Talk:Musculoskeletal System - Bone Development Timeline: Difference between revisions
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The Workshop was considered a significant success. Many new ideas and concepts were presented. For example, two cellular structures were described that appear to influence growth plate chondrocyte behavior. The first are actin-based signaling hubs that are activated by integrins; the second are calcium channels formed from polycystin-1 and polycystin-2 at the base of cilia. The output from these functional structures may influence cell orientation in the postmitotic phase of chondrocyte maturation. Renewed interest in vascular access to the growth plate including a rediscovered perichondrial capillary bed that surrounds the growth plate provides a fresh view of how circulating and perichondrial growth factors physically reach growth plate cells. This finding has important implications for growth plate therapeutics in the future. | The Workshop was considered a significant success. Many new ideas and concepts were presented. For example, two cellular structures were described that appear to influence growth plate chondrocyte behavior. The first are actin-based signaling hubs that are activated by integrins; the second are calcium channels formed from polycystin-1 and polycystin-2 at the base of cilia. The output from these functional structures may influence cell orientation in the postmitotic phase of chondrocyte maturation. Renewed interest in vascular access to the growth plate including a rediscovered perichondrial capillary bed that surrounds the growth plate provides a fresh view of how circulating and perichondrial growth factors physically reach growth plate cells. This finding has important implications for growth plate therapeutics in the future. | ||
Several new insights were gained into the potential interplay between growth plate regulatory circuits. For example, genetic interactions between Sox9, Sox5 and Sox 6 and between Sox9 and Runx2, were better defined, allowing one to envision how chondrocyte proliferation and terminal differentiation are coordinated and fine-tuned. Continuing on the theme of pathway integration, evidence was presented that both Smad-dependent and Smad-independent BMP pathways are involved in regulating the Ihh/PTHrP circuitry, that BMPs exert their effects on chondrogenesis through retinoic acid intermediates and also through activation of Sox9, Sox 5 and Sox6, and that canonical Wnt signaling acts through altering Ihh expression to influence chondrocyte maturation. | Several new insights were gained into the potential interplay between growth plate regulatory circuits. For example, genetic interactions between Sox9, Sox5 and Sox 6 and between Sox9 and Runx2, were better defined, allowing one to envision how chondrocyte proliferation and terminal differentiation are coordinated and fine-tuned. Continuing on the theme of pathway integration, evidence was presented that both Smad-dependent and Smad-independent BMP pathways are involved in regulating the Ihh/PTHrP circuitry, that BMPs exert their effects on chondrogenesis through retinoic acid intermediates and also through activation of Sox9, Sox 5 and Sox6, and that canonical Wnt signaling acts through altering Ihh expression to influence chondrocyte maturation. | ||
Revision as of 18:00, 2 February 2011
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Cite this page: Hill, M.A. (2026, August 14) Embryology Musculoskeletal System - Bone Development Timeline. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Musculoskeletal_System_-_Bone_Development_Timeline |
2009
An image-based skeletal tissue model for the ICRP reference newborn
Phys Med Biol. 2009 Jul 21;54(14):4497-531. Epub 2009 Jun 26.
Pafundi D, Lee C, Watchman C, Bourke V, Aris J, Shagina N, Harrison J, Fell T, Bolch W.
Department of Nuclear and Radiological Engineering, University of Florida, Gainesville, FL, USA.
Abstract Hybrid phantoms represent a third generation of computational models of human anatomy needed for dose assessment in both external and internal radiation exposures. Recently, we presented the first whole-body hybrid phantom of the ICRP reference newborn with a skeleton constructed from both non-uniform rational B-spline and polygon-mesh surfaces (Lee et al 2007 Phys. Med. Biol. 52 3309-33). The skeleton in that model included regions of cartilage and fibrous connective tissue, with the remainder given as a homogenous mixture of cortical and trabecular bone, active marrow and miscellaneous skeletal tissues. In the present study, we present a comprehensive skeletal tissue model of the ICRP reference newborn to permit a heterogeneous representation of the skeleton in that hybrid phantom set-both male and female-that explicitly includes a delineation of cortical bone so that marrow shielding effects are correctly modeled for low-energy photons incident upon the newborn skeleton. Data sources for the tissue model were threefold. First, skeletal site-dependent volumes of homogeneous bone were obtained from whole-cadaver CT image analyses. Second, selected newborn bone specimens were acquired at autopsy and subjected to micro-CT image analysis to derive model parameters of the marrow cavity and bone trabecular 3D microarchitecture. Third, data given in ICRP Publications 70 and 89 were selected to match reference values on total skeletal tissue mass. Active marrow distributions were found to be in reasonable agreement with those given previously by the ICRP. However, significant differences were seen in total skeletal and site-specific masses of trabecular and cortical bone between the current and ICRP newborn skeletal tissue models. The latter utilizes an age-independent ratio of 80%/20% cortical and trabecular bone for the reference newborn. In the current study, a ratio closer to 40%/60% is used based upon newborn CT and micro-CT skeletal image analyses. These changes in mineral bone composition may have significant dosimetric implications when considering localized marrow dosimetry for radionuclides that target mineral bone in the newborn child.
PMID: 19556686
High and low birth weight and its implication for growth and bone development in childhood and adolescence
J Pediatr Endocrinol Metab. 2009 Jan;22(1):19-30.
Fricke O, Semler O, Stabrey A, Tutlewski B, Remer T, Herkenrath P, Schoenau E.
Children's Hospital, University of Cologne, Cologne, Germany. frickeo@uni-koeln.de Abstract AIM: To investigate the relationship of birth weight (BW) to anthropometric measures, local body composition and bone development.
POPULATION AND METHODS: 284 individuals (age 5-19 yr, 145 females) were recruited from the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) study. Parameters of bone development (cortical bone mineral density [BMDcort], endosteal circumference [CE]) and of local body composition (cross-sectional fat area [FA]) were analyzed by pQCT at the forearm. Parameters were transformed into SD scores to adjust for age or height.
RESULTS: BW predicted weight-SDS (R = 0.221), height-SDS (R = 0.260) and FA-SDS (R = 0.150). Individuals with lower BW (< 10th percentile) had lower weight-SDS (p < 0.01), height-SDS (p < 0.01), BMDcort-SDS (p = 0.02) and higher CE-SDS (p = 0.05). BMDcort was correlated with BW (r = -0.319) and FA (r = -0.283) in pubertal females.
CONCLUSION: BW is characterized by direct and indirect effects on growth, body composition and bone development.
PMID: 19344071 http://www.ncbi.nlm.nih.gov/pubmed/19344071
2008
Growth and bone development
Nestle Nutr Workshop Ser Pediatr Program. 2008;61:53-68.
Cooper C, Harvey N, Javaid K, Hanson M, Dennison E.
MRC Epidemiology Resource Centre and Centre for Developmental Origins of Health and Adult Disease, University of Southampton, Southampton General Hospital, Southampton, UK. cc@mrc.soton.ac.uk Abstract Osteoporosis is a major cause of morbidity and mortality through its association with age-related fractures. Although most effort in fracture prevention has been directed at retarding the rate of age-related bone loss, and reducing the frequency and severity of trauma among elderly people, evidence is growing that peak bone mass is an important contributor to bone strength during later life. The normal patterns of skeletal growth have been well characterized in cross-sectional and longitudinal studies. It has been confirmed that boys have higher bone mineral content, but not volumetric bone density, than girls. Furthermore, there is a dissociation between the peak velocities for height gain and bone mineral accrual, in both genders. Puberty is the period during which volumetric density appears to increase in both axial and appendicular sites. Many factors influence the accumulation of bone mineral during childhood and adolescence, including heredity, gender, diet, physical activity, endocrine status, and sporadic risk factors such as cigarette smoking. In addition to these modifiable factors during childhood, evidence has also accrued that fracture risk might be programmed during intrauterine life. Epidemiological studies have demonstrated a relationship between birthweight, weight in infancy, and adult bone mass. This appears to be mediated through modulation of the set-point for basal activity of pituitary-dependent endocrine systems such as the hypothalamicpituitary-adrenal and growth hormone/insulin-like growth factor-1 axes. Maternal smoking, diet (particularly vitamin D deficiency), and physical activity also appear to modulate bone mineral acquisition during intrauterine life; furthermore, both low birth size and poor childhood growth are directly linked to the later risk of hip fracture. The optimization of maternal nutrition and intrauterine growth should also be included within preventive strategies against osteoporotic fracture, albeit for future generations.
PMID: 18196944
2006
International Workshop on the Skeletal Growth Plate Stevenson, Washington June 11–15, 2006
The Workshop was considered a significant success. Many new ideas and concepts were presented. For example, two cellular structures were described that appear to influence growth plate chondrocyte behavior. The first are actin-based signaling hubs that are activated by integrins; the second are calcium channels formed from polycystin-1 and polycystin-2 at the base of cilia. The output from these functional structures may influence cell orientation in the postmitotic phase of chondrocyte maturation. Renewed interest in vascular access to the growth plate including a rediscovered perichondrial capillary bed that surrounds the growth plate provides a fresh view of how circulating and perichondrial growth factors physically reach growth plate cells. This finding has important implications for growth plate therapeutics in the future.
Several new insights were gained into the potential interplay between growth plate regulatory circuits. For example, genetic interactions between Sox9, Sox5 and Sox 6 and between Sox9 and Runx2, were better defined, allowing one to envision how chondrocyte proliferation and terminal differentiation are coordinated and fine-tuned. Continuing on the theme of pathway integration, evidence was presented that both Smad-dependent and Smad-independent BMP pathways are involved in regulating the Ihh/PTHrP circuitry, that BMPs exert their effects on chondrogenesis through retinoic acid intermediates and also through activation of Sox9, Sox 5 and Sox6, and that canonical Wnt signaling acts through altering Ihh expression to influence chondrocyte maturation.
New approaches for keeping track of the human chondrodysplasias that integrate developmental, clinical, genetic and pathological observations were presented. Disturbances responsible for these disorders are now beginning to be understood at the molecular level. For instance, failure to hydroxylate proline residues at the 3 position of type I collagen leads to recessive osteogenesis imperfecta, and induction of the unfolded protein response to mutant type X collagen and COMP contributes to the pathogenesis of Schmid metaphyseal dysplasia, pseudoachondroplasia and multiple epiphyseal dysplasia. Similarly, delineating the intersection of two signaling pathways, the pathway downstream of the CNP receptor, which is mutated in acromesomelic dysplasia, and the pathway downstream from FGFR3, which is mutated in achondroplasia, provides a conceptual basis for treatment of achondroplasia. Mutations are being found in more and more of the genes that play important roles in growth plate development and function. Similarly, a growing number of human chondrodysplasias are being modeled through genetic engineering in mice.
Several new research tools were presented including genetically engineered mice that allow specific events important to growth plate formation and function to be dissected. Of particular note were new mouse strains harboring osterix-cre-ERT2, collagen I (3/2kb)-cre and Col10-LacZ transgenic reporter mice. A number of new analytical techniques were discussed, including real-time multiphoton imaging of growth plate and articular cartilage of live mice, microsurgical techniques to dissect and transplant rodent growth plate zones, three-dimensional culture systems to study interactions between cartilage and vascular cells, and improved high-resolution imaging technologies to assess bone structure and mineralization in mice.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1992437
The abstracts of the poster sessions are available at http://www.growthplate.org.
2004
Studies on the time frame for ossification of the medial clavicular epiphyseal cartilage in conventional radiography
Int J Legal Med. 2004 Feb;118(1):5-8. Epub 2003 Oct 8.
Schmeling A, Schulz R, Reisinger W, Mühler M, Wernecke KD, Geserick G.
Institut für Rechtsmedizin, Universitätsklinikum Charité der Humboldt-Universität zu Berlin, Hannoversche Strasse 6, 10015 Berlin, Germany. andreas.schmeling@charite.de
Abstract
Radiological assessment of the degree of ossification of the medial clavicular epiphyseal cartilage plays a vital part in forensic age diagnosis of living adolescents and young adults. A total of 873 plain chest radiographs requested by the staff medical officer for members of staff aged 16-30 at the University Hospital Charité were evaluated retrospectively. Of these X-rays 699 permitted an assessment of ossification of at least 1 side of the clavicle. In addition to the customary stages (1: non-ossified epiphysis, 2: discernible ossification centre, 3: partial fusion, 4: total fusion) a stage 5 was also defined, characterised by the disappearance of the epiphyseal scar following total fusion. The earliest age at which stage 3 was detected in either gender was 16 years. Stage 4 was first observed in women at 20 years and in men at 21 years. In both genders, the earliest observation of stage 5 was at 26 years. It was concluded that plain chest radiographs can essentially be used to assess clavicular ossification. In practice, if overlap in posterior-anterior views impedes evaluation, a lateral view should also be taken to facilitate age estimation. In forensic practice the reference values of the present paper should be applied.
PMID: 14534796 http://www.ncbi.nlm.nih.gov/pubmed/14534796
