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11: Module 9- The Appendicular Skeleton - Biology
A skeletal system is necessary to support the body, protect internal organs, and allow for the movement of an organism. There are three different skeleton designs that fulfill these functions: hydrostatic skeleton, exoskeleton, and endoskeleton.
- Identify the three common skeleton designs
- Identify the components of the human axial skeleton
- Identify the components of the human appendicular skeleton
Online medical course that equips you with the skills to interpret radiological images correctly, improving patient outcomes and reducing risks.
Image Interpretation online medical course equips you with the skills to interpret radiological images correctly, improving patient outcomes and reducing risks. The programme has been developed in the UK by the College of Radiographers and Health Education England e-Learning for Healthcare. This online medical course covers a wide range of techniques used in radiography, with sessions already available for X-ray, ultrasound and cross-sectional imaging.
The Image Interpretation programme is part of the UK College of Radiographers’ continuing professional development scheme – CPD now. So, it meets UK quality standards for professional training in this area.
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The Image Interpretation project is a fantastic resource for radiographers’ continuing professional development.
Nick Woznita, reporting radiographer at Homerton University Hospital
Healthcare staff will find the sessions invaluable as a tool to assist them to understand the wide ranging and complex appearances of both normal images and those showing pathology.
Dorothy Keane, Image Interpretation Clinical Lead
It is not only refreshing my memory of anatomy and biomechanics learnt on qualification and in my years of practice but it is teaching me new things to look for in the patient’s history and what to look out for in the resulting image.
Image Interpretation user
Vertebrate Skeletal Development
David M. Ornitz , Pierre J. Marie , in Current Topics in Developmental Biology , 2019
2.1 Expression of FGF and FGF receptors in the developing appendicular skeleton
In the developing appendicular skeleton , Fgf ligands and receptors are expressed and function at all stages, from formation of the limb bud through growth, remodeling, homeostasis, and repair of mature bone. In the distal limb bud, Fgfr1 and Fgfr2 are present in mesenchymal cells, before any morphological or molecular indication of a mesenchymal condensation (also called a chondrogenic condensation) ( Orr-Urtreger, Givol, Yayon, Yarden, & Lonai, 1991 Sheeba, Andrade, Duprez, & Palmeirim, 2010 ). At this precondensation stage, expression of Fgfr3 and Fgfr4 is not detected ( Sheeba et al., 2010 ).
The apical ectodermal ridge (AER) is a signaling center at the distal edge of the limb bud. The AER expresses several FGFs (primarily FGF4 and FGF8 but also FGF2, FGF9 and FGF17). One model of AER FGF function suggests that AER FGFs signal to limb mesenchymal FGFRs and function to delay cell differentiation, increasing the time cells have to proliferate, and thus promoting limb bud outgrowth ( Martin, 1998 Sun et al., 2000 Tabin & Wolpert, 2007 ). In this model, mesenchymal cells begin to differentiate when they are too far away from the AER to receive an AER derived FGF signal ( Benazet & Zeller, 2009 Tabin & Wolpert, 2007 ). Differentiation of the limb mesenchyme that is out of range of AER FGFs results in the formation of a mesenchymal (chondrogenic) condensation, the primary event that initiates appendicular skeletogenesis.
The formation of a chondrogenic condensation is marked by expression of Sox9 and increased expression of Fgfr2 (compared to the surrounding mesenchyme) ( Delezoide et al., 1998 Eswarakumar et al., 2002 Orr-Urtreger et al., 1991 Peters, Werner, Chen, & Williams, 1992 Sheeba et al., 2010 Szebenyi, Savage, Olwin, & Fallon, 1995 Yu & Ornitz, 2008 ). Fgfr1 remains more uniformly expressed throughout limb bud mesenchyme. Fgfr3 and Fgfr4 are excluded from distal limb bud mesenchyme however, these Fgfrs are expressed in more proximal locations in the growing limb in developing muscle tissue ( Delezoide et al., 1998 Orr-Urtreger et al., 1991 Peters et al., 1992 Sheeba et al., 2010 Szebenyi et al., 1995 ). The perichondrium and periosteum are derived from cells in the periphery of the condensation. These cells express both Fgfr1 and Fgfr2 ( Delezoide et al., 1998 Eswarakumar et al., 2002 ). Centrally, cells commit to a chondrogenic fate and begin to express Fgfr3 along with Sox9 and type II collagen ( Peters et al., 1992 Peters, Ornitz, Werner, & Williams, 1993 Purcell et al., 2009 ). As chondrocytes begin to hypertrophy at the center of the developing skeletal segment along the proximal-distal axis, Fgfr3 expression is decreased and Fgfr1 expression is increased ( Deng, Wynshaw-Boris, Zhou, Kuo, & Leder, 1996 Jacob, Smith, Partanen, & Ornitz, 2006 Karolak, Yang, & Elefteriou, 2015 Naski, Colvin, Coffin, & Ornitz, 1998 Peters et al., 1993, 1992 ).
Although the initiation of the mesenchymal chondrogenic condensation requires escape from AER FGFs, the subsequent development of the condensation is at least partially dependent on FGFR signaling ( Kumar & Lassar, 2014 Mariani, Ahn, & Martin, 2008 Murakami, Kan, McKeehan, & de Crombrugghe, 2000 Yu & Ornitz, 2008 ). In support of this idea, FGF signaling increases Sox9 expression in primary chondrocytes and in undifferentiated mesenchymal cell lines ( Murakami et al., 2000 Shung, Ota, Zhou, Keene, & Hurlin, 2012 ). Additionally, ERK1/2 activation maintains competence of limb bud mesenchyme to differentiate into chondrocytes by blocking Wnt-induced methylation and silencing of the Sox9 promoter ( Kumar & Lassar, 2014 Ten Berge, Brugmann, Helms, & Nusse, 2008 ). Fgfr3 expression in proliferating chondrocytes is maintained through Sox9 binding sites in the Fgfr3 gene ( Oh et al., 2014 ). The mechanisms that regulate the transition from AER derived FGF signaling to local FGF signaling in condensing mesenchyme and FGF signaling in the skeletal primordium are not known. However, factors that could regulate this transition include proximity of ligand sources and responding tissue, ligand binding specificity of different FGFs and FGFRs, and regulation of heparan sulfate sulfation patterns which could regulate FGF diffusion through the extracellular matrix and the binding affinity to FGFRs ( Nogami et al., 2004 Ornitz, 2000 ).
The perichondrium and periosteum that will give rise to the bone collar and cortical bone express Fgfr1 in mesenchymal progenitors and FGFR2 in differentiating osteoblasts ( Britto, Evans, Hayward, & Jones, 2001 Coutu, Francois, & Galipeau, 2011 Jacob et al., 2006 Molteni, Modrowski, Hott, & Marie, 1999b Ohbayashi et al., 2002 ). Fgfr3 is expressed more intensely in chondroprogenitor cells located in the groove of Ranvier and ring of LaCroix ( Robinson et al., 1999 ) and FGFR1 and FGFR3 are expressed in mouse and human articular chondrocytes ( Fig. 1 A ) ( Weng et al., 2012 Yan et al., 2011 ).
Fig. 1 . Expression patterns of FGF receptors in endochondral bone (A) and membranous bone (B) during development. Diagram shows a schematic of a growth plate with color coded expression patterns of FGF receptors.
The growth plate is established when chondrocytes in the center of the mesenchymal condensation begin to hypertrophy and when vascular invasion of the hypertrophic zone chondrocytes forms a primary ossification center. These immature chondroprogenitors express FGFR3. In the established growth plate, Fgfr3 expression remains high in proliferating and prehypertrophic zone chondrocytes. As chondrocytes begin to hypertrophy, Fgfr3 expression is shut down and Fgfr1 expression is increased ( Fig. 1 ) ( Delezoide et al., 1998 Eswarakumar et al., 2002 Hamada, Suda, & Kuroda, 1999 Jacob et al., 2006 Karolak et al., 2015 Karuppaiah et al., 2016 Lazarus, Hegde, Andrade, Nilsson, & Baron, 2007 Ornitz & Marie, 2002 Peters et al., 1993 Yu et al., 2003 ).