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Статті в журналах з теми "Bone Physiology"

Щоб переглянути інші типи публікацій з цієї теми, перейдіть за посиланням: Bone Physiology.

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 11 березня 2023

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1

Chowdhury, Biplob. "Bone Remodeling: The Molecular Mechanism of Bone Physiology- A Review." International Journal of Scientific Research 3, no. 4 (June 1, 2012): 305–6. http://dx.doi.org/10.15373/22778179/apr2014/105.

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2

Alexandre, Christian. "Bone physiology." Current Opinion in Rheumatology 3, no. 3 (June 1991): 452–56. http://dx.doi.org/10.1097/00002281-199106000-00018.

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3

Morone, Michael A. "Bone physiology and bone healing." Neurosurgical Focus 13, no. 6 (December 2002): 1. http://dx.doi.org/10.3171/foc.2002.13.6.1.

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4

Martin, T. J., Kong Wah Ng, and Tatsuo Suda. "Bone Cell Physiology." Endocrinology and Metabolism Clinics of North America 18, no. 4 (December 1989): 833–58. http://dx.doi.org/10.1016/s0889-8529(18)30346-3.

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5

Buck, Donald W., and Gregory A. Dumanian. "Bone Biology and Physiology." Plastic and Reconstructive Surgery 129, no. 6 (June 2012): 950e—956e. http://dx.doi.org/10.1097/prs.0b013e31824ec354.

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6

Buck, Donald W., and Gregory A. Dumanian. "Bone Biology and Physiology." Plastic and Reconstructive Surgery 129, no. 6 (June 2012): 1314–20. http://dx.doi.org/10.1097/prs.0b013e31824eca94.

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7

Clarke, Bart L., and Sundeep Khosla. "Physiology of Bone Loss." Radiologic Clinics of North America 48, no. 3 (May 2010): 483–95. http://dx.doi.org/10.1016/j.rcl.2010.02.014.

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8

El-Farrash, Rania Ali, Radwa Hassan Ali, and Noha Mokhtar Barakat. "Post-natal bone physiology." Seminars in Fetal and Neonatal Medicine 25, no. 1 (February 2020): 101077. http://dx.doi.org/10.1016/j.siny.2019.101077.

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9

DeLacure, Mark D. "Physiology Of Bone Healing And Bone Grafts." Otolaryngologic Clinics of North America 27, no. 5 (October 1994): 859–74. http://dx.doi.org/10.1016/s0030-6665(20)30613-7.

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10

Doherty, Alison H., Cameron K. Ghalambor, and Seth W. Donahue. "Evolutionary Physiology of Bone: Bone Metabolism in Changing Environments." Physiology 30, no. 1 (January 2015): 17–29. http://dx.doi.org/10.1152/physiol.00022.2014.

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Анотація:

Bone evolved to serve many mechanical and physiological functions. Osteocytes and bone remodeling first appeared in the dermal skeleton of fish, and subsequently adapted to various challenges in terrestrial animals occupying diverse environments. This review discusses the physiology of bone and its role in mechanical and calcium homeostases from an evolutionary perspective. We review how bone physiology responds to changing environments and the adaptations to unique and extreme physiological conditions.

11

Gross, Ted S., Ariff A. Damji, Stefan Judex, Robert C. Bray, and Ronald F. Zernicke. "Bone hyperemia precedes disuse-induced intracortical bone resorption." Journal of Applied Physiology 86, no. 1 (January 1, 1999): 230–35. http://dx.doi.org/10.1152/jappl.1999.86.1.230.

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An in vivo model was used to determine whether bone hyperemia precedes increased intracortical porosity induced by disuse. Twenty-four adult male roosters (age 1 yr) were randomly assigned to intact-control, 7-days-sham-surgery, 7-days-disuse, and 14-days-disuse groups. Disuse was achieved by isolating the left ulna diaphysis from physical loading via parallel metaphyseal osteotomies. The right ulna served as an intact contralateral control. Colored microspheres were used to assess middiaphyseal bone blood flow. Bone blood flow was symmetric between the left and right ulnae of the intact-control and sham-surgery groups. After 7 days of disuse, median (±95% confidence interval) standardized blood flow was significantly elevated compared with the contralateral bone (6.5 ± 5.2 vs. 1.0 ± 0.8 ml ⋅ min−1 ⋅ 100 g−1; P = 0.03). After 14 days of disuse, blood flow was also elevated but to a lesser extent. Intracortical porosity in the sham-surgery and 7-days-disuse bones was not elevated compared with intact-control bones. At 14 days of disuse, the area of intracortical porosity was significantly elevated compared with intact control bones (0.015 ± 0.02 vs. 0.002 ± 0.002 mm2; P = 0.03). We conclude that disuse induces bone hyperemia before an increase in intracortical porosity. The potential interaction between bone vasoregulation and bone cell dynamics remains to be studied.

12

Clarke, Bart. "Normal Bone Anatomy and Physiology." Clinical Journal of the American Society of Nephrology 3, Supplement 3 (November 2008): S131—S139. http://dx.doi.org/10.2215/cjn.04151206.

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13

Post, Teun M., Serge C. L. M. Cremers, Thomas Kerbusch, and Meindert Danhof. "Bone Physiology, Disease and Treatment." Clinical Pharmacokinetics 49, no. 2 (February 2010): 89–118. http://dx.doi.org/10.2165/11318150-000000000-00000.

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14

Roberts, W. Eugene. "Introduction: bone physiology in orthodontics." Seminars in Orthodontics 10, no. 2 (June 2004): 99. http://dx.doi.org/10.1053/j.sodo.2004.01.002.

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15

Zallone, Alberta Zambonin, and Anna Teti. "Animal models of bone physiology." Current Opinion in Rheumatology 5, no. 3 (May 1993): 363–67. http://dx.doi.org/10.1097/00002281-199305030-00017.

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16

Smaldone, Silvia, and Francesco Ramirez. "Fibrillin microfibrils in bone physiology." Matrix Biology 52-54 (May 2016): 191–97. http://dx.doi.org/10.1016/j.matbio.2015.09.004.

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17

Hays, Kathleen. "Physiology of normal bone marrow." Seminars in Oncology Nursing 6, no. 1 (February 1990): 3–8. http://dx.doi.org/10.1016/s0749-2081(05)80127-5.

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18

Davies, John E. "Physiology of onlay bone healing." Journal of Oral and Maxillofacial Surgery 61, no. 8 (August 2003): 3. http://dx.doi.org/10.1016/s0278-2391(03)00336-7.

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19

Marx, Robert E., and Arun K. Garg. "Bone Structure, Metabolism, and Physiology." Implant Dentistry 7, no. 4 (1998): 267–76. http://dx.doi.org/10.1097/00008505-199807040-00004.

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20

Chapurlat, Roland D., and Cyrille B. Confavreux. "Novel biological markers of bone: from bone metabolism to bone physiology." Rheumatology 55, no. 10 (January 20, 2016): 1714–25. http://dx.doi.org/10.1093/rheumatology/kev410.

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21

Chattopadhyay, Naibedya. "Adiponectin Signaling Regulates Skeletal Physiology." INDIAN JOURNAL OF PHYSIOLOGY AND ALLIED SCIENCES 74, no. 02 (June 15, 2022): 39–40. http://dx.doi.org/10.55184/ijpas.v74i02.57.

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Bone remodelling is important to maintain the skeletal physiology. Bone loss with aging and hormonal pathologies may be result ofaltered bone remodelling leading to osteoporosis. Even in presence of existing therapies, there is an unmet clinical need to look forideal alternatives that would stimulate bone formation and keep resorption in check. Adiponectin and its derivatives could be a possiblecandidate for such therapy. Orally active small molecule AdipoR agonists may be a proposed solution for this.

22

MCCARTHY, IAN. "THE PHYSIOLOGY OF BONE BLOOD FLOW." Journal of Bone and Joint Surgery-American Volume 88 (November 2006): 4–9. http://dx.doi.org/10.2106/00004623-200611001-00002.

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23

PROLO, DONALD J., and JUAN J. RODRIGO. "Contemporary Bone Graft Physiology and Surgery." Clinical Orthopaedics and Related Research &NA;, no. 200 (November 1985): 322???342. http://dx.doi.org/10.1097/00003086-198511000-00036.

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24

Raisz, L. G. "Prostaglandins and bone: physiology and pathophysiology." Osteoarthritis and Cartilage 7, no. 4 (July 1999): 419–21. http://dx.doi.org/10.1053/joca.1998.0230.

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25

Alkire, Kathe, and Janet Collingwood. "Physiology of blood and bone marrow." Seminars in Oncology Nursing 6, no. 2 (May 1990): 99–108. http://dx.doi.org/10.1016/s0749-2081(05)80142-1.

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26

STEINWEG, K. "Menopause, Bone Physiology, and Osteoporosis Prevention." Clinics in Family Practice 4, no. 1 (March 2002): 89–111. http://dx.doi.org/10.1016/s1522-5720(03)00053-9.

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27

Smith, R. "Bone physiology and the osteoporotic process." Respiratory Medicine 87 (February 1993): 3–7. http://dx.doi.org/10.1016/s0954-6111(05)80250-1.

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28

Hughes, D. E., and B. F. Boyce. "Apoptosis in bone physiology and disease." Molecular Pathology 50, no. 3 (June 1, 1997): 132–37. http://dx.doi.org/10.1136/mp.50.3.132.

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29

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

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30

Hu, Bo, Taofen Wu, Yongxu Zhao, Guangtao Xu, Ruilin Shen, and Guiqian Chen. "Physiological Signatures of Dual Embryonic Origins in Mouse Skull Vault." Cellular Physiology and Biochemistry 43, no. 6 (2017): 2525–34. http://dx.doi.org/10.1159/000484496.

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Background/Aims: The mammalian skull vault is a highly regulated structure and consists of several membrane bones of different tissue origins (e.g. neural crest derived frontal bone and mesoderm derived parietal bone). Although membrane bones form through intramembranous ossification, neural crest derived frontal bone has superior osteoblast activity and bone regeneration ability, triggering a novel conception for craniofacial reconstruction and bone regeneration called endogenous calvarial regeneration. However, a comprehensive landscape of the genes and signaling pathways involved in this process is not clear. Methods: Transcriptome analysis within the two bone elements is firstly performed to determine the physiological signatures of differential gene expressions in mouse skull vault. Results: Frontal bone tissues and parietal bone tissues maintain tissue origin through special gene expression similar to neural crest vs mesoderm tissue, and physiological functions between these two tissues are also found in differences related to proliferation, differentiation and extracellular matrix production and clustered signaling pathways. Conclusion: Our data provide novel insights into the potential gene regulatory network in regulating the development of neural crest-derived frontal bone and mesoderm-derived parietal bone.

31

Carter, Jason R., and John B. West. "Space physiology within an exercise physiology curriculum." Advances in Physiology Education 37, no. 3 (September 2013): 220–26. http://dx.doi.org/10.1152/advan.00035.2013.

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Compare and contrast strategies remain common pedagogical practices within physiological education. With the support of an American Physiological Society Teaching Career Enhancement Award, we have developed a junior- or senior-level undergraduate curriculum for exercise physiology that compares and contrasts the physiological adaptations of chronic terrestrial exercise (TEx) and microgravity (μG). We used a series of peer-reviewed publications to demonstrate that many of the physiological adaptations to TEx and μG are opposite. For example, TEx typically improves cardiovascular function and orthostatic tolerance, whereas μG can lead to declines in both. TEx leads to muscle hypertrophy, and μG elicits muscle atrophy. TEx increases bone mineral density and red blood cell mass, whereas μG decreases bone mineral density and red blood cell mass. Importantly, exercise during spaceflight remains a crucial countermeasure to limit some of these adverse physiological adaptations to μG. This curriculum develops critical thinking skills by dissecting peer-reviewed articles and discussing the strengths and weaknesses associated with simulated and actual μG studies. Moreover, the curriculum includes studies on both animals and humans, providing a strong translational component to the curriculum. In summary, we have developed a novel space physiology curriculum delivered during the final weeks of an exercise physiology course in which students gain critical new knowledge that reinforces key concepts presented throughout the semester.

32

Thompson, Bithika, and Dwight A. Towler. "Arterial calcification and bone physiology: role of the bone–vascular axis." Nature Reviews Endocrinology 8, no. 9 (April 3, 2012): 529–43. http://dx.doi.org/10.1038/nrendo.2012.36.

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33

Haug, R. H. "Facial bone healing and bone grafts: A review of clinical physiology." Journal of Oral and Maxillofacial Surgery 53, no. 1 (January 1995): 95–96. http://dx.doi.org/10.1016/0278-2391(95)90524-3.

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34

Imai, Yuuki, Min-Young Youn, Kazuki Inoue, Ichiro Takada, Alexander Kouzmenko, and Shigeaki Kato. "Nuclear Receptors in Bone Physiology and Diseases." Physiological Reviews 93, no. 2 (April 2013): 481–523. http://dx.doi.org/10.1152/physrev.00008.2012.

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During the last decade, our view on the skeleton as a mere solid physical support structure has been transformed, as bone emerged as a dynamic, constantly remodeling tissue with systemic regulatory functions including those of an endocrine organ. Reflecting this remarkable functional complexity, distinct classes of humoral and intracellular regulatory factors have been shown to control vital processes in the bone. Among these regulators, nuclear receptors (NRs) play fundamental roles in bone development, growth, and maintenance. NRs are DNA-binding transcription factors that act as intracellular transducers of the respective ligand signaling pathways through modulation of expression of specific sets of cognate target genes. Aberrant NR signaling caused by receptor or ligand deficiency may profoundly affect bone health and compromise skeletal functions. Ligand dependency of NR action underlies a major strategy of therapeutic intervention to correct aberrant NR signaling, and significant efforts have been made to design novel synthetic NR ligands with enhanced beneficial properties and reduced potential negative side effects. As an example, estrogen deficiency causes bone loss and leads to development of osteoporosis, the most prevalent skeletal disorder in postmenopausal women. Since administration of natural estrogens for the treatment of osteoporosis often associates with undesirable side effects, several synthetic estrogen receptor ligands have been developed with higher therapeutic efficacy and specificity. This review presents current progress in our understanding of the roles of various nuclear receptor-mediated signaling pathways in bone physiology and disease, and in development of advanced NR ligands for treatment of common skeletal disorders.

35

Moll, Natalia M., and Richard M. Ransohoff. "CXCL12 and CXCR4 in bone marrow physiology." Expert Review of Hematology 3, no. 3 (June 2010): 315–22. http://dx.doi.org/10.1586/ehm.10.16.

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36

Dougall, William C. "RANKL signaling in bone physiology and cancer." Current Opinion in Supportive and Palliative Care 1, no. 4 (December 2007): 317–22. http://dx.doi.org/10.1097/spc.0b013e3282f335be.

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37

Prior, Jerilynn C. "FSH and bone – important physiology or not?" Trends in Molecular Medicine 13, no. 1 (January 2007): 1–3. http://dx.doi.org/10.1016/j.molmed.2006.11.004.

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38

Aris, Robert M., Gayle E. Lester, and David A. Ontjes. "Bone Loss Physiology in Critically III Patients." Chest 114, no. 4 (October 1998): 954–55. http://dx.doi.org/10.1378/chest.114.4.954.

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39

Roberts, W. Eugene, Kirt E. Simmons, Lawrence P. Garetto, and Rolando A. DeCasto. "BONE PHYSIOLOGY AND METABOLISM IN DENTAL IMPLANTOLOGY." Implant Dentistry 1, no. 1 (1992): 11–24. http://dx.doi.org/10.1097/00008505-199200110-00002.

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40

Kushdilian, Michael V., Lauren M. Ladd, and Richard B. Gunderman. "Radiology in the Study of Bone Physiology." Academic Radiology 23, no. 10 (October 2016): 1298–308. http://dx.doi.org/10.1016/j.acra.2016.06.001.

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41

White, C. P., N. A. Morrison, E. M. Gardiner, and J. A. Eisman. "Vitamin D receptor alleles and bone physiology." Journal of Cellular Biochemistry 56, no. 3 (November 1994): 307–14. http://dx.doi.org/10.1002/jcb.240560306.

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42

Martin, T. John, and Natalie A. Sims. "RANKL/OPG; Critical role in bone physiology." Reviews in Endocrine and Metabolic Disorders 16, no. 2 (January 4, 2015): 131–39. http://dx.doi.org/10.1007/s11154-014-9308-6.

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43

Keçeci, Tolga. "Structure and physiology of the subchondral bone." TOTBİD Dergisi 22, no. 2 (March 15, 2023): 75–77. http://dx.doi.org/10.5578/totbid.dergisi.2023.12.

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44

Köhler, Meike, Nekane Marín-Moratalla, Xavier Jordana, and Ronny Aanes. "Seasonal bone growth and physiology in endotherms shed light on dinosaur physiology." Nature 487, no. 7407 (June 27, 2012): 358–61. http://dx.doi.org/10.1038/nature11264.

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45

Sui, Xin, Shijian Deng, Mengmeng Liu, Linlin Fan, Yunfei Wang, Huaxing Xu, Yao Sun, Anil Kishen та Qi Zhang. "Constitutive Activation of β-Catenin in Differentiated Osteoclasts Induces Bone Loss in Mice". Cellular Physiology and Biochemistry 48, № 5 (2018): 2091–102. http://dx.doi.org/10.1159/000492549.

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Background/Aims: Activation of the Wnt/β-catenin signalling pathway has been widely investigated in bone biology and shown to promote bone formation. However, its specific effects on osteoclast differentiation have not been fully elucidated. Our study aimed to identify the role of β-catenin in osteoclastogenesis and bone homeostasis. Methods: In the present study, exon 3 in the β-catenin gene (Ctnnb1) allele encoding phosphorylation target serine/threonine residues was flanked by floxP sequences. We generated mice exhibiting conditional β-catenin activation (Ctsk-Cre;Ctnnb1flox(exon3)/+, designated CA-β-catenin) by crossing Ctnnb1flox(exon3)/flox(exon3) mice with osteoclast-specific Ctsk-Cre mice. Bone growth and bone mass were analysed by micro-computed tomography (micro-CT) and histomorphometry. To further examine osteoclast activity, osteoclasts were induced from bone marrow monocytes (BMMs) isolated from CA-β-catenin and Control mice in vitro. Osteoclast differentiation was detected by tartrate-resistant acid phosphatase (TRAP) staining, immunofluorescence staining and reverse transcription-quantitative PCR (RT–qPCR) analysis. Results: Growth retardation and low bone mass were observed in CA-β-catenin mice. Compared to controls, CA-β-catenin mice had significantly reduced trabecular bone numbers under growth plates as well as thinner cortical bones. Moreover, increased TRAP-positive osteoclasts were observed on the surfaces of trabecular bones and cortical bones in the CA-β-catenin mice; consistent results were observed in vitro. In the CA-β-catenin group, excessive numbers of osteoclasts were induced from BMMs, accompanied by the increased expression of osteoclast-associated marker genes. Conclusion: These results indicated that the constitutive activation of β-catenin in osteoclasts promotes osteoclast formation, resulting in bone loss.

46

Frost, Harold M. "NEW TARGETS FOR THE STUDIES OF BIOMECHANICAL, ENDOCRINOLOGIC, GENETIC AND PHARMACEUTICAL EFFECTS ON BONES: BONE'S "NEPHRON EQUIVALENTS", MUSCLE, NEUROMUSCULAR PHYSIOLOGY." Journal of Musculoskeletal Research 04, no. 02 (June 2000): 67–84. http://dx.doi.org/10.1142/s0218957700000173.

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As age, experience and common sense look at biomechanical, hormonal, genetic and other roles in bone physiology and its disorders, two questions can arise: (a) How did we fail? (b) How could we make it better? The acerbic Sam Johnson said that to teach new things, we should use examples of already known ones. If so, an analogy might help to clarify this article's message for people who work with bones and their disorders. Assume this: (a) Mythical physiologists were taught that renal physiology depends on "kidney cells" but were taught nothing about nephrons; (b) so they explained renal health and disorders in those terms. (c) For many decades, they "knew" that view was correct (as the ancients "knew" the world was flat). (d) But then others described nephrons and some errors their properties revealed in those views about renal physiology; (e) so controversies began. Today, an analogous situation confronts real biomechanicians and physiologists. (i) Most of them were taught that osteoblasts and osteoclasts (bone's "effector cells") explain bone physiology without "nephron-equivalent" input, so they explained bone disorders and mechanical effects in those terms. (ii) Yet nephron-equivalent mechanisms and functions, including biomechanical ones, in bones have the same operational relationship to their cells, health and disorders as nephrons and their functions do to renal cells, health and disorders. (iii) Adding that knowledge to former views led to the Utah paradigm of skeletal physiology. It also revealed errors in many former views about bone physiology; (iv) so real controversies have begun. Biomechanicians, physiologists, clinicians and pharmacologists from whom poor interdisciplinary communication hid that paradigm could think the view in (i) above remains valid, and keep analyzing data and designing studies within its constraints. Like Wegner's idea of plate tectonics in geology, the Utah paradigm came before its field was ready, so others fought it. But while the plate-tectonics war was won, it has just begun for the Utah paradigm. This article reviews how such things could apply to bone and some of their implications. Its conclusion offers succinct answers to the italicized questions above.

47

Morey-Holton, Emily R., Bernard P. Halloran, Lawrence P. Garetto, and Stephen B. Doty. "Animal housing influences the response of bone to spaceflight in juvenile rats." Journal of Applied Physiology 88, no. 4 (April 1, 2000): 1303–9. http://dx.doi.org/10.1152/jappl.2000.88.4.1303.

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The rat has been used extensively as an animal model to study the effects of spaceflight on bone metabolism. The results of these studies have been inconsistent. On some missions, bone formation at the periosteal bone surface of weight-bearing bones is impaired and on others it is not, suggesting that experimental conditions may be an important determinant of bone responsiveness to spaceflight. To determine whether animal housing can affect the response of bone to spaceflight, we studied young growing (juvenile) rats group housed in the animal enclosure module and singly housed in the research animal holding facility under otherwise identical flight conditions (Spacelab Life Science 1). Spaceflight reduced periosteal bone formation by 30% ( P < 0.001) and bone mass by 7% in single-housed animals but had little or no effect on formation (−6%) or mass (−3%) in group-housed animals. Group housing reduced the response of bone to spaceflight by as much as 80%. The data suggest that housing can dramatically affect the skeletal response of juvenile rats to spaceflight. These observations explain many of the discrepancies in previous flight studies and emphasize the need to study more closely the effects of housing (physical-social interaction) on the response of bone to the weightlessness of spaceflight.

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Wongdee, Kannikar, Nateetip Krishnamra, and Narattaphol Charoenphandhu. "Endochondral bone growth, bone calcium accretion, and bone mineral density: how are they related?" Journal of Physiological Sciences 62, no. 4 (May 25, 2012): 299–307. http://dx.doi.org/10.1007/s12576-012-0212-0.

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Oppenheimer, Adam J., Lawrence Tong, and Steven R. Buchman. "Craniofacial Bone Grafting: Wolff's Law Revisited." Craniomaxillofacial Trauma & Reconstruction 1, no. 1 (November 2008): 49–61. http://dx.doi.org/10.1055/s-0028-1098963.

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Bone grafts are used for the reconstruction of congenital and acquired deformities of the facial skeleton and, as such, comprise a vital component of the craniofacial surgeon's armamentarium. A thorough understanding of bone graft physiology and the factors that affect graft behavior is therefore essential in developing a more intelligent use of bone grafts in clinical practice. This article presents a review of the basic physiology of bone grafting along with a survey of pertinent concepts and current research. The factors responsible for bone graft survival are emphasized.

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Matsuda, J. J., R. F. Zernicke, A. C. Vailas, V. A. Pedrini, A. Pedrini-Mille, and J. A. Maynard. "Structural and mechanical adaptation of immature bone to strenuous exercise." Journal of Applied Physiology 60, no. 6 (June 1, 1986): 2028–34. http://dx.doi.org/10.1152/jappl.1986.60.6.2028.

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To investigate the adaptive responses of immature bone to increased loads, young (3-wk-old) White Leghorn roosters were subjected to moderately intense treadmill running for 5 or 9 wk. The training program induced significant increases in maximal O2 consumption and muscle fumarase activity in the 12-wk-old birds, demonstrating that growing chickens have the ability to enhance their aerobic capacity. The structural and mechanical properties of the runners' tarsometatarsus bones were compared with sedentary age-matched controls at 8 and 12 wk of age. Suppression of circumferential growth occurred with exercise at both ages, whereas exercise enhanced middiaphysial cortical thickening, especially on the bones' concave surfaces. Although cross-sectional area moments of inertia did not change with exercise, significant decreases in bending stiffness, energy to yield, and energy to fracture were observed. It was concluded that strenuous exercise may retard long-bone maturation, resulting in more compliant bones.