Curcumin has been shown to have chondroprotective potential in vitro. However, its effect on disease and symptom modification in osteoarthritis (OA) is largely unknown. This study aimed to determine whether curcumin could slow progression of OA and relieve OA-related pain in a mouse model of destabilization of the medial meniscus (DMM).

The objective of this study was to assess the association between obesity and osteoarthritis (OA) of the knee, hip, and hand. OA patterns were studied in 809 patients with knee or hip joint replacement due to OA. Patients with OA were categorized as having bilateral or generalized OA according to the presence of radiographic OA in the contralateral joint or different finger joints, and as normal weight, overweight, or obese according to their body mass index (BMI). Odds ratios (OR) and 95% confidence intervals (CI) for relative weight and OA patterns were estimated with multivariable logistic regression. Eighty-five percent of participants had bilateral OA, 26% had generalized OA, and 31% were obese. Obesity (BMI >/= 30 kg/m(2); OR = 8.1; 95% CI: 2.4-28) and overweight (BMI >/= 25 kg/m(2); OR = 5.9; 95% CI: 2.0-18) were strongly associated with bilateral knee OA. No association between obesity and bilateral hip OA (OR = 0.7; 95% CI: 0.3-1.7) nor generalized OA (OR = 1.1; 95% CI: 0.6-2.1) was observed. Obesity seems to be a mechanical rather than a systemic risk factor for OA with the knee joint being especially susceptible.

Osteoarthritis genetics has been transformed in the past decade through the application of large-scale genome-wide association scans. So far, over 100 polymorphic DNA variants have been associated with this common and complex disease. These genetic risk variants account for over 20% of osteoarthritis heritability and the vast majority map to non-protein coding regions of the genome where they are presumed to act by regulating the expression of target genes. Statistical fine mapping, in silico analyses of genomics data, and laboratory-based functional studies have enabled the identification of some of these targets, which encode proteins with diverse roles, including extracellular signaling molecules, intracellular enzymes, transcription factors, and cytoskeletal proteins. A large number of the risk variants correlate with epigenetic factors, in particular cartilage DNA methylation changes in cis, implying that epigenetics may be a conduit through which genetic effects on gene expression are mediated. Some of the variants also appear to have been selected as humans adapted to bipedalism, suggesting that a proportion of osteoarthritis genetic susceptibility results from antagonistic pleiotropy, with risk variants having a positive role in joint formation but a negative role in the long-term health of the joint. Although data from an osteoarthritis genetic study has not yet directly led to a novel treatment, some of the osteoarthritis associated genes code for proteins that have available therapeutics. Genetic investigations are therefore revealing fascinating fundamental insights into osteoarthritis and can expose options for translational intervention.

The optimal treatment for isolated patellofemoral osteoarthritis is unclear at present. We systematically reviewed the highest level of available evidence on the nonoperative and operative treatment of isolated patellofemoral osteoarthritis to develop an evidenced-based discussion of treatment options.

The objective of this systematic review was to describe trapeziectomy outcomes and complications in the context of osteoarthritis of the base of the thumb after a five-year minimum follow-up.

No abstract available

Accelerated knee osteoarthritis may be a unique subset of knee osteoarthritis, which is associated with greater knee pain and disability. Identifying risk factors for accelerated knee osteoarthritis is vital to recognizing people who will develop accelerated knee osteoarthritis and initiating early interventions. The geometry of an articular surface (e.g., coronal tibial slope), which is a determinant of altered joint biomechanics, may be an important risk factor for incident accelerated knee osteoarthritis. We aimed to determine if baseline coronal tibial slope is associated with incident accelerated knee osteoarthritis or common knee osteoarthritis.

With the ageing of the population and the major advances in targeted drug treatments, there is in medicine a shift in attention from survival towards quality of life. Therefore new challenges are emerging in modern health care. Preventive and personalized medicine have been identified as key steps in this context. New targeted biologicals for musculoskeletal diseases such as chronic arthritis have entered daily clinical practice, thereby not only controlling symptoms and signs, inflammation and destruction, but also maintaining function of the joints. The last aspect is essential for the independence of the individual and critical for the quality of life. Since the lifespan of prosthetic devices will always remain limited, new treatment approaches to repair skeletal structures need to be devised for the young and middle aged individuals with skeletal and joint damage caused by either congenital, traumatic, or inflammatory conditions. It is believed that regenerative medicine and more specifically tissue engineering may fill this void to some extent. Indeed, recent cellular therapeutics and combination products, now resorting under a new regulatory class of Advanced Medicinal Therapeutic Products, provide indications that progress is being made with clinically relevant outcomes in well-defined patient populations. For osteoarthritis, a joint disease leading to joint decompensation, novel tissue engineering therapies are being explored and, although most of the developments are still in early phase clinical studies, there are sufficient positive signals to pursue these novel therapeutic approaches in clinics. This article is part of a Special Issue entitled "Osteoarthritis".

Systemic inflammatory factors have been implicated in symptomatic hand osteoarthritis (OA). Gut microbiome dysbiosis promotes systemic inflammation. The aim of this study was to examine the association between the gut microbiome and the presence of symptomatic hand OA in a population-based study.

Resveratrol is a non‑flavonoid polyphenol compound with a stilbene structure. As a type of phytoalexin produced under stress in plants, it improves the plant's resistance against pathogens and environment deterioration, and performs important functions beneficial to human health, such as anti‑cancer, anti‑oxidation, regulating blood lipid levels and prolonging life span. The effects of resveratrol were examined in a rat model of osteoarthritis (OA) and observed to ameliorate inflammatory damage and protect against OA. In the present study, resveratrol significantly inhibited the induction of clinical scores in rats with OA. Resveratrol inhibited tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6 and IL‑18 expression levels, and decreased caspase‑3/9 activity in rats with OA. Inducible nitric oxide synthase, nuclear factor (NF)‑κB, phosphorylated‑(p)‑AMP‑activated protein kinase and sirtuin 1 protein expression were significantly suppressed and heme oxygenase 1 (HO‑1) and nuclear factor erythroid 2‑related factor 2 (Nrf‑2) protein expression was stimulated in rats with OA treated with resveratrol. The current results indicate that resveratrol ameliorates inflammatory damage and protects against OA in a rat model of OA via NF‑κB and HO‑1/Nrf‑2 signaling.

Osteoarthritis is currently one of the most common chronic diseases. As life expectancy increases, its prevalence and incidence are expected to rise. At present, more and more evidences prove the correlation between the complement system and osteoarthritis (OA). This study aims to investigate complement C5's influence on the effect of MK801 on osteoarthritis synovial fibroblasts (OA-SFs).

There is no cure for knee osteoarthritis (KOA) and typically patients live approximately 30-years with the disease. Most common medical treatments result in short-term palliation of symptoms with little consideration of long-term risk. This systematic review aims to appraise the current evidence for the long-term (≥12 months) safety of common treatments for knee osteoarthritis (KOA).

The objective of this study is to identify circulating microRNAs that distinguish fast-progressing radiographic knee osteoarthritis (OA) in the Osteoarthritis Initiative cohort by applying microRNA-sequencing.

Often affecting knee joints, osteoarthritis (OA) is the most common type of arthritis and by 2020 is predicted to become the fourth leading cause of disability globally. Without cure, medication management is symptomatic, mostly with simple analgesics such as acetaminophen and non-steroidal anti-inflammatory drugs (NSAIDs), and glucosamine sulfate. Adherence to arthritis medications is generally low. Intentional non-adherence, that is deliberate decision-making about the use of analgesics, occurs in OA patients. To date, a limited number of studies have explored medication-taking decisions in people with OA nor the extent to which individuals' trade off one treatment factor for another in their decision-making using quantitative techniques. This study aimed to estimate the relative influence of medication-related factors and respondent characteristics on decisions to continue medications among people with symptomatic OA.

Osteoarthritis (OA) is a degenerative joints disorder influenced by genetic predisposition. We reported that rs11718863 DVWA SNP was represented in Sicilian with a more severe Kellgren and Lawrence (KL) radiographic grade, displaying its predictive role as OA marker progression. Here, we describe the DVWA SNPs: rs11718863, rs7639618, rs7651842, rs7639807 and rs17040821 probably able to induce protein functional changes.

Knee osteoarthritis is a degenerative arthritis that mainly affects older adults. Over time, osteoarthritis can result in significant and sustained discomfort, pain, and disability. Current treatment focuses on the alleviation of pain and functional impairment. While arthroplasty is the definitive management option, it subjects patients to surgical complications, and the possibility of surgical revisions. In addition, many patients are not surgical candidates. Instead, pharmacological therapy is recommended first-line for most patients. On top of pharmacological therapy, there are a range of non-operative procedural options available. However, leading professional guidelines vary in their recommendations for these agents. Therefore, we present a review of recent randomized controlled trials and meta-analyses on injectable corticosteroids, hyaluronic acid (HA), platelet-rich plasma (PRP), mesenchymal stem cell injections, and ozone therapy. The preliminary data reveal the strongest evidence in favour of corticosteroid injections, although there are promising findings regarding the long-term efficacy of HA and PRP.

In recent years, markers research has focused on the structural components of cartilage matrix. Specifically, a second generation of degradation markers has been developed against type II collagen neoepitopes generated by specific enzymes. A particular effort has been made to measure the degradation of minor collagens III and X of the cartilage matrix. However, because clinical data, including longitudinal controlled studies, are very scarce, it remains unclear whether they will be useful as an alternative to or in combination with current more established collagen biological markers to assess patients with osteoarthritis (OA). In addition, new approaches using high-throughput technologies allowed to detect new types of markers and improve the knowledge about the metabolic changes linked to OA. The relative advances coming from phenotype research are a first attempt to classify the heterogeneity of OA, and several markers could improve the phenotype characterization. These phenotypes could improve the selection of patients in clinical trials limiting the size of the studies by selecting patients with OA characteristics corresponding to the metabolic pathway targeted by the molecules evaluated. In addition, the inclusion of rapid progressors only in clinical trials would facilitate the demonstration of efficacy of the investigative drug to reduce joint degradation. The combination of selective biochemical markers appears as a promising and cost-effective approach to fulfill this unmet clinical need. Among the various potential roles of biomarkers in OA, their ability to monitor drug efficacy is probably one of the most important, in association with clinical and imaging parameters. Biochemical markers have the unique property to detect changes in joint tissue metabolism within a few weeks.

The main aim is to develop transcutaneous tenoxicam (TNX) loaded vesicles to control osteoarthritis (OA) without common side effects. Different vesicles were prepared by the emulsification technique, where poloxamer and glyceryl monooleate used for cubosomes. Then, hyalcubosomes were prepared by adding sodium hyaluronate to cubosomes components. Different characterization techniques were used. The selected formulations were tested using an ex-vivo permeation study to evaluate the ability to penetrate and retained in skin layers. Also, in-vitro cell studies using human skin fibroblasts were evaluated the safety of the formulation. The anti-inflammatory efficiency was tested using an in-vivo carrageenan-induced rat paw edema model. Finally, the efficiency to control OA symptoms was tested on three patients with a medical history of knee OA. Results confirmed the successful development of spherical cubosomes with particle size <250 nm, -14.5 mV, high entrapment efficiency percentage (>90%). Moreover, the addition of sodium hyaluronate to selected cubosomes improved viscosity and spreadability. Permeation study confirmed drug penetration and deposition. Cell studies proved the safety of the selected formulation. The animal model showed high anti-inflammatory activity. Finally, the preliminary clinical study demonstrates the potential efficacy and safety of the formulation in controlling OA symptoms over 8 weeks of therapy.

We describe here the development and validation of the Osteoarthritis Symptom Inventory Scale (OASIS), a new self-administered questionnaire specifically designed to evaluate the various osteoarthritis (OA) pain symptoms with different dimensions related to OA pain mechanisms. The initial development phase and qualitative study generated a list of 17 descriptors reflecting OA pain and other associated symptoms, leading to the first version of the questionnaire (OASIS17). Each item was quantified on a 0 to 10 Numerical Scale. Validation was performed using 123 consecutive patients with OA pain recruited at 28 centers in France, mainly general practitioner offices. Validation involved (1) determining the questionnaire's factorial structure through exploratory and confirmatory analyses, (2) analyzing convergent and divergent validities (ie, construct validity), (3) assessing each item's test-retest reliability, and (4) evaluating OASIS ability to detect treatment effects (ie, sensitivity to change). The final OASIS version includes 9 items discriminating and quantifying 3 distinct, clinically relevant OA pain dimensions sensitive to treatment. OASIS9 psychometric properties suggest that it could improve the characterization of OA pain profiles for 3 clinically relevant domains: localized, neuropathic-like, and deep pain. The OASIS9 questionnaire could be used to phenotype OA pain patients and identify responders to various therapeutic interventions as a function of OA pain dimensions.

Osteoarthritis is, at least in a subset of patients, associated with hypertrophic differentiation of articular chondrocytes. Recently, we identified the bone morphogenetic protein (BMP) and wingless-type MMTV integration site (WNT) signaling antagonists Gremlin 1 (GREM1), frizzled-related protein (FRZB) and dickkopf 1 homolog (Xenopus laevis) (DKK1) as articular cartilage's natural brakes of hypertrophic differentiation. In this study, we investigated whether factors implicated in osteoarthritis or regulation of chondrocyte hypertrophy influence GREM1, FRZB and DKK1 expression levels.