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Journal articles on the topic 'Inflammation of the Bone'

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1

Liu, Yiyan. "Bone Marrow Granulomatous Inflammation." Clinical Nuclear Medicine 33, no. 10 (2008): 707–8. http://dx.doi.org/10.1097/rlu.0b013e318184b423.

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2

Gu, Qiaoli, Huilin Yang, and Qin Shi. "Macrophages and bone inflammation." Journal of Orthopaedic Translation 10 (July 2017): 86–93. http://dx.doi.org/10.1016/j.jot.2017.05.002.

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3

Güler-Yüksel, Melek, Jos N. Hoes, Irene E. M. Bultink, and Willem F. Lems. "Glucocorticoids, Inflammation and Bone." Calcified Tissue International 102, no. 5 (2018): 592–606. http://dx.doi.org/10.1007/s00223-017-0335-7.

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4

Ofotokun, Ighovwerha, Emily McIntosh, and M. Neale Weitzmann. "HIV: Inflammation and Bone." Current HIV/AIDS Reports 9, no. 1 (2011): 16–25. http://dx.doi.org/10.1007/s11904-011-0099-z.

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5

Haynes, D. R. "Bone lysis and inflammation." Inflammation Research 53, no. 11 (2004): 596–600. http://dx.doi.org/10.1007/s00011-004-1303-z.

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6

Jakab, Lajos. "Bone tissue: Rebuilding and inflammation." Orvosi Hetilap 155, no. 40 (2014): 1575–83. http://dx.doi.org/10.1556/oh.2014.30015.

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In this review the author summarizes the knowledge related to structural elements of bone tissue. The process of bone reorganisation and knowledge about the special feature of bone metabolism in human are also discussed. It is noted that due to the reorganisation, there is a complete renewal of bone tissue in every 10 years, and this renewal lasts throughout the life. However, there are life periods when osteoclast activity is low, e.g. in childhood and the second decade of life when the gain of bone mass may be as much as 40% of the final bone mass. Overactivity of osteoclasts occurs at age 6
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7

Essers, Marieke A. G. "Inflammation Mediated Bone Marrow Remodeling." Blood 134, Supplement_1 (2019): SCI—2—SCI—2. http://dx.doi.org/10.1182/blood-2019-121050.

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Infection is a common, natural form of stress, with which the body is regularly challenged. During infection or inflammation, cells of the immune system are responsible for fighting the invading pathogens. This leads to consumption of blood and immune cells due to mobilization of these cells to the site of infection, or by apoptosis as part of the host response to invading pathogens. Restoration of the balance of the hematopoietic system following successful elimination of the infection is a crucial part of the recovery of the body. In addition, both clinical and experimental data indicate tha
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8

Gibon, Emmanuel, Laura Y. Lu, Karthik Nathan, and Stuart B. Goodman. "Inflammation, ageing, and bone regeneration." Journal of Orthopaedic Translation 10 (July 2017): 28–35. http://dx.doi.org/10.1016/j.jot.2017.04.002.

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9

Lingam, Ravi Kumar, Raekha Kumar, and Ram Vaidhyanath. "Inflammation of the Temporal Bone." Neuroimaging Clinics of North America 29, no. 1 (2019): 1–17. http://dx.doi.org/10.1016/j.nic.2018.08.003.

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10

Loi, Florence, Luis A. Córdova, Jukka Pajarinen, Tzu-hua Lin, Zhenyu Yao, and Stuart B. Goodman. "Inflammation, fracture and bone repair." Bone 86 (May 2016): 119–30. http://dx.doi.org/10.1016/j.bone.2016.02.020.

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11

Abu-Amer, Yousef. "Inflammation, cancer, and bone loss." Current Opinion in Pharmacology 9, no. 4 (2009): 427–33. http://dx.doi.org/10.1016/j.coph.2009.06.007.

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12

Hill, Geoffrey R. "Inflammation and Bone Marrow Transplantation." Biology of Blood and Marrow Transplantation 15, no. 1 (2009): 139–41. http://dx.doi.org/10.1016/j.bbmt.2008.11.008.

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13

SMOLEN, JOSEF S., and GEORG SCHETT. "Inflammation and Bone in RA." Rheumatology News 7, no. 10 (2008): 14–15. https://doi.org/10.1016/s1541-9800(08)70583-0.

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14

Wu, David H., and Antonis K. Hatzopoulos. "Bone morphogenetic protein signaling in inflammation." Experimental Biology and Medicine 244, no. 2 (2019): 147–56. http://dx.doi.org/10.1177/1535370219828694.

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Bone morphogenetic protein signaling has long been established as a crucial pathway during embryonic development. In recent years, our knowledge of the function of bone morphogenetic protein signaling has expanded dramatically beyond solely its important role in development. Today, the pathway is known to have important homeostatic functions across multiple different tissues in the adult. Even more importantly, bone morphogenetic protein signaling is now known to function as a driver of diseases in the adult spanning different organ systems. In this review, we will explore the functions of bon
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15

Aditya Rahman, Perdana. "Inflammation, Chronic Diseases and “Bone Quality”." Clinical and Research Journal in Internal Medicine 2, no. 1 (2021): 113–15. http://dx.doi.org/10.21776/ub.crjim.2021.002.01.1.

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16

Scholtysek, Carina, Gerhard Kronke, and Georg Schett. "Inflammation-Associated Changes in Bone Homeostasis." Inflammation & Allergy-Drug Targets 11, no. 3 (2012): 188–95. http://dx.doi.org/10.2174/187152812800392706.

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17

Denburg, Judah A., Lorna Wood, Gail Gauvreau, Roma Sehmi, Mark D. Inman, and Paul M. O'Byrne. "Bone marrow contribution to eosinophilic inflammation." Memórias do Instituto Oswaldo Cruz 92, suppl 2 (1997): 33–35. http://dx.doi.org/10.1590/s0074-02761997000800006.

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18

Bergmann, Berglind, Johan Mölne, and Inger Gjertsson. "The Bone-Inflammation-Cartilage (BIC) Stain." Journal of Histochemistry & Cytochemistry 63, no. 9 (2015): 737–40. http://dx.doi.org/10.1369/0022155415591599.

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19

Lerner, Ulf H., and Goran Sundquist. "Mediators of inflammation-induced bone resorption." Dental Traumatology 7, no. 4 (1991): 186. http://dx.doi.org/10.1111/j.1600-9657.1991.tb00206.x.

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20

Agrawal, Manasi, Shitij Arora, Jianjun Li, et al. "Bone, Inflammation, and Inflammatory Bowel Disease." Current Osteoporosis Reports 9, no. 4 (2011): 251–57. http://dx.doi.org/10.1007/s11914-011-0077-9.

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21

Steffens, J., B. Herrera, L. Coimbra, et al. "Testosterone Regulates Bone Response to Inflammation." Hormone and Metabolic Research 46, no. 03 (2014): 193–200. http://dx.doi.org/10.1055/s-0034-1367031.

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22

Adamopoulos, Iannis E. "Inflammation in bone physiology and pathology." Current Opinion in Rheumatology 30, no. 1 (2018): 59–64. http://dx.doi.org/10.1097/bor.0000000000000449.

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23

Collison, Joanna. "Low-level inflammation promotes bone growth." Nature Reviews Rheumatology 14, no. 5 (2018): 249. http://dx.doi.org/10.1038/nrrheum.2018.52.

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24

Haynes, D. R. "Erratum to: Bone lysis and inflammation." Inflammation Research 60, no. 10 (2011): 997. http://dx.doi.org/10.1007/s00011-011-0369-7.

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25

Mazzaferro, Sandro, Natalia De Martini, Silverio Rotondi, et al. "Bone, inflammation and chronic kidney disease." Clinica Chimica Acta 506 (July 2020): 236–40. http://dx.doi.org/10.1016/j.cca.2020.03.040.

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26

Schett, Georg. "Rheumatoid arthritis: inflammation and bone loss." Wiener Medizinische Wochenschrift 156, no. 1-2 (2006): 34–41. http://dx.doi.org/10.1007/s10354-005-0244-7.

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27

Görtz, Birgit, Silvia Hayer, Kurt Redlich, et al. "Arthritis Induces Lymphocytic Bone Marrow Inflammation and Endosteal Bone Formation." Journal of Bone and Mineral Research 19, no. 6 (2004): 990–98. http://dx.doi.org/10.1359/jbmr.040205.

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28

Hardy, R., and M. S. Cooper. "Bone loss in inflammatory disorders." Journal of Endocrinology 201, no. 3 (2009): 309–20. http://dx.doi.org/10.1677/joe-08-0568.

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Chronic inflammatory diseases of almost any cause are associated with bone loss. Bone loss is due to direct effects of inflammation, poor nutrition, reduced lean body mass, immobility and the effects of treatments, especially glucocorticoids. These mechanisms are complex and interrelated but are ultimately mediated through effects on the bone remodelling cycle. Inflammatory disease can increase bone resorption, decrease bone formation but most commonly impacts on both of these processes resulting in an uncoupling of bone formation from resorption in favour of excess resorption. This review wil
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29

Alippe, Yael, and Gabriel Mbalaviele. "Omnipresence of inflammasome activities in inflammatory bone diseases." Seminars in Immunopathology 41, no. 5 (2019): 607–18. http://dx.doi.org/10.1007/s00281-019-00753-4.

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Abstract The inflammasomes are intracellular protein complexes that are assembled in response to a variety of perturbations including infections and injuries. Failure of the inflammasomes to rapidly clear the insults or restore tissue homeostasis can result in chronic inflammation. Recurring inflammation is also provoked by mutations that cause the constitutive assembly of the components of these protein platforms. Evidence suggests that chronic inflammation is a shared mechanism in bone loss associated with aging, dysregulated metabolism, autoinflammatory, and autoimmune diseases. Mechanistic
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30

Kasi, Sundeep K., H. Jane Kim, Ryan P. Basham, et al. "Idiopathic Orbital Inflammation Associated With Necrotizing Scleritis and Temporal Bone Inflammation." Ophthalmic Plastic and Reconstructive Surgery 32, no. 4 (2016): e77-e79. http://dx.doi.org/10.1097/iop.0000000000000251.

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31

ElHawary, Hassan, Aslan Baradaran, Jad Abi-Rafeh, Joshua Vorstenbosch, Liqin Xu, and Johnny Ionut Efanov. "Bone Healing and Inflammation: Principles of Fracture and Repair." Seminars in Plastic Surgery 35, no. 03 (2021): 198–203. http://dx.doi.org/10.1055/s-0041-1732334.

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AbstractBones comprise a significant percentage of human weight and have important physiologic and structural roles. Bone remodeling occurs when healthy bone is renewed to maintain bone strength and maintain calcium and phosphate homeostasis. It proceeds through four phases: (1) cell activation, (2) resorption, (3) reversal, and (4) bone formation. Bone healing, on the other hand, involves rebuilding bone following a fracture. There are two main types of bone healing, primary and secondary. Inflammation plays an integral role in both bone remodeling and healing. Therefore, a tightly regulated
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32

Heckmann, S. M., J. J. Linke, F. Graef, Ch Foitzik, M. G. Wichmann, and H. P. Weber. "Stress and Inflammation as a Detrimental Combination for Peri-implant Bone Loss." Journal of Dental Research 85, no. 8 (2006): 711–16. http://dx.doi.org/10.1177/154405910608500805.

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The causes of peri-implant bone loss continue to be controversial. To determine the impact of biomechanical stress and inflammation, we investigated a total of 80 interforaminal implants in situ for more than 10 years. Two stress groups, with 14 patients each, were established: a low-stress situation with single-standing implants, and an increased-stress situation with splinted implants. To categorize inflammation, we introduced a Composite Inflammation Score using 4 inflammatory parameters. Peri-implant bone loss was calculated from digital panoramic radiographs. To differentiate between the
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33

Irwin, Regina, Sandi Raehtz, Narayanan Parameswaran, and Laura R. McCabe. "Intestinal inflammation without weight loss decreases bone density and growth." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 311, no. 6 (2016): R1149—R1157. http://dx.doi.org/10.1152/ajpregu.00051.2016.

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Increasing evidence indicates a strong link between intestinal health and bone health. For example, inflammatory bowel disease can cause systemic inflammation, weight loss, and extra-intestinal manifestations, such as decreased bone growth and density. However, the effects of moderate intestinal inflammation without weight loss on bone health have never been directly examined; yet this condition is relevant not only to IBD but to conditions of increased intestinal permeability and inflammation, as seen with ingestion of high-fat diets, intestinal dysbiosis, irritable bowel syndrome, metabolic
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34

Leimkühler, Nils B., and Rebekka K. Schneider. "Inflammatory bone marrow microenvironment." Hematology 2019, no. 1 (2019): 294–302. http://dx.doi.org/10.1182/hematology.2019000045.

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Abstract Self-renewing hematopoietic stem cells and their progeny, lineage-specific downstream progenitors, maintain steady-state hematopoiesis in the bone marrow (BM). Accumulating evidence over the last few years indicates that not only primitive hematopoietic stem and progenitor cells (HSPCs), but also cells defining the microenvironment of the BM (BM niche), sense hematopoietic stress signals. They respond by directing and orchestrating hematopoiesis via not only cell-intrinsic but also cell-extrinsic mechanisms. Inflammation has many beneficial roles by activating the immune system in tis
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35

Ke, Ke, Manoj Arra, and Yousef Abu-Amer. "Mechanisms Underlying Bone Loss Associated with Gut Inflammation." International Journal of Molecular Sciences 20, no. 24 (2019): 6323. http://dx.doi.org/10.3390/ijms20246323.

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Patients with gastrointestinal diseases frequently suffer from skeletal abnormality, characterized by reduced bone mineral density, increased fracture risk, and/or joint inflammation. This pathological process is characterized by altered immune cell activity and elevated inflammatory cytokines in the bone marrow microenvironment due to disrupted gut immune response. Gastrointestinal disease is recognized as an immune malfunction driven by multiple factors, including cytokines and signaling molecules. However, the mechanism by which intestinal inflammation magnified by gut-residing actors stimu
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36

Wang, Junjie, Bo Yuan, Ruixue Yin, and Hongbo Zhang. "Inflammation Responses to Bone Scaffolds under Mechanical Stimuli in Bone Regeneration." Journal of Functional Biomaterials 14, no. 3 (2023): 169. http://dx.doi.org/10.3390/jfb14030169.

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Physical stimuli play an important role in one tissue engineering. Mechanical stimuli, such as ultrasound with cyclic loading, are widely used to promote bone osteogenesis; however, the inflammatory response under physical stimuli has not been well studied. In this paper, the signaling pathways related to inflammatory responses in bone tissue engineering are evaluated, and the application of physical stimulation to promote osteogenesis and its related mechanisms are reviewed in detail; in particular, how physical stimulation alleviates inflammatory responses during transplantation when employi
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37

Geusens, Piet. "The role of RANK ligand/osteoprotegerin in rheumatoid arthritis." Therapeutic Advances in Musculoskeletal Disease 4, no. 4 (2012): 225–33. http://dx.doi.org/10.1177/1759720x12438080.

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In the complex system of bone remodeling, the receptor activator of nuclear factor κB ligand (RANKL)/osteoprotegerin (OPG) pathway is the coupling factor between bone formation and bone resorption. RANKL binds to the RANK receptor of pre-osteoclasts and mature osteoclasts and stimulates their activation and differentiation. The production of RANKL/OPG by osteoblasts is influenced by hormones, growth factors and cytokines, which each have a different effect on the production of RANKL and OPG. Ultimately, the balance between RANKL and OPG determines the degree of proliferation and activity of th
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38

BØYESEN, PERNILLE, FIONA M. McQUEEN, FRÉDÉRIQUE GANDJBAKHCH, et al. "The OMERACT Psoriatic Arthritis Magnetic Resonance Imaging Score (PsAMRIS) Is Reliable and Sensitive to Change: Results from an OMERACT Workshop." Journal of Rheumatology 38, no. 9 (2011): 2034–38. http://dx.doi.org/10.3899/jrheum.110420.

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Objective.The aim of this multireader exercise was to assess the reliability and sensitivity to change of the psoriatic arthritis magnetic resonance imaging score (PsAMRIS) in PsA patients followed for 1 year.Methods.MRI was acquired from 12 patients with PsA before initiation of treatment and after 12 months. MR images were scored according to PsAMRIS (for synovitis, tenosynovitis, periarticular inflammation, bone marrow edema, bone erosion, and bone proliferation) under standardized conditions, in unknown chronological order. Intraobserver/interobserver reliability was examined by intraclass
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39

Grahnemo, L., K. L. Gustafsson, K. Sjögren, et al. "Increased bone mass in a mouse model with low fat mass." American Journal of Physiology-Endocrinology and Metabolism 315, no. 6 (2018): E1274—E1285. http://dx.doi.org/10.1152/ajpendo.00257.2018.

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Mice with impaired acute inflammatory responses within adipose tissue display reduced diet-induced fat mass gain associated with glucose intolerance and systemic inflammation. Therefore, acute adipose tissue inflammation is needed for a healthy expansion of adipose tissue. Because inflammatory disorders are associated with bone loss, we hypothesized that impaired acute adipose tissue inflammation leading to increased systemic inflammation results in a lower bone mass. To test this hypothesis, we used mice overexpressing an adenoviral protein complex, the receptor internalization and degradatio
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40

Nakashima, Tomoki, and Hiroshi Takayanagi. "Osteoimmunology: the effect of inflammation on bone." Inflammation and Regeneration 31, no. 5 (2011): 404–12. http://dx.doi.org/10.2492/inflammregen.31.404.

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41

Mohler, Emile R., Francis Gannon, Carol Reynolds, Robert Zimmerman, Martin G. Keane, and Frederick S. Kaplan. "Bone Formation and Inflammation in Cardiac Valves." Circulation 103, no. 11 (2001): 1522–28. http://dx.doi.org/10.1161/01.cir.103.11.1522.

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42

Croes, M., MC Kruyt, L. Loozen, et al. "Local induction of inflammation affects bone formation." European Cells and Materials 33 (February 27, 2017): 211–26. http://dx.doi.org/10.22203/ecm.v033a16.

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43

Cochran, David L. "Inflammation and Bone Loss in Periodontal Disease." Journal of Periodontology 79, no. 8s (2008): 1569–76. http://dx.doi.org/10.1902/jop.2008.080233.

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44

Revu, Shankar, Vivekananda Gupta Sunkari, Akilan Krishnamurthy, Ileana Ruxandra Botusan, Sergiu-Bogdan Catrina, and Anca I. Catrina. "Hypoxia and inflammation synergistically promote bone destruction." Annals of the Rheumatic Diseases 71, Suppl 1 (2012): A61.1—A61. http://dx.doi.org/10.1136/annrheumdis-2011-201237.1.

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45

Knapik, Derrick M., Priyangi Perera, Jin Nam, et al. "Mechanosignaling in Bone Health, Trauma and Inflammation." Antioxidants & Redox Signaling 20, no. 6 (2014): 970–85. http://dx.doi.org/10.1089/ars.2013.5467.

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46

Burian, M. "Inflammation and tumors of the temporal bone." Der Radiologe 37, no. 12 (1997): 964–70. http://dx.doi.org/10.1007/s001170050308.

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47

Baker-LePain, Julie C., Mary C. Nakamura, and Nancy E. Lane. "Effects of inflammation on bone: an update." Current Opinion in Rheumatology 23, no. 4 (2011): 389–95. http://dx.doi.org/10.1097/bor.0b013e3283474dbe.

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48

Giannoudis, Peter V., David Hak, David Sanders, Erin Donohoe, Theodoros Tosounidis, and Chelsea Bahney. "Inflammation, Bone Healing, and Anti-Inflammatory Drugs." Journal of Orthopaedic Trauma 29 (December 2015): S6—S9. http://dx.doi.org/10.1097/bot.0000000000000465.

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49

Liu, Hongrui, Dongfang Li, Yi Zhang, and Minqi Li. "Inflammation, mesenchymal stem cells and bone regeneration." Histochemistry and Cell Biology 149, no. 4 (2018): 393–404. http://dx.doi.org/10.1007/s00418-018-1643-3.

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50

Zhou, Jiyin, Zuo Zhang, and Guisheng Qian. "Neuropathy and inflammation in diabetic bone marrow." Diabetes/Metabolism Research and Reviews 35, no. 1 (2018): e3083. http://dx.doi.org/10.1002/dmrr.3083.

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