Relevant bibliographies by topics / Adjuvant arthritis

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

Academic literature on the topic 'Adjuvant arthritis'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Adjuvant arthritis"

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Conforti, A., S. Lussignoli, S. Bertani, R. Ortolani, G. Verlato, and P. Bellavite. "Intraperitoneal Administration of Adjuvant Inhibits the Development of Adjuvant Arthritis in Rats." International Journal of Immunopathology and Pharmacology 8, no. 2 (May 1995): 113–21. http://dx.doi.org/10.1177/039463209500800206.

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In recent years, considerable efforts have been made to develop effective therapy for autoimmune diseases by specific suppression of the autoreactive immune process without affecting the remainder of the immune system. In our study we evaluated the protective effects and therapeutic potential of Mycobacterium butyricum (Mb), the causative antigen inducing adjuvant arthritis (AA), an experimental model of autoimmune disease in the rat. The antigen was administered to rats by a different route and at concentrations 10 and 100 times lower than the inducing one. Arthritis was induced by injection of 0.6 mg of Mb in paraffin oil into the hindpaw, and the severity of disease was assessed by measurement of contralateral paw swelling every three days and primary and secondary lesions were scored on an arbitrary scale after 14, 21, and 28 days. Animals were assigned to different groups and treated intraperitoneally with different doses and schedules of Mb. The administration of 60 μg of Mb every two days, starting 6 days before arthritogenic injection until the second day after, led to a significant inhibition of the arthritic process (p< 0.001 of the arthritic index). Treatment of animals with 60 μg of Mb every two days, from day 2 to day 21 after arthritis induction caused almost total suppression of lesions. However, in both treatment schedules, animals showed important signs of peritoneal inflammation. The administration of single injection of 60 or 6 μg of Mb 10 days after arthritis induction led to an inhibition of arthritic index reaching the maximum percentage on day 14 (26% and 24% with 60 and 6 μg respectively) and was able to delay the development of oedema foot volume, without signs of local inflammation. These results confirm the ability to modulate the autoimmune process even when the immunological response is far advanced, suggesting new strategies in the therapy of human autoimmune diseases.
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Neeraj, Srivastava, Dashora Nipun, Menaria Jyoti, and Kumar Neeraj. "Evaluation of Anti-inflammatory and Anti-arthritic Activity of Ajmodadi Churna- A Polyherbal Formulation." International Journal of Pharmaceutical and Phytopharmacological Research 6, no. 5 (October 30, 2016): 72. http://dx.doi.org/10.24896/eijppr.2016651.

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Anti-inflammatory and anti- arthritic activity of aqueous extract of Ajmodadi Churna (AJM) were evaluated by three methods namely, Carrageenan paw edema, Carrageenan induced Air Pouch Model in Rats and Freunds’ complete adjuvant Arthritis. The Carrageenan paw edema was carried out to test the effect of the extract on acute phase of inflammation. Carrageenan induced Air Pouch Model was used for local inflammation and Freunds’ complete adjuvant Arthritis was used for evaluation of chronic inflammation. Results showed that AJM have significant anti-inflammatory activity and Anti-arthritic Activity in both the doses (200 mg/kg and 400 mg/kg) when compared to the Diclofenac but higher dose was found more effective.Key Words: Anti-inflammatory, Anti-arthritic Activity, Freunds’ complete adjuvant Arthritis, Ajmodadi churna.
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Davis, RH, KY Rosenthal, LR Cesario, and GR Rouw. "Vitamin C influence on localized adjuvant arthritis." Journal of the American Podiatric Medical Association 80, no. 8 (August 1, 1990): 414–18. http://dx.doi.org/10.7547/87507315-80-8-414.

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This work attempts to determine the influence of vitamin C on locally induced inflammation and arthritis in rat paws, as measured by rat paw swelling, polymorphonuclear leukocyte infiltration, pain, and surface skin temperature. Daily subcutaneous administration of 150 mg/kg of vitamin C over 20 days reduced arthritic swelling, increased pain tolerance, and decreased polymorphonuclear leukocyte infiltration, with no significant change in surface temperature. Vitamin C may provide podiatrists with a supplemental or alternative treatment for patients with rheumatoid arthritis.
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Ibanez De Caceres, I., MA Villanua, L. Soto, AI Martin, and A. Lopez-Calderon. "IGF-I and IGF-I-binding proteins in rats with adjuvant-induced arthritis given recombinant human growth hormone." Journal of Endocrinology 165, no. 3 (June 1, 2000): 537–44. http://dx.doi.org/10.1677/joe.0.1650537.

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Adjuvant-induced arthritis in rats is associated with growth failure, hypermetabolism and accelerated protein breakdown. We have previously reported that adjuvant-induced arthritis in rats results in a decrease in body weight gain, pituitary GH mRNA, circulating GH and IGF-I together with an increase in serum IGF-binding proteins (IGFBPs). The aim of this study was to analyze the role of GH in the decrease in body weight and in the alterations in the IGF-I system observed in chronic inflammation. Male Wistar rats were injected with complete Freund's adjuvant and 16 days later arthritic rats were injected daily with recombinant human GH (rhGH) (3 IU/kg s.c.) for 8 days; control rats received 250 microl saline. Arthritis significantly decreased body weight gain and serum IGF-I. These decreases were not due to the reduced food intake, since in pair-fed rats they were not observed. Furthermore, administration of rhGH to arthritic rats increased body weight gain without modifying food intake. To further investigate the effect of GH administration, 14 days after adjuvant injection both control and arthritic rats were treated with 0, 1.5, 3 or 6 IU/kg of rhGH. GH treatment at the dose of 3 and 6 IU/kg significantly increased body weight gain in arthritic rats. GH administration, at the higher dose of 6 IU/kg, increased hepatic and serum concentrations of IGF-I in both control and arthritic rats. In control rats, rhGH at the three doses assayed increased circulating IGFBP-3. GH treatment in arthritic rats decreased IGFBP-1 and -2, and did not modify IGFBP-4. GH treatment at the dose of 3 IU/kg also decreased circulating IGFBP-3 in arthritic rats. These data suggest that GH treatment can ameliorate the catabolism observed in adjuvant-induced arthritis, an effect mediated, at least in part, by modifications in the circulating IGFBPs.
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Chen, Xi, Cheng Yi Zhang, and Hao Gang Xue. "Effect of Arthrigia on Adjuvant Arthritis Rats’ IL-12." Applied Mechanics and Materials 140 (November 2011): 43–47. http://dx.doi.org/10.4028/www.scientific.net/amm.140.43.

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Rheumatoid Arthritis （RA） is a systemic chronic autoimmune disease. To study the therapeutic mechanism of effects of Skullcap Brightviolet （SB），glucosamine/chondroitin （GC），and the combination of them (named Arthrigia) on RA. With the adjuvant arthritis (AA) rat models, we observed the protective effects of oral SB, GC and Arthrigia in different concentrations on AA in rats. We further examined the immunological mechanism of the combination of them by testing the rats’ secretion of IL-12. The results showed that Arthrigia inhibited the production and secretion of IL-12 factors in some extent, and its effects are more potent the single SB or GC. The present study provides the experimental evidences for Arthrigia for its further development, clinical prevention and treatment of RA.
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Castillero, Estíbaliz, María Paz Nieto-Bona, Carmen Fernández-Galaz, Ana Isabel Martín, María López-Menduiña, Miriam Granado, María Angeles Villanúa, and Asunción López-Calderón. "Fenofibrate, a PPARα agonist, decreases atrogenes and myostatin expression and improves arthritis-induced skeletal muscle atrophy." American Journal of Physiology-Endocrinology and Metabolism 300, no. 5 (May 2011): E790—E799. http://dx.doi.org/10.1152/ajpendo.00590.2010.

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Arthritis is a chronic inflammatory illness that induces cachexia, which has a direct impact on morbidity and mortality. Fenofibrate, a selective PPARα activator prescribed to treat human dyslipidemia, has been reported to decrease inflammation in rheumatoid arthritis patients. The aim of this study was to elucidate whether fenofibrate is able to ameliorate skeletal muscle wasting in adjuvant-induced arthritis, an experimental model of rheumatoid arthritis. On day 4 after adjuvant injection, control and arthritic rats were treated with 300 mg/kg fenofibrate until day 15, when all rats were euthanized. Fenofibrate decreased external signs of arthritis and liver TNFα and blocked arthritis-induced decreased in PPARα expression in the gastrocnemius muscle. Arthritis decreased gastrocnemius weight, which results from a decrease in cross-section area and myofiber size, whereas fenofibrate administration to arthritic rats attenuated the decrease in both gastrocnemius weight and fast myofiber size. Fenofibrate treatment prevented arthritis-induced increase in atrogin-1 and MuRF1 expression in the gastrocnemius. Neither arthritis nor fenofibrate administration modify Akt-FoxO3 signaling. Myostatin expression was not modified by arthritis, but fenofibrate decreased myostatin expression in the gastrocnemius of arthritic rats. Arthritis increased muscle expression of MyoD, PCNA, and myogenin in the rats treated with vehicle but not in those treated with fenofibrate. The results indicate that, in experimental arthritis, fenofibrate decreases skeletal muscle atrophy through inhibition of the ubiquitin-proteasome system and myostatin.
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WARD, P. A. "Neutrophils and adjuvant arthritis." Clinical & Experimental Immunology 107, no. 2 (February 1997): 225–26. http://dx.doi.org/10.1111/j.1365-2249.1997.00276.x.

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Castillero, Estíbaliz, María López-Menduiña, Ana Isabel Martín, María Ángeles Villanúa, and Asunción López-Calderón. "Comparison of the effects of the n-3 polyunsaturated fatty acid eicosapentaenoic and fenofibrate on the inhibitory effect of arthritis on IGF1." Journal of Endocrinology 210, no. 3 (June 29, 2011): 361–68. http://dx.doi.org/10.1530/joe-11-0170.

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Adjuvant-induced arthritis is a chronic inflammatory illness that induces muscle wasting and decreases circulating IGF1. Eicosapentaenoic acid (EPA) and fenofibrate, a peroxisome proliferator-activated receptors α agonist, have anti-inflammatory actions and ameliorate muscle wasting in arthritic rats. The aim of this work was to elucidate whether EPA and fenofibrate administration are able to prevent the effect of arthritis on the IGF1–IGFBP system. On day 4 after adjuvant injection control, arthritic rats were gavaged with EPA (1 g/kg) or fenofibrate (300 mg/kg) until day 15 when all rats were killed. Arthritis decreased body weight gain, serum IGF1, and liverIgf1mRNA, whereas it increased gastrocnemiusIgfbp3mRNA. EPA, but not fenofibrate, administration prevented arthritis-induced decrease in serum IGF1 and liverIgf1mRNA. In the rats treated with EPA arthritis increasedIgfbp5mRNA in the gastrocnemius. Fenofibrate treatment decreased IGF1 andIgf1mRNA in the liver and gastrocnemius. In arthritic rats, fenofibrate increased body weight gain and decreased gastrocnemiusIgfbp3andIgfbp5mRNA. These data suggest that the mechanisms through which EPA and fenofibrate act on the IGF1 system and ameliorate muscle wasting in arthritic rats are different. EPA administration increased circulating levels of IGF1, whereas fenofibrate decreased theIgfbp3andIgfbp5in the gastrocnemius muscle.
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Al-Okbi, S. Y., and D. A. Mohamed. "Preparation and evaluation of functional foods in adjuvant arthritis." Grasas y Aceites 63, no. 4 (October 25, 2012): 394–402. http://dx.doi.org/10.3989/gya.130811.

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Zhang, Maoquan, Baolong Liu, and Zonghui Ji. "Effect of Wu-Wei-Gui-Shao decoction on complete Freund's adjuvant-induced arthritis rats." Tropical Journal of Pharmaceutical Research 19, no. 9 (November 24, 2020): 1977–83. http://dx.doi.org/10.4314/tjpr.v19i9.25.

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Purpose: To investigate the anti-rheumatic potential of Wu-Wei-Gui-Shao decoction (WGD) and its possible mechanism of action. Methods: Adjuvant arthritis (AA) rats were established using complete Freund's adjuvant. The rats were then given different doses of WGD (100, 200, and 400 mg/kg, for 28 days). The anti-arthritic effects of WGD were evaluated. Furthermore, the in vitro anti-arthritic effects of WGD and its related mechanisms were also determined in MH7A cells. Results: WGD (100 - 400 mg/kg) exhibited significant anti-rheumatic properties after 28 days of treatment, inhibiting paw edema in AA rats, reducing arthritis score and thymus and spleen index, and inhibiting the tumor necrosis factor (TNF)-α and the interleukin (IL)-6. In addition, the results of in vitro cell experiments also confirmed that WGD reduced the release of cytokines, as well as mRNA levels of matrix metalloproteinase (MMP) -2, -3, and -9. Conclusion: These findings suggest that WGD can be further developed as a traditional Chinese medicine to treat rheumatic arthritis. Keywords: Wu-Wei-Gui-Shao decoction, Complete Freund's adjuvant, Arthritis, Molecular mechanism, Traditional Chinese Medicine
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Dissertations / Theses on the topic "Adjuvant arthritis"

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Holm, Barbro. "Pathogenetic studies of adjuvant-induced arthritis /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-347-3/.

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Jansson, Åsa. "Immunologic and genetic studies of rat adjuvant-induced arthritis /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4323-0/.

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Sverdrup, Berit. "Aspects of the role of mineral oil as immunological adjuvant in rheumatoid arthritis /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-112-8/.

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Wu, Qinyang. "Galanin and leu-enkephalin in the rat with special reference to adjuvant arthritis /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-977-3/.

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Walker, K. A. "An investigation into the mechanisms responsible for altered drug disposition in adjuvant-induced arthritis." Thesis, University of Aberdeen, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372625.

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Shipton, Deborah. "Autoimmune disease in rodents : control and specificity." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326005.

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Gauldie, Stephan D. "The role of some putative mediators of peripheral nociceptor activation in adjuvant-induced experimental arthritis." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/23013.

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In this thesis behavioural and electrophysiological techniques in both the rat and the mouse were used to determine the effect of a number of mediators and/or pharmacological receptors reported to be involved in chronic inflammation and nociception. The specific aims of the thesis centred on testing the following hypotheses: a) The neuropeptide somatostatin inhibits sensory nerve function in both normal and arthritic knee joints, b) the endocannabinoid anandamide activates peripheral nociceptors via its reported action at the vanilloid receptor (VR1), c) chronic unilateral inflammation of the knee joint can be induced in mice using Freund’s Complete Adjuvant (FCA), and d), the purinoceptor P2X7 plays a role in the induction of inflammation and hyperalgesia associated with experimental arthritis in mice. An additional aim of the thesis was in vivo neural recording from nociceptors innervating the mouse knee joint with a view to examining transgenic mice in future studies. In summary, in relation to the hypothesis being tested, the results showed that: a) the reported anti-nociceptive effect of somatostatin is not mediated by action on peripheral nociceptors or the inhibition of tested algogens, b) anandamide is able to directly activate sensory afferents via VR1 receptors, c) chronic, unilateral arthritis can be induced in mice by repeated intra-articular injections of FCA, and d P2X7 purinoceptors do not play a role in the induction of inflammation and hyperalgesia associated with the FCA model of unilateral arthritis. Innovation in this thesis included a novel model of murine unilateral arthritis and the development of a new technique for direct measurement of evoked discharge from peripheral nociceptors innervating the mouse knee joint. These advances in knowledge provide information relevant to understanding inflammatory joint disease and for future drug development.
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Birner, Ulrieke. "Cell adhesion molecule mechanisms for neutrophil and monocyte migration to joints of rats with adjuvant arthritis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0017/MQ49315.pdf.

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Lariviere, William R. "The role of the hypothalamic-pituitary-adrenal axis in the susceptibility to adjuvant-induced polyarthritis in the rat /." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36631.

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The hypothalamic-pituitary-adrenal (HPA) axis, a system activated by stress, is traditionally considered to affect the susceptibility to chronic pain via effects on peripheral processes. This study investigates whether the HPA axis contributes to the development of chronic pain in an animal model via direct effects on central pain mechanisms.
First, correlations between pain processes and the susceptibility to chronic pain in an animal model that is correlated with HPA-axis function were examined. The results show that, in the Fischer rat, the amount of pain suppression observed during the formalin interphase depression is negatively correlated with susceptibility to polyarthritis. Since the formalin interphase depression mechanisms are within the central nervous system, the results suggest a role for central pain mechanisms in the development of polyarthritis.
Hypophysectomy inhibits the development of adjuvant-induced arthritis. To test whether hypophysectomy inhibits adjuvant-induced polyarthritis via central pain mechanisms, the analgesic effect of hypophysectomy was examined in the formalin test. The results show that hypophysectomy specifically prolongs the formalin interphase depression, further supporting that the underlying central pain suppression mechanisms are associated with resistance to adjuvant-induced polyarthritis.
Corticotropin-releasing factor (CRF) was then investigated as a possible underlying mechanism of the effects of hypophysectomy. Peripheral injection of CRF into inflamed tissue affects pain mechanisms unrelated to the susceptibility to adjuvant-induced polyarthritis. However, central and intravenous administration of CRF preferentially affect the formalin interphase depression mechanisms. The observed dose-response relationships indicate that these effects are due to direct actions of CRF within the central nervous system.
In conclusion, the results strongly suggest that the HPA axis modulates the susceptibility to adjuvant-induced polyarthritis via direct effects on supraspinal pain suppression mechanisms. Thus, the HPA axis may contribute to the development of chronic pain syndromes associated with HPA-axis abnormalities, such as rheumatoid arthritis and fibromyalgia, via effects on pain mechanisms within the central nervous system.
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Guillot, Xavier. "Effets thérapeutiques et anti-inflammatoires de la cryothérapie dans les rhumatismes inflammatoires." Thesis, Besançon, 2016. http://www.theses.fr/2016BESA3009/document.

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La cryothérapie est utilisée de manière large et empirique à visée adjuvante dans les rhumatismes inflammatoires, avec un niveau de preuve faible. Dans une revue systématique de la littérature, en poolant les données de 6 études non contrôlées, nous avons pu démontrer que la cryothérapie (locale ou corps entier) appliquée deux fois par jour pendant 7 à 15 jours réduisait significativement l'EVA douleur et le score d'activité DAS25 dans la polyarthrite rhumatoïde. La cryothérapie locale (glace ou gaz froide) montrait par ailleurs des effets taille intra-classes supérieurs à ceux obtenus en utilisant la cryothérapie corps entier. L'objectif de ce travail était de mesurer les effets de la cryothérapie locale sur al douleur, l'inflammation synoviale et systémique chez les patients arthritiques et dans le modèle murin d'arthrite à l'adjuvant. Dans les études randomisées CDRI et ALGGAR, nous avons évalué les effets de deux applications locales de froid (glace versus gaz froid) sur la douleur, l'activité Doppler et les taux protéiques de cytokines intra-articulaires controlatéraux non souffrant d'arthrites de genou non septiques. Les genoux arthritiques controlatéraux non traités étaient utilisés comme contrôles. Nous avons par ailleurs étudié in vitro les effets de l'hypothermie modérée (30°C pendant 2heures) sur l'expression protéique des cytokines dans un modèle de culture de rotules de rats arthritiques. Nous avons enfin étudié in vitro dans l'arthrite à l'adjuvant les effets de l'application sub-chronique de glace ou de gaz froid (2 fois par jour pendant 14 jours versus contrôles arthritiques non traités) sur le score d'arthrite, le diamètre de cheville, la transcription des gènes codant pour les cytokines pro-inflammatoires dans les pattes arrières (Q-RT-PCR) et l'expression protéique des cytokines dans le plasma (Multiplex et ELISA) après 14 jours de traitement. Dans l'étude CDRI, la cryothérapie locale (glace et gaz froid) réduisait significativement l'EVA douleur ainsi que le score Doppler dans les genoux traités, ces effets persistant le lendemain des deux applications. Dans une analyse intermédiaire des résultats de l'étude ALGGAR, en combinant les deux groupes de traitement (glace et gaz de froid), nous avons observé une baisse des taux d'IL-6, d'IL-1β et de VEGF dans le liquide articulaire arès deux applications. dans les cultures d'explants de rotules de rats arthritiques, l'hypothermie ponctuelle réduisait significativement les taux d'IL-6, IL-17A et IL-1β dans les pattes arrières après 14 jours de traitement. Les deux modalités réduisaient significativement les niveaux plasmatiques d'IL-17A et la glace réduisait en outre les taux d'IL-6 et de VEGF. Nous n'avons observé aucun effet de la cryothérapie locale sur le voie du TNF-α chez l'homme ni chez l'animal. Nos résultats démontrent pour la première fois un effet thérapeutique et anti-inflammatoire de la cryothérapie locale dans l'arthrite. Les effets biologiques était IL-6/IL-147 dépendants et TNF-α indépendants. Des études complémentaires permettront de mieux caractériser les mécanismes moléculaires sous-jacents et de déterminer su la cryothérapie locale pourrait être une alternative aux AINS et corticoïdes dans les rhumatismes inflammatoires
Cryotheapy i widely and empirically used in an adjuvant setting in inflammatory rheumatic diseases, with a low level of evidence. We performed a systematic review of the literature and, by pooling data from 6 non-controlled studies, we could show that local cryotherapy (local or whole-body cryotherapy) applaied twice a day for 7-15 days significantly reduced the pain VAS and the DAS28 activity score in rheumatoid arthritis. Furthermore, local cryotherapy (ice packs or cold gas) showed significantly greater intra)class effect-sizes compared to whole-body cryotherapy. The aim of this work was to measure the effects of local cryotherapy on pain, synovial and systemic inflammation in arthrici patients and in the murine model of adjuvant-induced arthritis. First, in the CDRI and ALGGAR randomized studies, we evaluated the effects of 2 local cold applications (ice versus cold gas) on pain, power Doppler activity and intra-joint cytokine protein levels in 46 patients suffering from non-septic knee arthritides. Contralateral arthritic knee were used as control. Secondly, we studied the in vitro effects of mild hypothermia (30°C for 2 hours) on cytokine protein expression in a model of cultured arthritic rat patellae. Thidly, we studied the in vitro effects of sub-chronically applied ice or cold gas (twice a day for 14 days versus non-treated arthritic controls) on the arthritis score, the ankle diameter, pro-inflammatory cytokine gene transcription levelsin hind paws (Q-RT-PCR) and cytokine plasma protein levelx (Multiplex and ELISA) after 14 days of treatment. In the CDRI study, local cryotherapy (ice and cold gas) significantly reduced the pain VAS and the power Doppler score in treated kness, and these effects remained significant the day afetr 2 cold applicaitions. In an intermediate analysis of the ALGGAR study results, by pooling the 2 treatment groups, we could show significant decreases in IL-6 protein, IL-1β and VEGF synovial fluid protein levels after 2 cold applicatios. In arthritic rat patella explangt culture experiments, punctual hypothermia significantly reduced IL-6 protein levels. In vivon ice was more efficient on the clinical parameters and better tolerated compared to cold gas. Both techniques significantly reduced IL-6, IL-17A ans IL-1β gene transcription levels in hind paws after 14 days of treatment. Both techniques redcued IL-17A plasma protein levles, while ice also reduced IL-6 and VEGF plasma protein levels. Conversely, we observed no effect of local cryotherapy on the TNF-α pathway, neither in patients nor in our animal model. Here we demonstrate for the first time therapeutic and anti-inflammatory effet-cts of local cryothepary in arthritis. The biological effects were IL-6/IL-17-driven and TNF-α independent. Further studies will help elucidate the underlying molecular mlechanisms involved and detemrine whether local cryotherapy might be a safer alternative to NSAIDs ans corticosteroids in inflammatory rheumatic diseases
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Books on the topic "Adjuvant arthritis"

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Dasgupta, Bhaskar. Polymyalgia rheumatica. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0134.

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This chapter reviews advances in pathogenesis; European League Against Rheumatism/American College of Rheumatology (EULAR/ACR) classification criteria with clinical, laboratory, and ultrasound criteria for classification as polymyalgia rheumatica (PMR); the heterogeneity and overlap between PMR, inflammatory arthritis, and large-vessel vasculitis as illustrated by representative cases; recent guidelines on early and correct recognition, investigations, and management of PMR; the scope of disease-modifying agents; socio-economic impact, outcomes, and patient experience in PMR. It also discusses areas for future research including clinical trials with biological agents and newer steroid formulations, standardized outcome assessments, and the search for better biomarkers in PMR. PMR is one of the common inflammatory rheumatic diseases of older people and represents a frequent indication for long-term glucocorticoid (GC) therapy. It is characterized by abrupt-onset pain and stiffness of the shoulder and pelvic girdle muscles. Its management is subject to wide variations of clinical practice and it is managed in primary or secondary care by general practitioners (GPs), rheumatologists, and non-rheumatologists. The evaluation of PMR can be challenging, as many clinical and laboratory features may also be present in other conditions, including other rheumatological diseases, infection, and neoplasia. PMR is usually diagnosed in the primary care setting, but standard clinical investigations and referral pathways for suspected PMR are unclear. The response to standardized therapy is heterogeneous, and a significant proportion of patients do not respond completely. There is also an overlap with inflammatory arthritis and large-vessel vasculitis for which adjuvant disease-modifying medications are often used. Prolonged corticosteroid therapy is associated with a variety of side effects, especially when high-dose glucocorticoid therapy is employed. Giant cell arteritis (GCA) is also often linked to PMR. It is a vasculitis of large- and medium-sized vessels causing critical ischaemia. GCA is a medical emergency because of the high incidence of neuro-ophthalmic complications. Both conditions are associated with a systemic inflammatory response and constitutional symptoms. The pathogenesis is unclear. The initiating step may be the recognition of an infectious agent by aberrantly activated dendritic cells. The key cell types involved are CD4+ T cells and macrophages giving rise to key cytokines such as interferon-γ‎ (implicated in granuloma formation), PDGF (intimal hyperplasia), and interleukin (IL)-6 (key to the systemic response). The pathogenesis of PMR may be similar to that of GCA, although PMR exhibits less clinical vascular involvement. The mainstay of therapy is corticosteroids, and disease-modifying therapy is currently indicated in relapsing disease.
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Felquer, Laura Acosta, and Enrique R. Soriano. Approach to management and symptomatic (including non-pharmacologic) management of psoriatic arthritis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0027.

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Psoriatic arthritis (PsA) is a heterogenous disease with multiple manifestations and comorbidities, and requires a collaborative management with other specialists. The major symptoms bordering patients are pain stiffness, and swelling, but fatigue, depression, embarrassment and fear are frequent and not always assessed by treating physicians. Non-steroidal anti-inflammatory drugs and local glucocorticosteroid injections remain important treatment options that should be used, although with caution, in the appropriate patient. Since the pre-biologic era, physical therapy has been part of non-pharmacological treatment in patients with rheumatic disease. Unfortunately there is little evidence of the efficacy of rehabilitation in PsA with no study with high grade of evidence. Surgery should be reserved for advanced cases as the new paradigms in the treatment of PsA (early diagnosis and treatment, remission as an objective, and treat to target), would very probably reduce the already low number of patients that need this last treatment option. In PsA patients surgery outcomes are similar to those of surgical management of other forms of arthritis. Symptomatic and non-pharmacologic management of PsA remain as important adjuvants of PsA treatment, although with little evidence.
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1942-, Furst Daniel E., and Weinblatt Michael E, eds. Immunomodulators in the rheumatic diseases. New York: M. Dekker, 1990.

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Book chapters on the topic "Adjuvant arthritis"

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Chillingworth, N. L., and L. F. Donaldson. "Arthritis Model, Adjuvant-Induced Arthritis." In Encyclopedia of Pain, 185–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_282.

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Kingston, A. E., S. L. Carney, C. A. Hicks, and M. E. J. Billingham. "In Vitro and in Vivo Effects of Proteoglycan Fractions in Adjuvant Treated Rats." In Joint Destruction in Arthritis and Osteoarthritis, 75–79. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-7442-7_7.

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Carlson, Richard P., and Peer B. Jacobson. "Comparison of adjuvant and streptococcal cell wall-induced arthritis in the rat." In In Vivo Models of Inflammation, 1–50. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-7775-6_1.

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Atlan, Henri, and Irun R. Cohen. "Paradoxical Effects of Suppressor T Cells in Adjuvant Arthritis: Neural Network Analysis." In Theoretical and Experimental Insights into Immunology, 379–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76977-1_25.

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van Eden, W., E. J. M. Hogervorst, E. J. Hensen, R. van der Zee, J. D. A. van Embden, and I. R. Cohen. "A Cartilage-Mimicking T-Cell Epitope on a 65K Mycobacterial Heat-Shock Protein: Adjuvant Arthritis as a Model for Human Rheumatoid Arthritis." In Current Topics in Microbiology and Immunology, 27–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74594-2_3.

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Naim, J. O., K. M. L. Ippolito, R. J. Lanzafame, and C. J. van Oss. "Induction of Type II Collagen Arthritis in the DA Rat Using Silicone Gel as Adjuvant." In Current Topics in Microbiology and Immunology, 103–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-85226-8_11.

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Huard, Johnny, Hajime Utsunomiya, Karen K. Briggs, and Marc J. Philippon. "Adjuvant Therapies in the Treatment of Pre-Arthritic Hip Disease." In Hip Dysplasia, 129–39. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-33358-4_9.

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Kröger, H., A. Dietrich, R. Grätz, M. Klewer, H. Wohlert, and W. Ehrlich. "The Influence of Antagonists of Poly(Adp-Ribose)Polymerase on the Activity Of Antirheumatic Drugs on the Development of Adjuvant Arthritis in Rats and on the Induction of Tyrosine Aminotransferase in the Liver of Rats." In Advances in Experimental Medicine and Biology, 523–26. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0381-7_81.

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Weidner, W., H. C. Becker, W. Mohr, and K. L. Schmidt. "Entzündungen im Urogenitaltrakt bei der Adjuvans-Arthritis der Ratte — ein Analogon zur „Uroarthritis“ beim Mann?" In Experimentelle Urologie, 242–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70524-3_34.

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Thierse, Hermann-Josef, Walter-Gunar Friebe, Werner Scheuer, Wolfgang Voelter, and Ulrich Tibes. "Evidence for Activation of Cyclooxygenase-1/-2 by Endogenous Nitric Oxide in Adjuvant Arthritic Lewis Rats." In Advances in Experimental Medicine and Biology, 343–48. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0179-8_55.

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Conference papers on the topic "Adjuvant arthritis"

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Chen, Xi, and Fan Li. "Effects of Arthrigia on adjuvant arthritis rats' serum TNF-α." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027993.

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Choi, Seok Cheol, Mi-Ha Joo, Gil-Hyun Lee, Joon-Sun Lee, Dae Sik Kim, Kyung Mo Oh, Jae-Hyun Choi, and Kyung Yae Hyun. "Effects of Anion in the Rat with Adjuvant-induced Arthritis." In Bioscience and Medical Research 2014. Science & Engineering Research Support soCiety, 2014. http://dx.doi.org/10.14257/astl.2014.56.04.

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Bordy, R., P. Totoson, F. Verhoeven, C. Prati, J. Moretto, M. Tournier-Nappey, and C. Demougeot. "FRI0039 Endothelial dysfunction in rheumatoid arthritis: which effect of methotrexate? a study in adjuvant induced arthritis model." 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.3234.

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Bordy, Romain, Perle Totoson, Marie-Lynda Bouressam, François Dupuis, Frank Verhoeven, Daniel Wendling, and Céline Demougeot. "AB0113 ARTHRITIS IS ASSOCIATED WITH CEREBROVASCULAR ENDOTHELIAL DYSFUNCTION: MECHANISTIC INSIGHTS IN THE RAT ADJUVANT-INDUCED ARTHRITIS MODEL." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.266.

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Wang, Xueding, Justin Rajian, Xia Shao, David L. Chamberland, and Gandikota Girish. "Characterization and treatment monitoring of inflammatory arthritis by photoacoustic imaging: a study on adjuvant-induced arthritis rat model." In SPIE BiOS, edited by Alexander A. Oraevsky and Lihong V. Wang. SPIE, 2014. http://dx.doi.org/10.1117/12.2037418.

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Danilov, AV, NI Korshunov, TG Danilova, VP Mikhailov, and LA Tsyganova. "AB0022 Lactoferrin – a potent anti-inflammatory agent for treatment of adjuvant arthritis." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.927.

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Jurčovičová, Jana, Olha Roman, Iveta Herichová, and Janette Šereš. "24-Hour profiles of pro-inflammatory adenopituitary hormones and interleukin-1β in rats with adjuvant arthritis." In VIIIth Conference Biologically Active Peptides. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2003. http://dx.doi.org/10.1135/css200306038.

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Hyun, Kyung Yae, Min Chull Park, Gil-Hyun Lee, Joon-Sun Lee, Mi-Ha Joo, Hwa-Sik Choi, Kyung Mo Oh, and Seok Cheol Choi. "An Ameliorative Effects of Swimming combined with Korean Berchemia roots on Adjuvant-induced Arthritis in Rats." In Bioscience and Medical Research 2014. Science & Engineering Research Support soCiety, 2014. http://dx.doi.org/10.14257/astl.2014.56.05.

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Bradunaite, R., E. Bernotiene, L. Leonaviciene, and D. Vaitkiene. "THU0078 Antiarthritic effect of salbutamol alone and in combination with pentoxyphiline on adjuvant arthritis in rats." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.955.

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Verhoeven, F., C. Prati, P. Totoson, R. Bordy, D. Wendling, and C. Demougeot. "FRI0044 Non-steroidal anti-inflammatory drugs are more beneficial than anti-tnfα drugs on the radiographic damage in arthritis: a study in adjuvant induced arthritis." 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.2611.

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You might also be interested in the extended bibliographies on the topic 'Adjuvant arthritis' for particular source types:
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