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Neuromechanical Alterations Due to Induced Knee Pain and Effusion During Functional MovementsPark, Jihong 09 December 2011 (has links) (PDF)
Purpose: Examine neuromechanical alterations due to isolated and/or combined knee pain and effusion in functional movements. Methods: A 4X3 randomised controlled laboratory study with repeated measures was used. Nineteen, healthy volunteers (age: 22.4 ± 2.4 years) underwent four different treatments (control, effusion, pain, and pain/effusion) with a week wash out period. Ten near-infrared cameras with 43 reflective markers, 12 surface EMG electrodes, and two ground-embedded force platforms were used to record neuromechanical changes during functional movements (walking and drop landing). To induce pain, 5% sodium chloride (1 ml) was injected into the infrapatellar fat pad. To induce effusion, 0.9% sodium chloride (50 ml) was injected into the knee joint capsule. To induce pain/effusion, both injections were employed. No injection was used for the control. Subjects performed walking and a single leg drop landing in three time intervals: precondition (prior to injection), condition (immediate post injection), and postcondition (30 min post injection). To quantify pain perception, the visual analogue scale was measured every two minutes. Results: Under pain/effusion treatment, subjects walked slowly with a shorter stride length. Joint moments of plantarflexion, knee extension, knee abduction, and hip abduction were reduced. Subjects also showed a decrease at 20% and 80% of stance phase, and an increase in 50% in vertical ground reaction force (VGRF). Under the same treatment, subjects landed with a less peak VGRF with increased time to peak VGRF, alterations of joint angles (ankle dorsiflexion, knee extension, and hip adduction), and moments (knee extension, knee abduction, and hip abduction). Conclusions: Joint pain and effusion cause neuromechanical alterations in the lower extremity during functional movements. These compensatory strategies may alter joint loading, potentially resulting in acceleration of the joint degenerative process. We also recommend use of crutches following injury to avoid modifications of movement strategies.
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Promotion of joint degeneration and chondrocyte metabolic dysfunction by excessive growth hormone in miceZhu, S., Liu, H., Davis, T., Willis, Craig R.G., Basu, R., Witzigreuter, L., Bell, S., Szewczyk, N., Lotz, M.K., Hill, M., Fajardo, R.J., O'Connor, P.M., Berryman, D.E., Kopchick, J.J. 03 April 2023 (has links)
Yes / Objective: Many patients with acromegaly, a hormonal disorder with excessive growth hormone (GH) production, report pain in joints. We undertook this study to characterize the joint pathology of mice with overexpression of bovine GH (bGH) or a GH receptor antagonist (GHa) and to investigate the effect of GH on regulation of chondrocyte cellular metabolism.
Methods: Knee joints from mice overexpressing bGH or GHa and wild-type (WT) control mice were examined using histology and micro–computed tomography for osteoarthritic (OA) pathologies. Additionally, cartilage from bGH mice was used for metabolomics analysis. Mouse primary chondrocytes from bGH and WT mice, with or without pegvisomant treatment, were used for quantitative polymerase chain reaction and Seahorse respirometry analyses.
Results: Both male and female bGH mice at ~13 months of age had increased knee joint degeneration, which was characterized by loss of cartilage structure, expansion of hypertrophic chondrocytes, synovitis, and subchondral plate thinning. The joint pathologies were also demonstrated by significantly higher Osteoarthritis Research Society International and Mankin scores in bGH mice compared to WT control mice. Metabolomics analysis revealed changes in a wide range of metabolic pathways in bGH mice, including beta-alanine metabolism, tryptophan metabolism, lysine degradation, and ascorbate and aldarate metabolism. Also, bGH chondrocytes up-regulated fatty acid oxidation and increased expression of Col10a. Joints of GHa mice were remarkably protected from developing age-associated joint degeneration, with smooth articular joint surface.
Conclusion: This study showed that an excessive amount of GH promotes joint degeneration in mice, which was associated with chondrocyte metabolic dysfunction and hypertrophic changes, whereas antagonizing GH action through a GHa protects mice from OA development. / Dr. Zhu's work was supported by Ohio University, the Arthritis National Research Foundation (grant 833836), a FIRST award from the American Society for Bone and Mineral Research, the NIH (grant R15-AR-080813), and a Hevolution Foundation AGE grant (AGE-008). Dr. Davis’ work was supported by a medical student seed grant from Ohio University. Dr. Lotz's work was supported by the NIH (grant R37-AG-059418). Dr. Berryman was supported by the NIH (grant R01-AG-059779). Dr. Kopchick was supported by the State of Ohio's Eminent Scholar Program that includes a gift from Milton and Lawrence Goll and the AMVETS, and by the NIH (grant R01-AG-059779).
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Influence of Mechanical Choices on Development and Persistence of Osteoarthritis: How Alexander Technique Can Promote Prevention and ManagementLowry, Rachelle E 01 May 2016 (has links)
Is osteoarthritis a fate unconditionally vested in genetic makeup, or are joints aggravated into inflammation by the way they are treated? Humans are a complicated conglomeration of experiences, decisions, and inheritance. Osteoarthritis, likewise, has evaded simplicity in any explanation of its causation, so it necessitates a multi-dimensional perspective.
This research considers the relevance of Alexander Technique in filling a void in which treatment and management of osteoarthritis is not equally equipped to answer this multi-dimensional causation. Alexander Technique is classified as a movement therapy, but this does not quite encompass the mindset of it—that it is indeed largely a mindset about movement. More concisely, Alexander Technique emphasizes self-awareness about how a person uses his or her body to perform daily tasks. It is physical minimalism, and involves continual recognition of muscle tension along with the ability to let go of any tension that is burdensome and unnecessary. This technique has diminished pain and increased the ease of movement for those who have experienced it, even people with osteoarthritis.
To build the argument that osteoarthritis can be hindered through a heightened consideration of how joints are treated, the initial component of this research investigated the vast amount of information already gleaned about the pathogenesis of this disease. The fields of physiology, genetics, immunology, and clinical practice already have much to share, and this knowledge has been combined with studies about the benefits and goals of Alexander Technique to discover the common ground of osteoarthritis treatment. The experimental component assesses the association of Alexander Technique to the minimization of pain from osteoarthritis. An online survey asks osteoarthritis cohorts about the history of their disease, the effect it has had on their pain levels and activities of daily living, and about the efficacy of their management strategies. Because each participant will be asked if he or she has received Alexander Technique lessons, the survey can be used to analyze each respondent’s experience of osteoarthritis with respect to that.
It was found that participants who had received Alexander Technique lessons reported an average of one more pain-free day per week, and experienced diminished pain levels for daily physical activities such as walking. Management strategies also indicated the benefit of Alexander Technique; those who had taken lessons less frequently used pain and anti-inflammatory medications and were able to be more physically active than the unexposed group. No statistical significance was achieved from the data, largely owing to small sample size (Alexander Technique, n=12, no Alexander Technique, n=25). This study is a step in the direction of better osteoarthritis management, promoting prevention-minded awareness of joint use and providing preliminary fuel for more extensive research.
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Långdistanslöpning och artros : En systematisk litteraturstudie / Long distance running and osteoarthritis : A systematic reviewde Flon, Peter January 2014 (has links)
Sammanfattning Syfte och frågeställningar Syftet med denna studie var att sammanställa kvalitet på och resultat av studier som undersökt om långdistanslöpning ger artros i höft-, knä- eller fotleder. Finns det vetenskaplig evidens för att långdistanslöpning ger artros i höft-, knä- eller fotleder? Vilka styrkor och svagheter har de studier som försökt utröna om samband finns mellan långdistanslöpning och artros i höft-, knä- eller fotleder? Metod Sökning av litteratur utfördes i PubMed, CINAHL, Cochrane Library och PEDro. Detta resulterade i att tio artiklar inkluderades för närmare granskning och sammanställning. Utifrån artiklarnas sammantagna bevisvärde poängsattes och graderades artiklarna efter evidensnivå enligt Statens Beredning för medicinsk Utvärderings (SBU) granskningsmallar för kohortstudier med kontrollgrupper. Resultat Endast en av tio studier visar ett positivt samband mellan långdistanslöpning och artros i höft-, knä- eller fotleder, i detta fall höftledsartros. Studierna har ingen tydlig och gemensam definition över vad långdistanslöpning är. De granskade studierna använder sig av olika mätmetoder för att bedöma leddegenerationen, både av självrapportering och av olika diagnostiska kriterier för artros. Alla studier har inslag av selektionsbias. Slutsats En indikation på att det inte finns ett vetenskapligt stöd för att långdistanslöpning ger höft-, knä- eller fotledsartros hos människor. Studierna har brister i hantering av confounders och selektionsbias och bedöms vara av låg eller medelhög kvalitet. / Abstract Aim The purpose of this study was to compile the quality and results of studies that examined if long-distance running gives osteoarthritis of the hip, knee or ankle joints. Is there scientific evidence that long-distance running gives osteoarthritis of the hip, knee or ankle? What strengths and weaknesses of the studies attempted to determine if the link between long-distance running and osteoarthritis of the hip, knee or ankle joints. Method Search of the literature was performed in PubMed, CINAHL, Cochrane Library, and PEDro. This resulted in ten articles that were included for further review and compilation. Based on the articles combined probative value was scored and graded articles for level of evidence according to the National Council on Technology Evaluation (SBU) examination templates for cohort studies with control groups. Results Only one of the ten studies showed a positive association between long distance running and osteoarthritis of the hip, knee or ankle joints, in this case hip joint. The studies have not a clear and common definition of what long-distance running is. The studies reviewed use different metrics to assess joint degeneration, both by self-report and of different diagnostic criteria for osteoarthritis. All studies have an element of selection bias. Conclusion An indication that there is no scientific evidence that long-distance running gives hip, knee or ankle osteoarthritis in humans. The studies were inadequate handling of confounders and selection bias and judged to be of low or medium quality.
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Développement d'un modèle animal de paralysie cérébrale : basé sur l'ischémie prénatale et l'expérience sensorimotrice anormaleDelcour, Maxime 02 October 2012 (has links)
La paralysie cérébrale (PC) regroupe un ensemble varié de troubles moteurs, sensoriels et cognitifs, liés à des lésions de la substance blanche (i.e. leucomalacie périventriculaire, PVL) survenant, le plus souvent, après un épisode hypoxo-ischémique autour de la naissance. Afin de reproduire la PVL chez l'animal, nous utilisons une ischémie prénatale (PI) qui induit des lésions des substances blanche et grise. Les rats ischémiés développent des déficits cognitifs visuo-spatiaux et une hyperactivité, également observés chez les patients atteints de PC, liés à des lésions du cortex entorhinal, préfrontal et cingulaire. La PI n'induit que des troubles locomoteurs modérés associés à des signes de spasticité, et une atteinte anatomique et fonctionnelle du cortex somesthésique primaire (S1), tandis que le cortex moteur (M1) reste intact. Ainsi, la PI reproduit les symptômes observés chez les enfants et adultes nés prématurément. La présence de mouvements spontanés anormaux au cours de la 1ère année conduisant à la PC suggère une implication de l'expérience sensorimotrice anormale dans le développement de cette pathologie. La combinaison d'une restriction sensorimotrice (SMR) durant le développement et de la PI induit des troubles cognitifs atténués mais une hyperactivité importante. Les rats combinant PI et SMR présentent des déficits posturo-moteurs drastiques et une spasticité, associés à une dégradation des tissus musculo-squelettiques, comparables à ceux observés chez les patients. Ces troubles moteurs, associés à une désorganisation importante des cartes corticales dans S1 et M1, suggèrent un dysfonctionnement important des boucles d'intégration sensorimotrice. / Cerebral palsy (CP) corresponds to various motor, sensory and cognitive disorders related to white matter damage (i.e. periventricular leucomalacia, PVL) often occurring after perinatal hypoxic-ischemic events. To reproduce PVL in rodents, we used a prenatal ischemia (PI) that induces white and gray matter damage. The ischemic rats exhibit visual-spatial cognitive deficits and hyperactivity, as observed in patients with CP, related to lesions of entorhinal, prefrontal and cingular cortices. Only mild locomotor disorders are induced by PI, associated to signs of spasticity, along with anatomical and functional degradation in the primary somatosensory cortex (S1), while the primary motor cortex (M1) remains unchanged. Thus, PI recapitulates the main symptoms found in children born preterm. Abnormal spontaneous movements (i.e. general movements) observed in infants who develop CP later on suggest that abnormal sensorimotor experience during maturation is key in the development of this catastrophic disease. The combination of a sensorimotor restriction (SMR) and PI in animal induces fewer cognitive deficits but still hyperactivity. Such a combination leads to severe postural and motor disorders, and spasticity, associated with musculoskeletal pathologies, as observed in patients with CP. In addition to motor disorders, drastic topographical disorganization of cortical maps in S1 and M1 suggest a major dysfunction of sensorimotor loops.
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