Deterioration Of Articular Cartilage Research Articles

Syndecans, Exostosins and Sulfotransferases as Potential Synovial Inflammation Moderators in Patients with Hip Osteoarthritis.

The gradual deterioration of articular cartilage was thought to be the central event in osteoarthritis (OA), but recent studies demonstrated the importance of low-grade synovitis in the progression of OA. The Syndecan (SDC) family of membrane proteoglycans is known to be involved in the regulation of inflammation, but there is limited evidence considering the role of syndecans in OA synovitis. Our study aimed to investigate the hip OA synovial membrane expression patterns of SDC1, SDC2 and SDC4, as well as exostosins and sulfotransferases (enzymes involved in the polymerisation and modification of syndecans' heparan sulphate chains). Synovial membrane samples of patients with OA (24) were divided into two groups according to their Krenn synovitis score severity. The immunohistochemical expressions of SDC1, SDC2, SDC4, EXT1, EXT2, NDST1 and NDST2 in synovial intima and subintima were then analysed and compared with the control group (patients with femoral neck fracture). According to our study, the immunoexpression of SDC1, NDST1 and EXT2 is significantly increased in the intimal cells of OA synovial membrane in patients with lower histological synovitis scores and SDC4 in patients with higher synovitis scores, in comparison with non-OA controls. The difference in the expression of SDC2 among the OA and non-OA groups was insignificant. SDC1, SDC4, NDST1 and EXT2 seem to be involved as inflammation moderators in low-grade OA synovitis and, therefore, should be further investigated as potential markers of disease progression and therapeutic goals.

A Dual Functional Bioinspired Lubricant for Osteoarthritis Treatment and Potential Prevention.

Osteoarthritis (OA), primarily characterized by the deterioration of articular cartilage, is a highly prevalent joint-disabling disease. The pathological onset and progression of OA are closely related to cartilage lubrication dysfunction and synovial inflammation. Synergistic options targeted at restorative lubrication and anti-inflammation are expected to be the most attractive candidates to treat OA and perhaps help prevent it. Herein, a bioinspired lubricant (HA/PA@Lipo) was fabricated by combining anionic hyaluronan-graft-poly(2-acrylamide-2-methylpropanesulfonic acid sodium salt) (HA/PA) with cationic liposomes (Lipo) via electrostatic interaction. HA/PA@Lipo mimicked the lubrication complex located on the outer cartilage surface and was endowed cartilage with excellent cartilage-lubricating performances. After the antioxidant gallic acid (GA) was loaded for dual functionality, HA/PA@Lipo-GA was prepared with added anti-inflammatory properties. HA/PA@Lipo-GA showed favorable biocompatibility with C28/I2 cells, inhibited the production of reactive oxygen, and regulated the expression levels of anabolic genes and proteins. The therapeutic effects of HA/PA@Lipo-GA were evaluated using a sodium iodoacetate-induced OA rat model, and the preventive effects of HA/PA@Lipo-GA were estimated in vivo. The results suggested the robust potential of HA/PA@Lipo-GA with dual functions as a candidate option for OA treatment and prevention.

A Comparative Study of Machine Learning Classifiers for Enhancing Knee Osteoarthritis Diagnosis

Knee osteoarthritis (KOA) is a leading cause of disability, particularly affecting older adults due to the deterioration of articular cartilage within the knee joint. This condition is characterized by pain, stiffness, and impaired movement, posing a significant challenge in medical diagnostics and treatment planning, especially due to the current inability for early and accurate detection or monitoring of disease progression. This research introduces a multifaceted approach employing feature extraction and machine learning (ML) to improve the accuracy of diagnosing and classifying KOA stages from radiographic images. Utilizing a dataset of 3154 knee X-ray images, this study implemented feature extraction methods such as Histogram of Oriented Gradients (HOG) with Linear Discriminant Analysis (LDA) and Min–Max scaling to prepare the data for classification. The study evaluates six ML classifiers—K Nearest Neighbors classifier, Support Vector Machine (SVM), Gaussian Naive Bayes, Decision Tree, Random Forest, and XGBoost—optimized via GridSearchCV for hyperparameter tuning within a 10-fold Stratified K-Fold cross-validation framework. An ensemble model has also been made for the already high-accuracy models to explore the possibility of enhancing the accuracy and reducing the risk of overfitting. The XGBoost classifier and the ensemble model emerged as the most efficient for multiclass classification, with an accuracy of 98.90%, distinguishing between healthy and unhealthy knees. These results underscore the potential of integrating advanced ML methodologies for the nuanced and accurate diagnosis and classification of KOA, offering new avenues for clinical application and future research in medical imaging diagnostics.

Curcuma longa L. extract exhibits anti-inflammatory and cytoprotective functions in the articular cartilage of monoiodoacetate-injected rats.

Osteoarthritis (OA), the most prevalent form of arthritis, is a degenerative joint disease marked by the progressive deterioration of articular cartilage, leading to clinical manifestations such as joint pain. This study investigated the effects of Curcuma longa L. extract (CL) containing curcumin, demethoxycurcumin, and bisdemethoxycurcumin on monosodium iodoacetate (MIA)-induced OA rats. Sprague-Dawley rats with MIA-induced OA received CL supplementation at doses of 5, 25, and 40 mg/kg body weight. CL extract administration suppressed mineralisation parameters and morphological modifications and decreased arachidonate5-lipoxygenase and leukotriene B4 levels in articular cartilage. Additionally, it decreased serum prostaglandin E2, NO, and glycosaminoglycanlevels as well as the protein expression of phosphorylated inhibitor kappa B-alpha, phosphorylated p65, cyclooxygenase-2, and inducible nitric oxide synthase in the cartilage of MIA-injected rats. Furthermore, it also reduced matrix metalloproteinases and elevated SMAD family member 3 phosphorylation, tissue inhibitor of metalloproteinases, aggrecan, collagen type I, and collagen type II levels in the articular cartilage of MIA-induced OA rats. This study's findings suggest that CL supplementation helps prevent OA development and is an effective therapy for OA.

Evaluating the Anti-Osteoarthritis Potential of Standardized Boswellia serrata Gum Resin Extract in Alleviating Knee Joint Pathology and Inflammation in Osteoarthritis-Induced Models.

Osteoarthritis is a widespread chronic degenerative disease marked by the deterioration of articular cartilage, modifications in subchondral bone, and a spectrum of symptoms, including pain, stiffness, and disability. Ultimately, this condition impairs the patient's quality of life. This study aimed to evaluate the therapeutic efficacy of standardized Boswellia serrata gum resin extract (BSRE) in a rat model of monosodium iodoacetate (MIA)-induced osteoarthritis. A total of 60 rats were allocated into six groups: normal control group (NC), osteoarthritis control (injected with MIA, OC), O + B50 (injected with MIA and treated with 50 mg/kg body weight (BW) BSRE), O + B75 (injected with MIA and treated with 75 mg/kg BW BSRE), O + B100 (injected with MIA and treated with 100 mg/kg BW BSRE), and O + M (injected with MIA and treated with 150 mg/kg BW methyl sulfonyl methane). Several parameters, including knee joint swelling, histopathological changes, and the expression of collagen type II alpha 1 (COL2A1) and aggrecan, were comprehensively assessed. Concurrently, the serum levels and mRNA expression of inflammatory mediators, cytokines, and matrix metalloproteinases (MMPs) were analyzed in both the serum and knee joint synovium. The results demonstrated that BSRE significantly mitigated knee joint swelling, cartilage destruction, and tissue deformation. Notably, BSRE administration markedly upregulated the expression of COL2A1 and aggrecan while concurrently reducing levels of nitric oxide, prostaglandin E2, leukotriene B4, interleukin (IL)-6, and tumor necrosis factor (TNF)-α. Furthermore, a substantial decrease was observed in the mRNA expression of inducible nitric oxide synthase, cyclooxygenase-2, 5-lipoxygenase, IL-6, TNF-α and MMP-3 and -13, thereby indicating promising therapeutic implications for osteoarthritis. In conclusion, BSRE exhibited anti-inflammatory properties and inhibited cartilage matrix degradation in a rat model of MIA-induced osteoarthritis, with the O + B100 group showing significant reductions in swelling and notable improvements in joint cartilage damage. These findings illuminate the preventive and therapeutic potential of BSRE for osteoarthritis treatment, emphasizing the criticality of exhaustive evaluation of novel compounds.

Articular cartilage corefucosylation regulates tissue resilience in osteoarthritis.

This study aimed to investigate the glycan structural changes that occur before histological degeneration in osteoarthritis (OA) and to determine the mechanism by which these glycan conformational changes affect cartilage degeneration. An OA model was established in rabbits using mannosidase injection, which reduced high-mannose type N-glycans and led to cartilage degeneration. Further analysis of glycome in human OA cartilage identified specific corefucosylated N-glycan expression patterns. Inhibition of N-glycan corefucosylation in mice resulted in unrecoverable cartilage degeneration, while cartilage-specific blocking of corefucosylation led to accelerated development of aging-associated and instability-induced OA models. We conclude that α1,6 fucosyltransferase is required postnatally to prevent preosteoarthritic deterioration of articular cartilage. These findings provide a novel definition of early OA and identify glyco-phenotypes of OA cartilage, which may distinguish individuals at higher risk of progression.

Articular cartilage corefucosylation regulates tissue resilience in osteoarthritis

This study aimed to investigate the glycan structural changes that occur before histological degeneration in osteoarthritis (OA) and to determine the mechanism by which these glycan conformational changes affect cartilage degeneration. An OA model was established in rabbits using mannosidase injection, which reduced high-mannose type N-glycans and led to cartilage degeneration. Further analysis of glycome in human OA cartilage identified specific corefucosylated N-glycan expression patterns. Inhibition of N-glycan corefucosylation in mice resulted in unrecoverable cartilage degeneration, while cartilage-specific blocking of corefucosylation led to accelerated development of aging-associated and instability-induced OA models. We conclude that α1,6 fucosyltransferase is required postnatally to prevent preosteoarthritic deterioration of articular cartilage. These findings provide a novel definition of early OA and identify glyco-phenotypes of OA cartilage, which may distinguish individuals at higher risk of progression.

Acupressure for Pain of Osteoarthritis : A Systematic Review

Background: Osteoarthritis can be defined as a disorder of movable joints characterized by deterioration of articular cartilage; osteophyte formation and bone remodeling; changes in periarticular tissues; and a low-grade, nonpurulent inflammation of variable degree. Acupressure is a traditional non-pharmacological intervention that promotes blood circulation and muscle activity. Purpose: This review aimed to investigate the efficacy of acupressure as a complementary therapy method for the pain of osteoarthritis. Methods: Four electronic databases were searched from PubMed, ProQuest, Scopus, and The Cochrane Library use PICO strategy. In studies comparing acupressure with sham acupuncture, no intervention, or conventional intervention was eligible for inclusion. Article study is published on 2012-2022, using English and design RCT and Quasi-experiment. Prisma analysis was used in selection process. The risk of bias in the included studies was assessed using the Joanna Briggs Institute Critical Appraisal Tools for Quasi-Experimental Studies and Randomized Controlled Trials. Results: There were 12 reports selected for review with the homogeny of knee Osteoarthritis. Outcomes were either objectively- or subjectively assessed improvements in specific pain parameters and safety for clinical use. Results showed more clinical trials with proper methodology are needed to confirm the effectiveness of acupressure for the pain of Osteoarthritis. The results of the review showed a positive effect in reducing pain level with acupressure intervention as either the main or complementary therapy. Conclusion: This systematic review shows that acupressure as a single or complementary intervention provides significant benefits in the management of Osteoarthritis. Further trials with a more rigorous design are needed to further validate and address the limitations of the current evidence.

Calcipotriol suppresses GPX4-mediated ferroptosis in OA chondrocytes by blocking the TGF-β1 pathway

Globally, tens of millions of individuals experience osteoarthritis (OA), a degenerative joint condition for which a definitive cure is currently lacking. This condition is characterized by joint inflammation and the progressive deterioration of articular cartilage. In this study, western blotting, quantitative reverse-transcription polymerase chain reaction, and immunofluorescence analysis were performed to elucidate the molecular mechanisms by which calcipotriol alleviates chondrocyte ferroptosis. The effect of calcipotriol on reactive oxygen species and lipid peroxidation levels in chondrocytes was assessed using dihydroethidium staining and the fluorescent dye BODIPY. To replicate OA, the destabilized medial meniscus model was employed, followed by the injection of calcipotriol into the knee articular cavity. Morphological analysis was conducted through hematoxylin and eosin staining, safranin O-Fast green staining, and micro-computed tomography analysis. Immunohistochemical analysis was performed to validate the effect of calcipotriol in vivo. Our results demonstrate that the expression of SOX9, col2a1, and Aggrecan, as well as MMP13 and ADAMTS5 protein expression levels, decrease upon treatment with calcipotriol in interleukin-1β stimulated chondrocytes. Despite these promising outcomes, the exact mechanism underlying calcipotriol's therapeutic effect on OA remains uncertain. We discovered that calcipotriol inhibits chondrocyte GPX4-mediated ferroptosis by suppressing the expression of transforming growth factor-β1. Furthermore, our study established an in vivo model of OA using rats with medial meniscus instability. Our experiments on rats with OA revealed that intra-articular calcipotriol injection significantly reduces cartilage degradation caused by the disease. Our findings suggest that calcipotriol can mitigate OA by impeding GPX4-mediated ferroptosis of chondrocytes, achieved through the suppression of the TGF-β1 pathway.

Impaired autophagy contributes to the aggravated deterioration of osteoarthritis articular cartilage by peroxisome proliferator-activated receptor α deficiency, associated with decreased ERK and Akt activation

BackgroundAlthough the chondroprotection of peroxisome proliferator-activated receptor α (PPARα) activation against osteoarthritis (OA) has been revealed, the regulatory mechanism of PPARα deficiency to aggravate osteoarthritic cartilage deterioration remains unclear. Here, we aimed to investigate whether and how autophagy is involved in OA pathological progression.MethodsModel of experimental OA was established using destabilization of the medial meniscus in PPARα-KO 129S4/SvJae male mice, followed by histopathological detection of articular cartilage and immunohistochemistry detection of extracellular matrix (ECM) or autophagy-related signal molecules. Meanwhile, human OA chondrocytes obtained from total knee replacement surgery patients with OA were cultured with the pretreatment of IL-1β, followed with the treatment of PPARα agonist WY14643 and the detection of related signal molecules.ResultsPPARα deficiency aggravated cartilage damage with decreased LC3B level in combination with an increase in P62 level, accompanied with reduced p-Akt and p-ERK levels in PPARα-KO mouse model of experimental OA. On the contrary, PPARα activation by WY14643 promoted ECM synthesis in IL-1β-treated human OA chondrocytes, accompanied with increased LC3B-II/I ratio and Beclin 1 level and decreased P62 and Bcl2 levels. Meanwhile, it was observed that activated ERK and Akt by PPARα activation contributed to the enhancement of autophagy and ECM synthesis in human OA chondrocytes.ConclusionsImpaired autophagy contributed to the aggravated deterioration of osteoarthritis articular cartilage by PPARα deficiency associated with the suppression of ERK and Akt, with an implication that triggering PPARα activation ought to be a potential promising therapeutic target for OA therapy.

Label-free, multi-parametric assessments of cell metabolism and matrix remodeling within human and early-stage murine osteoarthritic articular cartilage

Osteoarthritis (OA) is characterized by the progressive deterioration of articular cartilage, involving complicated cell-matrix interactions. Systematic investigations of dynamic cellular and matrix changes during OA progression are lacking. In this study, we use label-free two-photon excited fluorescence (TPEF) and second harmonic generation (SHG) imaging to assess cellular and extracellular matrix features of murine articular cartilage during several time points at early stages of OA development following destabilization of medial meniscus surgery. We detect significant changes in the organization of collagen fibers and crosslink-associated fluorescence of the superficial zone as early as one week following surgery. Such changes become significant within the deeper transitional and radial zones at later time-points, highlighting the importance of high spatial resolution. Cellular metabolic changes exhibit a highly dynamic behavior, and indicate metabolic reprogramming from enhanced oxidative phosphorylation to enhanced glycolysis or fatty acid oxidation over the ten-week observation period. The optical metabolic and matrix changes detected within this mouse model are consistent with differences identified in excised human cartilage specimens from OA and healthy cartilage specimens. Thus, our studies reveal important cell-matrix interactions at the onset of OA that may enable improved understanding of OA development and identification of new potential treatment targets.

Cardamonin alleviates chondrocytes inflammation and cartilage degradation of osteoarthritis by inhibiting ferroptosis via p53 pathway.

Osteoarthritis (OA) is a common degenerative joint disease, mainly presented by the deterioration of articular cartilage. Amounts of data demonstrated this deterioration is composed of oxidative stress, pro-inflammation and chondrocyte death events. Ferroptosis is a novel form of cell death that differs from apoptosis and autophagy, recent studies have shown that chondrocyte ferroptosis contributes to the development of osteoarthritis. Cardamonin (CAD) has been demonstrated to possess antioxidant and anti-inflammatory properties in several diseases, whether CAD may influence the OA progression is still obscure. Therefore, we aimed to determine whether CAD alleviates chondrocyte ferroptosis and its effect on OA with potential mechanism. In this study, we found that inflammation, cartilage degradation and ferroptosis induced by interleukin-1β (IL-1β) were significantly alleviated by CAD. Moreover, the administration of the ferroptosis inhibitor, Deferoxamine (DFO) reversed the inflammatory and cartilage degradation effects of IL-1β as well. Chondrocyte mitochondrial morphology and function were alleviated by both CAD and DFO. We found that CAD increased collagen II, p53, SLC7A11 GPX4 expression and decreased MMP13, iNOS, COX2 expression in chondrocytes, further investigation showed that the P53 signaling pathway was involved. In vivo, intra-articular injection of CAD significantly ameliorated cartilage damage in a rat OA model, induced collagen II and SLC7A11 expression by immunohistochemistry. Our study proves that CAD ameliorated OA cartilage degradation by regulating ferroptosis via P53 signaling pathway, suggesting a potential role of CAD in OA treatment.

Synergistic strategy constructed novel double-network scaffolds with active micro-environment pH stabilization and M2-macrophage polarization for cartilage defect repair

Due to the disorder in microenvironmental pH, the persistence in inflammation, and the incomplete structural functionality of the healing cartilage-bone interface, cartilage defect repair has become a serious issue that needs to be addressed urgently. Therefore, a promising approach for treating cartilage defects would be to create multifunctional cartilage scaffold capable of stabilizing pH in the microenvironment, reducing inflammation, and promoting healed structural integrity in joint. Herein, the cartilage scaffold (M-APUs) consisting of amino acid-based polyurethane and modified chitosan was constructed to achieve synergistic therapy through creating a congenial microenvironment, supporting stem cell adhesion and growth, and enhancing normal remodeling of the osteochondral interface. The APU features stabilizing the pH of the microenvironment during its biodegradation, providing a comfortable environment for cartilage repair. Besides, the MC could help to stabilize scaffold structure, which could be enhance the promotion of cartilage repair. The cartilage scaffold was verified in an animal model, and the results demonstrated that the M-APUs could prevent deterioration of articular cartilage and promote cartilage repair. Moreover, histologic ICRS score of healed cartilage increase significantly and the integrity of structure and functionality about joint were greatly improved. It can be speculated that the novel system constructed with the synergistic strategy could become a competitive biomaterial in cartilage damage treatment.

Injury-related cell death and proteoglycan loss in articular cartilage: Numerical model combining necrosis, reactive oxygen species, and inflammatory cytokines.

Osteoarthritis (OA) is a common musculoskeletal disease that leads to deterioration of articular cartilage, joint pain, and decreased quality of life. When OA develops after a joint injury, it is designated as post-traumatic OA (PTOA). The etiology of PTOA remains poorly understood, but it is known that proteoglycan (PG) loss, cell dysfunction, and cell death in cartilage are among the first signs of the disease. These processes, influenced by biomechanical and inflammatory stimuli, disturb the normal cell-regulated balance between tissue synthesis and degeneration. Previous computational mechanobiological models have not explicitly incorporated the cell-mediated degradation mechanisms triggered by an injury that eventually can lead to tissue-level compositional changes. Here, we developed a 2-D mechanobiological finite element model to predict necrosis, apoptosis following excessive production of reactive oxygen species (ROS), and inflammatory cytokine (interleukin-1)-driven apoptosis in cartilage explant. The resulting PG loss over 30 days was simulated. Biomechanically triggered PG degeneration, associated with cell necrosis, excessive ROS production, and cell apoptosis, was predicted to be localized near a lesion, while interleukin-1 diffusion-driven PG degeneration was manifested more globally. Interestingly, the model also showed proteolytic activity and PG biosynthesis closer to the levels of healthy tissue when pro-inflammatory cytokines were rapidly inhibited or cleared from the culture medium, leading to partial recovery of PG content. The numerical predictions of cell death and PG loss were supported by previous experimental findings. Furthermore, the simulated ROS and inflammation mechanisms had longer-lasting effects (over 3 days) on the PG content than localized necrosis. The mechanobiological model presented here may serve as a numerical tool for assessing early cartilage degeneration mechanisms and the efficacy of interventions to mitigate PTOA progression.

Eplerenone modulates the inflammatory response in monosodium iodoacetate-induced knee osteoarthritis in rats: Involvement of RANKL/OPG axis

AimsOsteoarthritis (OA) is a multifactorial degenerative disease marked by the progressive deterioration of articular cartilage with inflammation of the synovium. OA's main symptoms include pain and function loss. Monosodium Iodoacetate (MIA) experimental model is widely-used for OS induction since it produces symptoms comparable to those occurring in humans. Materials and methodsThirty-two rats were divided into four groups (n = 8). The 1st group received saline and included the normal-control rats. Groups 2–4 received intra-articular injections of MIA (3 mg/50 μL) in the rats' knee joints to induce OA. Group 2 included the MIA-control rats. Groups 3 and 4 received intra-articular MIA followed by a 14-day oral eplerenone (50 and 100 mg/kg); respectively. Key findingsIntra-articular injection of MIA in rats' knee joints caused significant inflammation and pain, elevation of Akt and ERK gene expression in knee joints along with significant alterations in the histological pictures of knee joints and OARSI scores. RANKL/OPG Axis was significantly disrupted. SignificanceEplerenone treatment produced a significant improvement in motor coordination and spontaneous locomotor activity in rats and modulated the key inflammatory mediators in OA (TNF-α, NF-κβ, and IL-6). Eplerenone also suppressed the qRT–PCR gene expression of Akt and ERK in knee joint tissues and improved the histological pictures and OARSI scores of knee joints of treated rats. Eplerenone caused a decline in RANKL concentration accompanied by a rise in OPG concentration thus modulating the RANKL/OPG Axis. Consequently, eplerenone is a candidate for OA therapy due to its potential anti-inflammatory effects.

Qualitative and Quantitative Evaluation of Morpho-Metabolic Changes in Bone Cartilage Complex of Knee Joint in Osteoarthritis Using Simultaneous 18F-NaF PET/MRI-A Pilot Study.

Background Articular cartilage (AC) loss and deterioration, as well as bone remodeling, are all symptoms of osteoarthritis (OA). As a result, an ideal imaging technique for researching OA is required, which must be sensitive to both soft tissue and bone health. Objective The aim of this study was to assess the potential of simultaneous 18F sodium fluoride (18F-NaF) positron emission tomography/magnetic resonance imaging (PET/MRI) to identify as well as classify osseous metabolic abnormalities in knee OA and to see if degenerative changes in the cartilage and bone on MRI might be correlated with subchondral 18F-NaF uptake on PET. Methods Sixteen (32 knees) volunteers with no past history of knee injury, with or without pain, were enrolled for the research from January to July 2021. The images of both knees were taken utilizing an molecular magnetic resonance (mMR) body matrix coil on a simultaneous PET/MRI biograph mMR. The acquisition was conducted after 45 minutes of intravenous infusion of 18F-NaF 185-370 MBq (5-10 mCi) over one PET bed for 40 minutes, while MRI sequences were performed simultaneously. Results All pathologies showed significantly higher maximum standardized uptake value (SUV max ) than the background. Thirty-four subchondral magic spots were identified on 18F-NaF PET without any structural alteration on MRI. Bone marrow lesions (BMLs) and osteophytes with higher MRI osteoarthritis knee score (MOAKS) score showed higher 18F-NaF uptake (grade1˂grade2˂grade3). BMLs had corresponding AC degeneration. There was discordance between grade 1 osteophytes (86.6%), sclerosis (53.7%) and grade 1 BML in cruciate ligament insertion site (91.66%); they did not have high uptake of 18F-NaF. In case of cartilage, there was significant difference between AC grades and average subchondral SUV max and T2* relaxometry (grade0˂grade1˂grade2˂grade3˂grade4). BMLs are much more metabolically active than other pathologies, while sclerosis is the least. We also found that the subchondral uptake was statistically increased in the areas of pathology: Conclusion 18F-NaF PET/MRI was able to detect knee abnormalities unseen on MRI alone and simultaneously assessed metabolic and structural markers of knee OA across multiple tissues in the joint. Thus, it is a promising tool for detection of early metabolic changes in OA.

Evaluation of the effect of platelet-rich plasma in early osteoarthritis knee using the oxford knee score: A short-term outcome

Introduction: Osteoarthritis (OA) is classically described as a noninflammatory, degenerative joint disease most commonly occurring in the elderly population. It is characterized by the deterioration of articular cartilage and by the formation of new bone at joint surfaces and margins. Our study aims at evaluating the efficacy of intra-articular platelet-rich plasma (PRP) injections in Grade I and II OA knees. Materials and Methods: A total of 46 patients with Grade I and II (Kellgren and Lawrence grading) primary OA knee were enrolled for a prospective study. Prior consent was taken for intra-articular injection of PRP from all patients. The study group was evaluated using the Oxford Knee Score (OKS) at 3 months and 6 months. Results: In our study, we found decreasing pain and improvement in activities of daily living with an increase in OKS at 3 and 6 months, follow-up indicating long-term pain relief, improvement in function, and decreased stiffness. Conclusion: Our study shows that intra-articular injection of PRP is safe and effective in treating Grade I and Grade II OA knee. We also observed improvement in daily living activities and a reduction in pain in patients with OA of the knee treated with two doses of PRP. PRP therapy is an easy, affordable, and minimally invasive treatment, which is practical to administer for treating degenerative OA of the knee with minimal associated adverse events.

Chronic Proliferative Osteoarthritis in the Horse - A Case Report

Chronic osteoarthritis of the pastern joint has a significant role in affecting the musculoskeletal system and is a recurrent cause of lameness in the equine athlete manifested by chronic lameness and thorough clinical and radiographic examination. This case report describes the evolution of chronic proliferative ossified osteoarthritis and periarthritis of the proximal interphalangeal joint of the front limb of a 12-year-old gelding. The careful clinical examination aimed to detect the site of the lesion, which is then confirmed by radiography that revealed extensive periarticular new bone formation over the proximal interphalangeal joint. This affection causes progressive deterioration of articular cartilage, accompanied by bone and soft-tissue periarticular changes. Control radiographic examination after a period of 10 months showed the extension of the lesion and the severe appearance of bone evolution and several medical approaches have been undertaken without improvement of the clinical condition of the horse. Several medical therapies are used in synergy with the palliative goal of reducing lameness and relieving pain, but most are of limited duration and do not stop the negative progression of the disease process. Once joint damage is advanced, it is difficult to remedy.

The combination of resveratrol and Bletilla striata polysaccharide decreases inflammatory markers of early osteoarthritis knee and the preliminary results on LPS-induced OA rats.

Osteoarthritis (OA) of the knee is characterized by progressive deterioration and loss of articular cartilage with associatedstructural andperformance changes in the entire joint, and current treatments for OA only aim to relieve symptoms, rather than to prevent or reverse disease progression. Recently, treatments targeting "early osteoarthritis" (EOA) have attracted attention. However, during EOA stage, chondrocytes may change behaviors to express pro-inflammatory cytokines and free radicals, which would cause detrimental effects to the synovial cavity and further cartilage wear. In this study, we combined resveratrol (Res) and Bletilla striata polysaccharide (BSP) as anti-inflammatories and antioxidants to diffuse free radicals and to alleviate inflammation from the synovial cavity both short term and long term. The current study introduced a new method for harvesting BSP from as-received Bletilla striata to achieve high yields, shortened extraction times, and maintained structure/functions. In addition, it combined Res and home-extracted BSP (Res-BSP) to alleviate oxidative stress and inflammation in a Lipopolysaccharide (LPS)-induced OA model. The gene expressions of inflammatory genes iNOs, IL-1β, IL-6, and MMP-13 were upregulated 5.7-fold, 6.5-fold, 8.6-fold, and 4.5-fold, respectively on OA-like chondrocytes and the gene expressions were significantly downregulated to 3.3-fold, 2.1-fold, 4.9-fold, and 0.1-fold, respectively, once OA-like chondrocytes were treated with Res-BSP (p < 0.05, compared with OA-like chondrocytes). The gene expressions of chondrogenic genes TGFβ1, SOX9, and type II collagen were downregulated by 0.8-fold, 2.2-fold, and 0.8-fold, respectively, based on the control group as a baseline. While it was significantly upregulated by 3.4-fold, 0.32-fold, and 0.4-fold, respectively, once OA-like chondrocytes were treated with Res-BSP. (p < 0.05, compared with OA-like chondrocytes). Finally, we elucidated the role of Res-BSP in EOA in suppressing COX-2 and activating p-Smad 2/3 and p-Erk1/2. We believe that the combination of Res and BSP has great potential as an alternative therapeutic strategy for EOA treatment in future.

Changes in Small Noncoding RNA Expression during Chondrocyte Senescence.

ObjectiveOsteoarthritis (OA) is characterized by the chronic and progressive deterioration of articular cartilage. Chondrocyte senescence could lead to a shift in the balance between extracellular matrix (ECM) component synthesis and degradation. Small noncoding RNAs (sncRNAs), including microRNAs (miRNAs), P-element-induced wimpy testis-(PIWI-) interacting RNAs (piRNAs), small nucleolar RNAs (snoRNAs), small nuclear RNAs (snRNAs), and repeat-associated siRNAs (rasiRNAs), are a class of important epigenetic molecules. We aimed to gain insights into the changes and roles of sncRNA in chondrocyte senescence.DesignHealthy mouse postnatal chondrocytes were isolated, and a replicative aging model was constructed. We used small RNA sequencing (small RNA-seq) to generate extensive small RNA data. We identified differentially expressed sncRNAs and performed tissue-specific analysis using real-time quantitative polymerase chain reaction (qRT-PCR). β-galactosidase staining was used to detect chondrocyte senescence. The results showed that the expression profiles of sncRNA in passage 5 chondrocytes were significantly different from those in passage 0 chondrocytes. The expression of sncRNA was tissue specific. We found that 40 miRNAs were upregulated and 70 miRNAs were downregulated during chondrocyte senescence, and that miR-132-5p expression inhibition prevented chondrocyte senescence. We found that 8 piRNAs were upregulated and 17 piRNAs were downregulated during chondrocyte senescence, and that piRNA piR_025576 overexpression delayed chondrocyte senescence. We found that 24 snoRNAs were upregulated and 28 snoRNAs were downregulated during chondrocyte senescence, and that snoRNA ENSMUSG00000087935 overexpression delayed chondrocyte senescence. We found that 5 snRNAs were upregulated and 6 snRNAs were downregulated during chondrocyte senescence, and that snRNA ENSMUSG00000064682 overexpression delayed chondrocyte senescence. We found that 1 rasiRNA was upregulated and 4 rasiRNAs were downregulated during chondrocyte senescence.ConclusionsThese findings might provide novel insights into OA pathogenesis and contribute to the development of candidates for targeted therapeutics in OA.