Disorders of the growth plate

Phornphutkul, Chanika; Gruppuso, Philip A.

doi:10.1097/med.0b013e328331dca2

Cited by 10 publications

(7 citation statements)

References 66 publications

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“…From our histological studies we evidenced that the clavicle's epiphyseal growth behaves in the same way as the development of a true physis in a long bone. We observed all areas described in the literature: reserve zone I, proliferation II, hypertrophy III, calcification IV, and vascular invasion V [5,[17][18][19]. Chondrocytes at the acromial end increased their organization in orderly columns with increasing age.…”

Section: Discussionsupporting

confidence: 58%

A Histological Study of Postnatal Development of Clavicle Articular Ends

et al. 2015

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The clavicle is the first bone to begin the process of ossification and the last one to complete it. Whilst histological studies of the clavicle have been focused mainly on embryonic events, our study focused on postnatal clavicle development. The objective of this study was to perform a qualitative description of the clavicle's epiphyseal growth to further shed light on the postnatal ossification process. Histological studies performed on clavicles obtained from cadavers confirmed medial and lateral extremities as true physes. Unlike the development of other long bones, no secondary ossification centre was present at the acromial end. Furthermore, appearance of the sternal end was observed after the age of 18, as evidenced in clavicles from a 19-year old individual. The articular surface of the clavicle's acromial end was fibrocartilage. Thus far no histological studies have been performed before describing postnatal development of clavicular ends. Our data confirm the absence of an acromial secondary ossification centre, the late development of a secondary ossification centre at the sternal end, and the presence of fibrocartilage at the acromial end.

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Section: Discussionsupporting

confidence: 58%

A Histological Study of Postnatal Development of Clavicle Articular Ends

et al. 2015

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“…Given the accelerated ossification, we next evaluated if Dot1l affects hypertrophic chondrocyte differentiation and subsequent endochondral ossification. mRNA in situ hybridization of Col10a1 , a marker of hypertrophic chondrocytes, was performed in the femur of P2 pups. Although there was comparable level of Col10a1 expression in the Dot1l ‐deleted and control growth plates, there was ectopic expression of Col10a1 in epiphyseal chondrocytes (Fig.…”

Section: Resultsmentioning

confidence: 99%

The Role of Dot1l in Prenatal and Postnatal Murine Chondrocytes and Trabecular Bone

Domowicz

Henry

et al. 2019

JBMR Plus

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Osteoarthritis and osteoporosis are widely prevalent and have far‐reaching public health implications. There is increasing evidence that epigenetics, in particular, histone 3 lysine 79 methyltransferase DOT1L, plays an important role in the cartilage and bone biology. In this study, we evaluated the role of Dot1l in the articular cartilage, growth plate, and trabecular bone utilizing conditional KO mouse models. We generated chondrocyte‐specific constitutive and inducible conditional Dot1l KO mouse lines using Col2a1‐Cre and Acan‐CreER systems. Prenatal deletion of Dot1l in mouse chondrocytes led to perinatal mortality, accelerated ossification, and dysregulation of Col10a1 expression. Postnatal deletion of Dot1l in mouse chondrocytes resulted in trabecular bone loss decreased extracellular matrix production, and disruption of the growth plate. In addition, pharmacological inhibition of DOT1L in a progeria mouse model partially rescued the abnormal osseous phenotype. In conclusion, Dot1l is important in maintaining the growth plate, extracellular matrix production, and trabecular bone. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.

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“…Given the complexity of the physiology of the normal growth plate, it is not surprising that over 300 congenital abnormalities of skeletal growth have been defined. 36 Hereditary multiple osteochondromas (HMO) and achondroplasia are two common disorders caused by disturbances in regulatory growth plate pathways that are understood at the molecular level. HMO, also known as hereditary multiple exostoses, is caused by autosomal dominant mutations in the exostosin-1 and -2 ( Ext-1 and Ext-2) genes.…”

Section: Disorders Of the Growth Platementioning

confidence: 99%

The growth plate: a physiologic overview

Ağırdil

2020

EFORT Open Reviews

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The growth plate is the cartilaginous portion of long bones where the longitudinal growth of the bone takes place. Its structure comprises chondrocytes suspended in a collagen matrix that go through several stages of maturation until they finally die, and are replaced by osteoblasts, osteoclasts, and lamellar bone. The process of endochondral ossification is coordinated by chondrocytes and a variety of humoral factors including growth hormone, parathyroid hormone, oestrogen, growth factors, cytokines, and various signalling pathways. Chondrocytes progress from a resting state to enter the phases of proliferation and hypertrophy. Under the influence of oestrogen, the proliferation of chondrocytes decreases as the resting chondrocytes are consumed. During the terminal phase of differentiation, cartilage is replaced by blood vessels and organized bone tissue, and once chondrocytes have died, the longitudinal growth of the bone ceases and the growth plate closes. The highly complex regulatory signals involved in this process are genetically determined, and genetic perturbations in any of the associated genes can result in abnormalities of bone growth. Hundreds of chondrodysplasias have been described, pointing to the complexity of the humoral control systems involved in endochondral ossification. While our knowledge of the mechanisms behind the various bone growth control systems is improving, a deeper understanding of the underlying processes could aid clinicians to better understand bone health and bone growth abnormalities. This review describes the current clinical research into the physiology of the growth plate. Cite this article: EFORT Open Rev 2020;5:498-507. DOI: 10.1302/2058-5241.5.190088

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Disorders of the growth plate

Cited by 10 publications

References 66 publications

A Histological Study of Postnatal Development of Clavicle Articular Ends

A Histological Study of Postnatal Development of Clavicle Articular Ends

The Role of Dot1l in Prenatal and Postnatal Murine Chondrocytes and Trabecular Bone

The growth plate: a physiologic overview

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