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Biochimie Oct 2012Despite growing evidence for adipose tissue regulation of bone mass, the role of the adipokine leptin in bone remodeling remains controversial. The majority of in vitro... (Review)
Review
Despite growing evidence for adipose tissue regulation of bone mass, the role of the adipokine leptin in bone remodeling remains controversial. The majority of in vitro studies suggest leptin enhances osteoblastic proliferation and differentiation while inhibiting adipogenic differentiation from marrow stromal cells. Alternatively, some evidence demonstrates either no effect or a pro-apoptotic action of leptin on stromal cells. Similarly, in vivo work has demonstrated both positive and negative effects of leptin on bone mass. Most of the literature supports the idea that leptin suppresses bone mass by acting in the brainstem to reduce serotonin-dependent sympathetic signaling from the ventromedial hypothalamus to bone. However, other studies have found partly or entirely contrasting actions of leptin. Recently one study found a significant effect of surgery alone with intracerebroventricular administration of leptin, a technique crucial for understanding centrally-mediated leptin regulation of bone. Thus, two mainstream hypotheses for the role of leptin on bone emerge: 1) direct regulation through increased osteoblast proliferation and differentiation and 2) indirect suppression of bone formation through a hypothalamic relay. At the present time, it remains unclear whether these effects are relevant in only extreme circumstances (i.e. models with complete deficiency) or play an important homeostatic role in the regulation of peak bone acquisition and skeletal remodeling. Ultimately, determining the actions of leptin on the skeleton will be critical for understanding how the obesity epidemic may be impacting the prevalence of osteoporosis.
Topics: Animals; Bone and Bones; Drug Resistance; Homeostasis; Humans; Leptin; Receptors, Leptin
PubMed: 22534195
DOI: 10.1016/j.biochi.2012.04.015 -
Journal of Musculoskeletal & Neuronal... Jun 2013Bone remodeling is regulated by the two branches of the autonomic nervous system: the adrenergic and the cholinergic branches. Adrenergic activity favors bone loss,... (Review)
Review
Bone remodeling is regulated by the two branches of the autonomic nervous system: the adrenergic and the cholinergic branches. Adrenergic activity favors bone loss, whereas cholinergic activity has been recently shown to favor bone mass accrual. In vitro studies have reported that cholinergic activity induces proliferation and differentiation of bone cells. In vivo studies have shown that the inhibition of cholinergic activity favors bone loss, whereas its stimulation favors bone mass accrual. Clinical studies have shown that bone density is associated with the function of many cholinergic-regulated tissues such as the hypothalamus, salivary glands, lacrimal glands and langerhans cells, suggesting a common mechanism of control. Altogether, these observations and linked findings are of great significance since they improve our understanding of bone physiology. These discoveries have been successfully used recently to investigate new promising therapies for bone diseases based on cholinergic stimulation. Here, we review the current understanding of the cholinergic activity and its association with bone health.
Topics: Autonomic Pathways; Bone Remodeling; Bone and Bones; Central Nervous System; Humans; Osteoporosis; Parasympathetic Nervous System
PubMed: 23728099
DOI: No ID Found -
Clinical Orthopaedics and Related... Aug 2011Bone strength depends on both bone quantity and quality. The former is routinely estimated in clinical settings through bone mineral density measurements but not the... (Review)
Review
BACKGROUND
Bone strength depends on both bone quantity and quality. The former is routinely estimated in clinical settings through bone mineral density measurements but not the latter. Bone quality encompasses the structural and material properties of bone. Although its importance is appreciated, its contribution in determining bone strength has been difficult to precisely quantify partly because it is multifactorial and requires investigation of all bone hierarchical levels. Fourier transform infrared spectroscopy provides one way to explore these levels.
QUESTIONS/PURPOSES
The purposes of our review were to (1) provide a brief overview of Fourier transform infrared spectroscopy as a way to establish bone quality, (2) review the major bone material parameters determined from Fourier transform infrared spectroscopy, and (3) review the role of Fourier transform infrared microspectroscopic analysis in establishing bone quality.
METHODS
We used the ISI Web of Knowledge database initially to identify articles containing the Boolean term "infrared" AND "bone." We then focused on articles on infrared spectroscopy in bone-related journals.
RESULTS
Infrared spectroscopy provides information on bone material properties. Their microspectroscopic versions allow one to establish these properties as a function of anatomic location, mineralization extent, and bone metabolic activity. It provides answers pertaining to the contribution of mineral to matrix ratio, mineral maturity, mineral carbonate substitution, and collagen crosslinks to bone strength. Alterations of bone material properties have been identified in disease (especially osteoporosis) not attainable by other techniques.
CONCLUSIONS
Infrared spectroscopic analysis is a powerful tool for establishing the important material properties contributing to bone strength and thus has helped better understand changes in fragile bone.
Topics: Bone Density; Bone and Bones; Collagen; Humans; Spectroscopy, Fourier Transform Infrared
PubMed: 21210314
DOI: 10.1007/s11999-010-1751-4 -
BioMed Research International 2014Periodontitis and other bone loss diseases, decreasing bone volume and strength, have a significant impact on millions of people with the risk of tooth loss and bone... (Review)
Review
Periodontitis and other bone loss diseases, decreasing bone volume and strength, have a significant impact on millions of people with the risk of tooth loss and bone fracture. The integrity and strength of bone are maintained through the balance between bone resorption and bone formation by osteoclasts and osteoblasts, respectively, so the loss of bone results from the disruption of such balance due to increased resorption or/and decreased formation of bone. The goal of therapies for diseases of bone loss is to reduce bone loss, improve bone formation, and then keep healthy bone density. Current therapies have mostly relied on long-term medication, exercise, anti-inflammatory therapies, and changing of the life style. However there are some limitations for some patients in the effective treatments for bone loss diseases because of the complexity of bone loss. Interleukin-10 (IL-10) is a potent anti-inflammatory cytokine, and recent studies have indicated that IL-10 can contribute to the maintenance of bone mass through inhibition of osteoclastic bone resorption and regulation of osteoblastic bone formation. This paper will provide a brief overview of the role of IL-10 in bone loss diseases and discuss the possibility of IL-10 adoption in therapy of bone loss diseases therapy.
Topics: Animals; Bone Resorption; Bone and Bones; Humans; Interleukin-10; Periodontitis
PubMed: 24696846
DOI: 10.1155/2014/284836 -
Bone Sep 2010Postmenopausal osteoporosis and hyperparathyroidism are to two common forms of bone loss caused primarily by an expansion of the osteoclastic pool only partially... (Review)
Review
Postmenopausal osteoporosis and hyperparathyroidism are to two common forms of bone loss caused primarily by an expansion of the osteoclastic pool only partially compensated by a stimulation of bone formation. The intimate mechanisms by which estrogen deficiency and excessive production of PTH cause bone loss remain to be determined in part because in vitro studies do not provide the means to adequately reproduce the effects of ovx and PTH overproduction observed in vivo. This article examines the connection between T cells and bone in health and disease and reviews the evidence in favor of the hypothesis that T cells play an unexpected critical role in the mechanism of action of estrogen and PTH in bone.
Topics: Animals; Bone Diseases, Metabolic; Bone and Bones; Estrogens; Homeostasis; Humans; Menopause; Parathyroid Hormone; Signal Transduction; Stromal Cells; T-Lymphocytes; Tumor Necrosis Factor-alpha
PubMed: 20452473
DOI: 10.1016/j.bone.2010.04.611 -
The Anatomical Record. Part A,... Dec 2003The still-evolving mechanostat hypothesis for bones inserts tissue-level realities into the former knowledge gap between bone's organ-level and cell-level realities. It... (Review)
Review
The still-evolving mechanostat hypothesis for bones inserts tissue-level realities into the former knowledge gap between bone's organ-level and cell-level realities. It concerns load-bearing bones in postnatal free-living bony vertebrates, physiologic bone loading, and how bones adapt their strength to the mechanical loads on them. Voluntary mechanical usage determines most of the postnatal strength of healthy bones in ways that minimize nontraumatic fractures and create a bone-strength safety factor. The mechanostat hypothesis predicts 32 things that occur, including the gross anatomical bone abnormalities in osteogenesis imperfecta; it distinguishes postnatal situations from baseline conditions at birth; it distinguishes bones that carry typical voluntary loads from bones that have other chief functions; and it distinguishes traumatic from nontraumatic fractures. It provides functional definitions of mechanical bone competence, bone quality, osteopenias, and osteoporoses. It includes permissive hormonal and other effects on bones, a marrow mediator mechanism, some limitations of clinical densitometry, a cause of bone "mass" plateaus during treatment, an "adaptational lag" in some children, and some vibration effects on bones. The mechanostat hypothesis may have analogs in nonosseous skeletal organs as well.
Topics: Biomechanical Phenomena; Bone Density; Bone Development; Bone Remodeling; Bone and Bones; Fractures, Bone; Humans; Osteogenesis Imperfecta; Osteoporosis
PubMed: 14613308
DOI: 10.1002/ar.a.10119 -
Cell and Tissue Research May 2013Osteocytes establish an extensive intracellular and extracellular communication system via gap-junction-coupled cell processes and canaliculi throughout bone and the... (Review)
Review
Osteocytes establish an extensive intracellular and extracellular communication system via gap-junction-coupled cell processes and canaliculi throughout bone and the communication system is extended to osteoblasts on the bone surface. The osteocyte network is an ideal mechanosensory system and suitable for mechanotransduction. However, the overall function of the osteocyte network remains to be clarified, since bone resorption is enhanced by osteocyte apoptosis, which is followed by a process of secondary necrosis attributable to the lack of scavengers. The enhanced bone resorption is caused by the release of intracellular content, including immunostimulatory molecules that activate osteoclastogenesis through the canaliculi. Therefore, a mouse model is required in which the osteocyte network is disrupted but in which no bone resorption is induced, in order to evaluate the overall functions of the osteocyte network. One such model is the BCL2 transgenic mouse, in which the osteocyte network, including both intracellular and extracellular networks, is disrupted. Another model is the osteocyte-specific Gja1 knockout mouse, in which intercellular communication through gap junctions is impaired but the canalicular system is intact. Combining the findings from these mouse models with previous histological observations showing the inverse linkage between osteocyte density and bone formation, we conclude that the osteocyte network enhances bone resorption and inhibits bone formation under physiological conditions. Further, studies with BCL2 transgenic mice show that these osteocyte functions are augmented in the unloaded condition. In this condition, Rankl upregulation in osteoblasts and Sost upregulation in osteocytes are, at least in part, responsible for enhanced bone resorption and suppressed bone formation, respectively.
Topics: Animals; Bone Density; Bone and Bones; Humans; Mice; Osteocytes
PubMed: 23329124
DOI: 10.1007/s00441-012-1546-x -
Journal of Musculoskeletal & Neuronal... 2005Bone growth in length is primarily achieved through the action of chondrocytes in the proliferative and hypertrophic zones of the growth plate. Longitudinal growth is... (Review)
Review
Bone growth in length is primarily achieved through the action of chondrocytes in the proliferative and hypertrophic zones of the growth plate. Longitudinal growth is controlled by systemic, local paracrine and local mechanical factors. With regard to the latter, a feedback mechanism must exist which ensures that bone growth proceeds in the direction of the predominant mechanical forces. How this works is unknown at present. Bone growth in length is detrimental to bone stability, but this effect is counteracted by concomitant bone growth in width. This occurs through periosteal apposition, which is the responsibility of periosteal osteoblasts. The action of these cells is mainly controlled by local factors, with modulation by systemic agents. According to the mechanostat theory, periosteal apposition is regulated by mechanical requirements. An alternative model, called sizostat hypothesis, maintains that a master gene or set of genes regulate bone growth in width to reach a pre-programmed size, independent of mechanical requirements. The virtues of these two hypotheses have been the subject of much discussion, but experimental data are scarce. Future research will have to address the question how periosteal bone cells manage to integrate mechanical, hormonal and other input to shape bones that are as strong as they need to be.
Topics: Animals; Bone Development; Bone and Bones; Calcification, Physiologic; Chondrocytes; Gene Expression Regulation, Developmental; Growth Plate; Homeostasis; Humans; Osteoblasts; Osteogenesis; Periosteum
PubMed: 16172510
DOI: No ID Found -
Journal of Musculoskeletal & Neuronal... 2008This work proposes a mathematical model that qualitative describes the process of mechanically force-induced bone growth and adaptation. The mathematical model includes... (Review)
Review
This work proposes a mathematical model that qualitative describes the process of mechanically force-induced bone growth and adaptation. The mathematical model includes osteocytes as the key interfacing layer connecting tissue, cellular and molecular signaling levels. Specifically, in the presence of an increase in the mechanical stimuli, osteocytes respond by mechano-transduction releasing the local factors nitric oxide (NO) and prostaglandin E(2) (PGE(2)). These local factors act as the signaling recruitment signals for bone cells progenitors and influence the coupling activity among osteoblasts and osteoclasts during the process of bone remodeling. The model is in agreement with qualitative observations found in the literature concerning the process of bone adaptation and the cellular interactions during a local bone remodeling cycle induced by mechanical stimulation.
Topics: Adaptation, Physiological; Bone Remodeling; Bone and Bones; Humans; Models, Biological
PubMed: 18398254
DOI: No ID Found -
Advances in Experimental Medicine and... 2018The osteochondral tissue represents a complex structure composed of four interconnected structures, namely hyaline cartilage, a thin layer of calcified cartilage,... (Review)
Review
The osteochondral tissue represents a complex structure composed of four interconnected structures, namely hyaline cartilage, a thin layer of calcified cartilage, subchondral bone, and cancellous bone. Due to the several difficulties associated with its repair and regeneration, researchers have developed several studies aiming to restore the native tissue, some of which had led to tissue-engineered commercial products. In this sense, this chapter discusses the good manufacturing practices, regulatory medical conditions and challenges on clinical translations that should be fulfilled regarding the safety and efficacy of the new commercialized products. Furthermore, we review the current osteochondral products that are currently being marketed and applied in the clinical setting, emphasizing the advantages and difficulties of each one.
Topics: Animals; Bone Regeneration; Bone Substitutes; Bone and Bones; Humans; Hyaline Cartilage; Regenerative Medicine; Tissue Engineering
PubMed: 29691833
DOI: 10.1007/978-3-319-76711-6_19