Suggested Sequential Mode of Control of Changes in Cell Behaviour in Adult Bone Remodelling

Hattner, Robert S.; Epker, Bruce N.; Frost, Harold M.

doi:10.1038/206489a0

Cited by 297 publications

(196 citation statements)

References 2 publications

Supporting

Mentioning

192

Contrasting

Unclassified

Order By: Relevance

“…Cells in cancellous bone are subject to the influence of a variety of osteotropic cytokines, produced by local cells (mesenchymal cells, lymphocytes, macrophages, smooth muscle cells) in the marrow cavity, whereas cells in the cortical bone are more influenced by systemic osteotropic hormones (IGF-1, IGF-BP3, Platelet-Derived Growth Factor, Transforming Growth Factors). 42 The distribution of cancellous and cortical bone varies in the skeleton. In the lumbar spine, cancellous bone comprises more than 66% of the total bone content.…”

Section: Discussionmentioning

confidence: 99%

Bone metabolism and risk of secondary hyperparathyroidism 12 months after gastric banding in obese pre-menopausal women

et al. 2003

View full text Add to dashboard Cite

OBJECTIVE:To evaluate, during the first postoperative year in obese pre-menopausal women, the effects of laparoscopic gastric banding on calcium and vitamin D metabolism, the potential modifications of bone mineral content and bone mineral density, and the risk of development of secondary hyperparathyroidism. SUBJECTS: Thirty-one obese pre-menopausal women aged between 25 and 52 y with a mean body mass index (BMI) of 43.6 kg=m 2 , scheduled for gastric banding were included. Patients with renal, hepatic, metabolic and bone disease were excluded. METHODS: Body composition and bone mineral density (BMD) were measured at baseline, 6 and 12 months after gastric banding using dual-energy X-ray absorptiometry. Serum calcium, phosphate, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, g-glutamyltransferase, bilirubin, urea, creatinine, uric acid, proteins, parathormone, vitamin D 3 , IGF-1, IGF-BP3 and telopeptide, as well as urinary telopeptide, were measured at baseline and 1, 3, 6, 9 and 12 months after surgery. RESULTS: After 1 y vitamin D3 remained stable and PTH decreased by 12%, but the difference was not significant. Serum telopeptide C increased significantly by 100% (P < 0.001). There was an initial drop of the IGF-BP3 during the first 6 months (P < 0.05), but the reduction was no longer significant after 1 y. The BMD of cortical bone (femoral neck) decreased significantly and showed a trend of a positive correlation with the increase of telopeptides (P < 0.06). The BMD of trabecular bone, at the lumbar spine, increased proportionally to the reduction of hip circumference and of body fat. CONCLUSION: There is no evidence of secondary hyperparathyroidism 1 y after gastric banding. Nevertheless biochemical bone markers show a negative remodelling balance, characterized by an increase of bone resorption. The serum telopeptide seems to be a reliable parameter, not affected by weight loss, to follow up bone turnover after gastroplasty.

show abstract

Section: Discussionmentioning

confidence: 99%

Bone metabolism and risk of secondary hyperparathyroidism 12 months after gastric banding in obese pre-menopausal women

et al. 2003

View full text Add to dashboard Cite

show abstract

“…In addition to such factors derived from bone cells, the bone is additionally under the control of factors that are related to the immune, vascular and nervous systems. 2,6,8 Therefore, the understanding of the complicated network mediated by cell -cell communication would be extremely helpful for the design of novel treatments for bone diseases. …”

Section: Discussionmentioning

confidence: 99%

“…These activities occur in response to various hormones, cytokines, chemokines and biomechanical external stimuli. 1,2 This process, called bone remodeling, is a prerequisite for the normal bone homeostasis that maintains both bone quality and strength. 2 An imbalance of bone resorption and formation is often central to metabolic bone diseases in humans and animals.…”

Section: Introductionmentioning

confidence: 99%

“…1,2 This process, called bone remodeling, is a prerequisite for the normal bone homeostasis that maintains both bone quality and strength. 2 An imbalance of bone resorption and formation is often central to metabolic bone diseases in humans and animals. For example, excessive resorption by osteoclasts results in pathological bone destruction, as seen in osteoporosis, autoimmune arthritis, Paget ' s disease, periodontitis and bone tumors.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Bone cell communication factors and Semaphorins

Negishi-Koga

Takayanagi

2012

BoneKEy Reports

View full text Add to dashboard Cite

-6396/12 www.nature.com/bonekey IntroductionThe bony skeleton enables various crucial processes, such as locomotive activity, the storage of calcium and the harboring of hematopoietic stem cells. Bone is a dynamic organ that is continuously being broken down by osteoclasts and subsequently rebuilt with new bone by osteoblasts throughout the course of one ' s adult life. These activities occur in response to various hormones, cytokines, chemokines and biomechanical external stimuli. 1,2 This process, called bone remodeling, is a prerequisite for the normal bone homeostasis that maintains both bone quality and strength. 2 An imbalance of bone resorption and formation is often central to metabolic bone diseases in humans and animals. For example, excessive resorption by osteoclasts results in pathological bone destruction, as seen in osteoporosis, autoimmune arthritis, Paget ' s disease, periodontitis and bone tumors. 1,3,4 Therefore, bone remodeling must be regulated both temporally and spatially so that the aged or damaged bone is replaced by an essentially equivalent amount of new bone. 1,5,6 The bone remodeling is carried out within the temporary anatomic structures, so-called basic multicellular unit (BMU), which consists of a group of osteoclasts in front forming the cutting cone and a group of osteoblasts behind forming the closing cone, by associating with blood supply and the peripheral innervation. 7,8 The bone remodeling is a cycle consisting of three phases: ' initiation ' of bone resorption by osteoclasts, the ' transition ' from resorption to new bone formation (also well known as a ' reversal ' period) and the ' bone formation ' ( Figure 1 ). 6,9 The entire process is achieved by the coordinated actions of osteoclasts, osteoblasts and other osteoblast lineage cells, including bone-lining cells and osteocytes. The most obvious example is the osteoclastogenesis regulatory system by receptor activator of nuclear-B ligand (RANKL) and its decoy receptor osteoprotegerin (OPG), which are produced by osteoblast lineage cells. However, key questions remain REVIEW Bone cell communication factors and SemaphorinsTakako Negishi-Koga 1 , 2 , 3 and Hiroshi Takayanagi 1 , 2 , 3 , 4 Bone tissue is continuously renewed throughout adult life by a process called ' remodeling ' , which involves a dynamic interplay among bone cells including osteoclasts, osteoblasts and osteocytes. For example, a tight coupling between bone resorption and formation is essential for the homeostasis of the skeletal system. Studies on the coupling mechanism in physiological and pathological settings have revealed that osteoclasts or osteoclastic bone resorption promote bone formation through the production of diverse coupling factors. The classical coupling factors are the molecules that promote bone formation after resorption, but there may be distinct mechanisms at work in various phases of bone remodeling. A recent study revealed that the Semaphorin 4D expressed by osteoclasts inhibits bone formation, which represents a mechanism by which...

show abstract

“…Meanwhile, each part of a long bone has its own function: metaphyseal primary trabeculae are sites of bone modeling based on mineralized cartilage cores formed during endochondral ossification (3). Secondary trabeculae show bone remodeling mediated by cellular coupling between osteoclasts and osteoblasts (4,9,10,12). Cortical bone is a mature, well-mineralized hard tissue that composes the outer wall of the long bone.…”

Section: Methodsmentioning

confidence: 99%

<b>Chronological immunolocalization of sclerostin and FGF23 in the mouse metaphyseal trabecular and cortical </b><b>bone </b>

et al. 2017

View full text Add to dashboard Cite

To assess the chronological participation of sclerostin and FGF23 in bone metabolism, this study tracked the immunolocalization of sclerostin and FGF23 in the metaphyses of murine long bones from embryonic day 18 (E18) through 1 day after birth, 1 week, 2 weeks, 4 weeks, 8 weeks, and 20 weeks of age. We have selected two regions in the metaphyseal trabeculae for assessing sclerostin and FGF23 localization: close to the chondro-osseous junction, i.e., bone modeling site even in the adult animals, and the trabecular region distant from the growth plate, where bone remodeling takes place. As a consequence, sclerostin-immunopositive osteocytes could not be observed in both close and distant trabecular regions early at the embryonic and young adult stages. However, osteocytes gradually started to express sclerostin in the distant region earlier than in the close region of the trabeculae. Immunoreactivity for FGF23 was observed mainly in osteoblasts in the early stages, but detectable in osteocytes in the later stages of growth in trabecular and cortical bones. Fgf23 was weakly expressed in the embryonic and neonatal stages, while the receptors, Fgfr1c and αKlotho were strongly expressed in femora. At the adult stages, Fgf23 expression became more intense while Fgfr1c and aKlotho were weakly expressed. These findings suggest that sclerostin is secreted by osteocytes in mature bone undergoing remodeling while FGF23 is synthesized by osteoblasts and osteocytes depending on the developmental/growth stage. In addition, it appears that FGF23 acts in an autocrine and paracrine fashion in fetal and neonatal bones.By establishing a communication network between osteocytes and osteoblasts, osteocytes are situated at the center of bone turnover and help determine how bones adjust to mechanical stress through bone remodeling. Osteocytes exist inside osteocytic lacunae and connect to neighboring osteocytes and osteoblasts on the bone surfaces via fine cytoplasmic processes that run through osteocytic canaliculi. Osteocytes interconnect their cytoplasmic processes via gap junctions (2,6,7,33), thereby building functional syncytia referred to as osteocytic lacunar-canalicular system (OLCS) (5,15,16,31). In the last few decades, many studies have reported on important osteocyte-derived factors, such as sclerostin (which regulates osteoblastic activities) and fibroblast growth factor 23 (FGF23, which affects the proximal renal tubules to reduce serum

show abstract

Suggested Sequential Mode of Control of Changes in Cell Behaviour in Adult Bone Remodelling

Cited by 297 publications

References 2 publications

Bone metabolism and risk of secondary hyperparathyroidism 12 months after gastric banding in obese pre-menopausal women

Bone metabolism and risk of secondary hyperparathyroidism 12 months after gastric banding in obese pre-menopausal women

Bone cell communication factors and Semaphorins

<b>Chronological immunolocalization of sclerostin and FGF23 in the mouse metaphyseal trabecular and cortical </b><b>bone </b>

Contact Info

Product

Resources

About