Inhibition of complement C3 prevents osteoarthritis progression in guinea pigs by blocking STAT1 activation.

Osteoarthritis (OA) is one of the leading causes of disability, affecting over 500 million adults worldwide. Previous studies have found that various inflammatory factors can contribute to the pathogenesis of OA, including complement factors in the synovial fluid of OA patients. However, the pathogenesis of this disease is still not known, and the only therapy of severe OA is total joint replacements. Total joint replacements are invasive, expensive, and affect quality of life. Here we show that when human articular chondrocytes are stimulated with pro-inflammatory mediator interleukin-1ß (IL-1ß) there is an increase in inflammatory factors including complement component 3 (C3). We also found the transcription factor, signal transducer and activator of transcription 1 (STAT1), is responsible for increased C3 expression after IL-1ß stimulation in human articular chondrocytes. A specific STAT1 inhibitor, fludarabine, attenuates the hyper-expression of C3 and delays/prevents spontaneous OA in Dunkin-Hartley guinea pigs. Since fludarabine is already clinically used for chemotherapy, this study has great translational potential as a unique disease-modifying osteoarthritis drug (DMOAD) in treating primary OA.

Treatment with PB125® Increases Femoral Long Bone Strength in 15-Month-Old Female Hartley Guinea Pigs.

Nuclear factor-erythroid 2-related factor-2 (Nrf2) is a transcription factor that serves as a master regulator of anti-inflammatory agents, phase I xenobiotic, and phase II antioxidant enzymes, all of which provide a cytoprotective role during disease progression. We hypothesized that oral administration of a purported phytochemical Nrf2-activator, PB125®, would increase long bone strength in aging Hartley guinea pigs, a model prone to musculoskeletal decline. Male (N = 56) and female (N = 56) guinea pigs were randomly assigned to receive daily oral treatment with either PB125® or vehicle control. Animals were treated for a consecutive 3-months (starting at 2-months of age) or 10-months (starting at 5-months of age) and sacrificed at 5-months or 15-months of age, respectively. Outcome measures included: (1) ANY-maze™ enclosure monitoring, (2) quantitative microcomputed tomography, and (3) biomechanical testing. Treatment with PB125® for 10 months resulted in increased long bone strength as determined by ultimate bending stress in female Hartley guinea pigs. In control groups, increasing age resulted in significant effects on geometric and structural properties of long bones, as well as a trending increase in ultimate bending stress. Furthermore, both age and sex had a significant effect on the geometric properties of both cortical and trabecular bone. Collectively, this work suggests that this nutraceutical may serve as a promising target and preventive measure in managing the decline in bone mass and quality documented in aging patients. Auxiliary to this main goal, this work also capitalized upon 5 and 15-month-old male and female animals in the control group to characterize age- and sex-specific differences on long bone geometric, structural, and material properties in this animal model.

Effects of emulsified and non-emulsified palm tocotrienol on bone and joint health in ovariectomised rats with monosodium iodoacetate-induced osteoarthritis.

Postmenopausal women are susceptible to osteoporosis and osteoarthritis. Tocotrienol, a bone-protective nutraceutical, is reported to prevent osteoarthritis in male rats. However, its efficacy on joint health in oestrogen deficiency has not been validated. Besides, data on the use of emulsification systems in enhancing bioavailability and protective effects of tocotrienol are limited. Ovariectomised adult female Sprague-Dawley rats (3 months old) were treated with refined olive oil, emulsified (EPT, 100 mg/kg/day with 25% vitamin E content), non-emulsified palm tocotrienol (NEPT, 100 mg/kg/day with 50% vitamin E content) and calcium carbonate (1% w/v in drinking water) plus glucosamine sulphate (250 mg/kg/day) for 10 weeks. Osteoarthritis was induced with monosodium iodoacetate four weeks after ovariectomy. Baseline control was sacrificed upon receipt, while the sham group was not ovariectomised and treated with refined olive oil. EPT and NEPT prevented femoral metaphyseal and subchondral bone volume decline caused by ovariectomy. EPT decreased subchondral trabecular separation compared to the negative control. EPT preserved stiffness and Young's Modulus at the femoral mid-shaft of the rats. Circulating RANKL was reduced post-treatment in the EPT group. Joint width was reduced in all the treatment groups vs the negative control. The EPT group's grip strength was significantly improved over the negative control and NEPT group. EPT also preserved cartilage histology based on several Mankin's subscores. EPT performed as effectively as NEPT in preventing osteoporosis and osteoarthritis in ovariectomised rats despite containing less vitamin E content. This study justifies clinical trials for the use of EPT in postmenopausal women with both conditions.

Low-Molecular-Weight Fish Collagen Peptide (Valine-Glycine-Proline-Hydroxyproline-Glycine-Proline-Alanine-Glycine) Prevents Osteoarthritis Symptoms in Chondrocytes and Monoiodoacetate-Injected Rats.

The objective of this study was to investigate the effect of low-molecular-weight fish collagen (valine-glycine-proline-hydroxyproline-glycine-proline-alanine-glycine; LMWCP) on H2O2- or LPS-treated primary chondrocytes and monoiodoacetate (MIA)-induced osteoarthritis rat models. Our findings indicated that LMWCP treatment exhibited protective effects by preventing chondrocyte death and reducing matrix degradation in both H2O2-treated primary chondrocytes and cartilage tissue from MIA-induced osteoarthritis rats. This was achieved by increasing the levels of aggrecan, collagen type I, collagen type II, TIMP-1, and TIMP-3, while simultaneously decreasing catabolic factors such as phosphorylation of Smad, MMP-3, and MMP-13. Additionally, LMWCP treatment effectively suppressed the activation of inflammation and apoptosis pathways in both LPS-treated primary chondrocytes and cartilage tissue from MIA-induced osteoarthritis rats. These results suggest that LMWCP supplementation ameliorates the progression of osteoarthritis through its direct impact on inflammation and apoptosis in chondrocytes.

PG545 Prevents Osteoarthritis Development by Regulating PI3K/AKT/mTOR Signaling and Activating Chondrocyte Autophagy.

INTRODUCTION: Osteoarthritis (OA) is a degenerative disease common in the elderly and is characterized by joint pain, swelling, and restricted movement. In recent years, heparanase has been reported to play an important role in the development of osteoarthritic cartilage. PG545 is a heparan sulfate mimetic with heparanase inhibitory activity. In this study, the therapeutic effects and possible mechanisms of PG545 were investigated in a chondrocyte injury model induced by interleukin-1ß (IL -1ß). METHODS: Following treatment with PG545 or the autophagy inhibitor 3-methyladenine (3-MA), chondrocyte viability was detected using Cell Counting Kit-8 and fluorescein diacetate/propidium iodide double staining. The apoptosis rate of chondrocytes was determined by flow cytometry. Expression of light chain 3 and P62 was monitored by immunofluorescence labeling. Western blot, lentivirus infection with red fluorescent protein and green fluorescent protein, and quantitative real-time polymerase chain reaction were used to determine the expression levels of chondrocyte markers, apoptosis-related factors, autophagy proteins, and key proteins of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway. The expression and activity of stress-specific enzymes such as malondialdehyde, superoxide dismutase, and catalase (CAT) were investigated. Chondrocytes with ATG5 knockdown were used to investigate the relationship between the therapeutic effect of PG545 and autophagy. The therapeutic effect of PG545 was verified in vivo. RESULTS: PG545 had a significant protective effect on chondrocytes by reducing oxidative stress, apoptosis, and degradation of chondrocytes and increasing chondrocyte proliferation. PG545 was effective in inducing autophagy in IL-1ß-treated cells, while 3-MA attenuated the effect. The PI3K/Akt/mTOR pathway may be involved in the promotion of autophagy and OA treatment by PG545. CONCLUSION: PG545 was able to restore impaired autophagy and autophagic flux via the PI3K/Akt/mTOR pathway, thereby delaying the progression of OA, suggesting that PG545 may be a novel therapeutic approach for OA.

Geniposide stimulates autophagy by activating the GLP-1R/AMPK/mTOR signaling in osteoarthritis chondrocytes.

Osteoarthritis (OA) is a chronic joint disease characterized by cartilage degeneration. Autophagy is associated with chondrocyte homeostasis and exhibits a role in protecting against OA pathogenesis. Geniposide (GEN), an iridoid glycoside extracted from Eucommia ulmoides Oliv, acts as an activator of GLP-1R, which can stimulate autophagy. The AMPK/mTOR signaling pathway participates in the mediation of autophagy, and GLP-1R may act as an upstream factor of AMPK. However, whether GEN mediates the autophagic responses by activating the GLP-1R/AMPK/mTOR signaling pathway in OA chondrocytes is still unclear. In the current study, attenuated autophagy in MIA-induced rat OA models was observed, as shown by up-regulated expression of p62 and down-regulated expression of Beclin-1 and LC3-II/I. GEN stimulated autophagy and protected OA cartilage by up-regulating GLP-1R expression. In addition, GEN could enhance AMPK phosphorylation and down-regulate mTOR expression in IL-1ß-treated C28/I2 cells. Inhibition of AMPK or activation of mTOR could reverse the stimulatory effects of GEN on autophagy. Furthermore, a GLP-1R inhibitor Exendin 9-39 could eliminate the chondroprotective effects of GEN by suppressing the AMPK/mTOR signaling pathway. Conclusively, Geniposide exhibits protective effects against osteoarthritis development by stimulating autophagy via activating the GLP-1R/AMPK/mTOR signaling pathway.

Kukoamine A protects mice against osteoarthritis by inhibiting chondrocyte inflammation and ferroptosis via SIRT1/GPX4 signaling pathway.

AIMS: Osteoarthritis (OA) is one of the common chronic degenerative joint diseases, characterized by cartilage damage, subchondral bone changes, osteophyte formation, and synovitis. Kukoamine A (KuKA) is a bioactive compound isolated from Lycium chinense which is known as its anti-inflammatory activity. In this study, we detected the regulatory role of KuKA on OA both in vivo and in vitro. MATERIALS AND METHODS: Mouse chondrocytes were cultured and mouse model of OA was established. Inflammatory mediator was measured by ELISA. The signaling pathway was tested by western blot analysis. KEY FINDINGS: KuKA inhibited IL-1ß-induced PGE2 and NO production and iNOS and COX-2 expression. IL-1ß-induced MMP1 and MMP3 production was attenuated by KuKA. IL-1ß-induced MDA, iron, and ROS were alleviated by KuKA. Meanwhile, GSH content, GPX4, Ferritin, SIRT1, Nrf2, and HO-1 expression were upregulated by KuKA. Furthermore, the inhibitory role of KuKA on IL-1ß-induced inflammation, MMPs production, and ferroptosis were reversed by SIRT1 inhibitor. In vivo, KuKA could attenuate OA development in mouse model. KuKA markedly alleviated MMP1, MMP3, iNOS, and COX2 expression in OA mice. SIGNIFICANCE: In conclusion, KuKA could inhibit OA development through suppressing chondrocyte inflammation and ferroptosis via SIRT1/GPX4 signaling pathway.

Targeting the Inflammatory Hallmarks of Obesity-Associated Osteoarthritis: Towards Nutraceutical-Oriented Preventive and Complementary Therapeutic Strategies Based on n-3 Polyunsaturated Fatty Acids.

Obesity (Ob), which has dramatically increased in the last decade, is one of the main risk factors that contribute to the incidence and progression of osteoarthritis (OA). Targeting the characteristics of obesity-associated osteoarthritis (ObOA) may offer new chances for precision medicine strategies in this patient cohort. First, this review outlines how the medical perspective of ObOA has shifted from a focus on biomechanics to the significant contribution of inflammation, mainly mediated by changes in the adipose tissue metabolism through the release of adipokines and the modification of fatty acid (FA) compositions in joint tissues. Preclinical and clinical studies on n-3 polyunsaturated FAs (PUFAs) are critically reviewed to outline the strengths and weaknesses of n-3 PUFAs' role in alleviating inflammatory, catabolic and painful processes. Emphasis is placed on potential preventive and therapeutic nutritional strategies based on n-3 PUFAs, with a focus on ObOA patients who could specifically benefit from reformulating the dietary composition of FAs towards a protective phenotype. Finally, tissue engineering approaches that involve the delivery of n-3 PUFAs directly into the joint are explored to address the perspectives and current limitations, such as safety and stability issues, for implementing preventive and therapeutic strategies based on dietary compounds in ObOA patients.

Astaxanthin prevents osteoarthritis by blocking Rspo2-mediated Wnt/ß-catenin signaling in chondrocytes and abolishing Rspo2-related inflammatory factors in macrophages.

Chondrocyte degeneration and classically activated macrophage (AM)-related inflammation play critical roles in osteoarthritis (OA). Here, we explored the effects of astaxanthin and Rspo2 on OA in vitro and in vivo. We observed that the Rspo2 gene was markedly elevated in synovial tissues of OA patients compared with healthy controls. In 2D cultures, Rspo2 and inflammatory factors were enhanced in AMs compared with nonactivated macrophages (NMs), and the protein expression levels of Rspo2, ß-catenin, and inflammatory factors were increased, and anabolic markers were reduced in osteoarthritic chondrocytes (OACs) compared to normal chondrocytes (NCs). Astaxanthin reversed these changes in AMs and OACs. Furthermore, Rspo2 shRNA significantly abolished inflammatory factors and elevated anabolic markers in OACs. In NCs cocultured with AM, and in OACs cocultured with AMs or NMs, astaxanthin reversed these changes in these coculture systems and promoted secretion of Rspo2, ß-catenin and inflammatory factors and suppressed anabolic markers compared to NCs or OACs cultured alone. In AMs, coculture with NCs resulted in a slight elevation of Rspo2 and AM-related genes, but not protein expression, compared to culture alone, but when cocultured with OACs, these inflammatory mediators were significantly enhanced at both the gene and protein levels. Astaxanthin reversed these changes in all the groups. In vivo, we observed a deterioration in cartilage quality after intra-articular injection of Rspo2 associated with medial meniscus (DMM)-induced instability in the OA group, and astaxanthin was protective in these groups. Our results collectively revealed that astaxanthin attenuated the process of OA by abolishing Rspo2 both in vitro and in vivo.

[Peptides prevent the forming of secretory phenotype of chondrocytes associated with the aging.]

Secretory phenotype associated with the aging (SASP) of chondrocytes forms the conditions for the musculoskeletal system diseases development, in particular, osteoarthritis (OA). The search for effective methods for OA treating is an urgent task of molecular gerontology. The purpose of this work is to characterize the SASP of chondrocytes and to conduct a comparative assessment of the effect of AED peptide and the cartilage polypeptide complex (CPC). It was found that chondrocyte's SASP is characterized by an increase of the synthesis of p16, p21, p53 pro-apoptotic proteins, TNF-α, IL-1α pro-inflammatory cytokines and a decrease of Sirt1synthesis. Peptides AED and CPC normalize the synthesis of molecules that form SASP of chondrocytes. This effect may explain their geroprotective effect and effectiveness in studies of various pathologies of the musculoskeletal system, including OA.

Evidence Review for Preventing Osteoarthritis After an Anterior Cruciate Ligament Injury: An Osteoarthritis Action Alliance Consensus Statement.

CONTEXT: The Osteoarthritis Action Alliance formed a secondary prevention task group to develop a consensus on secondary prevention recommendations to reduce the risk of osteoarthritis after a knee injury. OBJECTIVE: Our goal was to provide clinicians with secondary prevention recommendations that are intended to reduce the risk of osteoarthritis after a person has sustained an anterior cruciate ligament injury. Specifically, this manuscript describes our methods, literature reviews, and dissenting opinions to elaborate on the rationale for our recommendations and to identify critical gaps. DESIGN: Consensus process. SETTING: Virtual video conference calls and online voting. PATIENTS OR OTHER PARTICIPANTS: The Secondary Prevention Task Group consisted of 29 members from various clinical backgrounds. MAIN OUTCOME MEASURE(S): The group initially convened online in August 2020 to discuss the target population, goals, and key topics. After a second call, the task group divided into 9 subgroups to draft the recommendations and supportive text for crucial content areas. Twenty-one members completed 2 rounds of voting and revising the recommendations and supportive text between February and April 2021. A virtual meeting was held to review the wording of the recommendations and obtain final votes. We defined consensus as >80% of voting members supporting a proposed recommendation. RESULTS: The group achieved consensus on 15 of 16 recommendations. The recommendations address patient education, exercise and rehabilitation, psychological skills training, graded-exposure therapy, cognitive-behavioral counseling (lacked consensus), outcomes to monitor, secondary injury prevention, system-level social support, leveraging technology, and coordinated care models. CONCLUSIONS: This consensus statement reflects information synthesized from an interdisciplinary group of experts based on the best available evidence from the literature or personal experience. We hope this document raises awareness among clinicians and researchers to take steps to mitigate the risk of osteoarthritis after an anterior cruciate ligament injury.

Sustained-Drug-Release, Strong, and Anti-Swelling Water-Lipid Biphasic Hydrogels Prepared via Digital Light Processing 3D Printing for Protection against Osteoarthritis: Demonstration in a Porcine Model.

Osteoarthritis is a serious disease affecting joint cartilage. Owing to poor blood supply, the meniscus and acetabular labrum of joints heal poorly after injury. However, the development of artificial alternatives to these components that have similar mechanical properties and cartilage-protection ability is challenging. In this study, a strong hydrogel with a biomimetic microstructure is prepared with an emulsion-type photosensitive resin, where both hydrophilic and hydrophobic monomers, photo-initiator, and drugs can be adopted. In this system, the hydrophobic monomer forms uniformly dispersed aggregates after curing, improving the mechanical properties of the hydrogel significantly. Furthermore, the coordination bonds between nontoxic Zr4+ cations and sulfonic acid groups prevent hydrogel swelling. In addition, the water-oil biphasic hydrogel ink enables the loading of water- and lipid-soluble drugs, yielding hydrogel scaffolds with sustained dual-drug release ability. Crucially, hydrogel scaffolds having excellent mechanical properties, low swelling, and sustained biphasic drug release ability can be prepared using digital light processing 3D printing technology, owing to the high curing rate of the hydrophobic photo-initiator. These hydrogel scaffolds are applied as meniscal and labral replacements in a porcine model and show great promise for the prevention of secondary osteoarthritis, demonstrating the broad potential clinical applications of this material.

The Role of Lubricin, Irisin and Exercise in the Prevention and Treatment of Osteoarthritis.

Osteoarthritis is a chronic degenerative musculoskeletal disease that worsens with age and is defined by pathological alterations in joint components. All clinical treatment recommendations for osteoarthritis promote exercise, although precise molecular pathways are unclear. The purpose of this study was to critically analyze the research on lubricin and irisin and how they relate to healthy and diseased joint tissue. Our research focused specifically on exercise strategies and offered new perspectives for future potential osteoarthritis treatment plans. Although lubricin and irisin have only recently been discovered, there is evidence that they have an impact on cartilage homeostasis. A crucial component of cartilage lubrication and integrity, lubricin is a surface-active mucinous glycoprotein released by the synovial joint. Its expression increases with joint movement. In healthy joints, lubricin molecules cover the cartilage surface to lubricate the boundary of the joint and inhibit protein and cell attachment. Patients with joint trauma, inflammatory arthritis, or genetically mediated lubricin deficiency, who do not produce enough lubricin to protect the articular cartilage, develop arthropathy. Irisin, sometimes known as the "sports hormone", is a myokine secreted primarily by skeletal muscle. It is a physiologically active protein that can enter the circulation as an endocrine factor, and its synthesis and secretion are primarily triggered by exercise-induced muscle contraction. We searched PubMed, Web of Science, Google Scholar, and Scopus using the appropriate keywords to identify the most recent research. The studies considered advance our knowledge of the role that exercise plays in the fight against osteoarthritis, serve as a valuable resource, and support the advancement of osteoarthritis prevention and therapy.

Quercetin prevents osteoarthritis progression possibly via regulation of local and systemic inflammatory cascades.

Due to the lack of effective treatments, osteoarthritis (OA) remains a challenge for clinicians. Quercetin, a bioflavonoid, has shown potent anti-inflammatory effects. However, its effect on preventing OA progression and the underlying mechanisms are still unclear. In this study, Sprague-Dawley male rats were divided into five groups: control group, OA group (monosodium iodoacetate intra-articular injection), and three quercetin-treated groups. Quercetin-treated groups were treated with intragastric quercetin once a day for 28 days. Gross observation and histopathological analysis showed cartilage degradation and matrix loss in the OA group. High-dose quercetin-group joints showed failure in OA progression. High-dose quercetin inhibited the OA-induced expression of MMP-3, MMP-13, ADAMTS4, and ADAMTS5 and promoted the OA-reduced expression of aggrecan and collagen II. Levels of most inflammatory cytokines and growth factors tested in synovial fluid and serum were upregulated in the OA group and these increases were reversed by high-dose quercetin. Similarly, subchondral trabecular bone was degraded in the OA group and this effect was reversed in the high-dose quercetin group. Our findings indicate that quercetin has a protective effect against OA development and progression possibly via maintaining the inflammatory cascade homeostasis. Therefore, quercetin could be a potential therapeutic agent to prevent OA progression in risk groups.

Amelioration of Osteoarthritis Development by Daily Oral Supplementation of Royal Jelly.

Royal jelly (RJ), an essential food for the queen honeybee, has a variety of biological activities. Although RJ exerts preventive effects on various lifestyle-related diseases, such as osteoporosis and obesity, no study evaluated the effect of RJ on the development of osteoarthritis (OA), the most common degenerative joint disease. Here, we showed that daily oral administration of raw RJ significantly prevented OA development in vivo following surgically-induced knee joint instability in mice. Furthermore, in vitro experiments using chondrocytes, revealed that raw RJ significantly reduced the expression of inflammatory cytokines and enzymes critical for the degradation of the extracellular matrix (ECM). Similar results were observed after treatment with 10-hydroxy-2-decenoic acid, the most abundant and unique fatty acid in raw RJ. Our results suggest that oral supplementation with RJ would benefit the maintenance of joint health and prophylaxis against OA, possibly by suppressing the activity of inflammatory cytokines and ECM-degrading enzymes.

Receptor-interacting protein 1 inhibition prevents mechanical stress-induced temporomandibular joint osteoarthritis by regulating apoptosis and later-stage necroptosis of chondrocytes.

OBJECTIVES: Temporomandibular joint osteoarthritis (TMJ OA) is a common degenerative joint disease that has multiple causes. The abnormal stress distribution is known to be an important trigger of TMJ OA. This article explored the pathological changes of the condylar cartilage under 60 g mechanical force and whether the inhibition of Receptor-interacting protein 1 (RIP1) can protect stress-induced TMJ OA. MATERIAL AND METHODS: We used a compressive mechanical force-induced-TMJ OA model and Lenti-virus targeting RIP1 to perform this study. A total of 72 male rats were used in the animal experiment. Each rat was injected with a negative control Lenti-shRNA in the right TMJ and Lenti-siRIP1 in the left TMJ and euthanized after 4 and 7 days, respectively. Quantitative real-time PCR, immunohistochemistry, Tunnel staining and Micro-CT were used to detect cartilage pathological changes and one way ANOVA with LSD analysis was used to determine statistical significance between groups. RESULTS: The results identified the characteristics of the spatio-temporal changes in stress-induced TMJ OA. Under mechanical force, inflammation and apoptosis, which occur in the whole layer of mandibular cartilage, appear on the 4th day and persist till the 7th day. Necroptosis arises in the later stage of mechanical force and is mainly located in the transition layer. RIP1 inhibition through Lenti-virus could protect stress-induced mandibular cartilage thinning by inhibiting persisted apoptosis and later-stage necroptosis in the transition layer. CONCLUSIONS: RIP1 plays an essential role in the destruction of mandibular cartilage under mechanical force. RIP1 inhibition through Lenti-virus could protect mechanical stress-induced TMJ OA.

2021 EULAR recommendations regarding lifestyle behaviours and work participation to prevent progression of rheumatic and musculoskeletal diseases.

OBJECTIVES: A European League Against Rheumatism taskforce was convened to review the literature and develop recommendations on lifestyle behaviours for rheumatic and musculoskeletal diseases (RMDs). METHODS: Six lifestyle exposures (exercise, diet, weight, alcohol, smoking, work participation) and seven RMDs (osteoarthritis, rheumatoid arthritis, axial spondyloarthritis, psoriatic arthritis, systemic lupus erythematosus, systemic sclerosis, gout) were considered. The taskforce included health professionals in rheumatology, geriatricians, epidemiologists, public health experts, people with RMDs and exposure domain experts. Systematic reviews were conducted to gather available evidence, from which recommendations were developed. RESULTS: Five overarching principles and 18 specific recommendations were defined based on available evidence. The overarching principles define the importance of a healthy lifestyle, how lifestyle modifications should be implemented, and their role in relation to medical treatments. Exercise recommendations highlight the safety and benefits of exercise on pain and disability, particularly among people with osteoarthritis and axial spondyloarthritis. The diet recommendations emphasise the importance of a healthy, balanced diet for people with RMDs. People with RMDs and health professionals should work together to achieve and maintain a healthy weight. Small amounts of alcohol are unlikely to negatively affect the outcomes of people with RMDs, although people with rheumatoid arthritis and gout may be at risk of flares after moderate alcohol consumption. Smokers should be supported to quit. Work participation may have benefits on RMD outcomes and should be discussed in consultations. CONCLUSIONS: These recommendations cover a range of lifestyle behaviours and can guide shared decision making between people with RMDs and health professionals when developing and monitoring treatment plans.

Guia de boas práticas do cuidado do quadril infantil do Hospital do Servidor Público Municipal de São Paulo / Good practice guide for children's hip care at the Hospital do Servidor Público Municipal de São Paulo

Introdução: A Displasia de Desenvolvimento do Quadril (DDQ) é uma condição que pode ocorrer durante o crescimento ou desenvolvimento embrionário, fetal e infantil. O diagnóstico precoce e o tratamento adequado são essenciais para evitar complicações futuras, como a osteoartrose. Atualmente, é estabelecido que o posicionamento pós-natal é um fator causal para a ocorrência da DDQ. Deste modo, o posicionamento pós-natal como no uso de dispositivos como "charutinhos" e "cangurus" influencia na incidência de DDQ. Promover a conscientização de profissionais de saúde e pais de recém-nascidos sobre estes cuidados pode contribuir para um desenvolvimento saudável do quadril e uma menor incidência de DDQ. Objetivo: Elaborar uma cartilha de conscientização a respeito de ações e cuidados com o quadril infantil a fim de diminuir a incidência de displasia do desenvolvimento do quadril em crianças. Método: Revisão da literatura pelos autores, com o objetivo de sistematizar o conteúdo relevante, de forma acessível e didática na forma de uma cartilha que será distribuída aos pais, responsáveis e profissionais de saúde que acompanham as crianças. Resultados: A elaboração da cartilha será estruturada em tópicos abrangendo explicações relacionadas a displasia do desenvolvimento de quadril em formato de textos e imagens de forma informative e acessível. Discussão: A implementação de políticas que conscientizem sobre as práticas adequadas relacionadas ao posicionamento do quadril das crianças poderá diminuir a incidência da DDQ, implicando na diminuição de casos de osteoartrose futuros secundários a esta doença. Isto poderá ter impacto positivo tanto na qualidade de vida e morbimortalidade futuros, como também nos custos de saúde relacionados a dor, locomoção e tratamentos definitivos para os quadris afetados. Conclusão: A conscientização a respeito dos cuidados com o quadril das crianças poderá resultar, além da diminuição da incidência de casos de DDQ, no aumento da adesão ambulatorial de pacientes e responsáveis; promoção de políticas e linhas de cuidados relacionados à prevenção da DDQ; conscientização de profissionais e responsáveis a respeito da DDQ; diminuição de custos relacionados a complicações de diagnósticos tardios da DDQ; possibilitar a realização de estudos futuros relacionadas a implementação das medidas propostas. Palavras-chave: Displasia do desenvolvimento dos quadris. Quadril. Ortopedia Pediátrica.

A novel Atlantic salmon (Salmo salar) bone collagen peptide delays osteoarthritis development by inhibiting cartilage matrix degradation and anti-inflammatory.

Nowadays, the biological activity of collagen peptides has been revealed, but the effect of Atlantic salmon (Salmo salar) bone-derived collagen peptide (CPs) on osteoarthritis remains unclear. In this study, CPs was identified as a small molecular weight peptide rich in Gly-X-Y structure. Meanwhile, interleukin-1ß (IL-1ß)-induced hypertrophic chondrocytes and partial medial meniscectomy (pMMx) surgery model in rats were performed. In IL-1ß stimulated chondrocytes, CPs significantly increased the type-II collagen content, reduced the type-X collagen abundance and chondrocytes apoptosis. Meanwhile, CPs reversed the increased expression of matrix metalloproteinase, metalloproteinase with thrombospondin motifs and RUNX family transcription factor 2 in chondrocytes induced by IL-1ß. In vivo, CPs increased pain tolerance of rats and without organ toxicity at 1.6 g/kg.bw. CPs significantly decreased the levels of COMP and Helix-II in serum. Furthermore, a significant decrease of IL-1ß in synovial fluid and cartilage tissue were observed by CPs intervention. From Micro-CT, CPs (0.8 g/kg.bw) significantly decreased Tb.sp and SMI value. Meanwhile, the expression of tumor necrosis factor and interleukin-6 were reduced by CPs administration both in vitro and in vivo. Together, CPs showed potential to be a novel and safe dietary supplement for helping anti-inflammatory and cartilage regeneration, ultimately hindering osteoarthritis development. However, the clear mechanism of CPs's positive effect on osteoarthritis needs to be further explored.

Effects of a Fall Prevention Program Based on Goal Attainment Theory for Homebound Older Adults With Osteoarthritis of the Lower Extremities.

This study implemented and evaluated a community-based fall prevention program based on goal attainment theory that targeted older adults with osteoarthritis. The program included education, exercise, and one-on-one counseling during which the participant and the provider set individual fall prevention goals. This study used a nonequivalent control group pre-/posttest design. Participants were older adults in senior centers with lower extremity osteoarthritis. A fall prevention program in the experimental group included group (70 minutes, once/week; education and exercise) and individual counseling (10 minutes, twice/week; emotional support and goal setting). Data analysis was conducted using SPSS/WIN 22.0 with the χ2 test, Fisher's exact test, independent t test, and Mann-Whitney U test. The experimental group experienced significantly fewer falls, less stiffness, less difficulty performing activity; more muscular strength, walking ability, and balance; as well as less fear of falling and higher falls efficacy in comparison with the control group. However, pain did not improve in either of the two groups. Fall prevention programs need to include the active involvement of carers in ensuring environmental changes to reduce fall risks. In addition, health professionals who care for community patients with osteoarthritis could strengthen interactions and exchanges to prevent falls and actively modify home hazards.