Talk:Musculoskeletal System - Shoulder Development

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Note - This sub-heading shows an automated computer PubMed search using the listed sub-heading term. References appear in this list based upon the date of the actual page viewing. Therefore the list of references do not reflect any editorial selection of material based on content or relevance. In comparison, references listed on the content page and discussion page (under the publication year sub-headings) do include editorial selection based upon relevance and availability. (More? Pubmed Most Recent)

Shoulder Embryology

<pubmed limit=5>Shoulder Embryology</pubmed>

Shoulder Development

<pubmed limit=5>Shoulder Development</pubmed>

2012

Body structures and physical complaints in upper limb reduction deficiency: a 24-year follow-up study

PLoS One. 2012;7(11):e49727. doi: 10.1371/journal.pone.0049727. Epub 2012 Nov 30.

Postema SG, van der Sluis CK, Waldenlöv K, Norling Hermansson LM. Source Centre for Rehabilitation Research, Örebro County Council, Örebro, Sweden ; Department of Rehabilitation Medicine, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.

Abstract

OBJECTIVE: To describe upper body structures associated with upper limb reduction deficiency and the development of these structures over time, to examine the presence of physical complaints in this population, and to compare body structures and complaints between groups based on prosthesis use. DESIGN: Prospective cohort study with a follow-up period of 24 years, with matched able-bodied controls. SUBJECTS: Twenty-eight patients with unilateral below-elbow reduction deficiency fitted with myoelectric prostheses, aged 8-18 years at inclusion. METHOD: Measurements of upper arm, trunk and spine were performed and study-specific questionnaires were answered at baseline and follow-up; the Brief Pain Inventory and the Quick Disability of Arm, Shoulder, and Hand questionnaires were answered at follow-up. RESULTS: Both at baseline and follow-up, within-subjects differences in structures of the arm and trunk were shown in patients but not in controls. Spinal deviations, although small, were greater in patients compared to controls. Self-reported disability was higher in patients compared to controls. Differences in back pain and effect of prostheses use could not be shown. CONCLUSIONS: Patients with unilateral below-elbow reduction deficiency have consistent differences in upper body structures. Deviations of the spine, probably of functional origin, do not progress to clinically relevant scoliosis.

PMID 23226218

2010

Commitment of chondrogenic precursors of the avian scapula takes place after epithelial-mesenchymal transition of the dermomyotome

BMC Dev Biol. 2010 Aug 31;10:91.

Wang B, Pu Q, De R, Patel K, Christ B, Wilting J, Huang R.

Department of Anatomy and Cell Biology, University of Goettingen, Kreuzbergring 36, 37075 Goettingen, Germany. baigang.wang@medizin.uni-goettingen.de Abstract BACKGROUND: Cells of the epithelially organised dermomyotome are traditionally believed to give rise to skeletal muscle and dermis. We have previously shown that the dermomyotome can undergo epithelial-mesenchymal transition (EMT) and give rise to chondrogenic cells, which go on to form the scapula blade in birds. At present we have little understanding regarding the issue of when the chondrogenic fate of dermomyotomal cells is determined. Using quail-chick grafting experiments, we investigated whether scapula precursor cells are committed to a chondrogenic fate while in an epithelial state or whether commitment is established after EMT.

RESULTS: We show that the hypaxial dermomyotome, which normally forms the scapula, does not generate cartilaginous tissue after it is grafted to the epaxial domain. In contrast engraftment of the epaxial dermomyotome to the hypaxial domain gives rise to scapula-like cartilage. However, the hypaxial sub-ectodermal mesenchyme (SEM), which originates from the hypaxial dermomyotome after EMT, generates cartilaginous elements in the epaxial domain, whereas in reciprocal grafting experiments, the epaxial SEM cannot form cartilage in the hypaxial domain.

CONCLUSIONS: We suggest that the epithelial cells of the dermomyotome are not committed to the chondrogenic lineage. Commitment to this lineage occurs after it has undergone EMT to form the sub-ectodermal mesenchyme.

PMID: 20807426

Scapula development is governed by genetic interactions of Pbx1 with its family members and with Emx2 via their cooperative control of Alx1

Development. 2010 Aug 1;137(15):2559-69.

Capellini TD, Vaccari G, Ferretti E, Fantini S, He M, Pellegrini M, Quintana L, Di Giacomo G, Sharpe J, Selleri L, Zappavigna V.

Department of Cell and Developmental Biology, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY 10021, USA. Abstract The genetic pathways underlying shoulder blade development are largely unknown, as gene networks controlling limb morphogenesis have limited influence on scapula formation. Analysis of mouse mutants for Pbx and Emx2 genes has suggested their potential roles in girdle development. In this study, by generating compound mutant mice, we examined the genetic control of scapula development by Pbx genes and their functional relationship with Emx2. Analyses of Pbx and Pbx1;Emx2 compound mutants revealed that Pbx genes share overlapping functions in shoulder development and that Pbx1 genetically interacts with Emx2 in this process. Here, we provide a biochemical basis for Pbx1;Emx2 genetic interaction by showing that Pbx1 and Emx2 can bind specific DNA sequences as heterodimers. Moreover, the expression of genes crucial for scapula development is altered in these mutants, indicating that Pbx genes act upstream of essential pathways for scapula formation. In particular, expression of Alx1, an effector of scapula blade patterning, is absent in all compound mutants. We demonstrate that Pbx1 and Emx2 bind in vivo to a conserved sequence upstream of Alx1 and cooperatively activate its transcription via this potential regulatory element. Our results establish an essential role for Pbx1 in genetic interactions with its family members and with Emx2 and delineate novel regulatory networks in shoulder girdle development.

PMID: 20627960

A Bayesian approach to age estimation in modern Americans from the clavicle

J Forensic Sci. 2010 May;55(3):571-83. Epub 2010 Apr 8.

Langley-Shirley N, Jantz RL.

Department of Anthropology, University of Tennessee, 250 South Stadium Hall, Knoxville, TN 37996, USA. nrshirley@gmail.com Abstract Clavicles from 1289 individuals from cohorts spanning the 20th century were scored with two scoring systems. Transition analysis and Bayesian statistics were used to obtain robust age ranges that are less sensitive to the effects of age mimicry and developmental outliers than age ranges obtained using a percentile approach. Observer error tests showed that a simple three-phase scoring system proved the least subjective, while retaining accuracy levels. Additionally, significant sexual dimorphism was detected in the onset of fusion, with women commencing fusion at least a year earlier than men (women transition to fusion at approximately 15 years of age and men at 16 years). Significant secular trends were apparent in the onset of skeletal maturation, with modern Americans transitioning to fusion approximately 4 years earlier than early 20th century Americans and 3.5 years earlier than Korean War era Americans. These results underscore the importance of using modern standards to estimate age in modern individuals.

PMID: 20384935 http://www.ncbi.nlm.nih.gov/pubmed/20384935

2009

Postnatal growth of the clavicle: birth to 18 years of age

J Pediatr Orthop. 2009 Dec;29(8):937-43.

McGraw MA, Mehlman CT, Lindsell CJ, Kirby CL.

Ohio University College of Osteopathic Medicine, Division of Pediatric Orthopaedic Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229-3039, USA. Abstract BACKGROUND: The purpose of our study was to perform a large cross-sectional study aimed at determining the postnatal growth pattern of the clavicle from birth to 18 years of age.

METHODS: We analyzed the digital chest radiographs of a convenience sample of 961 individuals between birth and 18 years of age. Malrotated radiographs were excluded. Right and left clavicle lengths were measured in millimeters from the most lateral ossified border to the most medial ossified border of each clavicle. Study patients were divided into 19 subgroups with the first group being labeled as "birth to 11 months of age" followed by 1-year-olds, 2-year olds, etc. Patients were also grouped by sex. There was a minimum of 25 patients in each group.

RESULTS: At 18 years of age the mean+/-SD clavicle length for females was 149+/-12 mm and for males it was 161+/-11 mm. Although a statistically significant difference (P=0.049) was noted between the length of right and left clavicles it was not clinically significant (0.036 mm). A steady growth rate was noted for both genders from birth to the age of 12 years (8.4 mm/y). Above the age of 12 years there were significant differences in the growth of the clavicles of girls (2.6 mm/y) versus boys (5.4 mm/y) (P<0.001). Our data suggest that females achieve 80% of their clavicle length by 9 years of age and boys by 12 years of age.

CONCLUSION: This cross-sectional study establishes that relatively little clavicle growth (20%) remains for girls beyond age 9 years and for boys beyond 12 years. The length of one clavicle may be properly judged by comparing it with the contralateral clavicle.

CLINICAL RELEVANCE: Remodeling of the clavicle shaft fractures is currently believed to be proportional to remaining growth. Our study questions the capacity of the clavicle to re-establish normal length beyond the age thresholds we have identified.

PMID: 19934713 http://www.ncbi.nlm.nih.gov/pubmed/19934713

A Runx2 threshold for the cleidocranial dysplasia phenotype

Hum Mol Genet. 2009 Feb 1;18(3):556-68. Epub 2008 Nov 20.

Lou Y, Javed A, Hussain S, Colby J, Frederick D, Pratap J, Xie R, Gaur T, van Wijnen AJ, Jones SN, Stein GS, Lian JB, Stein JL.

Department of Cell Biology, Cancer Center, University of Massachusetts Medical School, Worcester, MA 01655-0106, USA.

Cleidocranial dysplasia (CCD) in humans is an autosomal-dominant skeletal disease that results from mutations in the bone-specific transcription factor RUNX2 (CBFA1/AML3). However, distinct RUNX2 mutations in CCD do not correlate with the severity of the disease. Here we generated a new mouse model with a hypomorphic Runx2 mutant allele (Runx2(neo7)), in which only part of the transcript is processed to full-length (wild-type) Runx2 mRNA. Homozygous Runx2(neo7/neo7) mice express a reduced level of wild-type Runx2 mRNA (55-70%) and protein. This mouse model allowed us to establish the minimal requirement of functional Runx2 for normal bone development. Runx2(neo7/neo7) mice have grossly normal skeletons with no abnormalities observed in the growth plate, but do exhibit developmental defects in calvaria and clavicles that persist through post-natal growth. Clavicle defects are caused by disrupted endochondral bone formation during embryogenesis. These hypomorphic mice have altered calvarial bone volume, as observed by histology and microCT imaging, and decreased expression of osteoblast marker genes. The bone phenotype of the heterozygous mice, which have 79-84% of wild-type Runx2 mRNA, is normal. These results show there is a critical gene dosage requirement of functional Runx2 for the formation of intramembranous bone tissues during embryogenesis. A decrease to 70% of wild-type Runx2 levels results in the CCD syndrome, whereas levels >79% produce a normal skeleton. Our findings suggest that the range of bone phenotypes in CCD patients is attributable to quantitative reduction in the functional activity of RUNX2.

PMID: 19028669 http://www.ncbi.nlm.nih.gov/pubmed/19028669

2007

Critical role of the extracellular signal-regulated kinase-MAPK pathway in osteoblast differentiation and skeletal development

J Cell Biol. 2007 Feb 26;176(5):709-18.

Ge C, Xiao G, Jiang D, Franceschi RT.

Department of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI 48109, USA. Abstract The extracellular signal-regulated kinase (ERK)-mitogen-activated protein kinase (MAPK) pathway provides a major link between the cell surface and nucleus to control proliferation and differentiation. However, its in vivo role in skeletal development is unknown. A transgenic approach was used to establish a role for this pathway in bone. MAPK stimulation achieved by selective expression of constitutively active MAPK/ERK1 (MEK-SP) in osteoblasts accelerated in vitro differentiation of calvarial cells, as well as in vivo bone development, whereas dominant-negative MEK1 was inhibitory. The involvement of the RUNX2 transcription factor in this response was established in two ways: (a) RUNX2 phosphorylation and transcriptional activity were elevated in calvarial osteoblasts from TgMek-sp mice and reduced in cells from TgMek-dn mice, and (b) crossing TgMek-sp mice with Runx2+/- animals partially rescued the hypomorphic clavicles and undemineralized calvaria associated with Runx2 haploinsufficiency, whereas TgMek-dn; Runx2+/- mice had a more severe skeletal phenotype. This work establishes an important in vivo function for the ERK-MAPK pathway in bone that involves stimulation of RUNX2 phosphorylation and transcriptional activity.

PMID: 17325210 http://www.ncbi.nlm.nih.gov/pubmed/17325210

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2064027

1997

Mouse clavicular development: analysis of wild-type and cleidocranial dysplasia mutant mice

Dev Dyn. 1997 Sep;210(1):33-40.

Huang LF, Fukai N, Selby PB, Olsen BR, Mundlos S.

Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA. Abstract Cleidocranial dysplasia (CCD) is an autosomal dominant disease characterized by hypoplasia or aplasia of clavicles, open fontanelles, and other skeletal anomalies. A mouse mutant, shown by clinical and radiographic analysis to be strikingly similar to the human disorder and designated Ccd, was used as a model for the human disorder. Since malformation of the clavicle is the hallmark of CCD, we studied clavicular development in wild-type and Ccd mice. Histology and in situ hybridization experiments were performed to compare the temporal and spatial expression of several genes in wild-type and Ccd mutant mouse embryos. Bone and cartilage specific markers--type I, II, and X collagens, Sox9, aggrecan, and osteopontin were used as probes. The analyses covered the development of the clavicle from the initial mesenchymal condensation at embryonic day 13 (E13) to the late mineralization stage at embryonic day 15.5. At day 13.5, cells in the center of the condensation differentiate into characteristic precursor cells that were not observed in other bone anlagen. In the medial part of the anlage these cells express markers of the early cartilage lineage (type II collagen and Sox9), whereas cells of the lateral part express markers of the osteoblast lineage (type I collagen). With further development the medial cells differentiate into chondrocytes and start to express chondrocyte-specific markers such as aggrecan. Cells of the lateral part differentiate into osteoblasts as indicated by the production of bone matrix and the expression of osteopontin. At day 14.5 a regular growth plate has developed between the two parts where type X collagen expression can be demonstrated in hypertrophic chondrocytes. The data indicate that the medial part of the clavicle develops by endochondral bone formation while the lateral part ossifies as a membranous bone. The clavicle of Ccd mice showed a smaller band of mesenchymal cell condensation than in wild-type mice. Cells of the condensation failed to express type I and type II collagen at E13.5. In the lateral part of the clavicle type I collagen expression was not detected until E14.5 and osteopontin expression only appeared at E15.5. At E15.5, a small ossification center appears in the lateral part which is, in contrast to the wild-type clavicular bone, solid and without primary spongiosa as well as bone marrow. In the medial portion, type II collagen expression and endochondral ossification never occurs in Ccd mice; this portion of the clavicle is therefore missing in Ccd.

PMID: 9286593 http://www.ncbi.nlm.nih.gov/pubmed/9286593

1993

Conversion of bone marrow in the humerus, sternum, and clavicle: changes with age on MR images

Radiology. 1993 Jul;188(1):159-64. Zawin JK, Jaramillo D.

Department of Radiology, Children's Hospital, Boston, MA 02115. Abstract To study the normal conversion of bone marrow in the humerus, sternum, and clavicle, 101 T1-weighted magnetic resonance (MR) studies obtained in 91 patients aged 2 days to 37 years were retrospectively evaluated. Conversion from hypointense (red) to hyperintense (yellow) bone marrow was assessed by comparison of signal intensity of the bone marrow with that of muscle and fat. Conversion began in the proximal humeral epiphysis (in 16 of 21 adequate studies [76%]), humeral diaphysis (17 of 30 adequate studies [57%]), and distal metaphysis (16 of 25 adequate studies [64%]) before age 1 year and was nearly complete in these regions (20 of 22 adequate studies [91%], 20 of 21 adequate studies [95%], and five of seven adequate studies [71%]) in examinations of children aged 1-5 years. In the proximal humeral metaphysis, conversion was seen in 21 of 22 adequate studies (95%) in children aged 1-5 years and was nearly complete in all by age 20 years. Conversion began in the sternum (six of six studies [100%] in children aged 6-10 years) and clavicle (six of eight studies [75%] in children aged 6-10 years) before age 11 years but was never complete. Bone marrow conversion in the humerus, sternum, and clavicle follows a well-defined pattern and is depicted earlier by MR imaging than one would expect on the basis of histologic data.

PMID: 8511291

1988

The growth pattern of the clavicle in the rat

Rönning O, Kantomaa T.

Institute of Dentistry, University of Oulu, Finland. Abstract The mode of growth of the rat clavicle from 17 to 45 days of age was studied by means of vital staining (alizarin red S), histology and autoradiography (tritiated thymidine). In addition the clavicle on one side was subjected to periostomy at the age of 10 days and its length compared with that of its unoperated counterpart at the ages of 17 and 45 days. The alizarin red staining revealed that the medial end of the clavicle contributes to the length of the bone, while the lateral end appears to have mainly an articulatory function. Histologically, the medial end cartilage closely resembles the condylar cartilage of the mandible, whereas the lateral end appears to be composed of two cartilaginous structures separated by a mesenchymatous layer. Tritiated thymidine was deposited in the mesenchymal cells covering the medial end cartilage, whereas virtually no activity was observed in the mesenchyme of the lateral end cartilage. The periostomised clavicle was more slender in appearance than its control throughout the observation period. The two clavicles were of the same length at 17 days, but by 45 days the periostomised clavicle was significantly longer than the control. It is suggested that the growth of the clavicle is essentially comparable to the growth of the mandible. Length growth occurs in response to the action of the surrounding structures, while analogously to the mandibular condyle, the medial end cartilage actively translates the bone in a direction perpendicular to the articular surface, giving rise to its curved shape.

PMID: 3248965 J Anat. 1988 Aug;159:173-9.