Cartilage Loss Research Articles

Articular cartilage loss is an unmitigated risk of human spaceflight.

Microgravity and space radiation are hazards of spaceflight that have deleterious effects on articular cartilage. Since it is not widely monitored or protected through dedicated countermeasures, articular cartilage loss is an unmitigated risk of human spaceflight. Spaceflight-induced cartilage loss will affect an astronaut's performance during a mission and long-term health after a mission. Addressing concerns for cartilage health will be critical to the continued safe and successful exploration of space.

β-hydroxybutyrate ameliorates osteoarthritis through activation of the ERBB3 signaling pathway in mice.

The ketogenic diet (KD) has demonstrated efficacy in ameliorating inflammation in rats with osteoarthritis (OA). However, the long-term safety of the KD and the underlying mechanism by which it delays OA remain unclear. We found that while long-term KD could ameliorate OA, it induced severe hepatic steatosis in mice. Consequently, we developed two versions of ketogenic-based diets: KD supplemented with vitamin D and intermittent KD. Both KD supplemented with vitamin D and intermittent KD effectively alleviated OA by significantly reducing the levels of inflammatory cytokines, cartilage loss, sensory nerve sprouting, and knee hyperalgesia without inducing hepatic steatosis. Furthermore, β-hydroxybutyrate (β-HB), a convenient energy carrier produced by adipocytes, could ameliorate OA without causing liver lesions. Mechanistically, β-HB enhanced chondrocyte autophagy and reduced apoptosis through the activation of Erb-B2 receptor tyrosine kinase 3 (ERBB3) signaling pathway; a pathway which was down-regulated in the articular chondrocytes from both OA patients and mice. Collectively, our findings highlighted the potential therapeutic value of β-HB and KD supplemented with vitamin D and intermittent KD approaches for managing OA.

Regulation of ferroptosis in osteoarthritis and osteoarthritic chondrocytes by typical MicroRNAs in chondrocytes

Osteoarthritis (OA) is a progressive degenerative disorder impacting bones and joints, worsened by chronic inflammation, immune dysregulation, mechanical stress, metabolic disturbances, and various other contributing factors. The complex interplay of cartilage damage, loss, and impaired repair mechanisms remains a critical and formidable aspect of OA pathogenesis. At the genetic level, multiple genes have been implicated in the modulation of chondrocyte metabolism, displaying both promotive and inhibitory roles. Recent research has increasingly focused on the influence of non-coding RNAs in the regulation of distinct cell types within bone tissue in OA. In particular, an expanding body of evidence highlights the regulatory roles of microRNAs in OA chondrocytes. This review aims to consolidate the most relevant microRNAs associated with OA chondrocytes, as identified in recent studies, and to elucidate their involvement in chondrocyte metabolic processes and ferroptosis. Furthermore, this study explores the complex regulatory interactions between long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) in OA, with an emphasis on microRNA-mediated mechanisms. Finally, critical gaps in the current research are identified, offering strategic insights to advance the understanding of OA pathophysiology and guide therapeutic developments in this field.

Development of optimized standardized extracts of Echinodorus macrophyllus for arthritis management

Ethnopharmacological relevanceEchinodorus macrophyllus is a medicinal plant traditionally used in Brazil to treat rheumatic diseases. It is listed as a priority species for the development of herbal preparations for the Brazilian Unified Health System (SUS). Previous studies have demonstrated the anti-inflammatory and antiedematogenic properties of extracts and fractions from this species, but these preparations were neither standardized nor optimized for anti-arthritis effects. Aim of studyThis study aimed to investigate the anti-inflammatory and antiarthritic effects of various standardized extracts from the aerial parts of E. macrophyllus and to outline their mechanisms of action. The goal was to define an extract suitable for future scientific validation and clinical use. Material and methodsExtracts from the aerial parts of E. macrophyllus were prepared through percolation with 96°GL ethanol (EtOH) and hydroethanolic solutions at 90%, 70%, and 50% (v/v). They were standardized based on the contents of six chemical markers quantified by UPLC-DAD. Mice with acute or chronic antigen-induced arthritis (AIA) were treated with the extracts orally. The effects were evaluated by counting total and differential inflammatory cells, measuring cytokines by ELISA, and by histological analysis with toluidine blue staining. The mechanism of selected extracts was investigated in LPS-stimulated murine chondrocytes. ResultsAll extracts, except for the 90% EtOH extract, exhibited significant anti-inflammatory activity in acute AIA, reducing the migration of total inflammatory cells, neutrophils, and monocytes to the intra-articular cavity. In chronic AIA, both the 96°GL EtOH and 70% EtOH extracts markedly reduced the migration of total inflammatory cells, neutrophils, and monocytes to the intra-articular cavity, decreased IL-1β and CXCL1 levels in the periarticular tissue, and diminished proteoglycan loss in the articular cartilage. Both extracts reduced IL-6 release and MMP-3 expression in LPS-stimulated chondrocytes. The 70% EtOH and 50% EtOH extracts showed heightened activity and higher levels of chemical markers, notably cinnamoyl-tartaric acid derivatives. ConclusionsThe standardized 70% EtOH and 50% EtOH extracts from the aerial parts of E. macrophyllus, which contain higher levels of chemical markers, exhibit potent anti-inflammatory activity and reduce proteoglycan degradation. These extracts are potentially useful for developing herbal preparations to manage arthritic conditions and should be prioritized for further studies.

Ononin delays the development of osteoarthritis by down-regulating MAPK and NF-κB pathways in rat models.

Osteoarthritis (OA) is featured as cartilage loss, joint pain and loss of labor, which the inflammatory reaction may play critical roles. Ononin is an isoflavone isolating from medicinal plants and has anti-inflammatory effects. Our study investigated the anti-inflammation response of ononin on OA. Anterior cruciate ligament transection (ACLT)-induced OA operation was used to establish research model, then treated with ononin for 8 weeks. The condition of joint injury was assessed using pathological staining. The concentration of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in serum were measured by Elisa kit. The expression of collagen II and matrix metalloproteinase 13 (MMP-13) proteins to assess cartilage metabolism level by immunohistochemistry and Western blot. We detected the expression of proteins involved in the MAPK and NF-κB signaling pathways. Finally, we used molecular docking to assess the affinity of ononin for the target proteins ERK1/2, JNK1/2, p38 and p65. Our results confirmed that ononin ameliorated cartilage impairment through histopathological analysis by improving the morphological structures and cartilage tidal lines and decreasing Osteoarthritis Research Society International (OARSI) scores in OA rats. Moreover, ononin inhibited the secretion of above factors in OA rats. Furthermore, ononin has been shown to improve cartilage content levels in OA rats. In addition, ononin inhibited the reactivity of MAPK and NF-κB pathways in OA rats. And molecular docking indicated the ligand molecules could stably bind to the proteins of above receptors. Our results demonstrated that ononin may ameliorate cartilage damage and inflammatory response in OA rats by downgrading MAPK and NF-κB pathways, thus identifying ononin as a potential novel drug to treat OA.

Outcomes associated with hip preservation using osteochondral allograft transplants and acetabular labrum reconstruction.

Osteochondral allograft (OCA) transplantation with or without labral reconstruction is considered a hip preservation surgical treatment option for young, active patients. This study aims to report early outcomes for use of OCA and labrum allograft transplants for patients treated for symptomatic femoral head chondral damage and/or acetabular labrum deficiency after implementation of a comprehensive joint restoration approach. 33 patients from a lifelong registry were included for analysis. Outcomes were compared for statistically significant (p < 0.05) differences based on graft preservation methodology (standard preservation [SP] vs. Missouri Osteochondral Preservation System [MOPS]), and based on surfaces treated (femoral head only, labrum only, or femoral head and labrum). Mean follow-up duration was 44.8 (range 12-95) months. Success was documented in 28 (84.8%) patients. For the SP cohort, successful outcomes were documented in 5 cases (50%), while all 23 MOPS cases (100%) were deemed successful at least 1 year after surgery. Hip preservation surgeries performed using MOPS grafts were associated with significantly (p = 0.001; OR = 47x) higher success rates, including significant and clinically meaningful improvements in PROMs at 1 and 2 years after surgery. Revision was performed in 2 patients in the SP cohort and failure requiring total hip arthroplasty was documented in 3 SP patients. Mean time to revision or failure was 23.6 (range 4-43) months. The surfaces treated were significantly associated with failure when comparing patients undergoing a femoral head OCA with or without labral reconstruction to those undergoing labral reconstruction only (p = 0.03; OR = 8.3x). Patients with symptomatic femoral head cartilage loss and/or irreparable acetabular labrum deficiency undergoing femoral head OCA transplantation and/or labral reconstruction with meniscus allografts using MOPS-preserved tissues experienced statistically significant and clinically meaningful improvements in pain and function through at least 2 years after surgery.

Effectiveness of Ultrasound with Isometric Quadriceps Exercise and Retro walking in Osteoarthritis

Introduction: Knee osteoarthritis is a non-inflammatory, painful and degenerative joint disease; pathologic changes in osteoarthritis involve progressive hyaline joint cartilage loss with concomitant changes in subchondral bone and development of osteophyte. About symptomatic knee osteoarthritis affect 13% of women and 10% of men aged 60 years and older. Men have a lower prevalence of knee osteoarthritis than women. The tool used to measure pain intensity, physical functions in this study is WOMAC scale and to assess the range of motion by Universal goniometer. Aim : To Evaluate the Effectiveness of Ultrasound with Isometric quadriceps exercise and retro walking in osteoarthritis of knee. Method : A Total 30 both male and female participants between 45 to 65 years of age selected from RJS Group of institute of kopargaon , Kothari hospital kopargaon by using purposive sampling method according to the inclusion criteria. The total duration of the study is 3 weeks .total 30 participants allocated into two groups A and B 15 in each group. In group A were intervention Ultrasound with isometric quadriceps exercise and group B Ultrasound with retro walking were given for 3 weeks. Pre intervention and post intervention by WOMAC score and universal goniometer were taken analyzed compared using paired’ test. RESULT: As per statistical analysis both groups shown significant improvement but group B ( Ultrasound with Retro walking )was having most significant improvement as compare to group A ( Ultrasound with Isometric quadriceps exercises). CONCLUSION : This study concluded that Ultrasound with Retro walking was effective in participants with Osteoarthritis of knee .Hence there is reduction of pain, improving range of motion at knee joint and functional mobility, Activity of daily living in participants with osteoarthritis of knee.

Fluctuation of Bone Marrow Lesions and Inflammatory MRI Markers over 2 Years and Concurrent Associations with Quantitative Cartilage Loss.

To assess whether change of semiquantitatively magnetic resonance imaging (MRI)-defined bone marrow lesions (BMLs) and inflammatory markers is associated with change in quantitatively-assessed cartilage loss in the femorotibial joint (FTJ) in knees with radiographic osteoarthritis (OA) over 24 months. Participants were included from the IMI-APPROACH and the Osteoarthritis Initiative FNIH studies. Semiquantitative MRI assessment was performed for BMLs, Hoffa- and effusion-synovitis. Quantitative cartilage thickness measurements were performed manually. Definitions of change included number of subregions with BMLs, change in sum and change in maximum increase in size. Change in Hoffa-synovitis and effusion-synovitis was categorized in addition. Between-group comparisons regarding cartilage loss in the FTJ, medial and lateral compartments were performed using analysis of variance (ANOVA). A total of 629 participants were included. Knees without any BMLs at baseline (BL) and follow-up (FU) had significantly less cartilage loss compared to the other subgroups. Change in both directions in the sum score of BMLs was associated with increased rates of cartilage loss. Maximum increase in size of BMLs was associated with increased rates of cartilage loss (FTJ increase by 2 grades -0.183 mm, 95% CI [-0.335, -0.031], by 3 grades -0.306 mm, [-0.511, -0.101]). Worsening of Hoffa-synovitis was associated with increased rates of cartilage loss. Knees without BMLs at BL and FU showed lowest rates of cartilage loss. Knees with an increase in BML size showed increased rates of concurrent cartilage loss. Approaches with the aim to inhibit BML development, avoidance of increase in size and avoidance of Hoffa-synovitis worsening may have beneficial effects on cartilage loss.

Comprehensive classification and its value of capitellar cartilage injury concomitant with radial head fracture

BackgroundThere are defects in the existing classification of capitellar cartilage injury (CCI) concomitant with radial head fracture (RHF). This study aimed to introduce a comprehensive classification of CCI and to analyze its surgical guidance value.MethodsAccording to the affected site and severity, CCI was classified into four types: Type I - partial-thickness loss of articular cartilage, Type II - full-thickness loss of articular cartilage, Type III - full-thickness loss of articular cartilage with subchondral bone loss, Type IV - full-thickness loss of articular cartilage with thin cortex loss on the border of the capitellum; Different types suggest different surgical methods. Between January 2017 and January 2023, this comprehensive CCI classification was applied in 31 operated patients with CCI concomitant with RHF. The ranges of motion (ROM), Mayo Elbow Performance Index (MEPI) score, Hospital for Special Surgery (HSS) score and visual analog scale (VAS) for pain, were used to evaluate the functional recovery of the affected limb.ResultsMason Type I-IV RHF accounted for 6.45%, 38.71%, 48.39%, and 6.45%, respectively. Type I-IV CCI accounted for 12.90%, 35.48%, 45.16% and 6.45%, respectively. There was no relationship between the CCI and RHF types (p > 0.05). At the end of the follow-up period of 11–26 months with an average of 16 months, the elbow flexion and extension ROM recovered to (147.39 ± 9.84)°, forearm rotation ROM recovered to (168.74 ± 11.70)°, MEPI score recovered to (89.19 ± 4.17), HSS score recovered to (88.74 ± 4.62), VAS score recovered to (0.50 ± 0.57), indicating significant differences compared to preoperative measurements (p < 0.05). According to the MEPI and HSS scores, the excellent and good rate of functional recovery was 100%.ConclusionDifferent types of CCI differ not only in pathology but also in treatment methods. Surgical strategy according to the comprehensive CCI classification introduced in this paper may lead to a satisfactory outcome.

Osteopontin as a biomarker for diagnosing the severity of osteoarthritis

Osteoarthritis (OA) is the most common type of arthritis. It is characterized by the loss of cartilage and pain ultimately leading to difficulty in movement. Glycoprotein osteopontin (OPN) is an essential regulator that plays a critical role in developing osteoarthritis. The study aims to determine the level of OPN in the serum of patients with OA and its correlation with the content of calcium (Ca), phosphorus (P), and magnesium (Mg). The study was conducted on 92 male and female patients aged between 30 and 65, categorized into mild, moderate, and severe groups through clinical examination and X-rays. The control group consist of 58 healthy males and females 30-65-year old. OPN was measured using the ELISA technique, and minerals were estimated using spectrophotometry. It was shown that in OA patients, OPN level increased highly significant when compared with the control group (10.7 ± 3.4 ng/ml) and depended on OA severity. In patients with severe OA, it was higher (47.5 ± 8.1 ng/ml) than in groups with moderate (14.8 ± 4.5 ng/ml) and mild (12.1 ± 3.1 ng/ml) extent of the disease. We showed a significant positive relationship between OPN and phosphorus levels and a negative significant correlation between OPN and calcium, calcium/phosphorus ratio, and magnesium. These findings underscore the potential of OPN as a valuable biomarker for diagnosing the severity of osteoarthritis and monitoring the effectiveness of treatment. Keywords: calcium, magnesium, osteoarthritis, osteopontin, phosphorus.

Advances in diagnosing osteoarthritis: clinical applications of musculoskeletal ultrasonography

Background: Osteoarthritis (OA) is the most common arthritis globally. Besides cartilage loss, all surrounding structures of the joint, including the synovium, capsule, ligament, bone, nerve, and muscle, are affected by this disease, resulting in joint failure. The traditional diagnosis of OA depends on clinical symptoms, physical examination, and radiographic findings. Ultrasonography (US), computed tomography, and magnetic resonance imaging (MRI) are imaging modalities commonly used for assessing OA.Current Concepts: US findings of OA indicate synovitis, hyaline and fibrous cartilage damage, ligament and tendon changes, and bony abnormalities. US is clinically useful because it correlates with the clinical pain index and radiographic and MRI findings, differentiates the various causes of OA pain, helps diagnose early disease, predicts prognosis, and increases the accuracy and safety of intra-articular injections in OA joints.Discussion and Conclusion: Although US has some limitations as a tool for examining whole joint structures, its use is predicted to increase in the future because it is beneficial and easily accessible for assessing OA. To produce accurate US results, the examiner should have deep anatomical knowledge and skilled practice techniques, and a clinical diagnosis should be performed based on clinical symptoms and physical examination.

MTORC2 inhibition by JR-AB2-011 improves IL-1β-induced inflammation, catabolic response, and apoptosis in human chondrocytes through IκB-α/NF-κB p65.

Osteoarthritis (OA) is a very common chronic joint condition marked by inflammation and cartilage loss. mTOR is a well-known mediator of inflammation, cell survival, and aging; however, its role in OA has not been determined. To explore the role of mTORC2 in OA-and associated pathological changes, we examined the contribution of mTORC2-mediated Akt, rictor and IκB-α/NF-κB p65 pathway in interleukin (IL)-1β-treated human chondrocytes. We focused on the protein expression of proinflammatory cytokines and catabolic and apoptotic factors, including TNF-α, IL-6, iNOS, MMP13, Bax, and caspase3, which may occur through this signalling pathway in IL-1β-treated chondrocytes. Chondrocytes were cultured and treated with either 2 ng/mL IL‑1β alone or in combination with increasing concentrations of JR-AB2-011 (50, 100, or 250 µM), a selective mTORC2 inhibitor. The protein levels of phosphorylated (p)‑Akt, Akt, rictor, p-NF-κB p65, NF-κB p65, IκB-α, p-IκB-α, iNOS, MMP13, Bax, and caspase3 were evaluated by Western blotting. In IL-1β-stimulated chondrocytes, mTORC2 activity was increased with increased phosphorylation of Akt and expression of rictor. IL-1β increased the expression of p-IκBα, p-NF-κB p65, NF-κB p65, IL-6, TNF-α, iNOS, Bax, and caspase3 proteins and decreased the expression of IκB-α. All of these IL-1β-induced alterations were prevented by JR-AB2-011. The main novel finding in the present study is that selective mTORC2 inhibition by JR-AB2-011 prevents the inflammatory, catabolic, and apoptotic responses induced by IL-1β via modulation of IκB-α/NF-κB activity. Therefore, we demonstrated a previously unknown function of mTORC2 inhibition that seems to be a potential therapeutic target for OA.

Piezo1-driven mechanotransduction as a key regulator of cartilage degradation in early osteoarthritis.

Osteoarthritis (OA) is a prevalent degenerative disease characterized by pain and cartilage damage in its later stages, while early OA is marked by the loss of cartilage's mechanical function. Recent studies suggest that Piezo1, a mechanotransducer, may contribute to cartilage degradation under abnormal physical stress. This study investigates the mechanism by which Piezo1 mediates the loss of cartilage's mechanical properties. Using rat chondrocytes cultured in a 3D in vitro model, we found that fluid flow-induced physical stress activates constitutively expressed Piezo1, leading to increased catabolic activity and apoptosis, which, in turn, disrupts the matrix structure. Ex vivo cartilage experiments further demonstrated that the mechanical stress-induced loss of cartilage's physical properties (approximately 10% reduction in relaxation modulus) is mediated by Piezo1 and depends on cell viability. Notably, Piezo1 agonists alone did not alter the mechanical behavior of cartilage tissue. In vivo, using an OA rat model induced by anterior cruciate ligament transection, we observed cartilage integrity degradation and loss of mechanical properties, which were partially mitigated by Piezo1 inhibition. RNA sequencing revealed significant modulation of the PI3K signaling and matrix regulation pathways. Collectively, this study demonstrates that Piezo1-mediated catabolic activity in chondrocytes is a key driver of the loss of cartilage's mechanical function during the relaxation phase.

Articular cartilage debridement results in short-term significant improvements in patient-reported outcomes for large areas of cartilage loss of the femur in the setting of mild to moderate knee osteoarthritis

PurposeThis study aims to evaluate patient-reported outcomes (PROs) following chondroplasty in patients with larger chondral defects (≥2 cm2) of the femur in the setting of osteoarthritis. Materials and methodsRetrospective review of patients who underwent chondroplasty of the femur. All patients were radiographically assessed to have Kellgren-Lawrence (KL) grades of 2 or 3 and had a minimum of 1-year postoperative follow-up. Areas of chondral loss were estimated by arthroscopic measurements and by MRI. PROs included the International Knee Documentation Committee, Knee Injury and Osteoarthritis Outcome Score for Joint Replacement, and the Veterans Rand-12 Item. Statistical analysis was performed using paired t tests to compare baseline and follow-up data, as well as linear regressions to correlate lesion size with symptom improvement. ResultsA total of 39 patients were included. There were 20 KL grade 2 and 19 KL grade 3 knees. At both 1- and 2-year follow-ups, significant improvements were noted in International Knee Documentation Committee (34.9 ± 13.5 preoperative, 55.6 ± 18.8 at 2 years, P = .0025), Knee Injury and Osteoarthritis Outcome Score for Joint Replacement (56.3 ± 14.7 preoperative, 64.5 ± 17.0 at 2 years, P = .0243), and Veterans Rand-12 Item Physical Component Scores (38.0 ± 12.7 preoperative, 43.8 ± 8.6 at 2 years, P = .0044). All increases exceed previously reported Minimal Clinically Important Differences. Four (10.3%) conversions to arthroplasty were noted at most recent follow-up. ConclusionsArticular cartilage debridement for large areas of cartilage loss of the femur in the setting of mild to moderate knee osteoarthritis results in significant improvements in physical function and knee-specific PROs at 1- and 2-year follow-ups.

Labral pathology predicts cartilage loss over 2 years in young adult football players: findings from the femoroacetabular impingement and hip osteoarthritis cohort study

Labral pathology predicts cartilage loss over 2 years in young adult football players: findings from the femoroacetabular impingement and hip osteoarthritis cohort study

Disuse atrophy of articular cartilage can be restored by mechanical reloading in mice

BackgroundModerate mechanical stress generated by normal joint loading and movements helps maintain the health of articular cartilage. Despite growing interest in the pathogenesis of cartilage degeneration caused by reduced mechanical stress, its reversibility by mechanical reloading is less understood. This study aimed to investigate the response of articular cartilage exposed to mechanical reloading after unloading in vivo and in vitro.Methods and resultsDisuse atrophy was induced in the knee joint cartilage of adult mice through hindlimb unloading by tail suspension. For in vivo experiments, mice were subjected to reloading with or without daily exercise intervention or surgical destabilization of the knee joint. Microcomputed tomography and histomorphometric analyses were performed on the harvested knee joints. Matrix loss and thinning of articular cartilage due to unloading were fully or partially restored by reloading, and exercise intervention enhanced the restoration. Subchondral bone density decreased by unloading and increased to above-normal levels by reloading. The severity of cartilage damage caused by joint instability was not different even with prior non-weight bearing. For in vitro experiments, articular chondrocytes isolated from the healthy or unloaded joints of the mice were embedded in agarose gel. After dynamic compression loading, the expression levels of anabolic (Sox9, Col2a1, and Acan) and catabolic (Mmp13 and Adamts5) factors of cartilage were analyzed. In chondrocytes isolated from the unloaded joints, similar to those from healthy joints, dynamic compression increased the expression of anabolic factors but suppressed the expression of catabolic factors.ConclusionThe results of this study indicate that the morphological changes in articular cartilage exposed to mechanical unloading may be restored in response to mechanical reloading by shifting extracellular matrix metabolism in chondrocytes to anabolism.

Loss of collagen content is localized near cartilage lesions on the day of injurious loading and intensified on day 12.

Joint injury can lead to articular cartilage damage, excessive inflammation, and post-traumatic osteoarthritis (PTOA). Collagen is an essential component for cartilage function, yet current literature has limited understanding of how biochemical and biomechanical factors contribute to collagen loss in injured cartilage. Our aim was to investigate spatially dependent changes in collagen content and collagen integrity of injured cartilage, with an explant model of early-stage PTOA. We subjected calf knee cartilage explants to combinations of injurious loading (INJ), interleukin-1α-challenge (IL) and physiological cyclic loading (CL). Using Fourier transform infrared microspectroscopy, collagen content (Amide I band) and collagen integrity (Amide II/1338 cm-1 ratio) were estimated on days 0 and 12 post-injury. We found that INJ led to lower collagen content near lesions compared to intact regions on day 0 (p < 0.001). On day 12, near-lesion collagen content was lower compared to day 0 (p < 0.05). Additionally, on day 12, INJ, IL, and INJ + IL groups exhibited lower collagen content along most of tissue depth compared to free-swelling control group (p < 0.05). CL groups showed higher collagen content along most of tissue depth compared to corresponding groups without CL (p < 0.05). Immunohistochemical analysis revealed higher MMP-1 and MMP-3 staining intensities localized within cell lacunae in INJ group compared to CTRL group on day 0. Our results suggest that INJ causes rapid loss of collagen content near lesions, which is intensified on day 12. Additionally, CL could mitigate the loss of collagen content at intact regions after 12 days.

Research progress in Oxford unicompartmental knee arthroplasty for partial thickness cartilage loss in medial compartment of knee joint

To summarize the research progress of Oxford unicompartmental knee arthroplasty (UKA) in treating partial thickness cartilage loss (PTCL) in the medial compartment of the knee joint, aiming to further clarify the indications and optimize the effectiveness of Oxford UKA. A comprehensive review of recent domestic and international literature on Oxford UKA for PTCL in the medial compartment of the knee joint was conducted to summarize its application and research advancements. Based on current researches, the main indication for Oxford UKA is full thinckness cartilage loss in the medial compartment of the knee joint. Although it has shown certain effectiveness in treating PTCL in the medial compartment of the knee joint, there are also reports of opposite conclusions. Therefore, there is still controversy over whether Oxford UKA can be chosen for PTCL, and the large-sample and multi-center studies are needed to further clarify the controversy. Studies indicate that accurate preoperative assessment of cartilage damage severity is crucial for selecting appropriate candidates for Oxford UKA to optimize postoperative effectiveness. Oxford UKA may represent an effective treatment for patients with PTCL in the medial compartment of the knee joint. However, strict patient selection and precise preoperative evaluation are essential to ensure surgical success and long-term effectiveness.

Effects of Glucosamine in the Temporomandibular Joint Osteoarthritis: A Review.

Osteoarthritis in the temporomandibular joint (TMJ) is a chronic disease characterized by irreversible damage to articular surfaces, including inflammation, loss of articular cartilage, and subchondral bone alterations, which would be radiographically evident only in later stages. Symptomatic slow-acting so-called nutraceutical drugs have been proposed as a treatment for osteoarthritis in comparison to non-steroidal anti-inflammatory drugs (NSAID) because of their appreciable safety profile even in long-term intake. Glucosamine, being one among them, proved highly efficient in knee osteoarthritis. However, its application in TMJ osteoarthritis dates back only to 2001 and is still inconclusive in its efficiency even with systematic reviews, in restoring the structural and functional aspects of damaged TMJ. Glucosamine, being a natural compound and also a contributor to building the matrix of articular cartilage, can be utilized effectively for TMJ osteoarthritis as an adjunct along with other conventional treatment modalities available till now, which also have moderate prognosis in most of the clinical scenarios. This review summarizes data relating to the mechanism of osteoarthritis and its management using glucosamine formulations. The beneficial effects of glucosamine on the pathophysiology of TMJ osteoarthritis are possibly due to its contribution to hyaluronic acid regulation and in establishing a proper balance between anabolism/catabolism in the articular tissues.

Degradomics defines proteolysis information flow from human knee osteoarthritis cartilage to matched synovial fluid and the contributions of secreted proteases ADAMTS5, MMP13 and CMA1 to articular cartilage breakdown

ObjectivesProteolytic cartilage extracellular matrix breakdown is a major mechanism of articular cartilage loss in osteoarthritis (OA) pathogenesis. We sought to determine the overlap of proteolytic peptides in matched knee OA cartilage and synovial fluid on a proteome-wide scale to increase the prospective biomarker repertoire and to attribute proteolytic cleavages to specific secreted proteases. DesignMatched human knee OA cartilage and synovial fluid (n=5) were analyzed by N-terminomics using Terminal Amine Isotopic Labeling of Substrates (TAILS), comprising labeling and enrichment of protein N-termini, high-resolution mass spectrometry and positional peptide mapping. Donor non-OA articular cartilage was digested with CMA1, MMP13 or ADAMTS5, and TAILS was used to identify cleavage sites, which were matched against cartilage and synovial fluid degradomes. ResultsOf over 20,000 cleaved peptides in the combined OA cartilage and synovial fluid degradomes, 677 peptides, originating from 153 proteins, were present in all cartilage and synovial fluid samples. CMA1, MMP13 and ADAMTS5 digestion of cartilage identified numerous cleavage sites for each protease and distinct cleavage site preferences. Peptides resulting from the activities of these proteases were detected in OA cartilage and synovial fluid. ConclusionsProteolytic fragments from both cartilage and circulating proteins are detectable by synovial fluid degradomics. CMA1, MMP13 and ADAMTS5 activity profiles in cartilage are distinct from each other and the previously determined HtrA1 profile. This work expands the proteolytic biomarker space for OA investigation, suggests that multiple, diverse proteases contribute to cartilage destruction, and demonstrates that their specific contributions can each be defined by multiple biomarkers.