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Books on the topic 'Synovialis'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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1

J, Denton, ed. Atlas of synovial fluid cytopathology. Dordrecht: Kluwer Academic Publishers, 1991.

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2

M, Lazaro Deana, ed. Analysis of synovial fluid. Summit, N.J: CIBA-GEIGY, 1992.

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3

Freemont, A. J., and J. Denton. Atlas of Synovial Fluid Cytopathology. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3828-4.

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4

J, Reginato Antonio, ed. Atlas of synovial fluid analysis and crystal identification. Philadelphia: Lea & Febiger, 1991.

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5

Henderson, B. The synovial lining: In health and disease. London: Chapman and Hall, 1987.

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6

Brian, Henderson. The Synovial lining in health and disease. London: Chapman and Hall, 1987.

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7

Berëzkin, A. G. Sinovialʹnai͡a︡ zhidkostʹ sustavov konechnosteĭ mlekopitai͡u︡shchikh. Kiev: Nauk. dumka, 1987.

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8

1930-, Knight Joseph A., ed. Body fluids: Laboratory examination of amniotic, cerebrospinal, seminal, serous & synovial fluids. 3rd ed. Chicago: ASCP Press, 1993.

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9

Bailey, Lynne Christina. Isolation and characterisation of synovial T cell clones from patients with reactive arthritis. Birmingham: University of Birmingham, 1991.

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10

1930-, Knight Joseph A., ed. Body fluids: Laboratory examination of amniotic, cerebrospinal, seminal, serous & synovial fluids : a textbook atlas. 2nd ed. Chicago: American Society of Clinical Pathologists Press, 1986.

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11

Hua, Feng. Reactivity of synovial fluid antibodies from rheumatoid arthritis patients with chrondrocyte and cartilage matrix proteins. Ottawa: National Library of Canada, 1993.

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12

Gatter, Robert A. A practical handbook of joint fluid analysis. 2nd ed. Philadelphia: Lea & Febiger, 1991.

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13

Cherniakova, Yuliya Michailovna, and L. S. Pinchuk. Biophysics of synovia. Hauppauge, N.Y: Nova Science Publishers, 2011.

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14

Pitzalis, Costantino, Frances Humby, and Michael P. Seed. Synovial pathology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0052.

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Synovial pathology is seen in a variety of disease states, including rheumatoid arthritis (RA), osteoarthritis (OA), psoriatic arthritis, and systemic lupus erythmatosus (SLE). This chapter highlights recent advances that characterize the cellular composition of these tissues according to surface markers and chemokine and cytokine expression, and describes synovial functional status and response to therapeutics. In RA, after initiation, pannus migrates over and under cartilage, and into subchondral bone, in a destructive process. Cartilage-pannus junction (CPJ) is characterized as invasive or 'quiescent' or 'indistinct'. Invasive CPJ can comprise macrophages, fibroblast-like synoviocytes (FLS), mast cells, and/or neutrophils. CPJ activity is related to the state of activation of the overlying subintima. Subintimal inflammation can be graded to a variety of degrees (I–IV) according to established criteria and is illustrated. In some RA synovia, cellular aggregates organize into ectopic lymphoid structures (ELS) through the expression of lymphorganogenic signals, to exhibit T- or B-cell zones accompanied by dendritic cells and lymphangiogenesis. ELS synthesize rheumatoid factor (RF) and anti-citrullinated peptide antibodies (ACAP), considered to be indicative of aggressive disease. The selective cellular expression of macrophage and dendritic cell chemokines and cytokines such as TNF, GMCSF, TGFβ‎, IL-1, IL-6, IL-23, and chemokines can be seen in synovia, to form a regulated and cooperative environment that sustains the cellular organization and pathological function. Important to this process are FLS and CD68+ macrophages. CD68 expression correlates with disease severity and can be useful as a surrogate marker of disease modifying activity of therapeutics, such as anti-TNF and anti-B-cell biologics.
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15

Abdelattif, Engy, and Anthony J. Freemont. Assessment of synovial joint fluid. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0072.

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Assessment of synovial joint fluid is a simple, cheap, and relatively non-invasive test that can be applied to the whole spectrum of joint diseases, provided there is sufficient fluid within the joint to aspirate. The chapter outlines the key steps in undertaking microscopic analysis of synovial fluid in order to maximize the diagnostic and prognostic return, while placing the features seen within the context of some of the most important joint diseases. The chapter also examines the changing face of microbiological examination of synovial fluid to diagnose joint infection as a primary event and also the increasingly important problem of infection secondary to joint replacement surgery.
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16

Abdelattif, Engy, Anthony J. Freemont, and DC Mangham. Assessment of synovial joint fluid. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0072_update_002.

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Assessment of synovial joint fluid is a simple, cheap, and relatively non-invasive test that can be applied to the whole spectrum of joint diseases, provided there is sufficient fluid within the joint to aspirate. The chapter outlines the key steps in undertaking microscopic analysis of synovial fluid in order to maximize the diagnostic and prognostic return, while placing the features seen within the context of some of the most important joint diseases. The chapter also examines the changing face of microbiological examination of synovial fluid to diagnose joint infection as a primary event and also the increasingly important problem of infection secondary to joint replacement surgery.
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17

W, Archer Charles, ed. Biology of the synovial joint. Amsterdam, The Netherlands: Harwood Academic Publishers, 1999.

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18

Atlas of Synovial Fluid Cytopathology Current Histopathology. Springer, 2012.

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19

The Synovial Lining: In Health and Disease. Lippincott Williams & Wilkins Publishers, 1987.

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20

Nikolaev, Vladimir, Sergey Ermakov, Alexandr Beletskii, and Oleg Eismont. Liquid Crystals in Biotribology: Synovial Joint Treatment. Springer, 2015.

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21

Lentner, Cornelius. Analysis of Synovial Fluid (Diagnostic studies in rheumatology). 8th ed. Icon Learning Systems, 1986.

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22

Fick, Garret M. A new model describing the lubrication of synovial joints. 2006.

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23

Kjeldsberg, Carl. Laboratory Examination of Amniotic, Cerebrospinal, Seminal, Serous and Synovial Fluids. 2nd ed. Amer Society of Clinical, 1986.

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24

Pap, Thomas, Adelheid Korb, Marianne Heitzmann, and Jessica Bertrand. Joint biochemistry. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0056.

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Synovial joints are composed of different morphological structures that have their distinct cellular and biochemical properties. Articular cartilage and synovial membrane are key components of synovial joints and show a number of peculiarities that makes them different from other tissues in our body. An in-depth knowledge of these structural and biochemical peculiarities is not only important for understanding key features of articular function but also provides explanations for important characteristics of both degenerative and inflammatory joint diseases. This chapter reviews the structure and biochemical composition of cartilage and synovium and points to important links between physiology and pathological conditions, particularly arthritis.
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25

Gerald, Finerman, Noyes Frank R, American Academy of Orthopaedic Surgeons., National Institute of Arthritis and Musculoskeletal and Skin Diseases (U.S.), and American Orthopaedic Society for Sports Medicine., eds. Biology and biomechanics of the traumatized synovial joint: The knee as a model. Rosemont, IL: American Academy of Orthopaedic Surgeons, 1992.

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26

Veale, Douglas James. Clinical features and immunohistochemical studies of the skin and synovial membrane in psoriatic arthritis. 1992.

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27

Kamataki, Akihisa. Simple Method Using Gelatin-Coated Film for Comprehensively Assaying Gelatinase Activity in Synovial Fluid. INTECH Open Access Publisher, 2012.

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28

Pascual, Eliseo, and Francisca Sivera. Laboratory investigations in gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0042.

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Gout is a consequence of hyperuricaemia and the treatment goal is to dissolve the crystals by reducing serum urate levels. The first section of this chapter focuses on laboratory investigations on gout, reviewing serum urate levels and its determinants, methods of measurement, and urate renal handling. Additionally it reviews the use of inflammatory markers and synovial fluid cell counts. The second section of the chapter deals with the identification of monosodium urate and calcium pyrophosphate crystals in synovial fluid. It reviews the use of an optic microscope fitted with polarized filters and an analyser. A clear step-by-step process with useful tips is provided.
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29

Bhumbra, Rej S., Panagiotis D. Gikas, Sammy Hanna, Jakub Jagiello, and Stephen R. Cannon. Malignant tumours of soft tissues. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.002004.

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♦ Malignant vascular tumours of soft tissue♦ Synovial sarcoma♦ Malignant peripheral nerve sheath tumours♦ Rhabdomyosarcoma♦ Leiomyosarcoma♦ Epithelioid sarcoma♦ Clear cell sarcoma♦ Malignant fibrous histiocytoma♦ Chordoma.
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30

Sri-Ram, Kesavan, Anthony Mcgrath, Eric Yeung, Ben Spiegelberg, Nick Kalson, Barry Rose, Rob Pollock, and John Skinner. Benign tumours of soft tissues. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.002003.

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♦ Ganglion cyst♦ Intramuscular myxoma♦ Myositis ossificans♦ Nodular fasciitis♦ Haemangioma♦ Lipoma♦ Cavernous lymphangioma♦ Glomus tumour♦ Neurofibroma♦ Desmoid tumour♦ Elastofibroma♦ Schwannoma♦ Synovial chondromatosis.
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31

Thomas, Ranjeny, and Andrew P. Cope. Pathogenesis of rheumatoid arthritis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0109.

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In depth molecular and cellular analysis of synovial tissue and fluid from patients with rheumatoid arthritis has provided important insights into understanding disease pathogenesis. Advances in the 1980s and 1990s included modern cloning strategies, sensitive and specific assays for inflammatory mediators, production of high-affinity neutralizing monoclonal antibodies, advances in flow cytometry, and gene targeting and transgenic strategies in rodents. In the 21st century, technological platforms offer unparalleled opportunities for systematic and unbiased interrogation of the disease process at a whole-genome level. Here we describe the key molecular and cellular characteristics of the inflamed synovium and how infiltrating cells get there. With this background, we outline current concepts of the different phases of disease, how the first phase of genetic susceptibility evolves into autoimmunity, triggered by the exposome, prior to the onset of clinically apparent inflammatory disease. We then describe the pathways that actively contribute to this early inflammatory phase and document the key effector cells and molecules of the innate and adaptive immune systems that orchestrate and maintain chronic synovial inflammatory responses. We summarize how this inflammatory milieu translates to cartilage destruction and bone resorption in synovial joints, and conclude by reviewing those factors in inflamed synovium that promote immune homeostasis.
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32

Hullinger, Gordon A. A gp135 cellular receptor mediates infection of caprine synovial membrane cells by the lentivirus caprine arthritis-encephalitis virus. 1993.

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33

Wyatt, Laura A., and Michael Doherty. Morphological aspects of pathology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0003.

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Osteoarthritis (OA) is the commonest condition to affect synovial joints, but although any synovial joint can be affected, most studies of pathology relate to large joints (knees and hips). OA involves the whole joint and pathological alterations typically occur in all joint tissues. Established OA is characterized by a mixture of tissue loss and new tissue production resulting in focal loss of articular hyaline cartilage together with bone remodelling and osteophyte formation. Articular cartilage may show increased thickness in the earliest stages of OA with increased numbers of hypertrophic chondrocytes, followed by progressive decline in matrix components, thickness, and chondrocyte number. Surface fibrillation and vertical clefts become evident in mid- to end-stage OA and eventual complete loss of cartilage can occur, predominantly in maximum load-bearing regions, with subsequent eburnation and furrowing of bone. Bone remodelling may lead to alteration of bone shape and variable trabecular thickness in subchondral bone, whilst subchondral microfractures may result in localized osteonecrosis, fibrosis, and ‘cysts’. Endochondral ossification of new fibrocartilage produced predominantly at the joint margin produces characteristic bony osteophytes. The synovium shows areas of hyperplasia with varying amounts of lymphocyte aggregates and inclusion of osteochondral ‘loose’ bodies, and the outer fibrous capsule thickens to help stabilize the compromised joint. Synovial fluid increases in volume but decreases in viscosity. Periarticular changes include type II muscle atrophy and enthesophytes.
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34

Lafeber, Floris P. J. G., Nick J. Besselink, and Simon C. Mastbergen. Synovium and capsule. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0006.

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Synovium is an integrated tissue of the diarthrodial joints that interacts with all the other joint tissues and specifically is important in nourishment and lubrication of the articular cartilage, removal of waste products, and immunological surveillance. Chronic as well as recurrent low-grade synovial inflammation definitely contributes to progression and symptoms of certain patients with osteoarthritis. Low-grade inflammation may even be causative in the disease. The challenge is that osteoarthritis is a heterogeneous disorder with inflammation not only of the synovial tissue but with its mediators also present in cartilage and bone. Therefore, despite the presence of inflammatory mediators, in some cases synovitis may be seen as a bystander and not as a driving force in pathogenesis. Future research must be directed toward defining the risk-to-benefit ratio for (systemic) anti-inflammatory therapy, especially when targeting mediators of low-grade inflammation.
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35

Roberts, Simon. Articular cartilage. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199533909.003.0005.

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Synovial joints allow the efficient and controlled movement necessary for sport with a biological shock-absorbing bearing of hyaline cartilage. This is an extremely low friction surface, with a coefficient of one-sixth of that of ice on ice, lower than most man-made bearing materials. It has viscoelastic properties allowing dynamic congruity and minimization of transmitted pressure and impact....
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36

Colaco, Henry, Fares Haddad, and Cathy Speed. Knee injuries. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199533909.003.0031.

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The knee is a synovial hinge joint which achieves a range of movement of 0°–150° flexion with a complex combination of sliding, gliding, and rolling movements. The three components involved are the medial and lateral compartments of the tibiofemoral joint and the patellofemoral joint. The joint is lined with hyaline articular cartilage and stability is primarily provided by the joint capsule, menisci, ligaments, and muscles....
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37

Gerald A. M., M.D. Finerman (Editor), American Academy of Orthopaedic Surgeons (Corporate Author), National Institute of Arthritis and Musculoskeletal and Skin Diseases (Corporate Author), and Frank R., M.D. Noyes (Editor), eds. Biology and Biomechanics of the Traumatized Synovial Joint: The Knee As a Model/Workshop Scottsdale, Arizona November 1991 (Symposium). Amer Acad of Orthopaedic Surgeons, 1993.

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38

Doherty, Michael. Osteoarthritis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0266.

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Osteoarthritis (OA) is a disorder of synovial joints and is characterized by the combination of focal hyaline cartilage loss and accompanying subchondral bone remodelling and marginal new bone formation (osteophyte). It has genetic, constitutional, and environmental risk factors and presents a spectrum of clinical phenotypes and outcomes. OA commonly affects just one region (e.g. knee OA, hip OA). However, multiple hand interphalangeal joint OA, usually accompanied by posterolateral firm swellings (nodes), is a marker for a tendency towards polyarticular ‘generalized nodal OA’.
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39

Wheaton, Michael, Dustin Nowacek, and Zachary London. Radiculopathy and Plexopathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0125.

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Disorders of the nerve roots and neural plexi present with pain, numbness, or weakness in the neck, back, or extremities. Although the history and physical examination provide essential diagnostic information, imaging and electrodiagnostic studies may further aid in localizing and characterizing the underlying lesion. Causes of radiculopathy include intervertebral disc herniation, spondylosis, spinal synovial cysts, infection, metastatic disease, hematoma, or infiltrative disease. The brachial and lumbosacral plexi are susceptible to trauma, structural anomalies, neoplastic infiltration, and inflammatory processes. Management of these disorders is directed at treating the underlying cause, alleviating pain, and focused physical rehabilitation.
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40

Pilkington, Clarissa. Juvenile idiopathic arthritis: medical aspects. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.013002.

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♦ Juvenile idiopathic arthritis is defined as an arthritis persisting for at least 6 weeks♦ The cause may relate to the immune system response to a stimulus with a synovial or systemic manifestation♦ Classification depends on the clinical picture and the immunological markers♦ Joint sepsis is often a differential diagnosis♦ Most cases respond to simple measures, a few need a structured medical management plan. Surgery is indicated in 10% of cases. All require physiotherapy♦ Complications may occur secondary to the disease or its treatment.
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41

Pugh, Mark Timothy. Peripheral blood and synovial fluid immune responses to infectious agents and the E.coli Chaperone GroEL in children with juvenile chronic arthritis. 1996.

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42

Abhishek, Abhishek, and Michael Doherty. Investigations of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0051.

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Joint aspiration and microscopic examination of the aspirated synovial fluid remains the gold standard for the diagnosis of calcium pyrophosphate crystal deposition (CPPD). If synovial fluid aspiration is not feasible, plain radiography and/or ultrasound scanning may be used to detect chondrocalcinosis (CC) which predominantly occurs due to calcium pyrophosphate (CPP) crystals, and this can be used as a diagnostic surrogate for CPPD as suggested by the EULAR Task Force. Acute CPP crystal arthritis often associates with a brisk acute phase response (elevated C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR), plasma viscosity) and neutrophilia. A mildly raised CRP and/or ESR may be present in chronic CPP crystal inflammatory arthritis. On the contrary, asymptomatic CC, or CPPD with osteoarthritis does not cause raised acute phase reactants. As CPPD most commonly occurs due to increasing age and osteoarthritis, investigations to screen for underlying metabolic abnormalities should be carried out in those with early-onset CPPD (under 55 years), or in those with florid polyarticular CC. As hyperparathyroidism gets more common with ageing its presence should be specifically sought in all age groups. Tests for other predisposing metabolic conditions should only be carried out in the presence of specific clinical features. Genotyping for mutations, especially in the ANKH gene, may be warranted in those with a family history of premature CPPD and no evidence of inherited metabolic predisposition, but such testing is unavailable to most clinicians.
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43

van der Kraan, Peter M., and Esmeralda N. Blaney Davidson. Cartilage (including meniscus). Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0004.

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This chapter provides an overview of tissues unique to synovial joints, articular cartilage, and meniscus. The development and cellular and (bio)chemical composition are described, as well as the role of mechanical stimuli. In addition, the role of growth factors in cartilage and meniscus homeostasis, cellular differentiation, and chondrocyte hypertrophy are discussed. Furthermore, the involvement of aggrecanases and matrix metalloproteinases in cartilage and meniscus matrix degradation and osteoarthritis are described. Finally, the current status of repair of articular cartilage and meniscus is provided. This chapter reflects the changes in cellular differentiation, growth factor signalling, and altered matrix composition that contribute to osteoarthritis.
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44

Michaels, Frank H. Studies of the effects of infection by caprine arthritis-encephalitis virus of synovial macrophages: Activation, loss of accessory cell capability and increased expression of virus. 1989.

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45

Oikonomopoulou, Katerina, and Vinod Chandran. Biomarkers of psoriatic arthritis outcomes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0022.

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Psoriatic arthritis is an inflammatory musculoskeletal disease that occurs in patients suffering from psoriasis. The disease manifests with symptoms affecting the skin, peripheral and axial joints, and periarticular structures. Diagnosis and management of psoriatic arthritis is challenging due to its heterogeneous presentation. However, early diagnosis and subsequent appropriate treatment reduces disease activity, prevents joint damage, and improves long-term outcome. It is hoped that biomarkers for disease progression and activity will aid in cost-effective clinical management of patients. Potential biomarkers under investigation for psoriatic arthritis are disease-related components derived from skin and articular tissues, biological fluids, such as blood and synovial fluid, and arthritis-associated cell populations. Imaging including ultrasound and MRI are also being evaluated as biomarkers for diagnosis, activity and outcome. Despite the challenge of bringing these new markers into the clinic, many of these markers hold promise for the future management of patients with psoriatic arthritis.
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46

Cañete, Juan D., and Julio Ramírez. Enthesitis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0011.

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Enthesitis is common in psoriatic arthritis (PsA) occurring in50–60% of patients in clinical trials. Outcome measures for enthesitis have been developed, but its clinical diagnosis may be challenging at sites other than the Achilles and plantar insertions. Power Doppler ultrasound is more sensitive than clinical examination in detecting inflammatory and/or structural changes in asymptomatic patients, which have an unknown significance. Magnetic resonance imaging is useful to evaluate enthesitis and the best technique for osteitis. The concept of synovial–entheseal complex highlights the functional link between the entheseal site and synovium, supporting an important role for biomechanical stress in enthesitis, which is proposed as the primary lesion in PsA. Animal models have improved our understanding of molecular pathways, particularly TNF and IL-23/IL-17 cytokines, and new successful targeted therapies have been developed to treat enthesitis. Prospective studies integrating clinical and image examination will be crucial to better define the clinical implications of enthesitis changes.
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47

Dalbeth, Nicola. Epidemiology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198748311.003.0003.

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The aetiopathogenesis of gout is initiated by urate overproduction and uric acid under-excretion, leading to hyperuricaemia. Foods such as seafood, red meat, beer, and sugar-sweetened beverages contribute to overproduction. Under-excretion is mediated by renal and gut uric acid transporters such as SLC2A9, ABCG2, and URAT1. In hyperurcaemia, there is formation of monosodium urate (MSU) crystals in joints, with acute gouty arthritis mediated by the innate immune system occurring in response to these crystals. Factors such as urate concentration, proteins present in synovial fluid, temperature, and pH control crystal nucleation and growth. Activation of the inflammasome by MSU crystals and production of interleukin-1ß‎ is central to acute gouty arthritis. Advanced gout occurs when there is persistent gouty arthritis and tophus with the tophus being an organized immune tissue response to MSU crystals that involves both innate and adaptive immune cells. Progression through the gout checkpoints (hyperuricaemia, MSU crystal formation, and immune response) is governed by inherited genetic variants, lifetime environmental exposures, and their interaction.
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48

Cartin-Ceba, Rodrigo, and Udaya B. S. Prakash. Rheumatoid arthritis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0278.

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Rheumatoid arthritis is a progressive chronic inflammatory disease of autoimmune aetiology, characterized by joint swelling, tenderness, and destruction of synovial joints, leading to severe disability and premature mortality. The prevalence of rheumatoid arthritis has been estimated at 0.5–1% of the adult population and is the most common form of inflammatory joint disease. Rheumatoid arthritis frequently affects many non-articular systems, most commonly the cardiopulmonary, gastrointestinal, and haematological systems. Over recent years, the optimal use of disease-modifying anti-rheumatic drugs, in particular methotrexate, and the availability of several new biological agents, have dramatically enhanced the success of rheumatoid arthritis management. Multiple studies have demonstrated the efficacy of anti-TNF therapy, as well as other targeting, in reducing inflammatory activity, as well as inhibiting joint destruction in patients with active rheumatoid arthritis. A significant number of patients admitted to the intensive care unit (ICU) with autoimmune conditions have rheumatoid arthritis. The studies evaluating the outcome of rheumatoid arthritis patients admitted to the ICU have included other rheumatological conditions, but all have identified a high mortality (17–55%).
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49

Doherty, Michael, Johannes Bijlsma, Nigel Arden, David J. Hunter, and Nicola Dalbeth. Introduction: what is osteoarthritis? Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0001.

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This brief introductory chapter summarizes some of the key clinical and structural features of osteoarthritis (OA) and highlights some general observations and concepts concerning the nature of OA. General observations include the preservation of OA throughout human evolution; the occurrence of OA in many other animals; the dynamic, metabolically active nature of OA pathophysiology; the fact that most OA never associates with symptoms or functional impairment; and the good outcome in many cases of symptomatic OA. Such observations support the concept of OA as the inherent repair process of synovial joints, which can be triggered by a range of diverse insults and in which all the joint tissues are involved. Aetiologically, OA is a common complex disorder with recognized genetic, constitutional, and environmental risk factors, and these may combine in multiple ways to cause marked variation in phenotypic presentation and in some instances ‘joint failure’ with associated symptoms and disability. Within the spectrum of OA are some discrete subsets, the best defined being nodal generalized OA. However, in many people OA does not fit neatly into one type and its phenotypic characteristics may change as it evolves. Two striking associations of OA are with ageing and with crystal deposition, especially calcium crystals but also urate crystals, and there are a number of possible mechanisms to explain these.
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50

McDougall, Jason J., and Joel A. Vilensky. The innervation of the joint and its role in osteoarthritis pain. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0007.

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Diarthrodial joints possess an extensive network of sensory and sympathetic nerve fibres whose physiological functions are varied and complex. Nerves are primarily located in the synovium but also innervate the subchondral bone, the outer third of menisci, and the superficial surface of tendons and ligaments. Large-diameter, myelinated neurons are involved in joint position sense while small-diameter neurons with thin or no myelin typically sense pain. The small-diameter nerves in conjunction with sympathetic fibres control synovial blood flow and maintain joint homeostasis. In patients with osteoarthritis (OA), the sensory nerves become sensitized and increase their firing rate in response to normal movement. This peripheral sensitization is mediated by numerous algogenic agents released into the OA knee including neuropeptides, eicosanoids, and proteinases. A portion of joint afferents fire in the absence of mechanical stimuli and encode pain at rest. Interestingly, the firing rate of joint afferents does not correlate with OA severity, indicating that pain is a poor predictor of joint pathology. Evidence is accumulating to suggest that a subpopulation of OA patients who are unresponsive to classical non-steroidal anti-inflammatory drugs may be suffering from neuropathic pain in which there is damage to the joint nerves themselves. Better understanding of the biology of joint nerves could help in the development of patient-targeted therapies to alleviate OA pain and inflammation.
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