Search Results (288)

Osteochondritis Dissecans (OCD) is a joint condition characterized by damage to the surface of the joint and the underlying subchondral bone, leading to early-onset osteoarthritis. It predominantly affects the knee, elbow, and ankle, with higher prevalence in juveniles actively participating in sports, which complicates the condition due to slow healing processes and prolonged restrictions on physical activities. This review aims to summarize current knowledge on OCD in athletes, with emphasis on sport-specific risk factors, diagnosis, and treatment, to support clinical decision-making and future research. We conducted searches in the PubMed and Embase databases, covering the period from 2014 to 2024. The keywords used in the search covered most common sports in combination with term osteochondritis dissecans. This review examines the impacts of various sports on the development of OCD, analyzing prevalence and risk factors, with a focus on sports-specific risks across athletic disciplines like football, basketball, baseball, and gymnastics. The significance of early detection, intervention, and sport-specific conditioning is underscored to prevent the condition and manage it effectively. Moreover, the review highlights the positive prognosis for athletes, particularly adolescents, recovering from OCD, with a high rate of return to sport. Understanding the sports-specific risks, ensuring early intervention, and adopting a cautious, stepwise return to sport are critical for managing OCD effectively, thereby safeguarding the health and careers of athletes. Full article

Introduction/Objectives: Osteoarthritis (OA) is a chronic systemic disease that affects the entire array of joint structures. It is one of the most common chronic, socially significant diseases, associated with a decline in the quality of life of patients and constantly increasing the cost of treatment. Clinical trial outcomes are largely inconclusive, and OA remains one of the few musculoskeletal diseases without an established disease-modifying therapy. One potential explanation is the use of ineffective tools for OA classification, patient stratification, and the assessment of disease progression. There is growing interest in musculoskeletal ultrasonography (MSK US), as it enables the dynamic visualization of the examined structures and gives information about both inflammatory and structural changes that have occurred. Determining the leading ultrasound phenotype, which depends on the most damaged tissue at a given time (bone, cartilage, synovial membrane, joint capsule, ligaments, tendons, menisci, etc.), can rationalize therapy use by selecting patients more suitable for specific treatments. This article aims to evaluate and summarize the potential of MSK US in the process of determining the clinical phenotype of OA and to emphasize the importance of this imaging modality in evaluating further therapeutic strategies. Method: A single-center prospective study conducted in the period of September 2023–June 2024 enrolled 259 consecutive patients with proven OA. The statistical program Minitab version 22.2.1 (2025) was used to analyze the data. The predominant and secondary phenotypes were tabulated for each OA localization and were presented numerically and as relative proportions (%). The rate of the most frequently occurring phenotypes was compared against that of the less frequent ones through paired z-tests. The initially acceptable type I error was set at 5%; it was further adjusted for the number of comparisons (Bonferroni). Results: The most frequent and predominant US phenotype for patients with knee OA was intra-articular effusion (n = 47, 37.90%). It was significantly higher compared to the rest of the US phenotypes: synovial proliferation (n = 22, 17.70%; p < 0.001), cartilage destruction (n = 26, 21%; p = 0.001), altered subchondral bone (n = 8, 6.50%; p < 0.001), extra-articular soft tissue changes (n = 12, 9.70%; p < 0.001), crystal deposits (n = 6, 4.8%; p < 0.001), and post-traumatic (n = 3, 2.40%; p < 0.001). The most common US phenotype for hip OA was altered subchondral bone (n = 32, 47.1%), with significant differences from intra-articular effusion (n = 12, 17.60%; p = 0.001), synovial proliferation (n = 5, 7.40; p = 0.001), cartilage destruction (n = 12, 17.60%; p = 0.001), extra-articular soft tissue changes (n = 3, 4.40%; p = 0.001), crystal deposits (n = 3, 4.40%; p = 0.001), and post-traumatic (n = 0). Altered subchondral bone was also the leading US phenotype for hand OA (n = 31, 55.40%), with significant differences compared to intra-articular effusion (n = 1, 1.80%; p < 0.001), synovial proliferation (n = 7, 12.50%; p < 0.001), cartilage destruction (n = 11, 19.60%; p < 0.001), extra-articular soft tissue changes (n = 2, 3.60%; p < 0.001), crystal deposits (n = 3, 5.40%; p < 0.001), and post-traumatic (n = 1, 1.80%, p < 0.001). For shoulder OA, extra-articular soft tissue changes were the most frequent (n = 8, 46.20%), followed by post-traumatic (n = 4, 30.70%), as the rate of both phenotypes was significantly higher compared to that of intra-articular effusion (n = 0), synovial proliferation (n = 0), cartilage destruction (n = 1, 7.70%; p = 0.003), and crystal deposits (n = 0). Conclusions: The therapeutic approach for OA is a dynamic and intricate process, for which the type of affected joint and the underlying pathogenetic mechanism at a specific stage of the disease’s evolution is essential. MSK US is one of the options for the clinical phenotyping of OA. Some of the suggested ultrasound subtypes may serve as the rationale for selecting a particular treatment. Full article

This study described, assessed and correlated ultrasonographic, computed tomographic, and histological findings in the sacroiliac joints of adult Warmblood horse cadavers. In total, 25 joints from 15 horses were examined post-mortem using transrectal ultrasonography and helical computed tomography. Findings on computed tomography were graded in the caudal joint third (caudally) and for the entire joint as mild, moderate, or severe. In total, 11 joints from nine horses were evaluated histologically. All joints (100%) showed abnormalities on computed tomography, and 92% (23/25) displayed abnormal ultrasonographic findings. The most common ultrasonographic findings were osteophytes (92%), joint effusion (76%), and sacral/iliac bone modeling (76%). Computed tomography revealed osteophytes (92% caudally, 100% overall), sclerosis (72% caudally, 88% overall), subchondral bone lesions (60% caudally, 88% overall), and enthesophytes (60% caudally, 68% overall). The most severe CT findings occurred caudally (44%), whereas 24% occurred cranially,16% in the mid portion of the SIJ, and 16% were multifocally present in the SIJ Histological analysis showed degenerative changes in the cartilage, subchondral bone, and the joint capsule. Horses with more pronounced imaging abnormalities also showed corresponding histological degeneration. Significant correlations were found between computed tomographic findings caudally and in the entire joint (r_s = 0.915, p < 0.001, n = 25), and between imaging and histological findings (computed tomography: r_s = 0.731, p = 0.011, n = 11; ultrasonography: r_s = 0.67, p = 0.024, n = 11). Non-significant correlations were observed between mean ultrasonographic and computed-tomographic grades (r_s = 0.35, p = 0.087, n = 25). Findings suggest these structural changes may reflect adaptation to joint loading. Transrectal ultrasonography appears suitable as a first-line diagnostic tool. However, future studies are essential to compare the diagnostic imaging findings of SIJs in asymptomatic and symptomatic horses to elucidate their clinical relevance. Full article

Background/Objectives: Osteoarthritis is a degenerative joint disease that affects people worldwide. It is characterized by joint pain, synovial inflammation, and the degradation of articular cartilage with subchondral bone. Presently, there is no known cure, and pharmacological treatment options are limited. Blueberries contain phytochemicals, which have been linked to positive health benefits and may offer therapeutic benefits. Therefore, the purpose of this study was to examine the dose-dependent effects of whole blueberries on arthritis symptoms in a monosodium iodoacetate (MIA)-induced rat model of osteoarthritis. Methods: Forty female rats were used for this study. Thirty were injected with MIA to induce joint degradation associated with osteoarthritis. Ten served as controls without MIA induction. The MIA-induced rats were randomized into three groups. All groups were fed a casein-based diet, with two of the MIA-induced groups receiving an addition of whole-blueberry powder at 5% and 10%. Fasted blood specimens and tissues of interest were collected post-euthanasia for analysis. Mechanical allodynia and joint widths were assessed throughout this study. Results: MIA induction resulted in changes in pain behaviors and the development of mechanical allodynia. The MIA injection produced inflammation, pain symptoms, and behaviors that are representative of those observed in humans with osteoarthritis. The incorporation of whole blueberries into diets reduced pain behaviors and inflammation. Conclusions: Overall, whole blueberries showed limited, non-dose-dependent effects in the MIA-induced rat model of osteoarthritis. While some outcomes improved in blueberry-treated groups, the overall results were not consistently significant. These preliminary findings suggest potential biological activity and support the further investigation of blueberries’ therapeutic efficacy. Full article

Osteoarthritis (OA) is a prevalent and disabling joint disorder characterized by progressive cartilage degradation, subchondral bone changes, synovial inflammation, and chronic pain. While traditionally attributed to mechanical and age-related factors, increasing attention has been directed toward the role of nutritional components in disease modulation. This article critically examines the emerging role of three essential trace elements, zinc, copper, and selenium, in the pathophysiology of OA. These micronutrients are fundamental to antioxidant defense, immune modulation, and extracellular matrix (ECM) integrity. Altered systemic or local levels of zinc, copper, and selenium have been associated with oxidative stress, inflammation, and dysregulated cartilage metabolism in OA. Drawing on clinical studies, in vivo and in vitro experimental models, and population-based data, we synthesize evidence on trace element status in OA patients, mechanistic pathways, and therapeutic potential, including emerging nanomedicine strategies that enhance the targeted delivery and therapeutic efficacy of trace elements in joint tissues. This review highlights the need for integrated trace element profiling in OA research and clinical care and supports the exploration of targeted nutritional interventions in OA prevention and management. Full article

Articular cartilage (AC) plays an important role in the biomechanics of synovial joints. Its task is to enable smooth movement and transfer of mechanical loads with minimised friction. AC is characterised by unique mechanical properties resulting from its complex structure, in which the dominant components are type II collagen, proteoglycans and water. Healthy articular cartilage shows elasticity in compression, viscoelastic properties, and the ability to relax stresses under the influence of cyclic loads. In response to different loading modes, it shows anisotropic and non-uniform behaviour, which translates into its cushioning and protective function for the subchondral bone. Significant changes occur in the structure and mechanical properties of cartilage with age as a result of mechanical overload or degenerative diseases, such as osteoarthritis. This results in a deterioration of the cushioning and mechanical function, which leads to progressive degradation of joint tissues. Understanding the mechanical properties of AC is crucial for developing effective diagnostic methods. Analysis of changes in mechanical properties contributes to the early detection of pathological changes. The aim of this paper is to review the current state of knowledge regarding the structure and biomechanical properties of articular cartilage, and to analyse conventional and alternative diagnostic methods in the context of their suitability for assessing the state of AC, particularly in the early stages of degenerative processes. Full article

Osteoarthritis (OA) is the most prevalent degenerative joint disorder worldwide, causing significant declines in quality of life. The osteochondral junction (OCJ), a critical structural interface between deep cartilage and subchondral bone, plays an essential role in OA progression but is challenging to assess using conventional magnetic resonance imaging (MRI) due to its short T2 relaxation times. This study aimed to evaluate the utility of ultrashort echo time (UTE) MRI biomarkers, including macromolecular fraction (MMF), magnetization transfer ratio (MTR), and T2*, for in vivo quantification of OCJ changes in knee OA for the first time. Forty-five patients (mean age: 53.8 ± 17.0 years, 50% female) were imaged using 3D UTE-MRI sequences on a 3T clinical MRI scanner. Patients were stratified into two OA groups based on radiographic Kellgren–Lawrence (KL) scores: normal/subtle (KL = 0–1) (n = 21) and mild to moderate (KL = 2–3) (n = 24). Quantitative analysis revealed significantly lower MMF (15.8  ±  1.4% vs. 13.6 ± 1.2%, p < 0.001) and MTR (42.5 ± 2.5% vs. 38.2  ±  2.3%, p < 0.001) in the higher KL 2–3 group, alongside a higher trend in T2* values (19.7  ±  2.6 ms vs. 21.6  ±  3.8 ms, p = 0.06). Moreover, MMF and MTR were significantly negatively correlated with KL grades (r = −0.66 and −0.59; p < 0.001, respectively), while T2* showed a weaker positive correlation (r = 0.26, p = 0.08). Receiver operating characteristic (ROC) analysis demonstrated superior diagnostic accuracy for MMF (AUC = 0.88) and MTR (AUC = 0.86) compared to T2* (AUC = 0.64). These findings highlight UTE-MT techniques (i.e., MMF and MTR) as promising imaging tools for detecting OCJ degeneration in knee OA, with potential implications for earlier and more accurate diagnosis and disease monitoring. Full article

Osteoarthritis (OA) is now widely recognized not merely as a cartilage-centric disease but as a multifactorial disorder affecting the entire joint as an organ, including the articular cartilage, subchondral bone, synovium, ligaments, menisci, and the innervating neural elements. This review explores the complex pathophysiology of OA with a focus on the emerging mechanisms of pain and inflammation that extend beyond articular cartilage degradation. Joint inflammation driven by immune activation in response to cellular stress signals promotes the release of pro-inflammatory mediators and catabolic enzymes. Key signaling pathways such as NF-κB, MAPKs, and JAK/STAT amplify these responses, and pain is sustained through peripheral and central sensitization, contributing to exacerbating symptoms even in the absence of visible joint damage. This review also integrates molecular and cellular mechanisms to highlight innovative therapies aimed at modifying both the structural damage and neurosensory drivers of pain. These approaches offer the potential to not only alleviate symptoms but also alter disease progression, signaling a move toward personalized, mechanism-based treatments. Given the intricate interactions among joint tissues, immune activation, and sensory processing, a comprehensive strategy that targets both structural degeneration and neuroinflammation is essential for the future of OA management. Emphasizing the joint as an integrated organ, we advocate for translational research linking molecular pathology with clinically meaningful outcomes. Full article

Understanding the complex mechanical behavior of osteochondral tissues in silico is essential for improving experimental models and advancing research in joint health and degeneration. This review provides a comprehensive analysis of the constitutive models currently used to represent the different layers of the osteochondral region, from articular cartilage to subchondral bone, including intermediate regions such as the tidemark and the calcified cartilage layer. Each layer exhibits unique structural and mechanical properties, necessitating a layer-specific modeling approach. Through critical comparison of existing mathematical models, the viscoelastic model is suggested as a pragmatic starting point for modeling articular cartilage zones, the tidemark, and the calcified cartilage layer, as it captures essential time-dependent behaviors such as creep and stress relaxation while ensuring computational efficiency for initial coupling studies. On the other hand, a linear elastic model was identified as an optimal starting point for both the subchondral bone plate and the subchondral trabecular bone, reflecting their dense and stiff nature, and providing a coherent framework for early-stage multilayer integration. This layered modeling approach enables the development of physiologically coherent and computationally efficient representations of osteochondral region modeling. Furthermore, by establishing a layer-specific modeling approach, this review paves the way for modular in silico simulations through the coupling of computational models. Such an integrative framework supports scaffold design, in vitro experimentation, preclinical validation, and the mechanobiological exploration of osteochondral degeneration and repair. These efforts are essential for deepening our understanding of tissue responses under both physiological and pathological conditions. Ultimately, this work provides a robust theoretical foundation for future in silico and in vitro studies aimed at advancing osteochondral tissue regeneration strategies. Full article

Sclerostin (SOST) is a specific osteocyte protein. During the differentiation and proliferation of osteoblasts and osteoclasts, the high expression of SOST can inhibit bone formation and contribute to osteoporosis and the bone metastasis of malignant tumors. Most of the research on SOST has focused on bone cells, but studies have found that SOST is not a specific product of bone cells but that it is also expressed by articular chondrocytes. SOST can regulate the progression of osteoarthritis in bone and cartilage, promote subchondral bone sclerosis, and inhibit cartilage degeneration. A review of the literature found that SOST can not only regulate bone metabolism, but it is also expressed in cardiovascular, kidney, liver, and other tissues, influencing the occurrence and development of diseases in these organs and tissues. Studies have found that diseases of extra-bone organs, such as atherosclerosis, aneurysm, chronic kidney disease, and cirrhosis, may be related to the expression of SOST. Simultaneously, long-term exercise can reduce SOST levels, especially in areas of high bone strain. Prolonged exercise induces bone adaptation to mechanical stress, resulting in diminished responsiveness of bone cells to exercise and a reduction in serum SOST levels. Short-term acute exercise can elevate serum SOST levels, but these results are often limited by age, gender, and energy status. In general, serum SOST rises immediately after short-term acute exercise, returning to baseline or even decreasing after exercise. Full article

Degenerative joint disease remains a leading cause of global disability, with early diagnosis posing a significant clinical challenge due to its gradual onset and symptom overlap with other musculoskeletal disorders. This review focuses on emerging diagnostic strategies by synthesizing evidence specifically from studies that integrate biochemical biomarkers, advanced imaging techniques, and machine learning models relevant to osteoarthritis. We evaluate the diagnostic utility of cartilage degradation markers (e.g., CTX-II, COMP), inflammatory cytokines (e.g., IL-1β, TNF-α), and synovial fluid microRNA profiles, and how they correlate with quantitative imaging readouts from T2-mapping MRI, ultrasound elastography, and dual-energy CT. Furthermore, we highlight recent developments in radiomics and AI-driven image interpretation to assess joint space narrowing, osteophyte formation, and subchondral bone changes with high fidelity. The integration of these datasets using multimodal learning approaches offers novel diagnostic phenotypes that stratify patients by disease stage and risk of progression. Finally, we explore the implementation of these tools in point-of-care diagnostics, including portable imaging devices and rapid biomarker assays, particularly in aging and underserved populations. By presenting a unified diagnostic pipeline, this article advances the future of early detection and personalized monitoring in joint degeneration. Full article

Objectives: Osteoarthritis (OA) is a prevalent chronic degenerative joint disorder marked by cartilage degradation, subchondral bone remodeling, and synovial inflammation. Despite its widespread occurrence, effective pharmacological interventions to halt or reverse OA progression remain elusive. Thus, an in-depth understanding of its pathogenesis is imperative for developing novel therapeutic strategies. Methods: Sixty-four male Sprague-Dawley rats (8 weeks old, weighing 180–220 g) were randomly assigned to two groups: the anterior cruciate ligament transection (ACLT) group and the sham-operated group. Primary osteoblasts were isolated from the subchondral bone at 0, 4, 8, and 12 weeks after ACLT. Nuclear magnetic resonance (NMR)-based metabolomics was used to elucidate metabolic changes and the underlying mechanisms in osteoblasts. Results: A total of 26 metabolites were identified from the NMR spectra of osteoblasts. Distinct metabolic profiles were observed in the ACLT group at 0, 4, 8, and 12 weeks after surgery. In particular, several differential metabolites were identified, including glucose, lactate, NADP⁺, phosphocreatine, and alanine, as well as eight perturbed pathways, such as alanine, aspartate, and glutamate metabolism, phenylalanine metabolism, and taurine metabolism. Conclusions: Key energy-related metabolites, including glucose, lactate, creatine phosphate, and creatine, were identified as key markers of osteoblast dysfunction in OA, underscoring the profound metabolic perturbations induced by ACL injury. These disturbances in energy homeostasis are strongly implicated in the progression of OA. In addition, branched-chain amino acids emerged as potential biomarkers, further highlighting the metabolic dysregulation associated with the disease. Taken together, the metabolic changes observed in rat osteoblasts following ACL injury reveal a complex interplay between energy and amino acid metabolism, providing critical insights into the pathogenesis of post-traumatic OA and highlighting potential therapeutic targets. Full article

Objective: The aim of this work is to investigate the impact of exercise on gut microbiome composition, serum metabolites, and their correlation with osteoarthritis (OA) severity. Methods: Thirty-six Sprague-Dawley (SD) rats were randomly divided into four groups: Sham rats without treadmill walking (Sham/Sed group, n = 9), Sham rats with treadmill walking 2 months (Sham/TW2M group, n = 9), PTOA rats without treadmill walking (PTOA/Sed group, n = 9), and PTOA rats with treadmill walking 2 months (PTOA/TW2M group, n = 9). The PTOA model was induced by transection of the anterior cruciate ligament (ACLT) and destabilization of the medial meniscus (DMM). Histological evaluation and micro-CT analysis were performed to observe the pathological changes in cartilage and subchondral bone, respectively. Additionally, we conducted 16S rDNA sequencing of fecal samples and untargeted metabolomic analysis using liquid chromatography–mass spectrometry (LC–MS) of serum samples to detect the alteration of gut microbiota composition and metabolites. Results: Exercise effectively mitigated OA-related pathological changes, including articular cartilage degeneration and subchondral bone loss. Moreover, 16S rDNA sequencing analysis of gut microbiome revealed a decreased abundance of Bacteroidetes (p < 0.01), Bacteroidia (p < 0.01), Rikenellaceae (p < 0.01), [Paraprevotellaceae] (p < 0.01), and Paraprevotella (p < 0.01) but an increase in Firmicutes (p < 0.01) in PTOA/TW2M group rats compared with PTOA/Sed group as a response to exercise. In addition, the results of metabolomics analysis showed that exercise treatment contributed to the upregulation of Daidzein and Anthranilic acid and downregulation of 1-Palmitoyllysophosphatidylcholine. Moreover, the correlation analysis showed that Rikenellaceae significantly positively correlated with both OARSI (r = 0.81, p < 0.01) and Mankin score (r = 0.83, p < 0.01) and negatively correlated with the serum level of Anthranilic acid (r = −0.56, p < 0.01) and Daidzein (r = −0.46, p < 0.01). Conclusions: Exercise can effectively mitigate OA through slowing down articular cartilage degeneration and subchondral bone loss, modulating gut microbiota composition, and increasing beneficial metabolites. Full article

Micro-computed tomography assessment of osteochondral microstructural properties of the distal femur and proximal tibia was comprehensively conducted to compare adult patients with knee rheumatoid arthritis (RA) and primary knee osteoarthritis (KOA), with special focus on the effects of knee malalignment. This study encompassed 402 bone samples divided into three groups: the RA group [patients who were subjected to total knee arthroplasty (TKA) due to RA, n = 23, age: 61 ± 10 years], the KOA group [individuals subjected to TKA due to KOA, n = 24, age: 71 ± 9 years] and the control group [sex-matched cadavers without degenerative knee diseases, n = 20, age: 67 ± 11 years]. Our data revealed that the RA, KOA, and control groups differ significantly in osteochondral microstructural properties depending on the knee alignment. Specifically, increasing femoral and tibial cortical porosity, coupled with thinner articular cartilage, were noted in the RA and KOA groups, compared to the controls. Furthermore, larger femoral and tibial cortical pores, lower tibial and femoral subchondral trabecular bone fraction, and thinner tibial articular cartilage were noted in the RA group in comparison to the KOA group, implying that the medial-to-lateral load distribution in the knee joint could be most affected in these patients. Our data illustrated that the thinnest cartilage, a thicker and less porous cortex, along with lower trabecular bone volume, were present in the lateral femoral and tibial condyles of RA individuals with valgus knee alignment. Observed subchondral trabecular microarchitectural alterations could be morphological factors contributing to different effects of surgical treatment and variable implant stability in individuals with RA, warranting further research. Full article

Osteoarthritis (OA) is a chronically progressive degenerative arthropathy characterized by the loss of cartilage, changes in subchondral architecture, and ongoing inflammation resulting in reduced mobility and pain. This study assessed the treatment potential of a combination of chondroitin and glucosamine enriched with Curcumin C3 Complex (C3GC) in modulating the pathophysiological features in mouse models with surgically induced OA and in dogs with naturally occurring OA. A cohort of 24 male C57BL/6 mice aged 3 months old were surgically destabilized with medial meniscus (DMM) to cause osteoarthritis. These animals underwent a nutritional intervention with C3GC or with GC over a course of 8 weeks. In order to evaluate cartilage health and subchondral bone structure, we carried out a combination of behavioral tests, micro-computed tomography (micro-CT), and histopathological examinations. In addition, a cohort of 12 OA-diagnosed retired police dogs were administered C3GC supplements or conventional care over a course of 30 days, with pain measurement and serum concentrations of MMP-3 and TNF-α determined before and after treatment. According to our findings, the administration of C3GC was determined to preserve subchondral microarchitectural structure integrity (p < 0.05) and resulted in better motor function in comparison with GC. In animals taking nutritional supplements, the OARSI scores of joint tissue sections were reduced, with the medial tibial plateau OARSI score being particularly low in the C3GC group (p < 0.0001). In dogs, treatment with C3GC resulted in a 24.5% reduction in serum MMP-3 levels (p < 0.01), and there was also a 20.8% decrease in serum TNF-α levels (p < 0.05), along with a decrease in subjective pain assessment. The results are in support of the chondroprotective, anti-inflammatory, and analgesic properties of C3GC and justify future research on the potential utility of C3GC in treating osteoarthritis. Full article