficiently target chondrocytes and selectively remove subcellular dysfunctional mitochondria. As a result, this system demonstrated an advantage in mitochondria function restoration, reactive oxygen species scavenging, cell survival rescue, and chondrocyte homeostasis maintenance through increasing mitophagy. In a rat post-traumatic osteoarthritis model, the intra-articular injection of HM@WY-Lip/UA ameliorated cartilage matrix degradation, osteophyte formation, and subchondral bone sclerosis at 8 weeks. Overall, this study indicated that HM@WY-Lip/UA provided a protective effect on cartilage degeneration in an efficacious and clinically relevant manner, and a mitochondrial-oriented strategy has great potential in the subcellular therapy of osteoarthritis.
PubMed: 38274127
DOI: 10.34133/research.0306 -
Materials Today. Bio Apr 2024Osteoarthritis (OA) is a chronic inflammatory joint disease characterized by progressive cartilage degeneration, synovitis, and osteoid formation. In order to...
Osteoarthritis (OA) is a chronic inflammatory joint disease characterized by progressive cartilage degeneration, synovitis, and osteoid formation. In order to effectively treat OA, it is important to block the harmful feedback caused by reactive oxygen species (ROS) produced during joint wear. To address this challenge, we have developed injectable nanocomposite hydrogels composed of polygallate-Mn (PGA-Mn) nanoparticles, oxidized sodium alginate, and gelatin. The inclusion of PGA-Mn not only enhances the mechanical strength of the biohydrogel through a Schiff base reaction with gelatin but also ensures efficient ROS scavenging ability. Importantly, the nanocomposite hydrogel exhibits excellent biocompatibility, allowing it to effectively remove ROS from chondrocytes and reduce the expression of inflammatory factors within the joint. Additionally, the hygroscopic properties of the hydrogel contribute to reduced intra-articular friction and promote the production of cartilage-related proteins, supporting cartilage synthesis. In vivo experiments involving the injection of nanocomposite hydrogels into rat knee joints with an OA model have demonstrated successful reduction of osteophyte formation and protection of cartilage from wear, highlighting the therapeutic potential of this approach for treating OA.
PubMed: 38440110
DOI: 10.1016/j.mtbio.2024.100993 -
Chemico-biological Interactions Mar 2024Knee osteoarthritis (KOA) is a chronic, disabling knee joint lesion in which degeneration and defects in articular cartilage are the most important features. Casticin...
Knee osteoarthritis (KOA) is a chronic, disabling knee joint lesion in which degeneration and defects in articular cartilage are the most important features. Casticin (CAS) is a flavonoid extracted from the Chinese herb Vitex species that has anti-inflammatory and antitumor effects. The aim of this study was to investigate the therapeutic and mechanistic effects of CAS on cartilage damage in KOA. A KOA rat model was established by anterior cruciate ligament transection (ACLT), and cartilage morphological changes were assessed by histological analysis and micro-CT scans. Subsequently, chondrocytes were treated with 10 ng/mL IL-1β to establish an OA model. CCK-8 assays and EdU assays were performed to assess the viability of CAS-treated chondrocytes. Western blotting, flow cytometry and Hoechst 33342/PI Double Stain were used to detect chondrocyte apoptosis. Western blotting, qRT‒PCR and ELISA were used to detect changes in inflammatory mediators. In addition, cartilage matrix-related indices were detected by Western blotting, qRT‒PCR and immunofluorescence (IF) analysis. Immunohistochemistry (IHC) and Western blotting were performed to detect the expression of p-PI3K, p-AKT and HIF-1α in vivo and in vitro. Micro-CT, pathological sections and related scores showed that CAS improved the alterations in bony structures and reduced cartilage damage and osteophyte formation in the ACLT model. In vivo, CAS attenuated IL-1β-induced cartilage matrix degradation, apoptosis and the inflammatory response. In addition, CAS inhibited the expression of the PI3K/AKT/HIF-1α signaling pathway in the ACLT animal model and IL-1β cell model. CAS may ameliorate cartilage damage in OA by inhibiting the PI3K/AKT/HIF-1α signaling pathway, suggesting that CAS is a potential strategy for the treatment of OA.
Topics: Rats; Animals; Proto-Oncogene Proteins c-akt; Phosphatidylinositol 3-Kinases; Osteoarthritis, Knee; Signal Transduction; Flavonoids; Interleukin-1beta; Chondrocytes; Cartilage, Articular; Disease Models, Animal
PubMed: 38309612
DOI: 10.1016/j.cbi.2024.110897 -
International Journal of Oral and... Nov 2023This study was performed to compare the diagnostic accuracy of cone beam computed tomography (CBCT) alone and magnetic resonance imaging (MRI) alone in patients with...
Is magnetic resonance imaging or cone beam computed tomography alone adequate for the radiological diagnosis of symptomatic temporomandibular joint osteoarthritis? A retrospective study.
This study was performed to compare the diagnostic accuracy of cone beam computed tomography (CBCT) alone and magnetic resonance imaging (MRI) alone in patients with clinical symptoms of temporomandibular joint osteoarthritis (TMJ-OA). Fifty-two patients (83 joints) with clinical signs of TMJ-OA were included in the study. Two examiners evaluated CBCT and MRI images. McNemar and kappa tests and Spearman's correlation analysis were applied. Radiological findings of TMJ-OA were detected in all 83 joints on CBCT or MRI . Seventy-four joints (89.2%) were positive for degenerative osseous changes on CBCT. MRI findings were positive in 50 joints (60.2%). Osseous changes were found in 22 joints, joint effusion in 30 joints, and disc perforation/degeneration in 11 joints on MRI. CBCT was more sensitive than MRI in detecting condylar erosion (P = 0.001), osteophyte (P = 0.001), and flattening (P = 0.002) and flattening of the articular eminence (P = 0.013) . Poor agreement (κ = -0.21) and weak correlations were found between CBCT and MRI. The study findings suggest that CBCT is superior to MRI in evaluating osseous changes of TMJ-OA, and that CBCT is more sensitive than MRI in detecting condylar erosion, condylar osteophyte, and flattening of the condyle and articular eminence.
PubMed: 37208280
DOI: 10.1016/j.ijom.2023.04.005 -
Osteoarthritis and Cartilage Sep 2023Osteoarthritis (OA) is a disease with sex-dependent prevalence and severity in both human and animal models. We sought to elucidate sex differences in synovitis,...
OBJECTIVE
Osteoarthritis (OA) is a disease with sex-dependent prevalence and severity in both human and animal models. We sought to elucidate sex differences in synovitis, mechanical sensitization, structural damage, bone remodeling, and the synovial transcriptome in the anterior cruciate ligament rupture (ACLR) mouse model of post-traumatic OA (PTOA).
DESIGN
Male and female 12-week-old C57/BL6J mice were randomized to Sham or noninvasive ACLR with harvests at 7d or 28d post-ACLR (n = 9 per sex in each group - Sham, 7d ACLR, 28d ACLR). Knee hyperalgesia, mechanical allodynia, and intra-articular matrix metalloproteinase (MMP) activity (via intravital imaging) were measured longitudinally. Trabecular and subchondral bone (SCB) remodeling and osteophyte formation were assessed by µCT. Histological scoring of PTOA, synovitis, and anti-MMP13 immunostaining were performed. Na1.8-Cre;tdTomato mice were used to document localization and sprouting of nociceptors. Bulk RNA-seq of synovium in Sham, 7d, and 28d post-ACLR, and contralateral joints (n = 6 per group per sex) assessed injury-induced and sex-dependent gene expression.
RESULTS
Male mice exhibited more severe joint damage at 7d and 28d and more severe synovitis at 28d, accompanied by 19% greater MMP activity, 8% lower knee hyperalgesia threshold, and 43% lower hindpaw withdrawal threshold in injured limbs compared to female injured limbs. Females had injury-induced catabolic responses in trabecular and SCB, whereas males exhibited 133% greater normalized osteophyte volume relative to females and sclerotic remodeling of trabecular and SCB. Na1.8+ nociceptor sprouting in SCB and medial synovium was induced by injury and comparable between sexes. RNA-seq of synovium demonstrated similar injury-induced transcriptomic programs between the sexes at 7d, but only female mice exhibited a transcriptomic signature indicative of synovial inflammatory resolution by 28d, whereas males had persistent pro-inflammatory, pro-fibrotic, pro-neurogenic, and pro-angiogenic gene expression.
CONCLUSION
Male mice exhibited more severe overall joint damage and pain behavior after ACLR, which was associated with persistent activation of synovial inflammatory, fibrotic, and neuroangiogenic processes, implicating persistent synovitis in driving sex differences in murine PTOA.
PubMed: 37716404
DOI: 10.1016/j.joca.2023.07.012 -
Radiographics : a Review Publication of... Dec 2023Overhead throwing, particularly in baseball, subjects the shoulder and elbow to various unique injuries. Capsular contracture following repetitive external rotation...
Overhead throwing, particularly in baseball, subjects the shoulder and elbow to various unique injuries. Capsular contracture following repetitive external rotation shifts the humeral head posterosuperiorly, predisposing to glenohumeral internal rotation deficit (GIRD), Bennett, posterosuperior internal impingement (PSI), and superior labrum anterior-posterior (SLAP) lesions. GIRD represents loss of internal rotation at the expense of external rotation. Bennett lesion represents ossification of the posteroinferior glenohumeral ligament due to repetitive traction. PSI manifests with humeral head cysts and "kissing" tears of the posterosuperior cuff and labrum. Scapular dysfunction contributes to symptoms of PSI and predisposes to labral or rotator cuff disease. "Peel-back" or SLAP lesions occur when torsional forces detach the biceps-labral anchor from the glenoid. Finally, disorders of the anterior capsule, latissimus dorsi, teres major, and subscapularis are well recognized in overhead throwers. At the elbow, injuries typically involve the medial-sided structures. The ulnar collateral ligament (UCL) is the primary static restraint to valgus stress and can be thickened, attenuated, ossified, and/or partially or completely torn. Medial epicondylitis can occur with tendinosis, partial tear, or complete rupture of the flexor-pronator mass and can accompany UCL tears and ulnar neuropathy. Posteromedial impingement (PMI) and valgus extension overload syndrome are related entities that follow abundant valgus forces during late cocking or acceleration, and deceleration. These valgus stresses wedge the olecranon into the olecranon fossa, leading to PMI, osteophytes, and intra-articular bodies. Other osseous manifestations include olecranon stress fracture and cortical thickening of the humeral shaft. RSNA, 2023 Quiz questions for this article are available in the supplemental material.
Topics: Humans; Adult; Shoulder; Elbow Injuries; Rotator Cuff; Shoulder Joint; Scapula; Shoulder Injuries; Rotator Cuff Injuries; Athletic Injuries
PubMed: 37917538
DOI: 10.1148/rg.230094