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Purpose: The purpose of this study was to compare the long-term clinical and radiological outcomes between the immediate and delayed meniscus allograft transplantation (MAT)., Methods: Nine menisci were transplanted immediately after total meniscectomy (immediate group, IM), and 10 menisci were delayed transplanted in patients with the median of 35 months (range 9-92 months) after total meniscectomy (delayed group, DE). Patient's subjective clinical outcomes including VAS, IKDC, Lysholm and Tegner scores as well as muscle strength measures were compared. Joint degeneration was evaluated by both radiographs to assess joint space width narrowing, Kellegren-Lawrence (KL) grade and MRI with T2 mapping sequences to quantitatively analyze both cartilage and meniscal allograft degeneration., Results: The median follow-up time was 10.8 years (range 10-14 years). The IKDC (IM vs DE, 89.8 vs 80.9, n.s.) and Lysholm scores (IM vs DE, 87.7 vs 78.0, n.s.) were close in two groups, while the IM group showed slightly lower VAS (IM vs DE, 0.2 vs 1.5, p = 0.031), higher Tegner score (IM vs DE, 7 vs 3.5 p = 0.021) and better quadriceps muscle strength. The IM group had less joint space narrowing (IM vs DE, 0.35 mm vs 0.71 mm, n.s.), less KL grade progression (IM vs DE, 0.6 vs 1.7, p = 0.041) on radiographs and less chondral lesions development on MRIs (Cartilage Degeneration Index, IM vs DE, 252 vs 2038, p = 0.025). All meniscal grafts exhibited degeneration by showing grade 3 signal on MRI, and 4 (4/9) in the IM group and 8 (8/10) cases in the DE group. The T2 value of cartilage and meniscal allograft in the IM group was close to that of the healthy control and was significantly lower than that of the DE group., Conclusion: Compared to the conventional delayed MAT, the immediate MAT achieved better cartilage and meniscus protection in the long-term, while its superiority in patient-reported outcomes was limited., Level of Evidence: IV., (© 2022. The Author(s) under exclusive licence to European Society of Sports Traumatology, Knee Surgery, Arthroscopy (ESSKA).)

Objective: Suppurative chondritis is a potentially devastating complication of burns to the ear. The infection and inflammation can liquify cartilage, leading to significant aesthetic deformities which are difficult to treat. This article reviews published measures for preventing post-burn chondritis., Method: A comprehensive search of all available literature up to September 2020 was performed, according to PRISMA guidelines, for studies assessing preventive measures for post-burn chondritis. Randomised controlled trials (RCT), cohort studies, case-control studies, case reports and series were eligible for inclusion., Results: A total of 10 studies, including one RCT and nine retrospective observational analyses, were included, incorporating 1369 patients with burns to the ear. The most common interventions were pressure avoidance (70%), daily cleansing (60%), topical mafenide acetate (60%) and targeted debridement (30%). Packages of measures which included pressure avoidance were the most effective, all of which achieved a chondritis incidence of <6%., Conclusion: Low-level but strong published evidence suggests that important treatment principles include prevention by pressure relief, targeted debridement, prophylactic local antibiotics, local antisepsis and the avoidance of desiccation.

Competing Interests: The authors declare no conflict of interest.

Osteoarthritis (OA), a highly prevalent chronic joint disease, involves a complex network of inflammatory mediators that not only triggers pain and cartilage degeneration but also accelerates disease progression. Traditional Chinese medicinal shenjinhuoxue mixture (SHM) shows anti-inflammatory and analgesic effects against OA with remarkable clinical efficacy. This study explored the mechanism underlying anti-OA properties of SHM and evaluated its efficacy and safety via in vivo experiments. Through network pharmacology and published literature, we identified the key active phytochemicals in SHM, including β -sitosterol, oleanolic acid, licochalcone A, quercetin, isorhamnetin, kaempferol, morusin, lupeol, and pinocembrin; the pivotal targets of which are TLR-4 and NF- κ B, eliciting anti-OA activity. These phytochemicals can enter the active pockets of TLR-4 and NF- κ B with docking score ≤ -3.86 kcal/mol, as shown in molecular docking models. By using surface plasmon resonance assay, licochalcone A and oleanolic acid were found to have good TLR-4-binding affinity. In OA rats, oral SHM at mid and high doses (8.72 g/kg and 26.2 g/kg) over 6 weeks significantly alleviated mechanical and thermal hyperalgesia ( P < 0.0001). Accordingly, the expression of inflammatory mediators (TLR-4, interleukin (IL-) 1 receptor-associated kinase 1 (IRAK1), NF- κ B-p65, tumor necrosis factor (TNF-) α , IL-6, and IL-1 β ), receptor activator of the NF- κ B ligand (RANKL), and transient receptor potential vanilloid 1 (TRPV1) in the synovial and cartilage tissue of OA rats was significantly decreased ( P < 0.05). Moreover, pathological observation illustrated amelioration of cartilage degeneration and joint injury. In chronic toxicity experiment of rats, SHM at 60 mg/kg demonstrated the safety. SHM had an anti-inflammatory effect through a synergistic combination of active phytochemicals to attenuate pain and cartilage degeneration by inhibiting TLR-4 and NF- κ B activation. This study provided the experimental foundation for the development of SHM into a more effective dosage form or new drugs for OA treatment., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2021 Xiaoqin Ma et al.)

Osteoarthritis (OA) is a degenerative disease of the articular cartilage with subchondral bone lesions. Osteoarthritis etiologies are mainly related to age, obesity, strain, trauma, joint congenital anomalies, joint deformities, and other factors. Osteoarthritis seriously affects the quality of life; however, there is no effective way to cure osteoarthritis. Aerobic exercise refers to a dynamic rhythmic exercise involving the large muscle groups of the body with aerobic metabolism. More and more evidence shows that exercise has become a useful tool for the treatment of osteoarthritis. This chapter will discuss the role of exercise in the prevention and treatment of osteoarthritis.

Sinomenine (SIN) has been shown to protect against IL-1β-induced chondrocyte apoptosis in vitro. However, the role of SIN in the anterior cruciate ligament transection (ACLT)-induced osteoarthritis (OA) mouse model and its underlying molecular mechanisms remain unclear. In the present study, the protective effect of SIN on ACLT-induced articular cartilage degeneration and IL-1β-induced chondrocyte apoptosis miR-223-3p/NLRP3 signaling regulation was investigated. Safranin O staining was performed to evaluate the pathological changes of articular cartilage. Chondrocyte apoptosis was measured with Annexin V-fluorescein isothiocyanate/polyimide (annexin V-FITC/PI) staining using flow cytometry. Gene and protein expression were detected by RT-qPCR and Western blotting, respectively. SIN administration markedly improved articular cartilage degradation in mice undergoing ACLT surgery. In addition, SIN treatment downregulated the levels of inflammatory cytokines and the protein expression of NLRP3 inflammasome components and upregulated the expression of miR-223-3p in OA mice and IL-1β-stimulated chondrocytes. In vitro, we found that NLRP3 was a direct target of miR-223-3p, and overexpression of miR-223-3p blocked IL-1β-induced apoptosis and the inflammatory response in chondrocytes. These findings indicate that miR-223-3p/NLRP3 signaling could be used as a potential target of SIN for the treatment of OA.

Objective: The aim of the study was to examine how mechanical unloading affects articular cartilage degeneration in the patellofemoral (PF) and tibiofemoral (TF) joints of a monosodium iodoacetate (MIA)-induced rat model of osteoarthritis (OA)., Design: The study involved 60 male rats. OA was induced by intra-articular injecting MIA into both knee joints. All animals were equally divided into two groups: sedentary (SE) and hindlimb unloading (HU) groups. Histopathological changes in the articular cartilage of the PF and TF joints were evaluated using the Osteoarthritis Research Society International (OARSI) score and modified Mankin score at 2 and 4 weeks after MIA injection., Results: In the SE and HU groups, representative histopathological changes in OA were detected in the PF and TF joints. The OARSI and modified Mankin scores for the PF and TF joints tended to increase over time after the injection of 0.2 mg or 1.0 mg of MIA in the SE and HU groups. Both the scores for the HU group were significantly lower than those for the SE group [OARSI score: P < 0.0001 (1.0-mg injection at 4 weeks); modified Mankin score: P = 0.0116 (0.2-mg injection at 4 weeks); P = 0.0004 and < 0.0001 (1.0-mg injection at 2 and 4 weeks, respectively)]., Conclusion: This study revealed new histological evidence that indicates that unloading condition suppresses articular cartilage degeneration and is beneficial in many areas of basal and clinical research involving OA., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Total knee arthroplasty is a commonly performed safe procedure and typically executed in severe knee arthritis, but it also triggers ischemia-reperfusion injury (IRI). More recently, microRNAs (miRs) have been reported to play a contributory role in IRI through the key signaling pathway. Hence, the current study aimed to investigate the effect and specific mechanism of microRNA-23b (miR-23b), murine double minute 4 (MDM4), and the p53 signaling pathway in IRI rat models. First, the IRI model was established, and the expression pattern of miR-23b, MDM4, and the p53 signaling pathway-related genes was characterized in cartilaginous tissues. Then, miR-23b mimics or inhibitors were applied for the elevation or the depletion of the miR-23b expression and siRNA-MDM4 for the depletion of the MDM4 expression in the articular chondrocytes. By means of immunohistochemistry, quantitative real-time polymerase chain reaction, and Western blot analysis, IRI rats exhibited increased miR-23b expression, activated p53 signaling pathway, and decreased MDM4 expression. MDM4 was verified as a target gene of miR-23b through. Downregulated miR-23b increased the expression of MDM4, AKT, and Bcl-2, but decreased the expression of p53, p21, and Bax. In addition, a series of cell experiments demonstrated that downregulated miR-23b promoted articular chondrocyte proliferation and cell cycle entry, but inhibited articular chondrocyte apoptosis. The absence of the effects of miR-23b was observed after MDM4 knocked down. Our results indicate that silencing miR-23b could act to attenuate IRI and reduce the apoptosis of articular chondrocytes through inactivation of the p53 signaling pathway by upregulating MDM4, which provide basic therapeutic considerations for a novel target against IRI., (© 2018 Wiley Periodicals, Inc.)

Purpose: To evaluate the association between surgical timing and the incidence of secondary meniscal or chondral damage in children and adolescents with anterior cruciate ligament (ACL) ruptures., Methods: Three electronic databases, PubMed, MEDLINE, and EMBASE, were systematically searched from database inception until October 16, 2017 by two reviewers independently and in duplicate. The inclusion criteria were English language studies that reported the incidence of meniscal and articular cartilage damage in children or adolescent athletes with ACL injuries as well as the timing of their ACL reconstruction (ACLR). Risk ratios were combined in a meta-analysis using a random effects model., Results: A total of nine studies including 1353 children and adolescents met the inclusion criteria. The mean age of patients included was 14.2 years (range 6-19), and 45% were female. There was a significantly decreased risk of concomitant medial meniscal injury in those reconstructed early (26%) compared to those with delayed reconstruction (47%) [pooled risk ratio (RR) = 0.49, 95% CI 0.36-0.65, p < 0.00001]. There was also a significantly reduced risk of medial femoral chondral (RR = 0.48, 95% CI 0.31-0.75, p = 0.001), lateral femoral chondral (RR = 0.38, 95% CI 0.20-0.75, p = 0.005), tibial chondral (RR = 0.45, 95% CI 0.27-0.75, p = 0.002), and patellofemoral chondral (RR = 0.41, 95% CI 0.20-0.82, p = 0.01) damage in the early reconstruction group in comparison to the delayed group., Conclusion: Pooled results from observational studies suggest that early ACLR results in a significantly decreased risk of secondary medial meniscal injury, as well as secondary medial, lateral, and patellofemoral compartment chondral damage in children and adolescents. This study provides clinicians with valuable information regarding the benefits of early ACL reconstruction in children and adolescents, and can be used in the decision making for athletes in this population., Level of Evidence: IV.

Background and Objective: Rheumatoid arthritis (RA) is a predominant inflammatory autoimmune disorder. The incidence and prevalence of RA is increasing with considerable morbidity and mortality worldwide. The pathophysiology of RA has become clearer due to many significant research outputs during the last two decades. Many inflammatory cytokines involved in RA pathophysiology and the presence of autoantibodies are being used as potential biomarkers via the use of effective diagnostic techniques for the early diagnosis of RA. Currently, several disease-modifying anti-rheumatic drugs are being prescribed targeting RA pathophysiology, which have shown significant contributions in improving the disease outcomes., Discussion: Even though innovations in treatment strategies and monitoring are helping the patients to achieve early and sustained clinical and radiographic remission, the high cost of drugs and limited health care budgets are restricting the easy access of RA treatment. Both direct and indirect high cost of treatment are creating economic burden for the patients and affecting their quality of life., Conclusion: The aim of this review is to describe the updated concept of RA pathophysiology and highlight current diagnostic tools used for the early detection as well as prognosis - targeting several biomarkers of RA. Additionally, we explored the updated treatment options with side effects besides discussing the global economic burden., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)

Objective The objective of this study was to determine whether intra-articular injections of tenascin-C (TNC) could prevent cartilage damage in murine models of osteoarthritis (OA). Design Fluorescently labeled TNC was injected into knee joints and its distribution was examined at 1 day, 4 days, 1 week, 2 weeks, and 4 weeks postinjection. To investigate the effects of TNC on cartilage degeneration after surgery to knee joints, articular spaces were filled with 100 μg/mL (group I), 10 μg/mL (group II) of TNC solution, or control (group III). TNC solution of 10 μg/mL was additionally injected twice after 3 weeks (group IV) or weekly after 1 week, 2 weeks, and 3 weeks (group V). Joint tissues were histologically assessed using the Mankin score and the modified Chambers system at 2 to 8 weeks after surgery. Results Exogenous TNC was maintained in the cartilage and synovium for 1 week after administration. Histological scores in groups I and II were better than scores in group III at 4 and 6 weeks, but progressive cartilage damage was seen in all groups 8 weeks postoperatively. Sequential TNC injections (groups IV and V) showed significantly better Mankin score than single injection (group II) at 8 weeks. Conclusion TNC administered exogenously remained in the cartilage of knee joints for 1 week, and could decelerate articular cartilage degeneration in murine models of OA. We also showed that sequential administration of TNC was more effective than a single injection. TNC could be an important molecule for prevention of articular cartilage damage.

Hyperglycemia-induced cartilage degeneration induces osteoarthritis (OA). Since oleanolic acid (OLA) have several pharmacological effects such as anti-inflammatory, anti-oxidant, we hypothesized it possesses protection against high glucose injured cartilage. We now report that OLA decreased type X collagen and reversed the cartilage degeneration in growth plate from db/db mice. OLA increased type Ⅱ collagen expression in a concentration-dependent manner (10-50 μΜ) in high glucose-treated chondrocytes. OLA prevented the high glucose induced cell injury and decreased the level of MMP-13, PGE2 and IL-6 due to decreasing mitochondrial membrane potential and stimulated the ATP production. Moreover, OLA treatment inhibited apoptosis. And the reversed SOD2 expression and activity may be ascribed to decreased SOD2 protein degradation by OLA treatment, via PPPAγ. In conclusion, OLA protected against the high-glucose-induced cartilage injury via PPARγ/SOD2 pathway., (Copyright © 2017 Elsevier Inc. All rights reserved.)

This study compared patients who failed a cartilage restoration procedure and underwent ipsilateral knee arthroplasty with matched control subjects undergoing knee arthroplasty without prior cartilage restoration. Although patients with a failed cartilage procedure derived benefit from knee arthroplasty, their magnitude of improvement and final outcomes scores were lower than the matched control subjects. In this cohort, the cartilage patients also experienced little to no benefit from cartilage restoration, suggesting that unmeasured shared patient characteristics may play a role. This information can be used to counsel this difficult patient population on expected outcomes following arthroplasty procedures. Further research identifying characteristics of responders to treatment remains critical to refine clinical decision-making for this difficult patient group., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Background: Arthropathy is a prevalent and invalidating complication of acromegaly with a characteristic radiographic phenotype. We aimed to further characterize cartilage and bone abnormalities associated with acromegalic arthropathy using magnetic resonance imaging (MRI)., Methods: Twenty-six patients (23% women, mean age 56.8 ± 13.4 years), with active ( n  = 10) and controlled acromegaly ( n  = 16) underwent a 3.0 T MRI of the right knee. Osteophytes, cartilage defects, bone marrow lesions and subchondral cysts were assessed by the Knee Osteoarthritis Scoring System (KOSS) method. Cartilage thickness and cartilage T2 relaxation times, in which higher values reflect increased water content and/or structural changes, were measured. Twenty-five controls (52% women, mean age: 59.6 ± 8.0 years) with primary knee OA were included for comparison., Results: Both in active and controlled acromegaly, structural OA defects were highly prevalent, with thickest cartilage and highest cartilage T2 relaxation times in the active patients. When compared to primary OA subjects, patients with acromegaly seem to have less cysts (12% vs 48%, P  = 0.001) and bone marrow lesions (15% vs 80%, P  = 0.006), but comparable prevalence of osteophytosis and cartilage defects. Patients with acromegaly had 31% thicker total joint cartilage ( P  < 0.001) with higher cartilage T2 relaxation times at all measured sites than primary OA subjects ( P  < 0.01)., Conclusions: Patients with active acromegaly have a high prevalence of structural OA abnormalities in combination with thick joint cartilage. In addition, T2 relaxation times of cartilage are high in active patients, indicating unhealthy cartilage with increased water content, which is (partially) reversible by adequate treatment. Patients with acromegaly have a different distribution of structural OA abnormalities visualized by MRI than primary OA subjects, especially of cartilage defects., (© 2017 European Society of Endocrinology.)

Aim: The comparison of the efficiency of the standard scheme of a conservative medicinal therapy of an OA of a hip joint and the modified scheme (with the muscle relaxant of the central action - Tolperisone) was the research objective., Material and Methods: The prospective research of the complex conservative therapy of two pools of patients with initial stages of a coxarthrosis from 2014 for 2017 with the subject assessment articulary treatment components is conducted., Results: As a result of the studying of the clinical performance of the modified scheme in comparison with the standard scheme of the therapy at patients with the prevalence of an arthritic component of a disease established the best results of the therapy.

Unlabelled: Articular cartilage defects of the knee are common among athletes where the physical demands of sport result in significant stresses on joints. Chondral defects are associated with pain and functional impairment that limit sporting participation and may progress to joint degeneration and frank arthritis. Management of established chondral lesions aims to allow athletes to return to high-impact sports and can be considered in terms of protection of existing cartilage, chondrofacilitation, and resurfacing. Repaired and regenerated cartilage must closely resemble and function like normal hyaline cartilage, and this ability may be the most significant factor for the return to sport. Based on our experiences and the available literature, we outline how athletes can best protect their cartilage, how physicians can facilitate intrinsic repair of established lesions, and which methods of cartilage restoration or resurfacing should be used in different situations., Level of Evidence: IV.

Background: Cross-linked hyaluronan--also called Hylan G-F 20--is a medical device developed to treat osteoarthritis of the knee. However, it is still controversial whether Hylan G-F 20 has a cartilage protective effect in trauma-induced osteoarthritis. We investigated whether Hylan G-F 20 delayed osteoarthritis progression in a partial meniscectomized rat model., Methods: Lewis rats were used for the experiments. The anterior medial meniscus was resected at the level of the medial collateral ligament in both knees. From 1 week after the surgery, 50 μl of Hylan G-F 20 was injected weekly into the left knee and phosphate buffered saline was injected into the right knee. Cartilage was evaluated for macroscopic findings, histology with safranin-o, and expression of type II collagen at 2, 4, and 8 weeks. Synovitis was also evaluated, and immunohistochemical analysis was performed for ED1., Results: Macroscopic findings demonstrated that India ink positive area, representing fibrillated cartilage, was significantly smaller in the Hylan G-F 20 group than in the control group at 2, 4, and 8 weeks (n = 5). There were no significant differences in osteophyte score between the Hylan G-F 20 group and the control group at 2, 4, and 8 weeks. Histologically, the cartilage in the medial tibial plateau was destroyed at 8 weeks in the control group, while type II collagen expression was still observed at 8 weeks in the Hylan G-F 20 group. OARSI score for cartilage histology was significantly lower in the Hylan G-F 20 group than in the control group at 4 and 8 weeks (n = 5). There were no significant differences in synovial cell number or modified synovitis score between the Hylan G-F 20 group and the control group at 2, 4, and 8 weeks (n = 5). In the Hylan G-F 20 group, foreign bodies surrounded by ED1 positive macrophages were observed in the synovium., Conclusion: Weekly injections of Hylan G-F 20 starting 1 week after surgery delayed cartilage degeneration after meniscectomy in a rat model. Synovitis induced by meniscectomy was not alleviated by Hylan G-F 20. Insoluble gels were observed in the synovium after the Hylan G-F 20 injection.

Objective: To evaluate the efficacy of Danshen on histological parameters and antioxidative activity in the articular cartilage of rabbits with osteoarthritis (OA)., Design: Twenty-four rabbits were randomly divided into three groups (control, OA, and Danshen OA; eight rabbits per group). Anterior cruciate ligament transection (ACLT) of the left hind knees was performed in all rabbits in the OA and Danshen OA group for induction of OA. The rabbits in the control group underwent a sham operation. After surgery, 3 g/kg body weight of Danshen granules dissolved in 5 mL distilled water was administered by gastric intubation once per day and over a 6-week period to the Danshen OA group. The same volume of distilled water was administered to the OA and control groups. After 6 weeks, the medial femoral condyles and synoviums of the left hind knees in all three groups were harvested and used for histological and biochemical analyses., Results: Severe articular cartilage degeneration as well as lower proteoglycan (PG) content were noted in the OA group compared to the Danshen OA group (P < 0.05). The glutathione (GSH) levels in the synovium and articular cartilage of the rabbits in the Danshen OA group were significantly higher compared to the OA group (P < 0.001). The malondialdehyde (MDA) levels of the synovium and articular cartilage in the Danshen OA group was markedly depleted compared to the OA group (P < 0.001)., Conclusion: Danshen can prevent articular cartilage degeneration in OA through the defense against oxidative stress., (Copyright © 2015 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.)

Gastrectomy (Gx) leads to osteopenia/osteoporosis in humans and animals. However, little is known about the influence of Gx on the cartilage in this regard. Recent studies have demonstrated a protective effect of 2-oxoglutaric acid (2-Ox) on bone and cartilage. Hence, the purpose of this study was to investigate whether 2-Ox can mitigate eventual Gx-induced cartilage impairment. Twenty female Sprague-Dawley rats were subjected to Gx and randomly divided into two groups: Gx + 2-Ox and Gx. Another 20 rats were sham-operated (ShO) and randomly divided into two groups: ShO + 2-Ox and ShO. The daily dose of 2-Ox administered to the rats in the drinking water was 0.43 g per 100 g rat. After eight weeks, rats were euthanized and femora and tibiae were collected. Histology and histomorphometry analyses of the articular cartilage and the growth plate were done. Gx resulted in a 32% (±44.5 femur, ±35.8 tibia) decrease in overall thickness of articular cartilage in both bones (femur: ShO 279.1 ± 48.5 vs. Gx 190.2 ± 38.4 µm, tibia: ShO 222.9 ± 50.3 µm vs. Gx 151.3 ± 52.6 µm) (in some zones up to 58 ± 28.0%), and in the growth plate up to 20% (±22.4) (femur: ShO 243.0 ± 34.0 vs. Gx 207.0 ± 33.7 µm, tibia: ShO 220.0 ± 24.6 µm vs. Gx 171.1 ± 16.1 µm). Gx altered the spatial distribution of thick and thin collagen fibers, and chondrocyte shape and size. 2-Ox administration prevented the reduction in both cartilages thickness (Gx + 2-Ox: articular cartilage 265.2 ± 53.8 µm, 235.6 ± 42.7 µm, growth plate 236.7 ± 39.2 µm, 191.3 ± 16.5 µm in femur and tibia, respectively), and abolished the spatial changes in collagen distribution and structure induced by Gx. Gx affects cartilage structure and thickness, however, 2-Ox administration mitigates these effects and showed protective and stimulatory properties. Our observations suggest that dietary 2-Ox can be used to offset some of the changes in hyaline cartilage, in particular articular cartilage, following bariatric surgeries., (© 2016 by the Society for Experimental Biology and Medicine.)

This study investigated the effects of fucoidan (extract from Hizikia fusiforme) on symptoms and inflammatory cytokine activation in rats with monosodium iodoacetate (MIA)-induced osteoarthritis (OA). Forty male SD rats were divided into five groups, including normal, negative control (MIA), positive control (Lyprinol), and two experimental groups treated with 50 or 100 mg/kg fucoidan. Weight-bearing assessments were done after MIA injection into the right knee to induce OA. After 14 days of treatment, microcomputed tomographic (micro-CT) images were made of rat knee joints, and then animals were sacrificed for joint histology and inflammatory cytokine level assessments. MIA injection successfully induced OA by causing 40% weight-bearing imbalance, severe bone loss and cartilage degeneration, and markedly increased cytokine levels. However, fucoidan groups showed over 45% of imbalance and no articular cartilage surface lesions or change in subchondral trabecular bones in Micro-CT images. Histological analysis revealed that cartilage morphology and cell counts were also normal in the 100 mg/kg fucoidan group. In addition, the 100 mg/kg fucoidan groups exhibited lower serum tumor necrosis factor alpha (TNF-α) (30%), interleukin 1 beta (IL-1β) (48%), and matrix metalloproteinase-1 (MMP-1) (65%) compared to the MIA groups. These results suggest that administration of fucoidan prevents the progression of OA in a MIA-induced OA rat model.

Mechanical stress and aging are major risk factors of cartilage degeneration. Human studies have previously reported that oxidative damage increased, while SOD2 protein was reciprocally downregulated in osteoarthritic degenerated cartilage. However, it remains unclear whether mitochondrial superoxide imbalance in chondrocytes causes cartilage degeneration. We herein demonstrate that mechanical loading promoted mitochondrial superoxide generation and selective Sod2 downregulation in chondrocytes in vivo and that mitochondrial superoxide inducer also downregulated Sod2 expression in chondrocytes in vitro. A genetically manipulated model revealed that Sod2 deficiency in chondrocytes also resulted in mitochondrial superoxide overproduction and dysfunction, thus leading to cartilage degeneration. Intra-articular injection of a permeable antioxidant effectively suppressed the mechanical loading-induced mitochondrial superoxide generation and cartilage degeneration in mice. Our findings demonstrate that mitochondrial superoxide plays a pivotal role in the development and progression of osteoarthritis, and the mitochondrial superoxide balance may therefore be a promising target for the treatment of cartilage degeneration.

Introduction: Previous studies in animal models of osteoarthritis suggest that alendronate (ALN) has antiresorptive and chondroprotective effects, and can reduce osteophyte formation. However, these studies used non-physiologic injury methods, and did not investigate early time points during which bone is rapidly remodeled prior to cartilage degeneration. The current study utilized a non-invasive model of knee injury in mice to investigate the effect of ALN treatment on subchondral bone changes, articular cartilage degeneration, and osteophyte formation following injury., Methods: Non-invasive knee injury via tibial compression overload or sham injury was performed on a total of 90 mice. Mice were treated with twice weekly subcutaneous injections of low-dose ALN (40 μg/kg/dose), high-dose ALN (1,000 μg/kg/dose), or vehicle, starting immediately after injury until sacrifice at 7, 14 or 56 days. Trabecular bone of the femoral epiphysis, subchondral cortical bone, and osteophyte volume were quantified using micro-computed tomography (μCT). Whole-joint histology was performed at all time points to analyze articular cartilage and joint degeneration. Blood was collected at sacrifice, and serum was analyzed for biomarkers of bone formation and resorption., Results: μCT analysis revealed significant loss of trabecular bone from the femoral epiphysis 7 and 14 days post-injury, which was effectively prevented by high-dose ALN treatment. High-dose ALN treatment was also able to reduce subchondral bone thickening 56 days post-injury, and was able to partially preserve articular cartilage 14 days post-injury. However, ALN treatment was not able to reduce osteophyte formation at 56 days post-injury, nor was it able to prevent articular cartilage and joint degeneration at this time point. Analysis of serum biomarkers revealed an increase in bone resorption at 7 and 14 days post-injury, with no change in bone formation at any time points., Conclusions: High-dose ALN treatment was able to prevent early trabecular bone loss and cartilage degeneration following non-invasive knee injury, but was not able to mitigate long-term joint degeneration. These data contribute to understanding the effect of bisphosphonates on the development of osteoarthritis, and may support the use of anti-resorptive drugs to prevent joint degeneration following injury, although further investigation is warranted.

Effective lubrication of synovial joints is important to prevent cartilage degeneration and to keep the joints healthy. This paper sets out the basics of engineering lubrication with respect to the composition and properties of synovial fluid constituents. Two basic types of boundary lubrication are discussed: the presence of highly hydrophilic proteoglycans that provide a water liquid film, and the existence of multilamellar phospholipids lubricating layers at the surface ofarticular cartilage. Based on current knowledge, we may conclude that no single mechanism of boundary lubrication exists, and that effective boundary lubrication of synovial joints is maintained by the synergic effect of all synovial fluid constituents.

Slipped upper femoral epiphysis is a disabling condition with an annual incidence of 2-13 per 100,000. In situ surgical fixation is the preferred initial treatment for both stable and unstable slipped capital femoral epiphysis (SCFE) cases. The main aim is to avoid further slippage and complications such as osteonecrosis and chondrolysis. The choice of medical implants in managing this condition has changed along the years from large nail-like devices to cannulated screws. The biomechanical properties of different fixation techniques have been studied. All implants have been associated with complications that can occur intraoperatively as well as in the early and late postoperative periods. This report examines a number of different implants used and identifies complications and ways on how to avoid such complications. It also looks at the complications directly related to medical implants in the management of SCFE. We looked at published literature in peer-reviewed journals describing the use of the different medical implants and the documented complications. We also examined literature that suggests ways on how to avoid and manage these complications. A review of the current literature is presented in this text.

Slipped capital femoral epiphysis (SCFE) is a common hip disorder among adolescents, whereby the epiphysis is displaced posteriorly and inferiorly to the metaphysis. Treatment modalities aim to stabilize the epiphysis, prevent further slippage, and avoid complications associated with long-term morbidity, such as osteonecrosis and chondrolysis. Controversy exists with SCFE regarding prophylactic fixation of the contralateral, painless, normal hip, the role of femoroacetabular impingement with SCFE, and whether in situ fixation is the best treatment method for SCFE. This article presents and discusses the latest diagnostic and treatment modalities for SCFE., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Objective: To test whether inhibition of sclerostin by a targeted monoclonal antibody (Scl-Ab) protects from bone and cartilage damage in inflammatory arthritis. Sclerostin is a potent inhibitor of bone formation and may be responsible for the low level of bone repair in patients with rheumatoid arthritis., Methods: Human tumour necrosis factor transgenic mice (hTNFtg mice) developing inflammatory arthritis and local and bone loss were administered either vehicle, anti-TNF antibody, Scl-Ab, or a combination of both agents. Inflammation, systemic and periarticular bone loss, bone erosion and cartilage damage were evaluated at baseline (week 8) and after 3 weeks of treatment by clinical assessment, micro-CT and histology., Results: Scl-Ab did not affect joint swelling or synovitis. Systemic bone loss in the spine and periarticular bone loss in the proximal tibia were completely blocked and partially reversed by inhibition of sclerostin but not by inhibition of TNF. Moreover, Scl-Ab completely arrested the progression of bone erosion in hTNFtg mice and in combination with TNF inhibition even led to significant regression of cortical bone erosions. Protective effects of Scl-Ab were also observed for the articular cartilage., Conclusions: These data suggest that sclerostin inhibition is a powerful tool to enhance bone repair in inflammatory arthritis.

The combination of interleukin (IL)-4 and IL-10 protects against blood-induced cartilage damage in vitro. It has been hypothesized that the combination of these cytokines is effective if applied early in the process of cartilage damage. The present study investigated whether a single intra-articular injection of IL-4 plus IL-10 immediately after a joint bleed limits cartilage damage in an in vivo haemophilia mouse model of blood-induced joint damage. Factor VIII knockout mice with severe haemophilia A were punctured once with a needle below the patella to induce a joint haemorrhage. Subsequently IL-4 plus IL-10 (n = 24) or vehicle (n = 24) was injected intra-articularly. After 35 days, the time needed for development of detectable joint degeneration, knee joints were examined for cartilage damage by macroscopic and microscopic evaluation. A single intra-articular injection of IL-4 plus IL-10 ameliorated progression of cartilage degeneration caused by a single joint bleed to a certain extent. No effect on inflammation was observed at this time point. A single intra-articular injection of IL-4 plus Il-10 directly after a single joint bleed limits progression of cartilage degeneration over time. Improved bioavailability (half-life) of both cytokines might improve their protective ability in the development of cartilage degeneration, and probably also inflammation., (© 2012 Blackwell Publishing Ltd.)

Physical medicine and rehabilitation aim to evaluate, diagnose and treat disability in haemophiliac patients, while preventing injury or deterioration. They also aim to maintain the greatest degree of functional capacity and independence in patients with haemophilia, or to return them to that state. Rehabilitation, together with clotting factor replacement therapy, has revolutionized the management of these patients in developed countries and reduced their morbidity/mortality rates. A knowledge of the musculoskeletal signs and symptoms of haemophilia is essential for providing a treatment which is suitable and customized. Physical medicine and rehabilitation techniques, which are based on physical means, are intended to reduce the impact which these injuries and their consequences or sequelae can have on the quality of life of patients with haemophilia. Under ideal haemostatic control conditions (primary prophylaxis), people with haemophilia could achieve good physical condition which will allow them to enjoy both physical activity and a daily life without limitations. Currently, children undergoing primary prophylaxis are quite close to this ideal situation. For these physical activities to be carried out, the safest possible situations must be sought.

Objective: To evaluate the prevention of joint destruction and clinical efficacy of low-dose etanercept (ETN) (25 mg/week) compared with standard-dose ETN (50 mg/week) in RA., Methods: In this prospective, randomized, open-label study, 70 patients were assigned to receive ETN at either 50 or 25 mg/week for 52 weeks. The primary endpoint was the variation in modified total Sharp score (mTSS), and secondary endpoints were variations in disease activity score in 28 joints (DAS-28), modified HAQ and adverse event rate. Values of mTSS were calculated at baseline and after 52 weeks. Non-progression was estimated as ΔmTSS ≤0.5, and the non-progression rate was compared between groups., Results: Mean values at baseline were as follows: disease duration 9.2 years; DAS-28 5.45; and annual progression of mTSS 26.1. No significant differences in background were seen between groups. At 52 weeks, the non-progression rate was significantly less in the 25 mg/week group (36.7%) than in the 50 mg/week group (67.7%) (P = 0.041). Mean ΔmTSS was higher at 25 mg/week (1.03) than at 50 mg/week (-0.13). DAS-28 was significantly improved at 4 weeks, and the effect of treatment lasted for 52 weeks in both groups. No differences in adverse event rates were seen between groups., Conclusion: Low-dose ETN is not inferior to standard-dose ETN in terms of effects on clinical manifestations. However, in terms of the radiographic non-progression rate, the effects of low-dose ETN may be inferior to the effects of standard-dose ETN., Trial Registration: UMIN Clinical Trials Registry, http://www.umin.ac.jp/ctr/, UMIN000001798.

Although various drugs for the treatment of rheumatoid arthritis (RA) have been used in clinics, RA is not completely curable to date. Thus, to seek new drugs for the treatment of RA has been a hotspot. Hydroxynaphthoquinones are the major anti-inflammatory active constituents in Arnebia euchroma (Royle) Johnst. The present study aims to evaluate the anti-arthritic activity of a hydroxynaphthoquinone mixture (HM) of A. euchroma (Royle) Johnst, including its anti-inflammatory and analgesic effects. The anti-arthritic efficacy of HM was examined using complete Freund's adjuvant- and bovine type II collagen-induced arthritic models. The paw edema, polyarthritis index and histopathological change were evaluated. The analgesic effect was assessed using the chemical and thermal models of nociception. Results found that HM administered prophylactically and curatively showed marked anti-arthritic activity by suppressing the paw swelling and development of inflammation, lowering the levels of TNF-α and IL-1β and protecting cartilage and bone from damage. The protection of HM was superior to that of reference drugs such as prednisone acetate or etanercept, and showed no direct deleterious effect. Similarly, HM showed significant analgesic effects. In summary, HM possessed potent anti-arthritic activity. It could relieve inflammatory symptoms and protect against joint destruction. These findings indicate that HM would be a potential therapeutic agent for arthritic disease, which provide pharmacological evidence for its clinical application., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Purpose: This was a preliminary study performed in vivo to evaluate the viability and the chondroprotective effects of irradiated deep-frozen xenogeneic meniscal tissue as a novel substitute for meniscus transplantation., Methods: Medial meniscectomies were performed on the right knees of 48 New Zealand white rabbits. The inner one-third of pig meniscus was harvested and then irradiated and deeply frozen. The treated xenogeneic meniscal tissues were then transplanted to 24 right knees (Xeno group), whereas 24 other knees received meniscus allograft transplantations (Allo group). The left knees of the Xeno group and Allo group received meniscectomies (Meni group) and sham operations (Sham group), respectively. The rabbits were killed at weeks 6, 12, and 24 postoperatively. The newly formed structure of the implanted tissue and cartilage of the medial compartment of each group was assessed by gross and semiquantitative histologic analysis., Results: After 24 weeks, the implanted xenogeneic meniscal tissue completely healed to the synovium and formed meniscus-like tissue. The chondrocyte-like cell infiltrated into the tissue with extracellular matrix including type II collagen and proteoglycans. The Xeno group showed significantly less cartilage degeneration than that of the Meni group in the medial tibial plateau at week 24 (P < .05). No significant difference was found between the Xeno group and the Allo group except for the meniscus-covered regions at week 24. From week 12 to week 24, almost no advanced cartilage degeneration was found in weight-bearing regions of the medial tibial plateau of the Xeno group., Conclusions: The treated xenogeneic meniscal tissue healed to the synovium with tissue regeneration and slowed down articular cartilage degeneration in the short-term. The chondroprotection of xenograft transplantation was similar to that of allograft transplantation., Clinical Relevance: The treated xenogeneic meniscal tissue showed the potential for viability and slowed cartilage degeneration, but more studies are required for application in humans in the future., (Copyright © 2012 Arthroscopy Association of North America. Published by Elsevier Inc. All rights reserved.)

Inhibition of histone deacetylases (HDAC) has been shown to modulate gene expression and cytokine production after stimulation with several stimuli. In the present study, the antiinflammatory effect of a potent HDACi, ITF2357, was explored in different experimental models of arthritis. In addition, the bone protective effect of ITF2357 was investigated in vitro. Treatment of acute arthritis (Streptococcus pyogenes cell wall [SCW] arthritis) with ITF2357 showed that joint swelling and cell influx into the joint cavity were reduced. Furthermore, the chondrocyte metabolic function was improved by treatment of ITF2357. The production of proinflammatory cytokines by synovial tissue was reduced after ITF2357 treatment. To examine the effect of HDAC inhibition on joint destruction, ITF2357 was applied to both rat adjuvant arthritis and mouse collagen type II arthritis. ITF2357 treatment both ameliorates the severity scores in arthritis models and prevents bone destruction. In an in vitro bone destruction assay, ITF2357 was highly effective at a dose of 100 nmol/L. In conclusion, inhibition of HDAC prevents joint inflammation and cartilage and bone destruction in experimental arthritis.

Background: The anti-human Fas/APO-1/CD95 (Fas) mouse/human chimeric monoclonal IgM antibody ARG098 (ARG098) targets the human Fas molecule. The cytotoxic effects of ARG098 on cells isolated from RA patients, on normal cells in vitro, and on RA synovial tissue and cartilage in vivo using implanted rheumatoid tissues in an SCID mouse model (SCID-HuRAg) were investigated to examine the potential of ARG098 as a therapy for RA., Methods: ARG098 binding to each cell was analyzed by cytometry. The effects of ARG098 on several cells were assessed by a cell viability assay in vitro. Effects on the RA synovium, lymphocytes, and cartilage were assessed in vivo using the SCID-HuRAg mouse model., Results: ARG098 bound to cell surface Fas molecules, and induced apoptosis in Fas-expressing RA synoviocytes and infiltrating lymphocytes in the RA synovium in a dose-dependent manner. However, ARG098 did not affect the cell viability of peripheral blood mononuclear cells of RA patients or normal chondrocytes. ARG098 also induced apoptosis in RA synoviocytes and infiltrating lymphocytes in the RA synovium in vivo. The destruction of cartilage due to synovial invasion was inhibited by ARG098 injection in the modified SCID-HuRAg mouse model., Conclusions: ARG098 treatment suppressed RA synovial hyperplasia through the induction of apoptosis and prevented cartilage destruction in vivo. These results suggest that ARG098 might become a new therapy for RA.

Postarthroscopic glenohumeral chondrolysis is a devastating, poorly understood, and relatively rare complication. True chondrolysis involves the dissolution of articular cartilage, including the matrix and cellular elements, leading to premature and irreversible articular cartilage loss. Several factors have been implicated in this phenomenon; however, to date, no study has conclusively ascertained the causation. Potential causative agents include subclinical infection, high volume intra-articular infusion of certain anesthetics, arthroscopic implants, suture material, and thermal energy. One must also consider the possibility that chondrolysis represents an ongoing immunogenic process interrupted or possibly potentiated by surgical intervention. The complex homeostasis of articular cartilage is undoubtedly sensitive to agents introduced into the joint including mechanical, chemical, and temperature-dependent interventions. To date, several papers have described the phenomenon and the potential associations; however, there is no definitive answer although the use of high-dose bupivacaine as an intra-articular anesthetic seems to be contraindicated. The purpose of this article is to review the basic science regarding chondrolysis and to assess the current literature which focuses on postarthroscopic glenohumeral chondrolysis, as well as innovative treatment alternatives. It is unlikely that postoperative chondrolysis will be clearly understood until controlled studies are available, of which there are currently none.

Purpose of Review: Local anesthetics are not only used as drugs to block the sodium channel to provide analgesia and antiarrhythmic action. The purpose of this review is to highlight the new indications and limitations of this class of drugs., Recent Findings: Recent research has focused on the use of intravenous local anesthetics to improve bowel function after surgery or trauma, to protect the central nervous system, to find new clues about local anesthetic effects in chronic neuropathic pain, and to investigate the long-term effect of anesthesia/analgesia provided by local anesthetics on cancer recurrence. Recent facts dealing with myotoxicity and chondrotoxicity are presented., Summary: There is growing evidence that local anesthetics have a broad spectrum of indications in addition to analgesia and antiarrhythmic effect. Most of them are still insufficiently known and investigated. These new indications will no doubt be intensively studied in the coming years.

Introduction: In inflammatory joint disease, such as osteoarthritis (OA), there is an increased level of proinflammatory cytokines, such as interleukin (IL)-1β. These cytokines stimulate the production of matrix metalloproteinases (MMPs), which leads to the degradation of the cartilage extracellular matrix and the loss of key structural components such as sulphated glycosaminoglycan (sGAG) and collagen II. The aim of this study was to examine the therapeutic potential of n-3 polyunsaturated fatty acids (PUFAs) in an in vitro model of cartilage inflammation., Methods: Two specific n-3 compounds were tested, namely, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), each at 0.1, 1 and 10 μM. Full thickness bovine cartilage explants, 5 mm in diameter, were cultured for 5 days with or without IL-1β and in the presence or absence of each n-3 compound. The media were replaced every 24 hours and assayed for sGAG content using the 1,9-dimethylmethylene blue (DMB) method. Chondrocyte viability was determined at the end of the culture period using fluorescence microscopy to visualise cells labelled with calcein AM and ethidium homodimer., Results: Treatment with IL-1β (10 ng.ml⁻¹) produced a large increase in sGAG release compared to untreated controls, but with no effect on cell viability, which was maintained above 80% for all treatments. In the absence of IL-1β, both n-3 compounds induced a mild catabolic response with increased loss of sGAG, particularly at 10 μM. By contrast, in the presence of IL-1β, both EPA and DHA at 0.1 and 1 μM significantly reduced IL-1β-mediated sGAG loss. The efficacy of the EPA treatment was maintained at approximately 75% throughout the 5-day period. However, at the same concentrations, the efficacy of DHA, although initially greater, reduced to approximately half that of EPA after 5 days. For both EPA and DHA, the highest dose of 10 μM was less effective., Conclusions: The results support the hypothesis that n-3 compounds are anti-inflammatory through competitive inhibition of the arachidonic acid oxidation pathway. The efficacy of these compounds is likely to be even greater at more physiological levels of IL-1β. Thus we suggest that n-3 PUFAs, particularly EPA, have exciting therapeutic potential for preventing cartilage degradation associated with chronic inflammatory joint disease.

Objective: To assess the efficacy of selenium supplementation for prevention of Kashin-Beck Osteoarthropathy in children., Methods: We searched eight electronic databases and seven journals (upto July 2007) to identify randomized controlled trials (RCTs) and prospective non-RCTs comparing selenium supplementations with placebo or no intervention for preventing Kashin-Beck disease (KBD). The methodological qualities of included studies were assessed according to the guidelines of Cochrane Handbook for Systematic Reviews of Interventions for RCTs and the method described by Deeks et al. for non-RCTs. Outcomes were presented as Peto-odds ratios (Peto-ORs) with 95% confidence intervals (95% CIs) based on fixed effect model. The number needed to treat (NNT) was calculated. Meta-regression was also conducted to explore the possible impacts of potential confounding variables (place of study, age, selenium form, etc.) of included trials on the incidence of KBD., Results: Five RCTs and 10 non-RCTs were included in this review. The methodological quality of included studies was low. The pooled Peto-OR and NNT favoring selenium supplement was 0.13 (95% CI: 0.04-0.47) and 21 in RCTs, and 0.16 (95% CI: 0.09-0.30) and 26 in non-RCTs. Meta-regression indicated that the effect of potential confounding variables on KBD incidence was not statistically significant. One trial reported the side effects of nausea and vomiting in the process of selenium supplementation., Conclusions: Current evidence supports the benefits of selenium supplementation for prevention of KBD in children. However, the evidence was limited by potential biases and confounders. Large, well-designed trials are still needed.

Objective: To assess the preventive role of zinc chloride on toxicity of ciprofloxacin administration in Wistar albino rat litter. It was a Prospective experimental study. The study was carried out in the Department of Anatomy, Basic Medical Sciences Institute, Jinnah Postgraduate Medical Centre, Karachi, Pakistan during March 2002 to February 2003 one year study., Method: Ciprofloxacin and zinc chloride were administered to newly born albino rat litters separately and simultaneously at a dose of 20 mg/kg body weight and 1200 microg/Kg body weight respectively, intraperitonealy twice daily from 1 - 14 day after birth. The animals were sacrificed by deep ether anaesthesia. The fore and hind limbs were dis-articulated from the axial skeleton, soft tissue was removed and bones were fixed in 10% buffered formalin. Decalcification was done in 10% nitric acid and 10% formic acid changes. After paraplast embedding, 4 microm thick longitudinal sections of proximal & distal ends of long bones were cut by a rotary microtome. Routine staining with haemotoxylin and eosin was performed. Histomorphometery was done to measure the thickness of epiphyseal cartilage and was compared with similar values of the control animals. The results were statistically analyzed to evaluate the significance., Result: Our study revealed that ciprofloxacin administration in new born albino rat litter decreased the width of epiphyseal growth plate cartilage by 13.7 +/- 0.42 microm, 10.43% in humerus and 6.6 +/- 1.2 microm 4.72% in femur as compared to control, whereas, simultaneous zinc chloride administration restricted the decrease to 1.27 microm +/- SD in humerus and 2.05 microm +/- SD in femur., Conclusion: Simultanous zinc chloride administration minimized the epiphseal cartilage damage induced by ciprofloxacin in Wistar albino rat litter.

Objective: To characterize bone microarchitectural changes and to test the hypothesis that disrupting local cytokine equilibrium could modify cartilage degradation in a murine model of experimental osteoarthritis (OA)., Methods: Ten-week-old male C57BL/6 mice underwent medial meniscectomy of their right knees and a sham operation of their left knees. The mice received intraperitoneal injections of osteoprotegerin (OPG) (10 mg/kg), interleukin-1 receptor antagonist (IL-1Ra) (100 mg/kg), or phosphate buffered saline for 6 weeks. The microarchitecture of the trabecular bone, the OA score, and expression of ADAMTS-4 and ADAMTS-5 were assessed. Proteoglycan release was measured in cartilage explant cultures in the presence of IL-1Ra and OPG., Results: In the meniscectomized knees, bone volume/tissue volume (BV/TV) was lower, whereas trabecular separation, the OA score, and aggrecanase expression were higher than in the sham-operated knees. After treatment with OPG, BV/TV was significantly increased and trabecular separation was reduced in the knees that underwent meniscectomy. The OA score and the number of ADAMTS-positive cells were significantly decreased by treatment with OPG but were not affected by IL-1Ra. Moreover, OPG did not directly reduce the release of proteoglycans from cartilage explant cultures., Conclusion: In an experimental model of OA, meniscectomy induced bone loss and cartilage degradation at 6 weeks. Systemic administration of OPG prevented bone and cartilage degradation in vivo but had no effect on cartilage in vitro. These data collectively indicate that bone could be a contributor in the early stages of OA pathogenesis. They further suggest that disruption of RANKL/OPG balance might result in the degradation of cartilage subjected to mechanical loading. Specific targeting of the bone cytokine network might help to prevent OA.

Severe joint inflammation following trauma, arthroscopic surgery or infection can damage articular cartilage, thus every effort should be made to protect cartilage from the catabolic effects of pro-inflammatory cytokines and stimulate cartilage anabolic activities. Previous pre-clinical studies have shown that pulsed electromagnetic fields (PEMFs) can protect articular cartilage from the catabolic effects of pro-inflammatory cytokines, and prevent its degeneration, finally resulting in chondroprotection. These findings provide the rational to support the study of the effect of PEMFs in humans after arthroscopic surgery. The purpose of this pilot, randomized, prospective and double-blind study was to evaluate the effects of PEMFs in patients undergoing arthroscopic treatment of knee cartilage. Patients with knee pain were recruited and treated by arthroscopy with chondroabrasion and/or perforations and/or radiofrequencies. They were randomized into two groups: a control group (magnetic field at 0.05 mT) and an active group (magnetic field of 1.5 mT). All patients were instructed to use PEMFs for 90 days, 6 h per day. The patients were evaluated by the Knee injury and Osteoarthritis Outcome Score (KOOS) test before arthroscopy, and after 45 and 90 days. The use of non-steroidal anti-inflammatory drugs (NSAIDs) to control pain was also recorded. Patients were interviewed for the long-term outcome 3 years after arthroscopic surgery. Thirty-one patients completed the treatment. KOOS values at 45 and 90 days were higher in the active group and the difference was significant at 90 days (P < 0.05). The percentage of patients who used NSAIDs was 26% in the active group and 75% in the control group (P = 0.015). At 3 years follow-up, the number of patients who completely recovered was higher in the active group compared to the control group (P < 0.05). Treatment with I-ONE aided patient recovery after arthroscopic surgery, reduced the use of NSAIDs, and also had a positive long-term effect.

Quinolone-induced chondrotoxicity in juvenile rats and multiple other species has been demonstrated previously. Identical damages can be induced in immature rats by feeding them a magnesium-deficient diet. The objective of the present study was to investigate whether, in reverse, oral supplementation with magnesium, vitamin E, or both can diminish the typical quinolone-induced arthropathy in juvenile Wistar rats. Four groups of 12 (6 male, 6 female) 24-day-old Wistar rats were each fed either normal feed (group A), a vitamin E-enriched diet (group B), a magnesium-enriched diet (group C), or a diet enriched with both vitamin E and magnesium (group D) for 10 days. All rats received two subcutaneous ciprofloxacin doses of 600 mg/kg of body weight on postnatal day 32. Two days later, the rats were sacrificed and cartilage samples from knee joints were examined under a light microscope for the presence of typical quinolone-induced joint cartilage lesions. In addition, magnesium, calcium, and vitamin E concentrations in cartilage and plasma were determined. In the samples from rats fed a normal diet (group A), 17 quinolone-induced joint cartilage lesions were observed. In groups fed an enriched diet, the incidence of specific lesions (n) was significantly lower: group B, n = 10 (41% reduction compared to the incidence for group A; P < 0.05); group C, n = 6 (65% reduction; P < 0.01); and group D, n = 3 (82% reduction; P < 0.01). In comparison to the standard diet, diets with magnesium and vitamin E supplementation resulted in significantly higher magnesium and vitamin E concentrations in plasma and articular cartilage. Supplementation with magnesium and vitamin E alone or in combination may relevantly diminish joint cartilage lesions induced by quinolones in immature rats, with an additive effect of combined supplementation. The data further support the proposed pathomechanism of quinolone-induced arthropathy and the crucial role of magnesium in immature joint cartilage.

The aim of this work was the analysis of process of growth of degenerative changes of the hip joint based on present literature. Epidemiological data allow to consider it as a disease of civilization. The opinions about primary and secondary pathology of articular cartilage are presented. Changes in articular cartilage are presented with reference to morphological construction and physiology of cartilage. The author paid attention to the dynamics of changes and their relation to pathological factors in the range of intraarticular balance disturbances, as in systemic diseases and overload syndrome with reference to axial articular cartilage overload. Economical analysis related to degenerative hip disease dictates to initiate both causal and symptomatic prevention, as retarding dynamics of pathological process. The author presented modern methods of prevention of degenerative changes: gene therapy, molecular engineering.

Articular cartilage in adults has a limited capacity for self-repair after a substantial injury. Surgical therapeutic efforts to treat cartilage defects have focused on delivering new cells capable of chondrogenesis into the lesions. Autologous chondrocyte transplantation (ACT) is an advanced cell-based orthobiologic technology used for the treatment of chondral defects of the knee that has been in clinical use since 1987 and has been performed on 12,000 patients internationally. With ACT, good to excellent clinical results are seen in isolated post-traumatic lesions of the knee joint in the younger patient, with the formation of hyaline or hyaline-like repair tissue. In the classic ACT technique, chondrocytes are isolated from small slices of cartilage harvested arthroscopically from a minor weight-bearing area of the injured knee. The extracellular matrix is removed by enzymatic digestion, and the cells are then expanded in monolayer culture. Once a sufficient number of cells has been obtained, the chondrocytes are implanted into the cartilage defect, using a periosteal patch over the defect as a method of cell containment. The major complications are periosteal hypertrophy, delamination of the transplant, arthrofibrosis and transplant failure. Further improvements in tissue engineering have contributed to the next generation of ACT techniques, where cells are combined with resorbable biomaterials, as in matrix-associated autologous chondrocyte transplantation (MACT). These biomaterials secure the cells in the defect area and enhance their proliferation and differentiation.

Foley's catheter is used for post-nasal packing in severe epistaxis. Various methods have been described for securing the catheter in position, all of which can be associated with patient discomfort, risk of alar necrosis or unsightliness. We describe a new method to secure the Foley's catheter without these problems. The ribbon gauze used for anterior nasal packing is tied over the catheter in multiple knots to secure it in place. This has been successfully tried on over 50 patients.