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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 molecules on bone can help identify new targets and therapeutics to prevent and treat bone disorders. In this article, we have focused on molecules that are produced by osteoblasts, osteocytes, and osteoclasts and their mechanism of action on these cells. We have also summarized the different pharmacological osteoporosis treatments that target different molecular aspects of these bone cells to minimize osteoporosis.

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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, periodontal connective tissue, macrophages, and neutrophils, which have implications for the occurrence of periradicular lesions. Lipoteichoic acid is also involved in producing D-alanine, which stimulates signals to other bacteria to form biofilms. The E. faecalis will change the balance of oxygen radical production in the periapical lesion, fragment collagen. The fight host's defense mechanisms that cause periapical damage and worsening bone loss. Furthermore, cytolysin will respond to changes in oxygen conditions in the depleting root canals for the dominance of E. faecalis against other bacteria. The energy needs of E. faecalis that assisted by hyaluronidase, which degrades hyaluronan dentin. İt has to produce disaccharide degradation products that can be transported and metabolized intracellularly. These materials hydrolyzing the substrate to obtain essential carbon for its growth. This article aims to describe the molecular aspect of E. faecalis virulence that is involved in root canal infections.

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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 points and aspects of bone synthesis and/or bone resorption, leading to defective bone tissue highly prone to long bone bowing, stress fractures and pseudofractures, and/or fragility fractures. To date, over 100 different Mendelian-inherited metabolic bone disorders have been identified and included in the OMIM database, associated with germinal heterozygote, compound heterozygote, or homozygote mutations, affecting over 80 different genes involved in the regulation of bone and mineral metabolism. This manuscript reviews clinical bone phenotypes, and the associated bone fragility in rare congenital metabolic bone disorders, following a disease taxonomic classification based on deranged bone metabolic activity.

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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 of the central, neural regulation of bone mass. Initial studies of an adipose-derived hormone, leptin, helped define a direct, sympathetic pathway involving efferent neural signals from the hypothalamus to receptors on the osteoblast. Since the leptin-mediated pathway has been continuously modified to reveal a complex system involving neuromedin U, cocaine- and amphetamine-related transcript and serotonin interacting within the hypothalamus and brainstem to regulate both bone formation and resorption in cancellous bone, a number of other systems have also been identified. Neuropeptide Y, acting through hypothalamic Y2 receptors, is capable of skeleton-wide modulation of osteoblast activity, with important coordination between body weight and bone mass. Cannabinoids, acting through central cannabinoid receptor 1 and bone cell cannabinoid receptor 2 receptors, modulate osteoclast activity, thereby identifying pathways active on both aspects of the bone remodeling process. This review explores the key central pathways to bone and explores the complexity of the interactions being revealed by this emergent field of research.

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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 and cytoplasm, the mitotic spindle and midbody, and in association with the actin belt. We show that PKD inhibitors CRT0066101 and CID755673 inhibit several distinct aspects of osteoclast formation. Treating bone marrow macrophages with lower doses of the PKD inhibitors had little effect on M-CSF + RANKL-dependent induction into committed osteoclast precursors, but inhibited their motility and subsequent differentiation into multinucleated mature osteoclasts, whereas higher doses of the PKD inhibitors induced apoptosis of the preosteoclasts. Treating post-fusion multinucleated osteoclasts with the inhibitors disrupted the osteoclast actin belts and impaired their resorptive activity. In conclusion, these data implicate PKD kinases as positive regulators of osteoclasts, which are essential for multiple distinct processes throughout their formation and function.

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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 arthritis showed that complete resolution of inflammation (with maximal reduction in the expression of pro-inflammatory factors) is crucial for bone healing, performed by osteoblasts activity. In fact, abnormal activity of factors and systems involved in osteoblast function in these patients has been described. A better understanding of the pathogenic mechanisms involved in osteoblast dysregulation could contribute to explain the generalized and focal articular bone loss found in rheumatoid arthritis. Nevertheless, these aspects have not been frequently and directly evaluated in studies. This review article is focused on analysis of the current knowledge about the role of osteoblast dysregulation occurring in rheumatoid arthritis: a better knowledge of these mechanisms could contribute to the realization of new therapeutic strategies.

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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 cellular mechanisms of action of the LCPUFA are complex and involve modulation of fatty acid metabolites such as prostaglandins, resolvins and protectins, several signaling pathways, cytokines, and growth factors, although in certain aspects there is still some controversy. LCPUFA affect receptor activator of nuclear factorκβ(RANK), a receptor found on the osteoclast, causing bone resorption, which controls osteoclast formation.Conclusions. Since fatty acids are an endogenous source of reactive oxygen species, free radicals alter the process of bone turnover; however, although there are clinical evidences linking bone metabolism and dietary lipids, more clinical trials are necessary to prove whetherω-3 PUFA supplementation plays a major role in bone health.

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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 destruction, the immunological and bacteriological responses, and new treatments. In these studies, the activation of osteoclasts, upregulation of pro-inflammatory factors, and excessive immune response have been considered as major factors in periodontal disruption. Multiple genes identified in periodontal tissues partly reflect the complexity of the pathogenesis of periodontitis. The effects of novel treatment methods on periodontitis have also been evaluated in a ligature-induced periodontitis model in mice. This model cannot completely represent all aspects of periodontitis in humans but is considered an effective method for the exploration of its mechanisms. Through this review, we aimed to provide evidence and enlightenment for future studies planning to use this model.

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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 using various search engines like google scholar, scihub, sciencedirect, pubmed, etc. A thorough understanding of the mechanism of bone targeting strategies has been discussed and related literature has been studied and compiled. Results: Bone remodeling process has been described in detail including various approaches for targeting bone. Several bone targeting moieties have been stated in detail along with their mechanisms. Targeting of osteoclasts and osteoblasts using various nanocarriers has been discussed in separate sections. The toxicity issues or Biosafety related to the use of nanomaterials have been covered. Conclusion: The treatment of osteoporosis targets the inhibition of bone resorption and the use of agents that promote bone mineralization to slow disease progression. Current osteoporosis therapy involves the use of targeting moieties such as bisphosphonates and tetracyclines for targeting various drugs. Nanotechnology has been used for targeting various drug molecules such as RANKLinhibitors, parathyroid hormone analogues, estrogen agonists and antagonists, Wnt signaling enhancer and calcitonin specifically to bone tissue (osteoclast and osteoblasts). So, a multicomponent treatment strategy targeting both the bone cells will be more effective rather than targeting only osteoclasts and it will be a potential area of research in bone targeting used to treat osteoporosis. The first section of the review article covers various aspects of bone targeting. Another section comprises details of various targeting moieties such as bisphosphonates, tetracyclines; and various nanocarriers developed to target osteoclast and osteoblast cells and summarized data on in vivo models has been used for assessment of bone targeting, drawbacks of current strategies and future perspectives.

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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 of a human pre-osteoblast cell line (HOB) induced to differentiate, and then treated with dexamethasone as osteoporosis inducer. Aspects of differentiation and viability were assessed by immunofluorescence, Western blot, mass spectrometry, and histological assays. Since steroids induce oxidative stress, the levels of reactive oxygen species and of redox related proteins were evaluated. Results—AFSC-EV were able to ameliorate the differentiation ability of HOB both in the case of pre-osteoblasts and when the differentiation process was affected by dexamethasone. Moreover, the viability was increased and parallelly apoptotic markers were reduced. The presence of EV positively modulated the redox unbalance due to dexamethasone. Conclusion—these findings demonstrated that EV from hAFSC have the ability to recover precursor cell potential and delay local bone loss in steroid-related osteoporosis.

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11

Miyazaki, Tsuyoshi, Hideki Katagiri, Yumi Kanegae, Hiroshi Takayanagi, Yasuhiro Sawada, Aiichiro Yamamoto, Mattew P. Pando, et al. "Reciprocal Role of ERK and Nf-κb Pathways in Survival and Activation of Osteoclasts." Journal of Cell Biology 148, no. 2 (January 24, 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 preventing spontaneous apoptosis. Neither inhibition nor activation of ERK affected the bone-resorbing activity of OCLs. Inhibition of NF-κB pathway with IKKDN virus suppressed the pit-forming activity of OCLs and NF-κB activation by IKKCA expression upregulated it without affecting their survival. Interleukin 1α (IL-1α) strongly induced ERK activation as well as NF-κB activation. RasDN virus partially inhibited ERK activation, and OCL survival promoted by IL-1α. Inhibiting NF-κB activation by IKKDN virus significantly suppressed the pit-forming activity enhanced by IL-1α. These results indicate that ERK and NF-κB regulate different aspects of osteoclast activation: ERK is responsible for osteoclast survival, whereas NF-κB regulates osteoclast activation for bone resorption.

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12

Munugalavadla, Veerendra, Sasidhar Vemula, Emily Catherine Sims, Subha Krishnan, Shi Chen, Jincheng Yan, Huijie Li, et al. "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, no. 23 (September 22, 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 impaired growth and differentiation, which is associated with reduced activation of Akt and mitogen-activated protein kinase extracellular signal-regulated kinase 1 (Erk1)/Erk2 in vitro. Furthermore, a significant reduction in the ability of p85α−/− osteoclasts to adhere to as well as to migrate via integrin αvβ3 was observed, which was associated with reduced bone resorption. Microarray as well as quantitative real-time PCR analysis of p85α−/− osteoclasts revealed a significant reduction in the expression of several genes associated with the maturation and migration of osteoclasts, including microphathalmia-associated transcription factor, tartrate-resistant acid phosphatase, cathepsin K, and β3 integrin. Restoring the expression of the full-length form of p85α but not the version with a deletion of the Src homology-3 domain restored the maturation of p85α−/− osteoclasts to wild-type levels. These results highlight the importance of the full-length version of the p85α subunit of class IA PI3-K in controlling multiple aspects of osteoclast functions.

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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 correlated with an increased expression of TNF-α. At 8 and 15 days, the number of RANKL(+) cells decreased near the mesial alveolar bone crest (ABC) but increased at the distal ABC. TRAP(+) cells on both sides of the complex significantly increased at 8 days. A gradual change in fibronectin expression from the distal PDL-secondary cementum interfaces through precementum layers was observed when compared to increased and abrupt changes at the mesial PDL-cementum and PDL-bone interfaces in ligated and control groups. Based on our results, we hypothesize that compromised strain fields can be created in a diseased periodontium, which in response to prolonged function can significantly alter the original bone and apical cementum formations.

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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, association of condylar position with TMDs, association of craniofacial morphology with TMDs, and influences of TMDs, TMJ-osteoarthritis (TMJ-OA) in particular, were examined. In a biomechanical aspect, the nature of stress distribution in the TMJ from maximum clenching was analyzed with finite element method. In addition, the pattern of stress distribution was examined in association with varying vertical discrepancies of the craniofacial skeleton and friction between the articular disk and condyle. The results demonstrated an induction of large compressive stresses in the anterior and lateral areas on the condyle by the maximum clenching and the subsequent prominent increases in the same areas of the mandibular condyle as the vertical skeletal discrepancy became more prominent. Increase of friction at the articular surface was also indicated as a cause of larger stresses and the relevant disk displacement, which further induced an increase in stresses in the tissues posterior to the disks, indicating an important role of TMJ disks as a stress absorber. In a histological or biological aspect, increase in TMJ loading simulated by vertical skeletal discrepancy, which has already been revealed by the preceding finite element analysis or represented by excessive mouth opening, produced a decrease in the thickness of cartilage layers, an increase in the numbers of chondroblasts and osteoclasts and the subsequent degenerative changes in the condylar cartilage associated with the expression of bone resorption-related factors. In a biochemical or molecular and cellular aspect, excessive mechanical stimuli, irrespective of compressive or tensile stress, induced HA fragmentation, expression of proinflammatory cytokines, an imbalance between matrix metalloproteinases and the tissue inhibitors, all of which are assumed to induce lower resistance to external stimuli and degenerative changes leading to bone and cartilage resorption. Excessive mechanical stimuli also reduced the synthesis of superficial zone protein in chondrocytes, which exerts an important role in the protection of cartilage and bone layers from the degenerative changes. It is also revealed that various cytoskeletal changes induced by mechanical stimuli are transmitted through a stretch-activated or Ca2+ channel. Finally, on the basis of the results from a series of studies, it is demonstrated that optimal intra-articular environment can be achieved by splint therapy, if indicated, followed by occlusal reconstruction with orthodontic approach in patients with myalgia of the masticatory muscles, and TMJ internal derangement or anterior disk displacement with or without reduction. It is thus shown that orthodontic treatment is available for the treatment of TMDs and the long-term stability after treatment.

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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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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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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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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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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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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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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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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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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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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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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 endosteal niche components (osteoblasts, mesenchymal stem cells (MSCs), endothelial cells and tumor) from myeloma-bearing and control mice, followed by RNA-Seq transcriptome profiling and gene set enrichment analysis (GSEA). Endosteal MSCs showed greatest transcriptome differences between myeloma-bearing and control groups. MSCs from myeloma-bearing mice showed positive enrichment (p = 0.004) for a 200-gene bone remodeling gene set. The leading edge (highest contributors to enrichment) of this gene set contained 24% BMP pathway genes, far higher than the next nearest pathway represented (TGFb signaling and AP-1 complex, both 6.5%). Whereas various other signaling pathways identified in the leading edge are known to be of high importance in myeloma bone disease (e.g. RANKL, TGFb, Wnt, hedgehog), BMP signaling has not hitherto been reported as deregulated. To assess the role of BMP signaling in myeloma in vitro and in vivo, we used the BMP pathway inhibitor LDN-193189 (LDN), which has high affinity for type I BMP receptors Alk2, Alk3 and Alk6. In the myeloma-bearing KaLwRij/5TGM1 mouse model, LDN significantly improved trabecular (p=0.02) and cortical bone volume (p=0.004) and reduced serum TRAP levels (p=0.003). Histomorphometric analysis demonstrated that LDN reduced osteoclast numbers (p<0.0001) and increased osteoblast numbers (p=0.018) in myeloma-bearing mice. As BMPs are well known to be osteoinductive, the mechanism by which BMP inhibition might cause increased bone mass in this model was investigated. In vitro, expression of rankl was significantly decreased by LDN in osteoblasts cultured from myeloma-bearing mice (p=0.03). Transcriptome profiling of endosteal MSCs sorted from myeloma mice treated with LDN or vehicle, subjected to GSEA (MSigDB Hallmark gene set database), showed significant enrichment in gene sets representing epithelial-mesenchymal-transition (EMT) and apical junction formation with LDN use. The leading edge genes included those involved in matrix deposition and osteoblast differentiation, indicating LDN may lead to reversal of certain aspects of the osteoblast differentiation block seen in MSCs in myeloma. LDN had no effect on overall tumour burden in vivo, however altered the niche-preference (endosteal vs central marrow) of myeloma cells to favor the endosteal niche (ratio endosteal: central marrow myeloma distribution 0.23 vehicle group, 0.37 LDN group, p=0.034). LDN also significantly reduced expression in liver of the iron regulatory hormone hepcidin (p=0.0003). Increased hepcidin has been described in multiple myeloma and likely contributes to inflammatory anemia, of clinical relevance in many myeloma patients. The analysis of cell-type specific in vivo gene expression changes in the myeloma endosteal niche led to investigation of a pathway not previously recognized as deregulated in myeloma bone disease. This technique has not previously been applied to the myeloma niche or, to our knowledge, any non-myeloid tumor invading bone marrow. We demonstrate its use in highlighting type 1 BMP receptor signaling as a novel therapeutic target in myeloma bone disease. BMP inhibition enhances osteoblast differentiation and reduces osteoclast activity in this model, suggesting anabolic and anti-resorptive benefits. The resulting preservation of the endosteal niche may have potential to increase the dormant tumor fraction. In addition to amelioration of bone disease, we hypothesize other clinical benefits, including improvement of inflammatory anemia and prolongation of quiescent phases, e.g. MGUS and post-treatment remission. Disclosures Ramasamy: Celgene: Honoraria, Research Funding.

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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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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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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 discuss the involvement of the inflammatory cytokine network in the pathophysiological aspects and the therapeutic advances in inflammatory autoimmune diseases.

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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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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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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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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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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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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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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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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. This editorial summarizes and discusses the themes of the fifteen articles published in the Special Issue, Osteoporosis: From Molecular Mechanisms to Therapies 2019, as part of the global picture of the current understanding of osteoporosis.

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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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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 histological and immunohistochemical analyses. Additionally, the local database was searched for all cases of meningiomas, as well as osteosclerotic differential diagnoses—i.e., fibrous dysplasia, Paget’s disease of bone, and other benign osteosclerotic lesions.RESULTSIn this study, PIM represented 2.4% of all meningiomas with a predominant occurrence in females (85%). Regarding the initial manifestation, PIMs show a slightly earlier onset than meningiomas. While most PIMs are located in the sphenoid bone, associated calcifications were visible in 58% of the cases on CT scans. Most of the cases were classified as WHO grade I (93%) and meningotheliomatous meningiomas (91%). Tumor growth was associated with an increased bone resorption followed by massive osteoid deposition and consecutive sclerosis. The frequently observed frayed appearance results from multiple bony canals, which contain blood vessels for the blood supply of the highly vascularized tumor tissue.CONCLUSIONSPIM is a rare but important differential diagnosis for osteosclerotic lesions of the skull, especially in women. Tumor-induced, cellular-mediated bone resorption and formation may play a central role in the underlying pathogenesis.

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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 (IC50> 300 nm). Conversely, the cathepsin K selective inhibitor was potently active in both the cytochemical (IC50= 63 nm) and resorption (IC50= 71 nm) assays. A recently reported dipeptide aldehyde with activity against cathepsins L (Ki= 0.052 nm) and K (Ki= 1.57 nm) was also active in both assays (IC50= 110 and 115 nm, respectively) These data confirm that cathepsin K and not cathepsin L is the major protease responsible for human osteoclastic bone resorption.

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