Improve Osteoarthritis Symptoms Research Articles

Tumor Necrosis Factor α-Induced Protein 8-like 2 (TIPE2) Gene Transfer Ameliorates Aging Associated Osteoarthritis in a progeria mouse model by reducing inflammation and cellular senescence

Osteoarthritis (OA) pain is often associated with expression of tumor necrosis factor (TNF-α), suggesting that TNF-α is one of the main contributing factors that causes inflammation, pain and OA pathology. Thus, inhibition of TNF-α could potentially improve OA symptoms and slow disease progression. Anti-TNF-α treatments with antibodies, however, require multiple treatments and cannot entirely block TNF-α. Tumor necrosis factor α-induced protein 8-like 2 (TIPE2) was found to regulate the immune system’s homeostasis, and inflammation, through different mechanisms from anti-TNF-α therapies. With a single treatment of AAV-TIPE2 gene delivery in the accelerated aging Z24-/- mouse model, we found differences in Safranin O staining intensity within the AC region of knee between TIPE2 treated mice and control mice. The glycosaminoglycan content (orange-red) was degraded in the Z24-/- cartilage while shown to be restored in the TIPE2 treated Z24-/- cartilage. We also observed that chondrocytes in Z24-/- mice exhibited a variety of senescent-associated phenotypes. Treatment with TIPE2 decreased TNF-α positive cells, β-Gal activity and p16 expression seen in Z24 -/- mice. Our study demonstrated that AAV-TIPE2 gene delivery effectively blocked TNF-α induced inflammation and senescence and result resulting in the prevention or delay of knee OA in our accelerated aging Z24-/- mouse model.

Effects of Diclofenac Etalhyaluronate (SI-613/ONO-5704) on Cartilage Degeneration in Arthritic Rats and Inflammatory Cytokine-Stimulated Human Chondrocytes.

Cartilage degeneration is a key feature of osteoarthritis (OA) and rheumatoid arthritis and is thought to negatively impact patients' quality of life. Diclofenac etalhyaluronate (DEH, SI-613/ONO-5704) is a hyaluronic acid (HA) derivative chemically bound to diclofenac (DF) that has been reported to improve OA symptoms; however, its effect on cartilage degeneration remains unknown. In the present study, we investigated the chondroprotective effect of DEH in rats with collagen-induced arthritis and interleukin-1β-stimulated human chondrocytes. Rats with collagen-induced arthritis were administered DEH and HA intra-articularly, and DF orally. Knee joint swelling, histological scores of articular cartilage, and inflammatory (Il1b) and catabolic (Mmp3 and Mmp13) gene expression in the synovial tissue and cartilage were evaluated. In vitro direct effects of DEH on matrix metalloproteinase (MMP)-3 and MMP-13 expression were examined in interleukin-1β-stimulated human chondrocytes. In a rat model of collagen-induced arthritis, a single intra-articular dose of DEH inhibited knee joint inflammation and cartilage degeneration. Daily oral administration of DF had similar effects. Conversely, HA administered as a single intra-articular dose had no effect. Only DEH inhibited Mmp3 gene expression in the cartilage, whereas DEH and DF inhibited Mmp3 and Mmp13 mRNA expression in the synovial tissue. In interleukin-1β-stimulated human chondrocytes, DEH and HA inhibited MMP-3 and MMP-13 production, whereas DF had no effect. In this study, we demonstrated the chondroprotective effect of DEH in rats with collagen-induced arthritis and in interleukin-1β-stimulated human chondrocytes. Thus, DEH may suppress cartilage degeneration in patients with musculoskeletal diseases, such as OA.

Effects of extracorporeal shockwave therapy for mild knee osteoarthritis: A pilot study.

Extracorporeal shockwave therapy (ESWT) has been widely used for various musculoskeletal disorders, including knee osteoarthritis (OA), and has been shown in several studies to be a safe treatment. Although some studies have confirmed the pain-relieving effect of ESWT for knee OA, research on objectivity for structural changes in knee OA is lacking. The aim of this study was to evaluate the ESWT treatment mechanisms in patients with knee OA by means of clinical symptoms and ultrasound techniques as objective measures. Eighteen patients with mild knee OA were enrolled and randomized to 1 of 2 treatment groups: active or sham. Patients in the experimental group received 0.05 mJ/mm² total energy with 1000 pulses weekly for 3 weeks. We then assessed them before, immediately after, and 1-month after the last treatment using the following measurements: pain on a visual analog scale, Western Ontario and McMaster Universities Osteoarthritis Index, Lequesne index, knee joint range of motion, and ultrasonographic features (articular cartilage thickness, Doppler activity, and joint effusion height). All 18 patients completed the 3 treatment sessions without any complication. Both the experimental and control groups improved in terms of OA symptoms, as measured by the visual analog scale, Western Ontario and McMaster Universities Osteoarthritis Index score, and Lequesne index (P < .05). The height of the suprapatellar effusion decreased with time course in the experimental group (P < .05) and showed significant differences with control group at 1-month follow-up (P < .05). The experimental group showed an increase in knee flexion range of motion and Doppler activity immediately following the last treatment session (P < .05), but the effect was not sustained at the 1-month follow-up. Although the therapeutic activity itself could improve OA symptoms, objective improvements were only observed after ESWT. Suprapatellar effusion height was reduced after ESWT and the effect was maintained after 1-month. Our results suggest that ESWT may be effective in reducing suprapatellar effusion and improving symptoms in mild knee OA. However, studies with a larger sample size are required.

A static magnetic field enhances the repair of osteoarthritic cartilage by promoting the migration of stem cells and chondrogenesis.

To investigate the therapeutic effects of static magnetic field (SMF) and its regulatory mechanism in the repair of osteoarthritic cartilage. Fourteen-week-old female C57BL/6 mice were randomly divided into the sham operation group and the osteoarthritis (OA) groups with and without SMF application. SMF was applied at 200​mT for two consecutive weeks. Changes in knee cartilage were examined by histomorphometry, and the chondrogenesis and migration of endogenous stem cells were assessed. The expression of SRY-related protein 9 (SOX9), Collagen type II (COL2), matrix metallopeptidase 13 (MMP13), stromal cell-derived factor 1/C-X-C chemokine receptor type 4 (SDF-1/CXCR4), Piezo1 and other genes was evaluated, and the mechanism of SMF's action was tested using the CXCR4 inhibitor, AMD3100, and Piezo1 siRNA. SMF significantly decreased the OARSI scores after induction of OA. SMF was beneficial to chondrogenesis by elevating SOX9. In the OA mouse model, an increase in MMP13 with a decrease in COL2 led to the destruction of the cartilage extracellular matrix, which was suppressed by SMF. SMF promoted the migration of cartilage-derived stem/progenitor cells and bone marrow-derived mesenchymal stem cells (MSCs). It increased SDF-1 and CXCR4, while the CXCR4 inhibitor significantly suppressed the beneficial effects of SMF. The application of Piezo1 siRNA inhibited the SMF-induced increase of CXCR4. SMF enhanced chondrogenesis and improved cartilage extracellular matrices. It activated the Piezo1-mediated SDF-1/CXCR4 regulatory axis and promoted the migration of endogenous stem cells. Collectively, it attenuated the pathological progression of cartilage destruction in OA mice. The findings in this study provided convincing evidence that SMF could enhance cartilage repair and improve OA symptoms, suggesting that SMF could have clinical value in the treatment of OA.

Strategy for osteoarthritis therapy: Improved the delivery of triptolide using liposome-loaded dissolving microneedle arrays

Osteoarthritis (OA) is a chronic disease that seriously impairs people’s physical function and quality of life. Triptolide (TP), as a promising anti-inflammatory drug for the treatment of OA, has limited clinical application due to its severe systemic toxicity, poor solubility and rapid elimination in the body. To extend its application prospect for OA treatment. We have developed a liposome-loaded dissolving microneedle (DMN) system, which can effectively deliver poorly water-soluble TP and improve OA symptoms. To incorporate TP into DMNs, triptolide liposome (TP-Lipo) with entrapment efficiency of 90.25% was prepared by ethanol injection. Subsequently, TP-Lipo was concentrated by ultrafiltration tube and mixed with hyaluronic acid solution to prepare DMNs, TP-Lipo-loaded DMNs (TP-Lipo@DMNs) showed sufficient mechanical and insertion properties to penetrate about 200 μm of rat skin. The drug distribution in vivo showed that TP-Lipo@DMNs had a slow-release effect compared with intra-articular injection. In vivo pharmacodynamic research showed that TP-Lipo@DMNs significantly reduced knee joint swelling and the level of inflammatory cytokines (TNF-α, IL-1β, IL-6). Micro-CT and histological evaluation showed that TP-Lipo@DMNs effectively reduced cartilage destruction and alleviated OA symptoms. These results support that TP@Lipo@DMNs may be a promising option for OA treatment.

Mesenchymal stem cells genetically engineered to express platelet-derived growth factor and heme oxygenase-1 ameliorate osteoarthritis in a canine model

BackgroundMesenchymal stem cells (MSCs) are used for the treatment of osteoarthritis (OA), and MSC genetic engineering is expected to enhance cartilage repair. Here, we aimed to investigate the effect of MSCs overexpressing platelet-derived growth factor (PDGF) or heme oxygenase-1 (HO-1) in chondrocytes and synovial cells with an OA phenotype and assess the in vivo efficacy of intra-articular injections of these MSCs in canine OA models.MethodsCanine adipose-derived MSCs were transfected with canine PDGF (PDGF-MSCs) or HO-1 (HO-1-MSCs) using lentiviral vectors. Canine chondrocytes or synovial cells were stimulated with lipopolysaccharide (LPS) to mimic the inflammatory OA model and then co-cultured with MSCs, PDGF-MSCs, or HO-1-MSCs for 24 h and 72 h. The mRNA levels of pro-inflammatory, extracellular matrix-degradative/synthetic, or pain-related factors were measured after co-culture by real-time PCR. Furthermore, a surgery-induced canine OA model was established and the dogs were randomized into four groups: normal saline (n = 4), MSCs (n = 4), PDGF-MSCs (n = 4), and HO-1-MSCs (n = 4). The OA symptoms, radiographic OA severity, and serum matrix metallopeptidase (MMP)-13 levels were assessed before and 10 weeks after treatment, to evaluate the safety and efficacy of the modified MSCs.ResultsPDGF or HO-1 overexpression significantly reduced the expression of pro-inflammatory factors, MMP-13, and nerve growth factor elicited by LPS and increased that of aggrecan and collagen type 2 in chondrocytes (P < 0.05). In addition, the expression of aggrecanases was significantly downregulated in synovial cells, whereas that of tissue inhibitor of metalloproteinases was upregulated (P < 0.05). Furthermore, the co-cultured MSCs highly expressed genes that contributed to the maintenance of joint homeostasis (P < 0.05). In vivo studies showed that OA symptoms improved after administration of all MSCs. Also, PDGF-MSCs significantly improved limb function and reduced pain (P < 0.05). The results of the radiographic assessment and serum MMP-13 levels did not vary significantly compared to those of the control.ConclusionsGenetically modifying PDGF and HO-1 in MSCs is an effective strategy for treating OA, suggesting that PDGF-MSCs can be novel therapeutic agents for improving OA symptoms.

Astilbin-induced inhibition of the PI3K/AKT signaling pathway decelerates the progression of osteoarthritis.

Degeneration and destruction of articular cartilage are the key characteristics of osteoarthritis (OA). In recent studies, the use of astilbin (AST), the primary active ingredient of Astilbe chinensis, has been shown to correlate with a reduction in inflammatory disease symptoms. The present study aimed to investigate the effects and mechanisms of AST on OA. A rat model of OA was constructed and in vivo experiments were performed using the AST, PBS, OA and control groups. The cartilage tissues of each group were assessed by hematoxylin and eosin and toluidine blue staining. The gene expression levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, AKT, PI3K and other related proteins were analyzed by reverse transcription-quantitative PCR and western blot analysis. AST was found to significantly inhibit IL-1β and TNF-α protein expression; this further confirmed that IL-1β, TNF-α and PI3K mRNA expression was downregulated, indicating that the protective mechanism of AST is associated with the PI3K/AKT pathway. Overall, the results of the present study demonstrate that AST can improve OA symptoms by downregulating the PI3K/AKT signaling pathway, and may therefore be a potential therapeutic option for patients with OA.

TissueGene-C promotes an anti-inflammatory micro-environment in a rat monoiodoacetate model of osteoarthritis via polarization of M2 macrophages leading to pain relief and structural improvement

Osteoarthritis (OA) is the most common form of arthritis, characterized by cartilage destruction, pain and inflammation in the joints. Existing medications can provide relief from the symptoms, but their effects on the progression of the disease are limited. TissueGene-C (TG-C) is a novel cell and gene therapy for the treatment of OA, comprising a mixture of human allogeneic chondrocytes and irradiated cells engineered to overexpress transforming growth factor-β1 (TGF-β1). This study aims to investigate the efficacy and mechanism of action of TG-C in a rat model of OA. Using the monosodium-iodoacetate (MIA) model of OA, we examined whether TG-C could improve OA symptoms and cartilage structure in rats. Our results showed that TG-C provided pain relief and cartilage structural improvement in the MIA OA model over 56 days. In parallel with these long-term effects, cytokine profiles obtained on day 4 revealed increased expression of interleukin-10 (IL-10), an anti-inflammatory cytokine, in the synovial lavage fluid. Moreover, the increased levels of TGF-β1 and IL-10 caused by TG-C induced the expression of arginase 1, a marker of M2 macrophages, and decreased the expression of CD86, a marker of M1 macrophages. These results suggest that TG-C exerts a beneficial effect on OA by inducing a M2 macrophage-dominant micro-environment. Cell therapy using TG-C may be a promising strategy for targeting the underlying pathogenic mechanisms of OA, reducing pain, improving function, and creating a pro-anabolic micro-environment. This environment supports cartilage structure regeneration and is worthy of further evaluation in future clinical trials.

The Effectiveness of Exercise Therapy on Reducing Pain in Osteoarthritis Patients: Literature Review

Osteoarthritis (OA) is a chronic joint disorder with damage to the joint cartilage, this causes a decrease in the functional ability and perform daily activities. So intervention is needed in reducing these problems to increase and maintain independence in carrying out training activities. The research will aim to detect the influences of exercises that can be applied to OA patients to reduce pain. This research used a systematic literature study approach obtained from PubMed database and Science Direct. In total, the literature review systematic review concluded that exercise therapy can affect pain in osteoarthritis. The results of this systematic review revealed that yoga improves OA symptoms and can be done safely without supervision at home. In conclusion, the result of this study showed that there were Moderate physical activity at least three times per week can reduce the risk of arthritis-related disability. However, there is increasing evidence in the literature for the beneficial effects of exercise for managing OA. Evidence on the comparative effectiveness of different types of exercise, including exercise adherence and satisfaction in older adults with knee OA, is limited.

Hydrogen sulfide biosynthesis is impaired in the osteoarthritic joint.

Osteoarthritis (OA) is the most common form of arthritis and it is a leading cause of disability in the elderly. Its complete etiology is not known although there are several metabolic, genetic, epigenetic, and local contributing factors involved. At the moment, there is no cure for this pathology and treatment alternatives to retard or stop its progression are intensively being sought. Hydrogen sulfide (H2S) is a small gaseous molecule and is present in sulfurous mineral waters as its active component. Data from recent clinical trials shows that balneotherapy (immersion in mineral and/or thermal waters from natural springs) in sulfurous waters can improve OA symptoms, in particular, pain and function. Yet, the underlying mechanisms are poorly known. Hydrogen sulfide is also considered, with NO and CO, an endogenous signaling gasotransmitter. It is synthesized endogenously with the help of three enzymes, cystathionine gamma-lyase (CTH), cystathionine beta-synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3-MPST). Here, the expression of these three enzymes was demonstrated by quantitative real-time polymerase chain reaction (qRT-PCR) and their protein abundance [by immunohistochemistry and Western blot (WB)] in human articular cartilage. No significant differences were found in CBS or CTH expression or abundance, but mRNA and protein levels of 3-MPST were significantly reduced in cartilage form OA donors. Also, the biosynthesis of H2S from OA cartilage, measured with a specific microelectrode, was significantly lower than in OA-free tissue. Yet, no differences were found in H2S concentration in serum from OA patients and OA-free donors. The current results suggest that reduced levels of the mitochondrial enzyme 3-MPST in OA cartilage might be, at least in part, responsible for a reduction in H2S biosynthesis in this tissue and that impaired H2S biosynthesis in the joint might be a contributing factor to OA. This could contribute to explain why exogenous supplementation of H2S, for instance with sulfurous thermal water, has positive effects in OA patients.

Efficiency of platelet-rich plasma therapy in knee osteoarthritis does not depend on level of cartilage damage

ObjectivesOsteoarthritis of the knee is common and often leads to significant physical disability. While classic conservative therapeutic approaches aim for symptoms like pain and inflammation, procedures like the intraarticular application of hyaluronic acids (HA) or platelet-rich plasma (PRP) are thought to stimulate the endogenous HA production, stop catabolism of cartilage tissue, and promote tissue regeneration. To analyse whether the positive effects of PRP injections are associated with the level of cartilage damage, patient satisfaction with the treatment was correlated with the level of knee joint osteoarthritis quantified by MRI.MethodsPRP was performed with a low-leukocyte autologous conditioned plasma (ACP) system in 59 patients. A pre-treatment MRI was performed and a Whole-Organ MRI Score (WORMS) was used to score the level of knee osteoarthritis by 14 features: integrity of the cartilage, affection of the bone marrow, subcortical cysts, bone attrition, osteophytes, integrity of the menisci and ligaments, presence of synovitis, loose bodies, and periarticular cysts. A multivariate analysis with ordinary least squares regressions was used.ResultsAlthough pain symptoms and severity of clinical osteoarthritis symptoms decreased, regression analysis could not detect a correlation between the degree of cartilage damage measured by the WORMS score and a positive response to PRP therapy.ConclusionThis study suggests that intraarticular injection of PRP might improve osteoarthritis symptoms and reduces the pain in patients suffering from osteoarthritis of the knee joint independent from the level of cartilage damages quantified by the whole-organ MRI scoring method WORMS.

Effects of ultrasound therapy on the synovial fluid proteome in a rabbit surgery-induced model of knee osteoarthritis

BackgroundUltrasound (US) therapy may improve osteoarthritis symptoms. We investigated the effects of US on the synovial fluid (SF) proteome in a rabbit knee osteoarthritis (KOA) model to explore its therapeutic mechanisms.MethodsSixteen healthy 6-month-old New Zealand white rabbits (eight male, eight female), weighing 2.5–3.0 kg, were randomly divided into groups A and B with eight rabbits per group. Both groups were subjected to right anterior cruciate ligament transaction. Six weeks after surgery, we treated the operated knee joint of group A rabbits with US and of group B rabbits with sham US for 2 weeks. The proteomes of knee joint SF from groups A and B rabbits were then analyzed using a label-free mass spectrometry (MS) quantification method.ResultsWe identified 19 protein sequences annotated by 361 Gene Ontology (GO) items. According to the Kyoto Encyclopedia of Genes and Genomes (KEGG) database of rabbit protein sequences, we then annotated the KO numbers of homologous/similar proteins to 32 relevant KEGG pathways. We extracted 10 significantly differentially expressed proteins among the 32 relevant KEGG messages/metabolism pathways. The proteins whose levels were decreased were apolipoprotein A-I (AopA-1), transferrin (TF), carboxypeptidase B2 (CBP2), arylesterase/paraoxonase (PON), fibrinogen alpha chain, and alpha-2-macroglobulin (A2M). The proteins whose levels were increased were molecular chaperone HtpG/heat shock proteins (htpG, HSP90A), decorin (DCN), pyruvate kinase (PK, pyk), and fatty acid-binding protein 4/adipocyte (FABP4, aP2).ConclusionsUS therapy can alter protein levels in SF, which can decrease AopA-1, TF, CBP2, PON, fibrinogen alpha chain and A2M protein levels, and increase HtpG/HSP90A, DCN, PK/PKY, and FABP4/aP2 protein levels in SF of KOA, suggesting that the therapeutic mechanisms of US therapy on KOA may occur through changes in the SF proteome.

Effect of collagen supplementation on osteoarthritis symptoms: a meta-analysis of randomized placebo-controlled trials.

Osteoarthritis (OA) is one of the most common causes of disability and a prevalent chronic disease. The use of collagen is growing due to the satisfactory results in the treatment of OA. However, the possible beneficial effects of collagen for the treatment of OA are currently controversial. The aim of the present meta-analysis was to evaluate the effect of collagen-based supplements on OA symptoms. PubMed-Medline, Scopus, and Google Scholar databases were searched for randomized placebo-controlled trials evaluating the effect of orally administered collagen on OA symptoms using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) scale and/or the Visual Analog Scale (VAS). Meta-analysis was conducted using a random-effects model and ageneric inverse variance method. Heterogeneity was tested using the I2 statistic index. Collagen treatment showed a significant reduction in the score of total WOMAC index (WMD - 8.00; 95% CI - 13.04, - 2.95; p = 0.002). After subgroup analysis of the WOMAC subscores, the collagen supplementation revealed a significant decrease in the stiffness subscore (WMD - 0.41; 95% CI - 0.74, - 0.08; p = 0.01), whereas the pain (WMD - 0.22; 95% CI - 1.58, 1.13; p = 0.75) and functional limitation (WMD - 0.62; 95% CI - 5.77, 4.52; p = 0.81) subscores did not have significant differences. Finally, a significant reduction was found in the VAS score after collagen administration (WMD - 16.57; 95% CI - 26.24, - 6.89; p < 0.001). The results of this meta-analysis showed that collagen is effective in improving OA symptoms by the decrease of both total WOMAC index and VAS score.

Platelet-Rich Plasma and Cartilage Repair

To assess the utilization and efficacy of platelet-rich plasma (PRP), for the treatment of articular cartilage injury, most commonly characterized by progressive pain and loss of joint function in the setting of osteoarthritis (OA). PRP modulates the inflammatory and catabolic environment through a locally applied concentrate of platelets, leukocytes, and growth factors. Clinically, PRP has been shown to be possibly a viable treatment adjuvant for a variety of inflammatory and degenerative conditions. Recent efforts have focused on optimizing delivery methods that enable platelets to slowly degranulate their biological constituents, which may promote healing and improve OA symptoms for a longer duration. There are various factors that affect the progression of OA within joints, including inhibition of inflammatory cytokines and altering the level of enzymatic expression. PRP therapy aims to mediate inflammatory and catabolic factors in a degenerative environment through the secretion of anti-inflammatory factors and chemotaxic effects. There are a growing number of studies that have demonstrated the clinical benefit of PRP for non-operative management of OA. Additional randomized controlled trials with long-term follow-up are needed in order to validate PRP's therapeutic efficacy in this setting. Additionally, continued basic research along with well-designed pre-clinical studies and reporting standards are necessary in order to clarify the effectiveness of PRP for cartilage repair and regeneration for future clinical applications.

Olive leaf extract prevents cartilage degeneration in osteoarthritis of STR/ort mice

The chondroprotective effect of olive leaf extract (OLE) on knee osteoarthritis (OA) was studied with STR/ort mice (n=5). OLE was administrated with a dosage of 100mg/kg for 8weeks and the OA severity score of hind limb knee joints was then measured. The Mankin scores of the knee joints of the non-OA control group, OA control group and OLE-treated group were 3.50, 11.13 and 7.20, respectively. This suggests that oral OLE supplements help prevent cartilage degeneration in STR/ort mice. In vitro, the synthesis of high molecular weight hyaluronan in synovial cells (HIG-82) was increased by OLE stimulation. This suggests that OLE modulates hyaluronan metabolism in synovial cells and improves OA symptoms. Our findings indicate that OLE intake inhibits cartilage destruction by increasing high molecular weight hyaluronan and thus preventing OA progress.

Celecoxib for osteoarthritis.

Celecoxib for osteoarthritis.

The effect of exercise and sports on musculoskeletal health in the elderly.

There is insufficient information on the effect of exercise and sports on musculoskeletal health in the elderly. Although the effects of sports are still unclear, the effects of exercise could be significant. For example, exercise improves osteoporosis by increasing bone mineral density and ameliorates sarcopenia by increasing muscle mass, muscular strength, and walking speed. As a result, fall risk is reduced and fracture risk is also likely to improve. Tai Chi is reportedly effective for joint pain and stiffness, and may improve symptoms of osteoarthritis.

Impact of Physical Activity in Cardiovascular and Musculoskeletal Health: Can Motion Be Medicine?

Physical activity is a well-known therapeutic tool for various types of medical conditions, including vasculopathic diseases such as coronary artery disease, stroke, type 2 diabetes, and obesity. Additionally, increased physical activity has been proposed as a therapy to improve musculoskeletal health; however, there are conflicting reports about physical activity potentially leading to degenerative musculoskeletal disease, especially osteoarthritis (OA). Additionally, although physical activity is known to have its benefits, it is unclear as to what amount of physical activity is the most advantageous. Too much, as well as not enough exercise can have negative consequences. This could impact how physicians advise their patients about exercise intensity. Multiple studies have evaluated the effect of physical activity on various aspects of health. However, there is a paucity of systematic studies which review cardiovascular and musculoskeletal health as outcomes. Therefore, the purpose of this review was to assess how physical activity impacts these aspects of health. Specifically, we evaluated the effect of various levels of physical activity on: 1) cardiovascular and 2) musculoskeletal health. The review revealed that physical activity may decrease cardiovascular disease and improve OA symptoms, and therefore, motion can be considered a “medicine”. However, because heavy activity can potentially lead to increased OA risk, physicians should advise their patients that excessive activity can also potentially impact their health negatively, and should be done in moderation, until further study.

Is yoga better than aerobic/strengthening exercises for managing knee osteoarthritis in older adults?

Is yoga better than aerobic/strengthening exercises for managing knee osteoarthritis in older adults?

Capsule commentary on Agarwal et al., Healthcare Expenditures Associated with Depression among Individuals with Osteoarthritis: Post-Regression Linear Decomposition Approach.

Agarwal et al. estimate excess total healthcare expenditures associated with depression among adults with osteoarthritis, and use post-regression linear decomposition to examine which individual-level factors contribute to these costs, based on data from the 2010Medical Expenditure Panel Survey. The authors found that patients with comorbid osteoarthritis and depression had 38.8 % greater total healthcare costs compared to those without depression. These excess costs were attributable to comorbid anxiety, chronic conditions, and poor health status. Depression is common in primary care, and when present, exacerbates any symptom-based problems the patient may have. Numerous articles have shown that patients with depression have lower quality of life, lower functional status, more pain, and a greater number of physical symptoms. While antidepressant therapy can improve depressive symptoms, the evidence of benefit for pain and other physical symptoms is less robust; in general, depressed patients have improvement in functioning and comorbid symptoms when their depression is successfully treated. Whether treatment of depression in patients with comorbid osteoarthritis would reduce costs or improve osteoarthritis symptoms is uncertain, and is worthy of further research. Observational data are always subject to bias. For example, diabetics with depression have shown worse outcomes than patients without depression, but randomized trials investigating depression among diabetics showed disappointing results regarding the impact on diabetic outcomes. The most successful healthcare delivery systems for managing depression are collaborative. For example, the Depression Improvement Across Minnesota, Offering a NewDirection (DIAMOND) model used in Minnesota was found to be beneficial for improving treatment outcomes in patients withmajor depressive disorders. A similar model, the Massachusetts General Physicians Organization, reduced costs and improved care in high-utilizing patients with multiple chronic conditions, though depression was not specifically targeted in this population. Whether collaborative care models that target both depression and physical symptoms would do better than those focused solely on depression is worthy of future research.