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Introduction
Published in Ugo Ripamonti, The Geometric Induction of Bone Formation, 2020
Of note, partial purification of fine particle extracts on Sepharose CL-6B gel filtration chromatography showed that the reconstitution of column fractions of 20,000–50,000 mol. wt. with inactive coarse residue induced reproducible and prominent endochondral bone formation (Fig. 0.4d) (Sampath and Reddi 1984). Solubilized extracellular matrix components of coarse bone matrix (particle size of 74–420 µm) were reconstituted with fine matrix inactive residue (particle size 74–420 µm) and bioassayed for endochondral bone formation at subcutaneous bilateral sites in rodents (Sampath and Reddi 1984). The results showed that demineralized extracted collagenous matrices of coarse powders did not support the induction of bone formation when reconstituted with fine matrix (particle size 44–74 µm) (Sampath and Reddi 1984). On the other hand, the reconstitution of fine matrix extracts with coarse demineralized matrices (particle size 74–420 µm) restored the biological activity with the induction of endochondral bone formation (Fig. 0.4c) (Sampath and Reddi 1984).
Nutraceuticals for Bone Health in Pregnancy
Published in Priyanka Bhatt, Maryam Sadat Miraghajani, Sarvadaman Pathak, Yashwant Pathak, Nutraceuticals for Prenatal, Maternal and Offspring’s Nutritional Health, 2019
During embryonic and fetal development a great part of the skeleton starts as a cartilaginous scaffold, which is dynamically reabsorbed and replaced by bone. Endochondral bone formation proceeds until the development plates combine during puberty. At all life stages sufficient conveyance of mineral is required for the skeleton to accomplish and keep up suitable mineral substance and quality. During fetal development the placenta effectively transports calcium, phosphorus, and magnesium. Postnatally, passive and after that active absorption from the intestine turns into the primary supply of minerals to the skeleton. Animal and human data demonstrate that fetal bone development requires parathyroid hormone (PTH) and PTH-related protein but not vitamin D/calcitriol, calcitonin, or (perhaps) sex steroids. During the postnatal period, when intestinal calcium absorption becomes an active process, skeletal development begins to rely on vitamin D/calcitriol, however, this prerequisite can be circumvented by expanding the calcium substance of the eating routine or by controlling irregular calcium imbuement (König et al. 2018). The calciotropic hormones play different roles during the fetal and neonatal periods regulating skeletal improvement and mineralization. The epidemiological proof supporting a role for maternal dietary nutrient D and conceivably calcium in fetal, neonatal, and grown-up bone results was generally limited in the consultations of the audit board in modifying the DRIs for calcium and nutrient D (Rabin 2013).
Bone and Cartilage
Published in George W. Casarett, Radiation Histopathology: Volume II, 2019
The process of endochondral bone growth is radiosensitive because of the radiosen-sitivity of growing cartilage and bone marrow. Endochondral bone growth, i.e., bone growth in the wake of growth of cartilage is described here as exemplified in the longitudinal growth of the rat femur. The normal disc of hyaline cartilage (physis) in the center of endochondral bone growth, situated horizontally between the bony plate of the epiphysis and the cancellous bone of the metaphysis, may be described in terms of five zones, proceeding from the bony plate of the epiphysis to the metaphysis (Figure 5A):
Measurement of stapes footplate thickness in otosclerosis by ultra-high-resolution computed tomography
Published in Acta Oto-Laryngologica, 2020
Yukinori Akazawa, Akira Ganaha, Teruyuki Higa, Shunsuke Kondo, Yoshiki Oyakawa, Hitoshi Hirakawa, Mikio Suzuki, Tsuneo Yamashiro
Otosclerosis is a multifactorial temporal bone disorder with genetic and environmental causes involving endochondral bone of the otic and labyrinthine capsules. The prevalence of clinical otosclerosis is approximately 0.3–0.4% in the United States, although the prevalence of subclinical histologically confirmed disease is higher [1]. In 1841, Toynbee found stapes fixation in 39 of the 1659 temporal bones (2%) and thus established the link between deafness and stapes fixation [2]. It is important to clarify the fine architectural changes in the temporal bone in order to enable accurate differential diagnosis of several middle and inner ear disorders from otosclerosis [3]. The incidence of otosclerosis is estimated to be much lower in Japanese than in Caucasians [4]. This is considered to be due to the low incidence of involvement of foci anterior to the oval window, low activity, and small lesion size without involvement of the foot plate and/or membranous labyrinth of the inner ear [5]. Although otosclerosis is uncommon in the Japanese population, its incidence has been increasing [4].
Extracellular Matrix Remodeling During Palate Development
Published in Organogenesis, 2020
Xia Wang, Chunman Li, Zeyao Zhu, Li Yuan, Wood Yee Chan, Ou Sha
Type II collagen is the major extracellular matrix component of cartilage and essential for endochondral bone formation.5 In the palate mesenchyme, only a few osteoblast precursors express Col II in the palatal mesenchyme.8 Inactivate Type II collagen in mouse develops short bones and cleft palate.33-38 In these mutants, both chondrocyte differentiation and intramembranous ossification are disrupted. Augmented fibroblast growth factor 8 (FGF8) signaling in the anterior hard palate by using Shox2Cre causes a subset of palatal mesenchymal cells differentiating into Col II+ chondrogenic cells at the expense of osteogenic cell fate.8 These results indicate that appropriate level of Type II collagen is necessary for palate mesenchymal cell fate determination.
Cellular voids in the pathogenesis of otosclerosis
Published in Acta Oto-Laryngologica, 2023
Lars Juul Hansen, Sune Land Bloch, Mads Sølvsten Sørensen
The otic capsule is developed by the process of endochondral ossification. Normally, the primary or foetal characteristics of endochondral bone are removed by remodelling, thus replacing primary bone with secondary, more lamellar bone without calcified cartilage matrix remnants. However, a high concentration of OPG from the inner ear effectively inhibits modelling and remodelling around the inner ear. This explains the lifelong existence of foetal type bone features like primary trabeculae (osseous globules + interglobular spaces) embedded in primary woven type skein bone from cancellous compaction in the perilabyrinthine bone [11].