Inflamed Swelling 7 Letters
Inflamed Swelling 7 Letters – View ORCID profile ASA Eskelinen, View ORCID profile C Florea, View ORCID profile P Tanska, HK Hung, EH Frank, View ORCID profile S Mikkonen, View ORCID profile P Nieminen, View ORCID profile P Julkunen, View ORCID profile, AJ ORCIDsky Profile RK Korhonen
1 Department of Applied Physics, University of Eastern Finland, Yliopistonranta 1 F, 70210 Kuopio, Finland 2 Department of Bioengineering, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA
Inflamed Swelling 7 Letters
3 Institute of Biomedicine/Anatomy, University of Eastern Finland, Yliopistonranta 1 F, 70210 Kuopio, Finland 4 Department of Environmental and Biological Sciences, University of Eastern Finland, Yliopistokatu 2, 80100 Joensuu, Finland
Full Article: Anti Inflammatory And Hemostatic Effects Of Linaria Reflexa Desf
1 Department of Applied Physics, University of Eastern Finland, Yliopistonranta 1 F, 70210 Kuopio, Finland 5 Department of Clinical Neurophysiology, Kuopio University Hospital, Puijonlaaksontie 2, 70210 Kuopio, Finland
6 Departments of Biological Engineering, Electrical Engineering, and Computer Science and Mechanical Engineering, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA
Post-traumatic osteoarthritis is a musculoskeletal degenerative condition in which articular cartilage homeostasis is disrupted by lesions and inflammation, leading to abnormal loading at the tissue level. These mechanisms were rarely included simultaneously in
Models of osteoarthritis. We modeled early disease progression in bovine cartilage regulated by the cooperation of (1) mechanical injury, (2) pro-inflammatory interleukin-1α challenge and (3) cyclic loading that mimics walking and is considered beneficial (15% load, 1 Hz). Surprisingly, cyclic loading did not protect cartilage from accelerated glycosaminoglycan loss during 12 days of interleukin-1 culture despite promoting aggrecan biosynthesis. Our time-dependent data suggest that this loading regimen can be beneficial in the first few days after injury, but later become detrimental in interleukin-1-inflamed cartilage. As a result, early intervention of anti-catabolic drugs may delay, while cyclic loading during chronic inflammation may promote the progression of osteoarthritis. Our data on the early stages of post-traumatic osteoarthritis can be exploited in the development of countermeasures to the progression of the disease.
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Osteoarthritis is the most common musculoskeletal disorder after low back pain and fractures with hundreds of millions of patients suffering from pain and disability
. One of the hallmarks of this disease is the degeneration of the articular cartilage. The phenotype of the disease associated with the injury – post-traumatic osteoarthritis (PTOA) – manifests in the knee joint as the presence of chondral lesions
. Despite the vast body of literature, the mechanobiological response of cartilage to simultaneous mechanical damage, infiltration of proinflammatory cytokines, particularly interleukin-1 (IL-1), and physiological cyclic loading remains to be elucidated. Here, we used an experimental platform
To study these mechanisms in parallel for the first time with IL-1 in order to gain crucial insights into the complex and multifaceted progression of early-stage PTOA. The obtained time-dependent and cartilage depth-dependent data can be useful for developing methods and treatments that deal with the progression of the disease.
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The response of cartilage to injurious loading, inflammation and cyclic loading has been studied separately in recent decades. First, noxious loading has been shown to lead to an accelerated loss of sulfated glycosaminoglycans (GAG; found e.g. attached to aggrecan, the major proteoglycan in cartilage) in the extracellular matrix (ECM)
. Biosynthesis of new aggrecan with native GAG chains does not change significantly in the superficial cartilage nor in the deeper cartilage
But abnormal GAG aggrecan biosynthesis (changes in sulfation pattern of new chondroitin sulfate chains) may increase in deeper tissue shortly after injury
. Second, inflammation caused by pro-catabolic cytokines such as IL-1, IL-6 and tumor necrosis factor-α (TNFα) causes accelerated depletion of GAG from cartilage.
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. Furthermore, inflammatory factors induce a marked immune response in chondrocytes; The biosynthesis of aggrecan decreases and cell death increases
GAG content depends on the aggressiveness of loading. Aggressiveness of cyclic loading is defined by several mechanical variables, such as loading amplitude, frequency, waveform, and duration, which have received a wide variety of values and configurations in the literature
, voltage amplitude of 10-20%, loading frequency of 1 Hz, applied continuously for up to 48 hours or intermittently in three or four periods of one hour per day for up to 14 days) is thought to be beneficial for cartilage health, as demonstrated by the increased biosynthesis of new proteoglycans
Compared to more aggressive loading (such as a 30% stress amplitude that was considered overload and resulting in a pro-inflammatory cartilage response)
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. Although the physiological cyclic load can be within healthy and normal limits at the level of the whole joint, the load at the tissue level and cartilage deformation can be abnormal locally and thus lead to local GAG loss or apoptosis
. Such beneficial cyclic loading (10 and 20% strain amplitudes applied at 0.5 Hz, 1h on/5h off per day) has been shown to effectively reduce GAG loss after 4 and 8 days, even when antagonized by exogenous IL-6 and TNFα
. A similar protective effect of cyclic loading was also observed with the presence of exogenous IL-1, but this was only studied for 1–3 days without initial controlled injurious loading of cartilage.
. Without cyclic loading, a damaged tissue environment predisposes cartilage to more rapid inflammation-induced degeneration compared to a mechanically intact environment
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A study with bovine cartilage was to determine the effects of simultaneous noxious loading, IL-1 culture, and moderate cyclic loading on time-dependent bulk GAG loss, local GAG loss, aggrecan biosynthesis, and cell viability beyond the early response up to 12 days (Fig. 1). We aimed to fill a gap in previous literature regarding the behavior of IL-1 in an injured and cyclically loaded environment; The same was previously studied with cytokines IL-6 and TNFα
, we hypothesized that a combination of noxious loading and IL-1 challenge would be more degrading than either of these conditions alone, but the cyclic loading regimen you chose (15% voltage amplitude, 1 Hz, Heversin waveform, 1 hour on/5 hours off per day and including overnight rest; see Supplementary Material S1, Section S1, Fig. S1), considered beneficial based on earlier literature
, will improve the deterioration. Contrary to our hypothesis, we observed that moderate cyclic loading did not inhibit or only moderately inhibited the procatabolic response of cartilage to a relatively high concentration (1 ng/ml) of IL-1 for 12 days. Although cyclic loading increased aggrecan biosynthesis and significantly once led to locally elevated GAG levels away from lesions especially in the deep tissue, the data show that cyclic loading employed in our protocol cannot rescue the bulk cartilage from degradation during IL-1-mediated inflammation. Interestingly, increased GAG depletion shortly after injurious loading and IL-1 induction is also noted. , when cyclic loading was absent, but this early degradation was suppressed when cyclic loading was involved. Overall, our data suggest that a cyclic loading regimen previously thought to be beneficial may only be beneficial initially after joint trauma, but may become detrimental over time periods Prolonged in case the inflammatory response is not removed.
= 6 animals). The surface of each slot was divided into four areas, all of which provided samples for 1) cyclically unloaded and 2) cyclically loaded treatment groups, as well as control groups of free-swelling and position-matched animals. After a 2-day equilibration period, the samples were subjected to (b) six different culture conditions for up to 12 days: 1) free swelling used as a control (CTRL); Groups without cyclic loading were 2) injury only (INJ), 3) interleukin-1α-challenge exogenous only (IL), and 4) injured and IL-1α-challenge (INJ-IL); The cyclically challenged groups were 5) IL-1α-challenged and cyclically loaded (IL-CL) and 6) injured, IL-1α-challenged, and CYCEL-loaded (INJ-IL-CL). (c) To determine the response of the cartilage to the different culture conditions, we used a glycosaminoglycan assay of the entire plug (in total
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= 6 plugs corresponding to the location of two different animals for each treatment and analysis time point), optical density measurements indicating local glycosaminoglycan (GAG) loss (
In order to determine an appropriate concentration of IL-1α for further study, we first conducted 7-day and 12-day cultures of calf cartilage plugs with only the biochemical degradation mechanism present in the form of exogenous cytokine challenge (free-swelling as control (CTRL), 0.1, 0.5, 1 and 10 ng/ml of IL-1α). Cumulative GAG loss (%) – a measure of GAG release over time from a cartilage plug relative to the total GAG content of that plug (Equation 1; see methods subsection 4.3) – was higher and faster with increasing cytokine concentration. From day 4 onwards, 1 ng/ml of IL-1 caused significantly greater cumulative GAG loss compared to CTRL conditions; For example, at day 12, the mean cumulative GAG losses in the 1 ng/mL and CTRL groups were 21.7% and 15.7%, respectively (
= 0.003; Linear mixed effects model, detailed statistics are compiled into Supplementary Material S1). The concentration of 1 ng/ml of IL-1α was chosen for further study since this concentration was able to cause substantial and rapid degradation compared to the CTRL conditions. This concentration was also low enough not to be highly destructive to the ECM (as likely as 10 ng/ml, based on the pilot study) and therefore not to control for biomechanical degradation factors (injury, cyclic loading). For details For more, see Supplementary Material S1 (Sections S2.1–2.2, Figures S2 and S3, Tables S1–S6).
2.2 Cyclic loading reduces the GAG loss of cartilage affected by IL-1α initially, but its inhibitory effects are impaired