Relevant bibliographies by topics / Osteoarthritis and obesity

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Osteoarthritis and obesity'

Author: Grafiati
Published: 5 June 2025
Last updated: 24 June 2025

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Journal articles on the topic "Osteoarthritis and obesity"

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Yang, Tzi-Peng, Hsiao-Mei Chen, Chao-Chin Hu, et al. "Interaction of Osteoarthritis and BMI on Leptin Promoter Methylation in Taiwanese Adults." International Journal of Molecular Sciences 21, no. 1 (2019): 123. http://dx.doi.org/10.3390/ijms21010123.

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Leptin (LEP) regulates glucose metabolism and energy storage in the body. Osteoarthritis (OA) is associated with the upregulation of serum LEP. LEP promoter methylation is associated with obesity. So far, few studies have explored the association of BMI and OA with LEP methylation. We assessed the interaction between body mass index (BMI) and OA on LEP promoter methylation. Data of 1114 participants comprising 583 men and 558 women, aged 30–70 years were retrieved from the Taiwan Biobank Database (2008–2015). Osteoarthritis was self-reported and cases were those who reported having ever been clinically diagnosed with osteoarthritis. BMI was categorized into underweight, normal weight, overweight, and obesity. The mean LEP promoter methylation level in individuals with osteoarthritis was 0.5509 ± 0.00437 and 0.5375 ± 0.00101 in those without osteoarthritis. The interaction between osteoarthritis and BMI on LEP promoter methylation was significant (p-value = 0.0180). With normal BMI as the reference, the mean LEP promoter methylation level was significantly higher in obese osteoarthritic individuals (β = 0.03696, p-value = 0.0187). However, there was no significant association between BMI and LEP promoter methylation in individuals without osteoarthritis, regardless of BMI. In conclusion, only obesity was significantly associated with LEP promoter methylation (higher levels) specifically in osteoarthritic patients.
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Syifaa', Arifah, Zurriyani Zurriyani, and Zuheri Zuheri. "Prevalensi Obesitas terhadap Kejadian Osteoarthritis di Poliklinik Penyakit Dalam RS Pertamedika Ummi Rosnati Banda Aceh." MEDIA KESEHATAN MASYARAKAT INDONESIA 21, no. 3 (2022): 190–95. http://dx.doi.org/10.14710/mkmi.21.3.190-195.

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Latar belakang: Osteoarthritis sering terjadi pada kalangan masyarakat yang dapat menimbulkan nyeri dan kecacatan sehingga menggangu kegiatan sehari-hari. Satu dari beberapa faktor yang menyebabkan perkembangan osteoarthritis yaitu obesitas. Obesitas dapat meningkatkan perkembangan osteoarthritis pada sendi melalui dampak biomekanik dan biokimia. Tujuan dilaksanakannya penelitian ini adalah mengetahui prevalensi obesitas terhadap kejadian osteoarthritis pada pasien osteoarthritis di Poliklinik Penyakit Dalam yang ada di RS Pertamedika Ummi Rosnati Banda Aceh.Metode: Metode observasional deskriptif digunakan di penelitian ini dengan pendekatan cross sectional. Penelitian ini dilaksanakan pada periode Februari - April 2021 menggunakan data primer serta sekunder. Sampel secara total sampling berjumlah 70 responden.Hasil: Hasil penelitian berdasarkan kategori BMI didapatkan jumlah penderita osteoarthritis yang mengalami obesitas sebanyak 49 orang (70%). Penelitian ini menunjukkan bahwa penderita osteoarthritis yang mengalami obesitas, paling tinggi terjadi pada wanita yaitu 43 orang (87,8%), sebagian besar merupakan kelompok usia 50-60 tahun berjumlah 23 orang (46,9%), mayoritas adalah ibu rumah tangga yaitu 33 orang (67,3%), sebagian besar tidak memiliki riwayat genetik sejumlah 31 orang (63,3%), sebagian besar tidak ada riwayat trauma yaitu 35 orang (71,4%), dan sebagian besar mengalami osteoarthritis pada sendi lutut yaitu 35 orang (71,4%).Simpulan: Sebagian besar responden osteoarthritis mengalami obesitas.Kata kunci: Osteoarthritis; ObesitasABSTRACTTitle: Obesity Prevalence on Osteoarthritis Incidence in Internal Medicine Polyclinic of Pertamedika Ummi Rosnati Hospital Banda Aceh.Background: Osteoarthritis often occurs in the community which can cause pain and disability so that it interferes with daily activities. One of several factors that lead to the development of osteoarthritis is obesity. Obesity can promote the development of osteoarthritis by increasing the load on the joints through biomechanical and biochemical impacts. The purpose of this study was to determine the prevalence of obesity on the incidence of osteoarthritis in osteoarthritis patients at the Internal Medicine Polyclinic at Pertamedika Ummi Rosnati Hospital, Banda Aceh. Method:Descriptive observational method used in this study with a cross sectional approach. This research was conducted during the period February-April 2021 using primary and secondary data. The sample in total sampling amounted to 70 respondents. Result:The results of the study based on the BMI category showed that the number of patients with osteoarthritis who were obese was 49 people (70%). This study shows that obese osteoarthritis sufferers, the highest occurred in women, namely 43 people (87.8%), most of them were in the 50-60 year age group totaling 23 people (46.9%), the majority were housewives, namely 33 people (67.3%), most of them did not have a genetic history of 31 people (63.3%), most of them did not have a history of trauma as many as 35 people (71.4%), and most of them had osteoarthritis in the knee joint, namely 35 people (71.4%).Conclusion: Most of osteoarthritis respondent were obese.Keywords: Osteoarthritis; Obesity
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Kulkarni, Kunal, Timothy Karssiens, Vijay Kumar, and Hemant Pandit. "Obesity and osteoarthritis." Maturitas 89 (July 2016): 22–28. http://dx.doi.org/10.1016/j.maturitas.2016.04.006.

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Strebkova, E. A., and L. I. Alekseeva. "OSTEOARTHRITIS AND OBESITY." Rheumatology Science and Practice 53, no. 5 (2015): 542–52. http://dx.doi.org/10.14412/1995-4484-2015-542-552.

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Hawker, Gillian A. "Osteoarthritis & Obesity." Canadian Journal of Diabetes 37 (April 2013): S219—S220. http://dx.doi.org/10.1016/j.jcjd.2013.03.043.

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Anggraini, Niken Enestasia, and Lucia Yovita Hendrati. "The Relation of Obesity and Individual Factors with Knee Osteoarthritis." Jurnal Berkala Epidemiologi 2, no. 1 (2014): 93. http://dx.doi.org/10.20473/jbe.v2i1.2014.93-104.

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ABSTRACTOsteoarthritis represent disease at most found in the world, including in Indonesia. This disease cause pain in bone and disability at patient so disturb everyday activity. One of removed occurrence of knee Osteoarthritis was obesity. Other factors like age, gender, physical activity, and habit smoke were risk factors of knee Osteoarthritis . This research was the relationship of obesitas and individuals factors with occurrence knee osteoarthritis at Surabaya Islamic Hospital. The methods of this research was an observation with case control design. Level of sampel was 64 which consist of 32 case group and 32 control group from incomed patient to radiology unit Islamic Hospital Surabaya for X-Ray photo. The dependent variable was occurence of knee osteoarthritis . The independent variables were obesity, gender, age, physical activity, habit smoke. The instrument used was a questionnaire and form BMI measurement. Data analysis used Chi-Square test with α=0,05 and to know oods ratio (OR) used statclac. The results showed significant relationship between occurence of knee osteoartritis with obesity (p=0,001,OR=7,20), age (p=0,012,OR=3,67) , gender (p=0,005,OR=4,69). For the characteristic of habit smoke (p=0,268,OR=0,56) and physical activity (p=0.919,OR=0,71) were’nt associated with occurence of knee Osteoarthritis at Surabaya Islamic Hospital. The conclusion there is relationship between obesity with knee osteoarthritis at Surabaya Islamic Hospital. Risk factor knee osteoarthritis like gender and age also there were relation with occurence of knee osteoarthritis , for the risk factor of physical activity and habit smoke were’nt relation with occurence of knee osteoarthritis. Keyword : Knee osteoarthritis, obesity, individual factors
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Anggraini, Niken Enestasia, and Lucia Yovita Hendrati. "The Relation of Obesity and Individual Factors with Knee Osteoarthritis." Jurnal Berkala Epidemiologi 2, no. 1 (2014): 93. http://dx.doi.org/10.20473/jbe.v2i12014.93-104.

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ABSTRACTOsteoarthritis represent disease at most found in the world, including in Indonesia. This disease cause pain in bone and disability at patient so disturb everyday activity. One of removed occurrence of knee Osteoarthritis was obesity. Other factors like age, gender, physical activity, and habit smoke were risk factors of knee Osteoarthritis . This research was the relationship of obesitas and individuals factors with occurrence knee osteoarthritis at Surabaya Islamic Hospital. The methods of this research was an observation with case control design. Level of sampel was 64 which consist of 32 case group and 32 control group from incomed patient to radiology unit Islamic Hospital Surabaya for X-Ray photo. The dependent variable was occurence of knee osteoarthritis . The independent variables were obesity, gender, age, physical activity, habit smoke. The instrument used was a questionnaire and form BMI measurement. Data analysis used Chi-Square test with α=0,05 and to know oods ratio (OR) used statclac. The results showed significant relationship between occurence of knee osteoartritis with obesity (p=0,001,OR=7,20), age (p=0,012,OR=3,67) , gender (p=0,005,OR=4,69). For the characteristic of habit smoke (p=0,268,OR=0,56) and physical activity (p=0.919,OR=0,71) were’nt associated with occurence of knee Osteoarthritis at Surabaya Islamic Hospital. The conclusion there is relationship between obesity with knee osteoarthritis at Surabaya Islamic Hospital. Risk factor knee osteoarthritis like gender and age also there were relation with occurence of knee osteoarthritis , for the risk factor of physical activity and habit smoke were’nt relation with occurence of knee osteoarthritis. Keyword : Knee osteoarthritis, obesity, individual factors
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Efendi, Refangga Lova Nusantara, Zulfachmi Wahab, and M. Riza Setiawan. "Central and Peripheral Obesity on Severity Knee Osteoarthritis." MAGNA MEDICA Berkala Ilmiah Kedokteran dan Kesehatan 1, no. 3 (2021): 64. http://dx.doi.org/10.26714/magnamed.1.3.2016.64-68.

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Background: Obesity can affect severity of knee osteoarthritis sufferers. Several studies have examined relationship between obesity and osteoarthritis, but no one has examined the different types of obesity on osteoarthritis, therefore, researchers wanted to know differences of central and peripheral obesity on severity osteoarthritis.Methods: A retrospective studi, with cross-sectional, simple random sampling method, conducted between 1 August 2014 and 30 September 2014 in Semarang City. Samples people > 50 years old. Data were analyzed by rank Spearman and Anova correlation.Results: In this study, 45.7% (n = 32) reported severe osteoarthritis. The results of the statistical test obtained p1 = 0,000 (reject Ho). The correlation coefficient (r) is 0.857 (strong), and the linear pattern is positive. The coefficient of determination (r2) is obtained (0.857) 2 = 0.73 = 73%. And 37.1% (N = 26) reported being obese. p2 = 0.043 (reject Ho). The mean deviation (MD) was 0.048 (not significant) between central obesity and peripheral obesity.Conclusion: Obesity affects severity of knee osteoarthritis. The greater body mass index, greater severity of knee osteoarthritis. 73% of severity of knee osteoarthritis is influenced by obesity, but there is no significant effect between central and peripheral obesity on the occurrence of knee osteoarthritis.
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Holubkina, Ye O., and T. M. Tykhonova. "Pathogenetic features in patients with various phenotypic forms of obesity and osteoarthritis: focus on meta-inflammation." Journal of V. N. Karazin Kharkiv National University, Series "Medicine", no. 49 (June 28, 2024): 238–55. http://dx.doi.org/10.26565/2313-6693-2024-49-12.

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Background. Obesity occupies one of the leading places in the structure of non-communicable diseases and according to modern views it is a trigger factor for the occurrence of concomitant pathology, in particular, osteoarthritis. The driving force in osteoarthritis pathogenesis is not only an increase in mechanical load on the joints, but also the production of inflammatory mediators and hormones by adipose tissue, which subsequently leads to metabolic disorders in the osteoarticular system. In regard of the heterogeneity concept of obesity an important task is to study the relationship between the pathogenetic features of various obesity phenotypes and osteoarthritis development. However, despite numerous studies, there are many unresolved questions and controversial points of view on this problem. Purpose – based on the study of literary sources, mainly over the last 10 years, to analyze the pathogenetic features of obesity phenotypes and their relationship with the occurrence and progression of osteoarthritis, as well as to determine the role of inflammation in the structure of these disorders. Materials and Methods. Literature data obtained as a result of an electronic search in the MEDLINE/PubMed, Google Scholar and Web of Science databases using the following Keywords: «obesity», «metabolically healthy obesity», «metabolically unhealthy obesity», «osteoarthritis», «meta-inflammation» was studied and analyzed. Results. Obesity is characterized by a variety of phenotypes, such as: metabolically unhealthy obesity, metabolically healthy obesity, metabolic obesity with normal body weight. While metabolically healthy obesity has more favorable clinical features compared to metabolically unhealthy obesity due to the absence of metabolic disorders and lower levels of inflammatory markers, its verification is complicated with the absence of unified diagnosis criteria. The pathogenesis of osteoarthritis is closely related to obesity: the complex interaction of the metabolic syndrome components leads to the development of chronic low-level inflammation. These processes contribute to disruption of the blood and nerve supply to the joint, synovitis and cartilage destruction thus promoting osteoarthritis onset and progression. Patients with metabolically healthy obesity and metabolic obesity with normal body weight have a lower prevalence of osteoarthritis in comparison with metabolically unhealthy obesity. Conclusions. Involvement of inflammatory factors in the pathogenesis of osteoarthritis and its association with obesity and metabolic syndrome favor the relevance of studying the relationship between obesity and osteoarthritis. However, despite the results of numerous research works related to the influence of metabolic syndrome on the development of osteoarthritis, there is lack of studies on the relationship of osteoarthritis with other phenotypes of obesity, such as metabolically healthy obesity and metabolic obesity with normal body weight. The potential for transition from metabolically healthy to metabolically unhealthy obesity defines metabolically healthy obesity as a transient condition. Regarding this, further study is needed to develop unified and adequate criteria for obesity phenotypes to determine adequate management tactics and prevent the development of its complications and associated musculoskeletal system pathology.
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Marks, Ray. "Obesity, Osteoarthritis and Pain." Advances in Obesity, Weight Management & Control 2, no. 1 (2014): 1–6. http://dx.doi.org/10.15406/aowmc.2014.02.00006.

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Dissertations / Theses on the topic "Osteoarthritis and obesity"

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Harasymowicz, Natalia Sara. "Role of severe obesity in osteoarthritis." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/22930.

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Osteoarthritis (OA) is the most common degenerative joint disease affecting more than 40% of people above the age of 65 (Neogi et al., 2013). Obesity is one of the main risk factors of OA and has become a major problem in Western societies. With sedentary lifestyle and the aging of the population, it is estimated that more than 50% of British adults will be obese in 2030 (Wang et al., 2011). So far, the effect of obesity on joint degeneration has primarily been explained by the increased load on the joints. However, a growing number of studies have revealed that adipose tissue can affect cartilage and other joint tissues at a molecular level. The main goal of this thesis was to investigate the role of local knee joint tissues in obese patients with OA. The expression of molecular markers was investigated in local knee tissues: cartilage, synovium, infrapatellar fat pad (IPFP) and subchondral bone collected during Total Knee Replacement (TKR). A range of techniques (RT-PCR, Real Time qPCR, WB, IHC/ICC and ELISA) was used to examine the differences between genes and proteins expression in both lean and obese patients with OA. Further, the local immune cell infiltration was investigated in knee adipose tissue depots (synovium and IPFP) using flow cytometry. In addition, the subchondral bone microstructure was analysed using micro-Computed Tomography (μCT) and IHC techniques. Chondrocytes from OA patients were found to express a range of obesity-related genes. ADIPOR1 was produced significantly higher than ADIPOR2 in OA chondrocytes. Furthermore, CCL2 was produced at higher while PPARγ and visfatin were produced at a lower level in obese patients’ chondrocytes in comparison to lean ones. Synovium and IPFP also expressed a range of obesity-related genes. PPARγ and visfatin expression was lower in obese synovium and IPFP in comparison to lean. Surprisingly, adiponectin was expressed at a significantly lower level in obese patients’ synovium. In contrast, adiponectin was not differently expressed in lean and obese patients’ IPFP. The IPFP was found to be a significantly higher producer of PPARγ and adiponectin in comparison to synovium. Synovium, on the other hand, has an increased expression of VCAM-1, TLR4 and CCL2 in obese patients. An increased number of macrophages (defined by CD45+CD14+ and CD14+CD206+ markers expression) was detected in the synovium and IPFP from obese OA patients. Furthermore, there was an increased number of CD86+CD14+ cells in the synovium from obese patients. Other macrophage-related proteins including HLA-DR, CD36 were also expressed at a higher level in synovium from obese patients. T-lymphocyte detection revealed a higher number of CD3+CD4+ T cells in the synovium (but not IPFP) from obese patients but no change in the CD3+CD8+ population in both the synovium and IPFP. Subchondral bone analysis revealed possible differences in this tissue in obese male patients with OA in comparison to lean patients. μCT examination of subchondral bone showed a significantly lower bone mineral density (BMD) in obese in comparison to lean male OA patients. IHC analysis of bone sections suggested that there was an increased number of bone marrow adipose tissue macrophages. In addition, osteoblasts obtained from obese OA donors expressed a significantly higher level of ADIPOR2 and lower level of PPARγ mRNA in comparison to lean patients’ osteoblasts. The data obtained suggests that there were differences between lean and obese patients with OA at a molecular level. This proposes possible future directions for targeting these diseases. The limitation of the study were as follows: 1) possible different stages of end-stage OA between analysed patients, which could lead to differences in obtained data, 2) no non-OA control samples included in the study. However, the presented study may suggest that all tissues in the knee joint contribute to the interplay between OA and obesity. In addition, the data obtained is the first to suggest that there are differences in gene and protein expression in the synovium and IPFP from the same donor. Furthermore, there are differences in the immune cell populations in local adipose tissue depots (synovium and IPFP) from OA joints, which are linked to obesity. All of this data has helped to increase our understanding of the interaction between obesity and OA.
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Austin, Gretchen E. "Diet quality in older, overweight, and obese adults with knee osteoarthritis." Electronic thesis, 2002. http://dspace.zsr.wfu.edu/jspui/handle/10339/171.

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Pierce, Benjamin D. "The severity of obesity and knee osteoarthritis effects on strength and gait /." Winston-Salem, NC : Wake Forest University, 2009. http://dspace.zsr.wfu.edu/jspui/handle/10339/42589.

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Thesis (M.S.)--Wake Forest University. Dept. of Health and Exercise Science, 2009.<br>Title from electronic thesis title page. Thesis advisor: Stephen P. Messier. Vita. Includes bibliographical references (p. 66-73).
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Sun, Antonia Rujia. "Macrophage-mediated synovial inflammation is a key link to obesity-associated osteoarthritis." Thesis, Queensland University of Technology, 2018. https://eprints.qut.edu.au/123711/1/Antonia%20Rujia_Sun_Thesis.pdf.

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Obesity has been attributed in a major risk factor for developing and accelerating disease progression in osteoarthritis. To date, there is a lack of clinically proven therapies to halt osteoarthritis, the developments of such therapies are therefore a national as well as an international research priority. This research provides a new overview of the involvement of synovitis in promoting the destruction of synovial joints in obesity-induced osteoarthritis and might therefore by used as a therapeutic strategy for the development of disease-modifying anti-osteoarthritis drugs.
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Cléret, Damien. "Vascularisation et angiogenèse ostéochondrale dans différents phénotypes de souris arthrosiques." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSES037/document.

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L'obésité (Ob) est un facteur de risque majeur pour l'arthrose (OA). L'angiogenèse de l'os sous-chondral est impliquée dans la pathophysiologie de l'OA et peut réagir différemment aux facteurs de promotion de l'OA. L’objectif était de discriminer le rôle respectif de la charge liée au surpoids et des troubles métaboliques sur la dégradation articulaire et l'angiogenèse, dans un modèle de souris arthrosique. Des souris C57BL/6j ont subi une déstabilisation chirurgicale du ménisque médiale pour induire l'OA. Des souris OA-Mince ont ensuite été soumises à une hypergravité pour imiter les effets du surpoids. Les autres souris ont été conservées à 1g. Des souris OA-mince et des souris OA-Ob ont été traitées avec un anti-VEGF. Après la perfusion de baryum, le genou droit a été imagé et la microstructure osseuse, la moelle osseuse et les réseaux vasculaires sous-chondraux ont été quantifiés. L'histologie quantitative de l'os sous-chondral a été effectué. La dégradation du cartilage articulaire était similaire entre les groupes OA. L'hypergravité n'a pas aggravé l'amincissement du cartilage induit par l’OA mais a empêché l'épaississement lié à l'OA de la plaque osseuse sous-chondrale. Les souris OA-Ob avaient un volume osseux trabéculaire épiphysaire inférieur à celui des souris Mince-OA. L’OA a induit une angiogenèse à travers la plaque sous-chondrale dans les groupes OA-Mince 1g et 2g. En revanche, la densité vasculaire de la Mo était plus faible chez les OA-Ob que chez OA-Mince. L'obésité et le 2g ont eu des effets opposés sur la taille des vaisseaux. Le bevacizumab a empêché l'angiogenèse induite par l'OA dans le groupe OA-Mince mais n'a eu aucun effet dans le groupe Ob<br>Obesity is a major risk factor for osteoarthritis (OA). Subchondral bone angiogenesis is involved in OA pathophysiology and may respond differently to OA promoting factors. Aim was to discriminate the respective role of overweight-related-load and of metabolic disorders due to fat accumulation, in joint degradation and angiogenesis, in a mouse model of surgically Induced knee osteoarthritis. C57BL/6j male mice underwent surgical medial meniscus destabilization (MMD) to induce OA and Lean mice were sham operated (Sham-lean). At 2 Mo, gps were fed with high fat diet to induce insulino-resistance and obesity (Ob). OA-Lean mice were then submitted to 2g hypergravity in a centrifuge to mimic the effects of overweight. OA-lean mice and OA-Ob mice were treated with an anti-VEGF. After barium infusion, the right knee was imaged by high-resolution and bone microstructure, bone marrow (bm) and subchrondral vascular networks were quantified. After MMA embedding, OARSI scoring and subchondral bone quantitative histology were then carried out at the medial tibia plateau.Articular cartilage degradation was similar between the OA groups
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Soutakbar, Hessam. "The association of physical activity, obesity and injury on the risk of knee osteoarthritis." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/40281/.

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Title: The association of physical activity, obesity and injury on the risk of knee osteoarthritis (OA) Purpose: 1) To examine the effect of interactions between physical activity, obesity and injury on the incidence and progression of radiographic and symptomatic knee OA; 2) To establish age and gender specific normative data for knee pain, symptoms, function and knee related quality of life (QOL) as the clinical outcome measures in assessing people with knee OA and to examine their associations with OA risk factors including obesity, injury and physical activity. Methods: 1) Using existing cohort data from Osteoarthritis Initiative (OAI) and Multicenter Osteoarthritis Study (MOST) for interaction analyses Participants without radiographic knee OA at baseline were followed for the incidence of radiographic and symptomatic knee OA. In OAI, the focus was on the tibiofemoral joints (TF) only, so TF-OA was defined as a knee with a Kellgren and Lawrence (KL) grade 2 or greater. In MOST, knee OA was defined as a knee with TF-OA (KL ≥2) and/or patellofemoral- OA (osteophyte ≥2; or joint space narrowing ≥1 plus any cyst, osteophyte, or sclerosis using Osteoarthritis Research Society International atlas). The co-occurrence of radiographic knee OA and the frequent knee symptoms (pain, ache, or stiffness on most days of a month over the past 12 months) at the last follow-up was considered as the incidence of symptomatic knee OA. Progression of radiographic knee OA was determined as either one grade increase in KL score or one grade worsening in joint space narrowing at the last follow-up, in participants with radiographic knee OA at baseline. For the progression of symptomatic knee OA, participants with frequent knee symptoms at baseline were included. An increase of greater than 9.29 points in the total Western Ontario and McMaster Universities Osteoarthritis Index score from baseline to last follow-up was considered as a cut-off point (minimal clinical important worsening) for considering a person with symptom progression. Body mass index (obese/non-obese), injury (yes/no), physical activity (active/inactive), age and gender data were also collected at baseline in both databases. The measures of interactions on both additive and multiplicative scales were computed using the generalized estimation equation. 2) Establishing age and gender specific reference values data for Knee Injury and Osteoarthritis Outcome Score (KOOS) and Oxford Knee Score (OKS) Volunteer participants were recruited via a postal survey. From a list of 25,695 postcodes specified by Nottinghamshire local authorities and in the City of Nottingham, 2,500 postcodes were randomly selected. This was based on the proportion of the population in each local authority and in the City of Nottingham. 2,500 postcodes were then equally and randomly assigned into three age groups of 18-44, 45-69 and ≥70 years old. From each postcode assigned to the specific age group, one name and address was randomly selected. Participants were required to complete the questionnaire booklet once only. The questionnaire booklet consisted of the OKS and the KOOS questionnaires. It also collected information regarding participants’ age, gender, height, weight, history of injury and knee joint replacement and physical activity. Results: Interaction analysis In both cohorts, active and inactive people had a similar risk of incident radiographic or symptomatic knee OA (p > 0.05). This effect was not modified by obesity and/or injury in either cohort (p interactions > 0.05). No significant interactions were also found between physical activity, obesity and injury on the risk of radiographic or symptomatic knee OA progression (p interaction > 0.05). Obese people in both cohorts were significantly at a higher risk of incident radiographic and symptomatic knee OA when compared to non-obese people (p < 0.01); injury also increased the incident risk of knee OA (p < 0.01). There were some evidence of positive interactions between obesity and injury on the risk of incident knee OA. This reached statistical significance on additive and multiplicative scales in OAI (aOR-Symptomatic-multiplicative interaction: 2.83, 95%CI: 1.01 to 7.93; aOR-Symptomatic-additive interaction: 3.13, 95%CI: 0.05 to 6.21) and on additive scale in MOST (aOR- Radiological-additive interaction: 1.51, 95%CI: 0.10 to 2.93). There was no evidence of any statistically significant interaction between obesity and injury on the progressive risk of knee OA. Reference values data The overall response rate was 16.5% (n =414, 45% male, 55% female), with the highest in the middle age group with 24%, 18% in the old age and 8% in young age group. A significant dose response relationship was seen between increasing age and worsening scores of KOOS-Pain; KOOS- Activities of daily living (ADL); KOOS-QOL; and OKS (p < 0.05). The median (M) and inter quartile range (IQ) in old, middle and young age groups were as follows: KOOS-Pain (M, IQ: 91.6, 58.3-100; 94.4, 77.7-100; 100, 80.5-100), KOOS- ADL (M, IQ: 91.1, 59.3-100; 98.5, 77.2-100; 100, 89.7-100), KOOS-QOL (M, IQ: 81.2, 43.7-100; 87.5, 62.5-100; 87.5, 68.7-100), and OKS (M,IQ: 42.3, 29-48; 46, 38-48; 47, 42- 48). The oldest age group had the worst scores in KOOS-Pain, KOOS-ADL; KOOS-QOL; and OKS compared to the young or middle age groups (p < 0.05). However, the differences between young and middle age groups were not statistically significant in any KOOS or OKS scores (p > 0.05). Data were also stratified by gender. There was no gender difference in any KOOS or OKS scores (p > 0.05). Obesity and injury were also found as the strongest predictors for the worsening score in all KOOS and OKS subscale scores (p < 0.05), whereas physical activity was significantly associated with a lower risk of knee related complaints (p < 0.05). Conclusion: Physical activity did not increase the risk of incident or progressive knee OA at any level of obesity and/or injury in middle aged and older people with or at high risk of knee OA. In addition, meeting the minimum physical activity guidelines was significantly associated with lower self-reported knee complaints evaluated by KOOS and OKS. Therefore, moderate levels of physical activity appears to be safe to recommend to the general population and people with or at high risk of knee OA regardless of obesity and injury status. There was also some modest evidence of positive interaction between obesity and injury on the risk of incident knee OA. Hence, weight gain prevention strategies may protect injured people against further increase in the risk of knee OA. This study also provided normative data for KOOS and OKS. The self-reported knee complaints were found to vary with age (not gender) being highest in the oldest age group. This suggests that treatment outcomes in people with knee injury and knee OA should be compared against age-matched reference values from the general population.
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Liakhovych, O. D. "Some features of the clinical course of osteoarthritis in patients with comorbid nonalcoholic steatohepatitis and obesity." Thesis, БДМУ, 2022. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/19619.

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Dechaumet, Benoît. "Effets des troubles métaboliques et du surpoids liés à l’obésité sur le système musculo-squelettique murin arthrosique ou non : traitement potentiel par vibration corps entier." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSES045/document.

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L'obésité est associée à un risque de fragilité musculo-squelettique, en particulier d’arthrose (OA). Notre but est d’explorer leurs contributions des conditions métaboliques et du surpoids. L’obésité MM (mécanique et métabolique) est obtenue par un régime alimentaire. L’obésité M (mécanique) est mimée par hypergravité à 2g. L’OA est induite par acte chirurgicale. Nous avons exploré les effets des obésités MM et M sur le système musculo-squelettique de souris non OA. Les MM ont un os trabéculaire préservé, un os cortical détérioré et des muscles fragilisés. Chez les M, l’os est préservé et les muscles sont renforcés. Les troubles métaboliques sont responsables de la fragilisation de l’os cortical et du muscle. Dans une 2ème partie, les conséquences de l’OA sont évaluées chez des souris non obèses, MM ou M. L’OA chez les non obèses fragilise uniquement l’os trabéculaire. L’OA chez les MM accentue la diminution de l’épaisseur corticale. L’OA chez les souris M fragilise encore plus l’os cortical et le muscle que chez les souris MM. Cependant si on ne considère que les souris OA, la composante MM est toujours plus délétère que la composante M. Finalement, nous avons testé les vibrations corps entiers pendant les 4 dernières semaines comme traitement potentiel des détériorations musculo-squelettiques des MM couplée ou non à l’OA. Les vibrations n’impactent pas l’obésité et l’OA. Un effet musculaire est observé au niveau moléculaire, ces diminutions étant plus importantes chez les OA. Aucun changement de masse musculaire n’est observé. Le tissu osseux n’est pas influencé<br>Obesity is associated with a risk of musculoskeletal fragility, especially osteoarthritis (OA). Our goal is to explore their contributions of metabolic and overweight conditions. MM obesity (mechanical and metabolic) is obtained through a diet. Obesity M (mechanical) is mimed by hypergravity at 2g. OA is induced by surgery. We explored the effects of MM and M obesity on the non-OA mouse musculoskeletal system. MMs have preserved trabecular bone, deteriorated cortical bone and weakened muscles. In M, bone is preserved and muscles are strengthened. Metabolic disorders are responsible for the weakening of cortical bone and muscle. In a second part, the consequences of OA are evaluated in non-obese mice, MM or M. OA in non-obese only weakens the trabecular bone. OA in MM accentuates the decrease in cortical thickness. OA in M mice further weakens cortical bone and muscle than in MM mice. However, if we consider only the OA mice, the MM component is always more deleterious than the M component. Finally, we tested entire body vibrations during the last 4 weeks as a potential treatment for musculoskeletal deterioration of MM, whether or not coupled to OA. Vibrations do not affect obesity and OA. A muscular effect is observed at the molecular level, these decreases being greater in OA. No change in muscle mass is observed. The bone tissue is not influenced
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Nigoro, Kazuya. "Obesity with radiological changes or depression was associated with worse knee outcome in general population: a cluster analysis in the Nagahama study." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/264660.

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京都大学<br>新制・課程博士<br>博士(医学)<br>甲第23379号<br>医博第4748号<br>新制||医||1052(附属図書館)<br>京都大学大学院医学研究科医学専攻<br>(主査)教授 石見 拓, 教授 戸口田 淳也, 教授 中山 健夫<br>学位規則第4条第1項該当<br>Doctor of Medical Science<br>Kyoto University<br>DFAM
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Francin, Pierre-Jean. "Rôle des adipokines dans la physiopathologie de l'arthrose : exemple de la leptine et de l'adiponectine." Thesis, Nancy 1, 2010. http://www.theses.fr/2010NAN10057/document.

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L’arthrose est une maladie dégénérative des articulations et représente la deuxième cause d’invalidité en France. En raison des liens entre l’obésité et l’arthrose concernant à la fois les articulations portantes et non portantes, nous faisons l’hypothèse que des protéines produites par le tissu adipeux, les adipokines, constituent des facteurs clés impliqués dans cette arthropathie. En premier lieu, nous avons montré que l’expression de la leptine, de l’adiponectine et de leurs récepteurs évolue de façon inverse et dépend fortement de l’état de différenciation des chondrocytes. Dans une seconde étude, nous avons comparé la production des adipokines par le ligament adipeux de Hoffa à celle mesurée dans la graisse sous-cutanée et avons ainsi mis en évidence des différences entre les 2 tissus adipeux. Les travaux réalisés ensuite ont permis de préciser le rôle des adipokines dans l’arthrose. Ainsi, la production d’adiponectine par les chondrocytes augmente lorsque le cartilage se dégrade et apparaît directement reliée à celle de la MMP-13 et du TGF-[bêta]. En revanche, l’expression de son récepteur AdipoR1 est associée à l’expression d’éléments matriciels et d’un facteur de transcription spécifique du cartilage impliqué dans la synthèse de ces éléments. Le traitement des chondrocytes à l’adiponectine a permis de confirmer in vitro les données observées in vivo chez les patients atteints d’arthrose, à savoir que l’adiponectine induit l’expression du TGF-[bêta]et de la MMP-13. Les résultats obtenus avec la leptine indiquent par ailleurs que l’obésité influence fortement la réponse des chondrocytes à cette adipokine. Elle semble ainsi protéger le cartilage chez les patients non obèses en stimulant l’expression de l’IGF-1, du collagène de type 2 et du TIMP-2, mais contribue au processus dégénératif chez les patients obèses en augmentant l’expression de la MMP-13. Enfin l’induction d’une arthrose expérimentale chez le rat Zucker n’ayant pas de récepteur fonctionnel à la leptine a montré que cette adipokine est susceptible de préserver l’articulation des modifications du cartilage et surtout de l’os sous-chondral<br>Osteoarthritis (OA) is a degenerative joint disease and represents one of the most frequent and disabling disease. There is a positive association between obesity and OA, and not only for knee joints but also for non-weight-bearing joints suggesting that adipose-derived proteins, namely adipokines, may be some keys factors in OA pathophysiology. First, we found that leptin and adiponectin expression and their receptor evolves in an opposite way and depend on differenciation stage of chondrocyte. The production of adipokines were then compared according to adipose tissue and some differences were found between, the infrapatellat fat pad and subcutaneous adipose tissue. After this work, we aimed to further characterize the role of leptin and adiponectin in OA. Adiponectin production by chondrocytes increases when cartilage is damaged and seems to be directly related with MMP-13 and TGF-[bêta] expression. AdipoR1 expression is associated with the expression of matrix components and with Sox9, a transcription factor involved in their synthesis. Adiponectin treatment confirms data in OA patient, that is adiponectin can induce TGF-[bêta] and MMP-13. Then, we showed obesity influences the chondrocyte responsivness to leptin. This adipokine seems to protect cartilage collected from normal or overweight patient by stimulating IGF-1, type 2 collagen and TIMP-2 expression while leptin increases MMP-13 expression for obese patients. Finally, experimental OA in Zucker rat deficient in leptin receptor, showed the protective effect of leptin on cartilage and on subchondral bone
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Books on the topic "Osteoarthritis and obesity"

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Newell-Price, John, Alia Munir, and Miguel Debono. Obesity: differential diagnosis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0081.

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This topic addresses the causes and consequences of obesity, defined as a body mass index (BMI) of 30 or above. While BMI is the most commonly used measure of obesity, the waist-to-height ratio correlates better with visceral obesity. At least 1.1 billion adults are overweight worldwide, but a medical cause for obesity is found in less than 1 out of every 100 cases. The health consequences of obesity are diverse and serious. Approximately 50% of all hypertension is secondary to obesity, and the heart may also be harmed by obesity-induced chronic volume overload and ischaemic heart disease. Obesity contributes strongly to the pathophysiology of type II diabetes and its consequences. Obese patients have higher rates of stroke, osteoarthritis, obstructive sleep apnoea, gastro-oesophageal reflux, chronic liver disease, and infertility. In addition, obesity increases the incidence of some cancers (e.g. breast, prostate, and colorectal). The psychological and social effects of obesity include higher rates of depression and anxiety, and reduced employment.
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Henriksen, Marius, Robin Christensen, Berit L. Heitmann, and Henning Bliddal. Weight loss. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0023.

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Obesity is widely acknowledged as a risk factor for both the incidence and progression of osteoarthritis. Loss of at least 10% of body weight is recognized as a cornerstone in the management of obese patients with osteoarthritis, and can lead to significant improvement in symptoms, pain relief, physical function, and health-related quality of life. However, questions still remain surrounding optimal management and whether structural disease progression can be arrested. Given the significant health, social, and economic burden of osteoarthritis, especially in obese patients, it is imperative to advance our knowledge of osteoarthritis and obesity, and apply this to improve care and outcomes. This chapter overviews what is known about osteoarthritis, obesity, and weight loss and discusses current key challenges in management and maintenance of weight loss for overweight and obese individuals with osteoarthritis.
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Runhaar, Jos, and Sita M. A. Bierma-Zeinstra. Lifestyle. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0012.

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Modern lifestyles put a great burden on the human musculoskeletal system. Since 1980, the worldwide prevalence of obesity has tripled in many European countries. Obesity is known to affect both weight-bearing and non-weight-bearing joints due to a combination of mechanical overload and systemic inflammation. On the other hand, both to combat the obesity pandemic and to increase or maintain the quality of life, physical activity and sports are encouraged next to a healthy diet. Although both have a positive influence on cardiovascular risk factors, physical activity and especially sporting activities do lead to increased loading of the active joints and increased risk for joint injuries, which might lead to osteoarthritis development. This chapter provides an overview of the current knowledge on lifestyle risk factors for the development and progression of osteoarthritis as published in recent systematic reviews, complemented with several narrative reviews.
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Calisoff, Randy L., and David R. Walega. Chronic Knee Pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190271787.003.0010.

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Chronic knee pain affects 27 million people in the United States and is a leading cause of disability. Seventy percent of the population 65 years or older will have knee pain with radiographic evidence of osteoarthritis, and 12% will have clinical symptoms of osteoarthritis. Chronic knee pain after total knee replacement ranges from 10% to 20%. Patellofemoral pain syndrome (PFPS) refers to anterior knee pain exacerbated with knee joint loading activities (squatting, kneeling, prolonged sitting, ascending/descending stairs). PFPS is a clinical diagnosis, and treatment is directed toward pain alleviation and restoration of proper biomechanics. Pes anserine syndrome is common in runners, athletes, and individuals with osteoarthritis of the knee. Other risk factors include: female sex and a history of diabetes mellitus, obesity, or arthritis. Knowledge of the common knee pain etiologies, as well as key clinical manifestations, physical exam findings, differential diagnosis, and treatment options for each is important for pain specialists.
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Book chapters on the topic "Osteoarthritis and obesity"

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Eaton, Charles, and Roy K. Aaron. "Metabolic Syndrome, Obesity, and Osteoarthritis." In Diagnosis and Management of Hip Disease. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19905-4_3.

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Mediwala, Sanjay, and Dennis T. Villareal. "Obesity, Osteoarthritis, and Bone Disorders." In Handbook of Obesity, Two-Volume Set, 5th ed. CRC Press, 2024. http://dx.doi.org/10.1201/9781003437734-65.

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Mediwala, Sanjay, and Dennis T. Villareal. "Obesity, Osteoarthritis, and Bone Disorders." In Handbook of Obesity - Volume 1, 4th ed. CRC Press, 2023. http://dx.doi.org/10.1201/9781003437673-65.

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Miller, Peggy, Alexander Vincent, and Colin Murphy. "Obesity and Osteoarthritis of the Hip." In Musculoskeletal Disease and Obesity. Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-63310-2_7.

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Fu, Yao, and Timothy M. Griffin. "Obesity, Osteoarthritis and Aging: The Biomechanical Links." In The Mechanobiology of Obesity and Related Diseases. Springer International Publishing, 2014. http://dx.doi.org/10.1007/8415_2014_178.

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Mellion, Katelyn M., and Shanu N. Kothari. "The Role of Obesity and Bariatric Surgery in the Management of Knee and Hip Osteoarthritis." In Obesity and Diabetes. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-53370-0_60.

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Francisco, Vera, Clara Ruiz-Fernández, Jesús Pino, et al. "Obesity and Osteoarthritis: Are Adipokines Bridging Metabolism, Inflammation, and Biomechanics?" In Pathophysiology of Obesity-Induced Health Complications. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-35358-2_6.

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de Rooij, Mariëtte, Willem F. Lems, Marike van der Leeden, and Joost Dekker. "Comorbidity, Obesity, and Exercise Therapy in Patients with Knee and Hip Osteoarthritis." In Exercise and Physical Functioning in Osteoarthritis. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7215-5_10.

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Barr, Andrew J., and Philip G. Conaghan. "Osteoarthritis." In Oxford Textbook of Medicine, edited by Richard A. Watts. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0450.

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Clinical osteoarthritis (OA) is a syndrome of joint pain associated with structural deterioration of synovial joints that over time involves the whole joint organ. It is the most common form of arthritis and a leading cause of chronic pain, disability, and socioeconomic burden. Affected individuals report pain (especially on weight bearing) and joint stiffness leading to loss of muscle strength and poor joint function. This results in reduced participation in valued activities, low mood, sleep disturbance, and poor quality of life. The aetiology of joint deterioration, pain, and the interaction of the two remains unclear. OA is associated with a variety of both modifiable and non-modifiable risk factors including obesity, age, gender, occupational injury, trauma, and genetic predisposition. Obesity is the strongest potentially modifiable risk factor.
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Blanco, Francisco J. "Osteoarthritis." In Oxford Textbook of Geriatric Medicine. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198701590.003.0072.

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Osteoarthritis (OA) is the most common joint disease related to ageing involving cartilage degradation, synovial inflammation, subchondral bone sclerosis, degeneration of ligaments and, in the knee, the menisci and hypertrophy of the joint capsule. Other alterations, in periarticular muscles, nerves, bursa, and local fat pads, also contribute to OA. Some risk factors are associated with OA and it is possible to differentiate between risk factors that confer a generalized susceptibility to OA, such as age, osteoporosis, heredity, and gender, and the differing local biomechanical factors of joints, such as trauma, anatomical variance of the articulation, occupational exposures, and obesity. The treatment of osteoarthritis should be individualized and adjusted to the joint affected. The objectives are to control pain, maintain function, and to slow progression. Treatment of OA can be considered in symptom-modifying and structure-modifying treatments.
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Conference papers on the topic "Osteoarthritis and obesity"

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Hülser, M.-L., C. Schreiyaeck, Y. Luo, et al. "P086 Adipocytokines linking obesity and osteoarthritis." In 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.102.

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Berenbaum, F. "SP0157 Metabolic phenotype: the two faces of obesity in osteoarthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.7120.

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Strebkova, E., and L. Alekseeva. "SAT0558 Pharmacotherapy of obesity in patients with knee osteoarthritis and metabolic syndrome." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5072.

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Blazek, Katerina, Jessica Asay, Jennifer Erhart-Hledik, and Thomas Andriacchi. "Valgus Knee Alignment, Not Step Width or Toe-Out Cause Reduced Knee Adduction Moment in the Healthy Obese." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80375.

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Obesity is a strong risk factor for knee osteoarthritis (OA) [1], but the mechanism of OA initiation associated with obesity is not clear. Increases in ambulatory knee joint load due to obesity have been implicated as a cause of increased OA incidence, since an increased adduction moment has been associated with the severity and progression of medial compartment OA [2]. However, previous work has not consistently shown increases or decreases in the adduction moment in the obese. Step width and toe-out reduce the adduction moment [3] and are increased in the obese [4], suggesting that the adduction moment could also be reduced in the obese. Furthermore, obesity may be associated with knee malalignment, which may also alter the adduction moment. However, the cumulative effect of these gait alterations on the adduction moment is unclear, given the increased risk of medial knee OA in the obese. Understanding this interaction is important in understanding the link between obesity and knee OA.
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Cox, L. G. E., C. C. van Donkelaar, B. van Rietbergen, and K. Ito. "Mechanoregulated Bone Remodeling May Explain Bone Structural Changes Observed in Osteoarthritis." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19583.

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Osteoarthritis (OA) affects both the articular cartilage and the subchondral bone. It is a complicated disease, associated with conditions varying from obesity and strenuous exercise to joint malalignment, anterior cruciate ligament (ACL) injury, and even metabolic bone diseases. Patients suffer from chronic joint pain and limitation of motion, and no cure is yet available. For many years, medical therapies have been focused on cartilage, because bone changes were thought not to play a major role in the OA disease process. However, it has been shown that bone changes occur in an early stage of OA, and that alterations to subchondral bone can lead to cartilage degeneration [1]. Therefore, currently the bone is considered as a therapeutic target as well.
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Mckevitt, S., C. Jinks, E. L. Healey, and J. G. Quicke. "AB0972 The effectiveness of physical activityinterventions for people with osteoarthritis and obesity: a meta-analysis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6421.

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Fakhrazi, Ricky, and Tirza Z. Tamin. "The Correlation between Physical Activity with Body Mass Index in Obesity Patient with Knee Osteoarthritis." In The 11th National Congress and The 18th Annual Scientific Meeting of Indonesian Physical Medicine and Rehabilitation Association. SCITEPRESS - Science and Technology Publications, 2019. http://dx.doi.org/10.5220/0009090103160320.

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Strebkova, E., and L. Alekseeva. "SAT0510 Effect of pharmacological and non-pharmacological therapy of obesity on the clinical manifestations of osteoarthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.2819.

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Kinney, Allison L., Heather K. Vincent, Melinda K. Harman, James Coburn, Darryl D. D’Lima, and Benjamin J. Fregly. "Effects of Body Weight Modification on Internal Knee Contact Forces During Gait." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14727.

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Obesity is commonly considered a risk factor for the development of knee osteoarthritis [1]. Previous studies have shown that reductions in body weight correspond to reductions in total knee joint compressive forces (as calculated by inverse dynamics) [2–4]. A recent study showed that external knee load measurements are not strong predictors of internal knee contact forces [5]. Therefore, direct measurement of knee contact force is important for understanding how body weight changes impact knee joint loading. Force-measuring knee implants can directly measure internal knee contact forces [6].
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Ribeiro Rosa, Karoline, Martha Castaño-Betancourt, Catrine Rangel Maia, Monica Vannucci Nunes Lipay, and Evaldo Marchi. "CENTRAL OBESITY INFLUENCES JOINT PAIN SEVERITY IN OSTEOARTHRITIS AND RHEUMATOID ARTHRITIS CASES INDEPENDENT OF BODY MASS INDEX." In Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.17504.

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Reports on the topic "Osteoarthritis and obesity"

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Cao, Siyang, Yihao Wei, Huihui Xu, et al. Crosstalk between Ferroptosis and Chondrocytes in Osteoarthritis: A Systematic Review of in-vivo and in-vitro Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.3.0044.

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Review question / Objective: For the sake of better apprehending the nexus between ferroptosis and chondrocytes in osteoarthritis (OA), proffering novel insights and opening-up new orientation for in-depth research in both pre-clinical and clinical settings, it is warranted to initiate one rigorous and robust systematic review (SR) based upon up-to-date in-vivo and in-vitro research advances on this topic. To the best our knowledge, no SRs concerning ferroptosis and chondrocytes in OA have been published thus far. Condition being studied: Osteoarthritis (OA) is the most common form of arthritis, which menaces 7% of the human population globally. With the aged tendency of population and higher rates of obesity, the incidence of OA is anticipated to proliferate, which will entail a mounting impact and major challenges for global health care and each country’s public health systems unavoidably. In virtue of the onset of OA is mighty knotty, its etiology and underlying molecular mechanisms have not been expressly expounded. However, the salient role that cartilage degeneration acts in the progression of OA has been widely acknowledged. Chondrocytes are consequential for the safeguard of cartilage homeostasis and the functional integrity of the articular cartilage. Once the homeostatic equilibrium of the extracellular matrix (ECM) synthesis and degradation is smashed, OA comes up.
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