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Journal articles on the topic 'Bone resorption – Molecular aspects'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Gao, Yongguang, Suryaji Patil, and Jingxian Jia. "The Development of Molecular Biology of Osteoporosis." International Journal of Molecular Sciences 22, no. 15 (July 30, 2021): 8182. http://dx.doi.org/10.3390/ijms22158182.

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Osteoporosis is one of the major bone disorders that affects both women and men, and causes bone deterioration and bone strength. Bone remodeling maintains bone mass and mineral homeostasis through the balanced action of osteoblasts and osteoclasts, which are responsible for bone formation and bone resorption, respectively. The imbalance in bone remodeling is known to be the main cause of osteoporosis. The imbalance can be the result of the action of various molecules produced by one bone cell that acts on other bone cells and influence cell activity. The understanding of the effect of these m

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Asmah, Nur. "Molecular aspects of Enterococcus faecalis virulence." Journal of Syiah Kuala Dentistry Society 5, no. 2 (February 15, 2021): 89–94. http://dx.doi.org/10.24815/jds.v5i2.20020.

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The Enterococcus faecalis (E. Faecalis) virulence factor plays an essential role in the persistence of root canal infection. Virulence factors of Enterococcus faecalis such as lipoteichoic acid, extracellular superoxide, gelatinase, hyaluronidase, and cytolysin are known to increase the ability of Enterococcus faecalis to induce inflammatory processes, colonization formation, and increase resistance. The virulence factor of E. faecalis is mediated by LTA, which has pattern recognition receptors for cytokine release, bone resorption and triggers apoptosis of osteoblasts, osteoclasts, periodonta

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Marini, Francesca, Francesca Giusti, Teresa Iantomasi, and Maria Luisa Brandi. "Congenital Metabolic Bone Disorders as a Cause of Bone Fragility." International Journal of Molecular Sciences 22, no. 19 (September 24, 2021): 10281. http://dx.doi.org/10.3390/ijms221910281.

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Bone fragility is a pathological condition caused by altered homeostasis of the mineralized bone mass with deterioration of the microarchitecture of the bone tissue, which results in a reduction of bone strength and an increased risk of fracture, even in the absence of high-impact trauma. The most common cause of bone fragility is primary osteoporosis in the elderly. However, bone fragility can manifest at any age, within the context of a wide spectrum of congenital rare bone metabolic diseases in which the inherited genetic defect alters correct bone modeling and remodeling at different point

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Driessler, Frank, and Paul A. Baldock. "Hypothalamic regulation of bone." Journal of Molecular Endocrinology 45, no. 4 (July 26, 2010): 175–81. http://dx.doi.org/10.1677/jme-10-0015.

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On initial inspection, bone remodeling, the process whereby the skeleton adapts through time, appears to be relatively simple. Two cell types, the bone-forming osteoblasts and the bone-resorbing osteoclasts, interact to keep bone mass relatively stable throughout adult life. However, the complexity of the regulatory influences on these cells is continuing to expand our understanding of the intricacy of skeletal physiology and also the interactions between other organ systems and bone. One such example of the broadening of understanding in this field has occurred in the last decade with study o

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Leightner, Amanda C., Carina Mello Guimaraes Meyers, Michael D. Evans, Kim C. Mansky, Rajaram Gopalakrishnan, and Eric D. Jensen. "Regulation of Osteoclast Differentiation at Multiple Stages by Protein Kinase D Family Kinases." International Journal of Molecular Sciences 21, no. 3 (February 5, 2020): 1056. http://dx.doi.org/10.3390/ijms21031056.

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Balanced osteoclast and osteoblast activity is necessary for skeletal health, whereas unbalanced osteoclast activity causes bone loss in many skeletal conditions. A better understanding of pathways that regulate osteoclast differentiation and activity is necessary for the development of new therapies to better manage bone resorption. The roles of Protein Kinase D (PKD) family of serine/threonine kinases in osteoclasts have not been well characterized. In this study we use immunofluorescence analysis to reveal that PKD2 and PKD3, the isoforms expressed in osteoclasts, are found in the nucleus a

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6

Berardi, S., A. Corrado, N. Maruotti, D. Cici, and F. P. Cantatore. "Osteoblast role in the pathogenesis of rheumatoid arthritis." Molecular Biology Reports 48, no. 3 (March 2021): 2843–52. http://dx.doi.org/10.1007/s11033-021-06288-y.

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AbstractIn the pathogenesis of several rheumatic diseases, such as rheumatoid arthritis, spondyloarthritis, osteoarthritis, osteoporosis, alterations in osteoblast growth, differentiation and activity play a role. In particular, in rheumatoid arthritis bone homeostasis is perturbed: in addition to stimulating the pathologic bone resorption process performed by osteoclasts in course of rheumatoid arthritis, proinflammatory cytokines (such as Tumor Necrosis factor-α, Interleukin-1) can also inhibit osteoblast differentiation and function, resulting in net bone loss. Mouse models of rheumatoid ar

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Kajarabille, Naroa, Javier Díaz-Castro, Silvia Hijano, Magdalena López-Frías, Inmaculada López-Aliaga, and Julio J. Ochoa. "A New Insight to Bone Turnover: Role of -3 Polyunsaturated Fatty Acids." Scientific World Journal 2013 (2013): 1–16. http://dx.doi.org/10.1155/2013/589641.

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Background. Evidence has shown that long-chain polyunsaturated fatty acids (LCPUFA), especially theω-3 fatty acids such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are beneficial for bone health and turnover.Objectives. This review summarizes findings from bothin vivoandin vitrostudies and the effects of LC PUFA on bone metabolism, as well as the relationship with the oxidative stress, the inflammatory process, and obesity.Results. Some studies in humans indicate that LCPUFA can increase bone formation, affect peak bone mass in adolescents, and reduce bone loss. However, the

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8

Lin, Peiya, Hiromi Niimi, Yujin Ohsugi, Yosuke Tsuchiya, Tsuyoshi Shimohira, Keiji Komatsu, Anhao Liu, et al. "Application of Ligature-Induced Periodontitis in Mice to Explore the Molecular Mechanism of Periodontal Disease." International Journal of Molecular Sciences 22, no. 16 (August 18, 2021): 8900. http://dx.doi.org/10.3390/ijms22168900.

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Periodontitis is an inflammatory disease characterized by the destruction of the periodontium. In the last decade, a new murine model of periodontitis has been widely used to simulate alveolar bone resorption and periodontal soft tissue destruction by ligation. Typically, 3-0 to 9-0 silks are selected for ligation around the molars in mice, and significant bone loss and inflammatory infiltration are observed within a week. The ligature-maintained period can vary according to specific aims. We reviewed the findings on the interaction of systemic diseases with periodontitis, periodontal tissue d

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9

Kaur, Malkiet, Manju Nagpal, and Manjinder Singh. "Osteoblast-n-Osteoclast: Making Headway to Osteoporosis Treatment." Current Drug Targets 21, no. 16 (December 14, 2020): 1640–51. http://dx.doi.org/10.2174/1389450121666200731173522.

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Background: Bone is a dynamic tissue that continuously undergoes the modeling and remodeling process to maintain its strength and firmness. Bone remodeling is determined by the functioning of osteoblast and osteoclast cells. The imbalance between the functioning of osteoclast and osteoblast cells leads to osteoporosis. Osteoporosis is divided into primary and secondary osteoporosis. Generally, osteoporosis is diagnosed by measuring bone mineral density (BMD) and various osteoblast and osteoclast cell markers. Methods: Relevant literature reports have been studied and data has been collected us

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10

Gatti, Martina, Francesca Beretti, Manuela Zavatti, Emma Bertucci, Soraia Ribeiro Luz, Carla Palumbo, and Tullia Maraldi. "Amniotic Fluid Stem Cell-Derived Extracellular Vesicles Counteract Steroid-Induced Osteoporosis In Vitro." International Journal of Molecular Sciences 22, no. 1 (December 22, 2020): 38. http://dx.doi.org/10.3390/ijms22010038.

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Background—Osteoporosis is characterized by defects in both quality and quantity of bone tissue, which imply high susceptibility to fractures with limitations of autonomy. Current therapies for osteoporosis are mostly concentrated on how to inhibit bone resorption but give serious adverse effects. Therefore, more effective and safer therapies are needed that even encourage bone formation. Here we examined the effect of extracellular vesicles secreted by human amniotic fluid stem cells (AFSC) (AFSC-EV) on a model of osteoporosis in vitro. Methods—human AFSC-EV were added to the culture medium o

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11

Miyazaki, Tsuyoshi, Hideki Katagiri, Yumi Kanegae, Hiroshi Takayanagi, Yasuhiro Sawada, Aiichiro Yamamoto, Mattew P. Pando та ін. "Reciprocal Role of ERK and Nf-κb Pathways in Survival and Activation of Osteoclasts". Journal of Cell Biology 148, № 2 (24 січня 2000): 333–42. http://dx.doi.org/10.1083/jcb.148.2.333.

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To examine the role of mitogen-activated protein kinase and nuclear factor kappa B (NF-κB) pathways on osteoclast survival and activation, we constructed adenovirus vectors carrying various mutants of signaling molecules: dominant negative Ras (RasDN), constitutively active MEK1 (MEKCA), dominant negative IκB kinase 2 (IKKDN), and constitutively active IKK2 (IKKCA). Inhibiting ERK activity by RasDN overexpression rapidly induced the apoptosis of osteoclast-like cells (OCLs) formed in vitro, whereas ERK activation after the introduction of MEKCA remarkably lengthened their survival by preventin

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12

Munugalavadla, Veerendra, Sasidhar Vemula, Emily Catherine Sims, Subha Krishnan, Shi Chen, Jincheng Yan, Huijie Li та ін. "The p85α Subunit of Class IA Phosphatidylinositol 3-Kinase Regulates the Expression of Multiple Genes Involved in Osteoclast Maturation and Migration". Molecular and Cellular Biology 28, № 23 (22 вересня 2008): 7182–98. http://dx.doi.org/10.1128/mcb.00920-08.

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ABSTRACT Intracellular signals involved in the maturation and function of osteoclasts are poorly understood. Here, we demonstrate that osteoclasts express multiple regulatory subunits of class IA phosphatidylinositol 3-kinase (PI3-K) although the expression of the full-length form of p85α is most abundant. In vivo, deficiency of p85α results in a significantly greater number of trabeculae and significantly lower spacing between trabeculae as well as increased bone mass in both males and females compared to their sex-matched wild-type controls. Consistently, p85α−/− osteoclast progenitors show

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13

Lee, Ji-Hyun, Jeremy D. Lin, Justine I. Fong, Mark I. Ryder, and Sunita P. Ho. "The Adaptive Nature of the Bone-Periodontal Ligament-Cementum Complex in a Ligature-Induced Periodontitis Rat Model." BioMed Research International 2013 (2013): 1–17. http://dx.doi.org/10.1155/2013/876316.

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The novel aspect of this study involves illustrating significant adaptation of a functionally loaded bone-PDL-cementum complex in a ligature-induced periodontitis rat model. Following 4, 8, and 15 days of ligation, proinflammatory cytokines (TNF-αand RANKL), a mineral resorption indicator (TRAP), and a cell migration and adhesion molecule for tissue regeneration (fibronectin) within the complex were localized and correlated with changes in PDL-space (functional space). At 4 days of ligation, the functional space of the distal complex was widened compared to controls and was positively correlat

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14

Tanne, Kazuo, Yuki Okamoto, Shao-Ching Su, Tomomi Mitsuyoshi, Yuki Asakawa-Tanne, and Kotaro Tanimoto. "Current status of temporomandibular joint disorders and the therapeutic system derived from a series of biomechanical, histological, and biochemical studies." APOS Trends in Orthodontics 5 (December 29, 2014): 4–21. http://dx.doi.org/10.4103/2321-1407.148014.

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This article was designed to report the current status of temporomandibular joint disorders (TMDs) and the therapeutic system on the basis of a series of clinical, biomechanical, histological and biochemical studies in our research groups. In particular, we have focused on the association of degenerative changes of articular cartilage in the mandibular condyle and the resultant progressive condylar resorption with mechanical stimuli acting on the condyle during the stomatognathic function. In a clinical aspect, the nature and prevalence of TMDs, association of malocclusion with TMDs, associati

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15

Nair, S. P., S. Meghji, K. Reddi, S. Poole, A. D. Miller, and B. Henderson. "Molecular Chaperones Stimulate Bone Resorption." Calcified Tissue International 64, no. 3 (March 1, 1999): 214–18. http://dx.doi.org/10.1007/s002239900605.

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16

Teitelbaum, Steven L., Yousef Abu-Amer, and F. Patrick Ross. "Molecular mechanisms of bone resorption." Journal of Cellular Biochemistry 59, no. 1 (September 1995): 1–10. http://dx.doi.org/10.1002/jcb.240590102.

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17

Iqbal, Jameel, and Mone Zaidi. "Bone resorption goes green." Cell 184, no. 5 (March 2021): 1137–39. http://dx.doi.org/10.1016/j.cell.2021.02.023.

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18

HAMMARSTRÖM, LARS, and SVEN LINDSKOG. "General morphological aspects of resorption of teeth and alveolar bone." International Endodontic Journal 18, no. 2 (April 1985): 93–108. http://dx.doi.org/10.1111/j.1365-2591.1985.tb00426.x.

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19

Katsunuma, Nobuhiko. "Molecular mechanisms of bone collagen degradation in bone resorption." Journal of Bone and Mineral Metabolism 15, no. 1 (March 1997): 1–8. http://dx.doi.org/10.1007/bf02439448.

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20

Baron, Roland. "Molecular mechanisms of bone resorption An update." Acta Orthopaedica Scandinavica 66, sup266 (January 1995): 66–70. http://dx.doi.org/10.3109/17453679509157650.

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21

Väänänen, Kalero. "Cellular and molecular mechanisms of bone resorption." Pathophysiology 5 (June 1998): 130. http://dx.doi.org/10.1016/s0928-4680(98)80793-1.

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22

Suda, T., M. Inada, C. Miyaura, K. Kobayashi, N. Udagawa, and N. Takahashi. "The molecular mechanism of inflammatory bone resorption." Bone 27, no. 4 (October 2000): 4. http://dx.doi.org/10.1016/s8756-3282(00)80009-5.

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23

Gruber, Reinhard. "Molecular and cellular basis of bone resorption." Wiener Medizinische Wochenschrift 165, no. 3-4 (September 16, 2014): 48–53. http://dx.doi.org/10.1007/s10354-014-0310-0.

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24

Luukkonen, Jani, Meeri Hilli, Miho Nakamura, Ilja Ritamo, Leena Valmu, Kyösti Kauppinen, Juha Tuukkanen, and Petri Lehenkari. "Osteoclasts secrete osteopontin into resorption lacunae during bone resorption." Histochemistry and Cell Biology 151, no. 6 (January 14, 2019): 475–87. http://dx.doi.org/10.1007/s00418-019-01770-y.

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25

Gooding, Sarah, Siobhan Webb, Sam Olechnowicz, Seint Lwin, Andrew Armitage, Karthik Ramasamy, Claire M. Edwards, and Alexander Drakesmith. "Transcriptome Profiling of the Myeloma-Bone Niche Identifies BMP Signaling Role in Bone Destruction and Niche Maintenance, and Potential As a Therapeutic Target." Blood 128, no. 22 (December 2, 2016): 483. http://dx.doi.org/10.1182/blood.v128.22.483.483.

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Abstract In phases of myeloma dormancy such as MGUS (monoclonal gammopathy of uncertain significance) or post chemotherapy remission, certain characteristics of the bone marrow niche promote quiescence of the tumor. Myeloma cell dormancy has been proposed to be induced by contact with 'bone-lining' endosteal niche cells, which are destroyed by active disease. Preservation of dormancy could prevent disease relapse or MGUS progression to myeloma, however the molecular mechanisms and signaling pathways that maintain this bone-lining niche are unknown. We addressed this in vivo by sorting endostea

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26

ZAIDI, MONE, A. S. M. TOWHIDUL ALAM, VIJAI S. SHANKAR, BRIDGET E. BAX, CHRISTOPHER M. R. BAX, BALJIT S. MOONGA, PETER J. R. BEVIS, et al. "CELLULAR BIOLOGY OF BONE RESORPTION." Biological Reviews 68, no. 2 (May 1993): 197–264. http://dx.doi.org/10.1111/j.1469-185x.1993.tb00996.x.

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27

Hikiji, Hisako, Daisuke Endo, Kyoji Horie, Takeshi Harayama, Noriyuki Akahoshi, Hidemitsu Igarashi, Yasuyuki Kihara, et al. "TDAG8 activation inhibits osteoclastic bone resorption." FASEB Journal 28, no. 2 (November 12, 2013): 871–79. http://dx.doi.org/10.1096/fj.13-233106.

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28

Mundy, Gregory R. "Role of cytokines in bone resorption." Journal of Cellular Biochemistry 53, no. 4 (December 1993): 296–300. http://dx.doi.org/10.1002/jcb.240530405.

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29

Baron, Roland. "Molecular mechanisms of bone resorption by the osteoclast." Anatomical Record 224, no. 2 (June 1989): 317–24. http://dx.doi.org/10.1002/ar.1092240220.

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30

Amarasekara, Dulshara Sachini, Jiyeon Yu, and Jaerang Rho. "Bone Loss Triggered by the Cytokine Network in Inflammatory Autoimmune Diseases." Journal of Immunology Research 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/832127.

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Bone remodeling is a lifelong process in vertebrates that relies on the correct balance between bone resorption by osteoclasts and bone formation by osteoblasts. Bone loss and fracture risk are implicated in inflammatory autoimmune diseases such as rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel disease, and systemic lupus erythematosus. The network of inflammatory cytokines produced during chronic inflammation induces an uncoupling of bone formation and resorption, resulting in significant bone loss in patients with inflammatory autoimmune diseases. Here, we review and discus

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31

RIFKIN, BARRY R., ANTHONY T. VERNILLO, LORNE M. GOLUB, and NUNGAVARUM S. RAMAMURTHY. "Modulation of Bone Resorption by Tetracyclines." Annals of the New York Academy of Sciences 732, no. 1 Inhibition of (September 1994): 165–80. http://dx.doi.org/10.1111/j.1749-6632.1994.tb24733.x.

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32

SCHEPETKIN, IGOR. "Osteoclastic Bone Resorption: Normal and Pathological." Annals of the New York Academy of Sciences 832, no. 1 Phagocytes (December 1997): 170–93. http://dx.doi.org/10.1111/j.1749-6632.1997.tb46246.x.

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33

EVERTS, V., W. KORPER, A. J. P. DOCHERTY, and W. BEERTSEN. "Matrix Metalloproteinase Inhibitors Block Osteoclastic Resorption of Calvarial Bone but not the Resorption of Long Bone." Annals of the New York Academy of Sciences 878, no. 1 INHIBITION OF (June 1999): 603–6. http://dx.doi.org/10.1111/j.1749-6632.1999.tb07739.x.

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34

Hayashi, M. "Involvement of Calpain in Osteoclastic Bone Resorption." Journal of Biochemistry 137, no. 3 (March 1, 2005): 331–38. http://dx.doi.org/10.1093/jb/mvi036.

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35

Samee, Nadeem, Valérie Geoffroy, Caroline Marty, Corinne Schiltz, Maxence Vieux-Rochas, Philippe Clément-Lacroix, Cécile Belleville, Giovanni Levi, and Marie-Christine de Vernejoul. "Increased bone resorption and osteopenia inDlx5heterozygous mice." Journal of Cellular Biochemistry 107, no. 5 (August 1, 2009): 865–72. http://dx.doi.org/10.1002/jcb.22188.

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36

Suda, Tatsuo, Naoyuki Takahashi, and Etsuko Abe. "Role of vitamin D in bone resorption." Journal of Cellular Biochemistry 49, no. 1 (May 1992): 53–58. http://dx.doi.org/10.1002/jcb.240490110.

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37

Rani, C. S. Sheela, and Mary MacDougall. "Dental Cells Express Factors That Regulate Bone Resorption." Molecular Cell Biology Research Communications 3, no. 3 (March 2000): 145–52. http://dx.doi.org/10.1006/mcbr.2000.0205.

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38

Zeng, Guang-Zhi, Ning-Hua Tan, Xiao-Jiang Hao, Quan-Zhang Mu, and Rong-Tao Li. "Natural inhibitors targeting osteoclast-mediated bone resorption." Bioorganic & Medicinal Chemistry Letters 16, no. 24 (December 2006): 6178–80. http://dx.doi.org/10.1016/j.bmcl.2006.09.042.

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39

Tobe, Hiroyasu, Yoshifumi Muraki, Kazuyuki Kitamura, Osamu Komiyama, Yusuke Sato, Tatsuo Sugioka, Hiromi B. Maruyama, Eriko Matsuda, and Masahiro Nagai. "Bone Resorption Inhibitors from Hop Extract." Bioscience, Biotechnology, and Biochemistry 61, no. 1 (January 1997): 158–59. http://dx.doi.org/10.1271/bbb.61.158.

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40

Martin, T. John, Jonathan H. Gooi, and Natalie A. Sims. "Molecular Mechanisms in Coupling of Bone Formation to Resorption." Critical Reviews™ in Eukaryotic Gene Expression 19, no. 1 (2009): 73–88. http://dx.doi.org/10.1615/critreveukargeneexpr.v19.i1.40.

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41

Teitelbaum, Steven L., M. Mehrdad Tondravi, and F. Patrick Ross. "Osteoclasts, macrophages, and the molecular mechanisms of bone resorption." Journal of Leukocyte Biology 61, no. 4 (April 1997): 381–88. http://dx.doi.org/10.1002/jlb.61.4.381.

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42

Baron, R., M. Chakraborty, D. Chatterjee, W. C. Horne, A. Lomri, L. Neff, J. H. Ravesloot, and Y. Su. "Ion transport and the molecular mechanisms of bone resorption." Bone and Mineral 17 (April 1992): 81. http://dx.doi.org/10.1016/0169-6009(92)91681-8.

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43

Georgess, Dan, Irma Machuca-Gayet, Anne Blangy, and Pierre Jurdic. "Podosome organization drives osteoclast-mediated bone resorption." Cell Adhesion & Migration 8, no. 3 (February 7, 2014): 192–204. http://dx.doi.org/10.4161/cam.27840.

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Williams, John P., Harry C. Blair, Jay M. McDonald, Margaret A. McKenna, S. Elizabeth Jordan, Jodie Williford, and Robert W. Hardy. "Regulation of Osteoclastic Bone Resorption by Glucose." Biochemical and Biophysical Research Communications 235, no. 3 (June 1997): 646–51. http://dx.doi.org/10.1006/bbrc.1997.6795.

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45

Zhang, Jin, Mi-Jeong Ahn, Qi Shi Sun, Ki-Yoon Kim, Yun Ha Hwang, Jei Man Ryu, and Jinwoong Kim. "Inhibitors of bone resorption from Halenia corniculata." Archives of Pharmacal Research 31, no. 7 (July 2008): 850–55. http://dx.doi.org/10.1007/s12272-001-1237-y.

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46

Tang, Chih-Hsin. "Osteoporosis: From Molecular Mechanisms to Therapies." International Journal of Molecular Sciences 21, no. 3 (January 22, 2020): 714. http://dx.doi.org/10.3390/ijms21030714.

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Osteoporosis is a common skeletal disorder, occurring as a result of an imbalance between bone resorption and bone formation, with bone breakdown exceeding bone building. Bone resorption inhibitors, e.g., bisphosphonates, have been designed to treat osteoporosis, while anabolic agents such as teriparatide stimulate bone formation and correct the characteristic changes in the trabecular microarchitecture. However, all of these drugs are associated with significant side effects. It is therefore crucial that we continue to research the pathogenesis of osteoporosis and seek novel modes of therapy.

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47

Bacovsky, Jaroslav, Vlastimil Scudla, Marketa Vytrasova, Marie Budikova, and Miroslav Myslivecek. "Monitoring of bone resorption and bone formation in multiple myeloma." Biomedical Papers 146, no. 2 (December 1, 2002): 59–61. http://dx.doi.org/10.5507/bp.2002.012.

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48

Hohmann, ElizabethL, ArmenH Tashjian, Robert Elde, and Stanley Einzig. "VIP and bone: Evidence for neural control of bone resorption." Regulatory Peptides 10 (January 1985): S43. http://dx.doi.org/10.1016/0167-0115(85)90363-5.

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49

Butscheidt, Sebastian, Marielle Ernst, Tim Rolvien, Jan Hubert, Jozef Zustin, Michael Amling, and Tobias Martens. "Primary intraosseous meningioma: clinical, histological, and differential diagnostic aspects." Journal of Neurosurgery 133, no. 2 (August 2020): 281–90. http://dx.doi.org/10.3171/2019.3.jns182968.

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OBJECTIVEPrimary intraosseous meningioma (PIM) is a rare manifestation of meningioma, a benign, neoplastic lesion of the meninges. Its characteristic appearance is hyperostosis, while no or only minimal dural changes can be observed. This study aims to characterize this rare entity from both a clinical and histopathological point of view in order to improve clinical management.METHODSIn the years 2009–2017, 26 cases of PIM were diagnosed using MRI and CT scans. In 16 cases the indication for resection was given, and specimens were further examined using a multilevel approach, including histolo

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50

James, Ian E., Robert W. Marquis, Simon M. Blake, Shing Mei Hwang, Catherine J. Gress, Yu Ru, Denise Zembryki, et al. "Potent and Selective Cathepsin L Inhibitors Do Not Inhibit Human Osteoclast Resorptionin Vitro." Journal of Biological Chemistry 276, no. 15 (January 8, 2001): 11507–11. http://dx.doi.org/10.1074/jbc.m010684200.

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Cathepsins K and L are related cysteine proteases that have been proposed to play important roles in osteoclast-mediated bone resorption. To further examine the putative role of cathepsin L in bone resorption, we have evaluated selective and potent inhibitors of human cathepsin L and cathepsin K in anin vitroassay of human osteoclastic resorption and anin situassay of osteoclast cathepsin activity. The potent selective cathepsin L inhibitors (Ki= 0.0099, 0.034, and 0.27 nm) were inactive in both thein situcytochemical assay (IC50> 1 μm) and the osteoclast-mediated bone resorption assay (IC5

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