China
Africa
Explore chapters and articles related to this topic
Evidence-based radiology in child abuse
Published in Amaka C Offiah, Christine M Hall, Radiological Atlas of Child Abuse, 2018
Amaka C Offiah, Christine M Hall
The CML was originally thought to represent an avulsion injury of the periphery of the metaphysis.46 However, Kleinman, et al.8,47–51 have characterised these lesions histologically, and thus explained their radiological appearances and likely mechanism of injury. In brief, the CML is a series of planar microfractures through the most immature portion of the metaphyseal primary spongiosa. The fracture line extends in a planar fashion towards the periphery (cortex) of the bone. As it does so, it veers away from the physis (growth plate) undercutting a bony peripheral segment that encompasses the subperiosteal bone collar. As a consequence, the peripheral bony fragment(s) will be thicker than the central portion.
Principles of Skeletal Growth
Published in D. Dixon Andrew, A.N. Hoyte David, Ronning Olli, Fundamentals of Craniofacial Growth, 2017
Chondral ossification is the mode of ossification of the base of the skull, the vertebrae, the ribs, as well as of all the tubular bones (Figure 1.3). Cartilage here represents the first stage in bone development. Initially, a process of perichondral ossification results in the formation of a bone collar around the cartilage. Then the cartilage cells in the interior of the cartilage change into hypertrophic cartilage. Some of the cells are destroyed and the basic substance takes up calcium salts. Through endochondral ossification, mesenchyme cells from outside invade the cartilage and commence the formation of bone from the inside out. Concurrently, white blood cells (monocytes) become differentiated into chondroclasts which break down the cartilage, and mesenchyme cells become differentiated into osteoblasts which deposit bone matrix on the remaining cartilage.
Comparison of the Bone Regenerative Capacity of Three-Dimensional Uncalcined and Unsintered Hydroxyapatite/Poly-d /l -Lactide and Beta-Tricalcium Phosphate Used as Bone Graft Substitutes
Published in Journal of Investigative Surgery, 2021
Yunpeng Bai, Jingjing Sha, Takahiro Kanno, Kenichi Miyamoto, Katsumi Hideshima, Yumi Matsuzaki
The human OCN gene encodes bone γ-carboxyglutamic acid protein, a secreted protein produced primarily by osteoblasts [39]. Consequently, OCN is routinely used as a serum marker of well-differentiated osteoblastic bone formation and is thought to regulate mineralization within the bone matrix. During the bone-defect healing period, calcium granules first expand into the fracture containing callus chondrocytes and are then transported into the extracellular matrix (ECM), where they form the initial mineral deposits with phosphate [40]. During this process, soft callus is transformed into hard callus; generally, the peak of hard callus formation is reached by 14 days in animal models. This change can be defined not only by the histomorphometry of mineralized tissue but also by the detection of ECM markers such as OCN, type I procollagen, alkaline phosphatase, and osteonectin [30]. OCN is also considered an osteoblast-specific gene that is expressed during ossification, along with master transcriptional factors such as Runx2 and Osterix [41, 42]. During embryonic and postnatal bone development and fracture healing, intramembranous ossification consists mainly of osteogenic mesenchymal condensation and direct differentiation into osteoblasts, eventually producing bone [43, 44]. By contrast, the process of endochondral ossification is characterized not only by the differentiation of chondrocytes by mesenchymal condensation to form a cartilaginous template that is eventually replaced with bone but also by osteoblast cells that sometimes participate to form the bone collar, which subsequently becomes cortical bone [43].
Hereditary multiple exostoses: are there new plausible treatment strategies?
Published in Expert Opinion on Orphan Drugs, 2018
Another powerful pro-chondrogenic mechanism is the hedgehog signaling pathway that plays critical roles in skeletogenesis [45]. This pathway is active in the growth plate, regulates the rates of chondrocyte proliferation and maturation, and also induces bone collar formation around the hypertrophic zone [45,46]. HS and HS-rich proteoglycans control and restrict the range and boundaries of action by this pathway within the growth plate, a reflection of tight regulatory interactions of HS with hedgehog proteins via their HS-binding domains [47]. It is of interest that in the FGFR3-deficient mice described above, osteochondroma-like tissue development was preceded by up-regulation of Indian hedgehog (Ihh) gene expression and signaling [39], and the same was observed in Kif3a-deficient mice [48] in which the ectopic presence of Ihh in perichondrium was linked, and probably caused by, concurrent decreases in HS proteoglycan gene expression. Importantly, osteochondroma formation in the FGFR3-deficient mice was reduced by systemic treatment with GDC-0449 [39], a drug that inhibits the activity of the hedgehog transducing receptor Smoothened [49]. Mundy et al. showed that treatment with the hedgehog inhibitor HhAntag blocked both basal chondrogenesis as well as chondrogenesis that had been stimulated by HS depletion in vitro [50]. Together, these and other studies point to the possibility that the hedgehog pathway may be a reasonable target of therapeutic intervention in HME, and it is worth noting that hedgehog antagonists are already in clinical use and testing for other cancer conditions with acceptable safety profiles [51].
Growth factor signalling in osteoarthritis
Published in Growth Factors, 2018
Expression of dominant negative type II TGF-β receptor results in an OA-like phenotype and points to increased Indian hedgehog (IHH) expression that could be responsible for hypertrophic differentiation of articular chondrocytes observed in OA (Serra et al., 1997). IHH, sonic hedgehog (SHH) and desert hedgehog (DHH), are three members of the mammalian Hedgehog family (Ingham and McMahon, 2001). As secreted peptide ligands, Hedgehog (Hh) proteins act both locally and remotely in a dose- and duration-dependent manner as important morphogens in development and key players in tissue homeostasis. For Hh ligands, the primary receptor is Patched 1 (PTCH1), a transmembrane protein that inhibits activities of the Hh pathway if unbound to the Hh ligands. The repression of Hh pathway by PTCH1 is mediated by its inhibition of Smoothened (SMO), a member of the G protein-coupled receptor (GPCR) superfamily. Thus, upon Hh binding, SMO is relieved from PTCH1 suppression and activates transcriptional factors named Gli (Gli1, Gli2, and Gli3 in vertebrates) to conduct specific sets of gene expression. Among three ligands, IHH has been demonstrated to play multiple important functions in the development of bone and cartilage, including its regulatory role in proliferation and hypertrophic differentiation of chondrocytes (Kobayashi et al., 2002; Long et al., 2001; St-Jacques et al., 1999; Vortkamp et al., 1996), as well as in osteoblast differentiation (Chung et al., 2001; St-Jacques et al., 1999). Predominantly produced by prehypertrophic chondrocytes, IHH promotes the expression of parathyroid hormone-related protein (PTHrP) in periarticular chondrocytes, and keeps these chondrocyte proliferating without differentiating (St-Jacques et al., 1999; Vortkamp et al., 1996). IHH also induces the differentiation of periarticular chondrocytes into columnar chondrocytes independently of PTHrP (Kobayashi et al., 2005). Moreover, IHH is also required for the osteoblast differentiation of perichondrial cells that is essential to bone collar formation (Long et al., 2004). Because of its proliferation-stimulating effects on chondrocytes, IHH was tested for its cartilage repairing potential, by delivering bone marrow coagulates with adenoviral expression of IHH to osteochondral defects in the rabbit knees. The result was promising, suggesting the capability of IHH in cartilage repair (Sieker et al., 2015).