scholarly journals SHOX gene is expressed in vertebral body growth plates in idiopathic and congenital scoliosis: Implications for the etiology of scoliosis in turner syndrome

2008 ◽  
Vol 27 (6) ◽  
pp. 807-813 ◽  
Author(s):  
Gregory Day ◽  
Attila Szvetko ◽  
Lyn Griffiths ◽  
I. Bruce McPhee ◽  
John Tuffley ◽  
...  
Keyword(s):  
Turner Syndrome ◽  
Vertebral Body ◽  
Congenital Scoliosis ◽  
Body Growth ◽  
Growth Plates ◽  
Shox Gene

Glycosaminoglycans of the Vertebral Body Growth Plate in Patients with Idiopathic Scoliosis

2005 ◽  
Vol 139 (6) ◽  
pp. 738-740 ◽  
Author(s):  
T. V. Rusova ◽  
V. I. Rykova ◽  
A. V. Korel’ ◽  
A. M. Zaidman ◽  
D. S. Tkachev
Keyword(s):  
Idiopathic Scoliosis ◽  
Growth Plate ◽  
Vertebral Body ◽  
Body Growth

scholarly journals Coexisting diseases modifying each other’s presentation - lack of growth failure in Turner syndrome due to the associated pituitary gigantism

2016 ◽  
Vol 73 (10) ◽  
pp. 961-966
Author(s):  
Tamara Dragovic ◽  
Zorana Djuran ◽  
Svetlana Jelic ◽  
Dejan Marinkovic ◽  
Sasa Kikovic ◽  
...  
Keyword(s):  
Turner Syndrome ◽  
Genetic Disorder ◽  
Clinical Signs ◽  
Growth Failure ◽  
Delayed Puberty ◽  
Clinical Feature ◽  
Facial Dysmorphism ◽  
Primary Amenorrhea ◽  
Growth Plates ◽  
Gh Secretion

Introduction. Turner syndrome presents with one of the most frequent chromosomal aberrations in female, typically presented with growth retardation, ovarian insufficiency, facial dysmorphism, and numerous other somatic stigmata. Gigantism is an extremely rare condition resulting from an excessive growth hormone (GH) secretion that occurs during childhood before the fusion of epiphyseal growth plates. The major clinical feature of gigantism is growth acceleration, although these patients also suffer from hypogonadism and soft tissue hypertrophy. Case report. We presented a girl with mosaic Turner syndrome, delayed puberty and normal linear growth for the sex and age, due to the simultaneous GH hypersecretion by pituitary tumor. In the presented case all the typical phenotypic stigmata related to Turner syndrome were missing. Due to excessive pituitary GH secretion during the period while the epiphyseal growth plates of the long bones are still open, characteristic stagnation in longitudinal growth has not been demonstrated. The patient presented with delayed puberty and primary amenorrhea along with a sudden appearance of clinical signs of hypersomatotropinism, which were the reasons for seeking medical help at the age of 16. Conclusion. Physical examination of children presenting with delayed puberty but without growth arrest must include an overall hormonal and genetic testing even in the cases when typical clinical presentations of genetic disorder are absent. To the best of our knowledge, this is the first reported case of simultaneous presence of Turner syndrome and gigantism in the literature.

scholarly journals Cervical vertebral body growth and emergence of sexual dimorphism: a developmental study using computed tomography

2019 ◽  
Vol 234 (6) ◽  
pp. 764-777 ◽  
Author(s):  
Courtney A. Miller ◽  
Seong Jae Hwang ◽  
Meghan M. Cotter ◽  
Houri K. Vorperian
Keyword(s):  
Computed Tomography ◽  
Sexual Dimorphism ◽  
Vertebral Body ◽  
Body Growth ◽  
Developmental Study ◽  
Cervical Vertebral Body

Anterior lengthening in scoliosis occurs only in the disc and is similar in different types of scoliosis

2021 ◽  
Author(s):  
S de Reuver ◽  
RC Brink ◽  
JF Homans ◽  
L Vavruch ◽  
H Tropp ◽  
...  
Keyword(s):  
Vertebral Body ◽  
Sagittal Plane ◽  
Three Dimensional ◽  
Congenital Scoliosis ◽  
Intervertebral Discs ◽  
Ct Scans ◽  
Scoliotic Deformity ◽  
Different Types ◽  
Vertebral Bodies ◽  
Bony Abnormality

Relative anterior spinal overgrowth (RASO) was proposed as a generalized growth disturbance and a potential initiator of adolescent idiopathic scoliosis (AIS). However, anterior lengthening was also observed in neuromuscular (NM) scoliosis, was shown to be restricted to the apical areas and to be located in the intervertebral discs, not in the bone. In this study the goal was to determine if other scoliotic curves of known origin exhibit the similar mechanism of anterior lengthening without changes in the vertebral body. Therefore CT-scans of 18 patients in whom a short segment congenital malformation had led to a long thoracic compensatory curve without bony abnormality were included. Of each vertebral body and intervertebral disc in the compensatory curve, the anterior and posterior length was measured on CT-scans in the exact mid-sagittal plane, corrected for deformity in all three planes. The total AP% of the compensatory curve in congenital scoliosis showed a lordosis (+1.8%) that differed from the kyphosis in non-scoliotic controls (-3.0%; p<0.001), and was comparable to AIS (+1.2%) and NM scoliosis (+0.5%). This anterior lengthening was not located in the bone; the vertebral body AP% showed a kyphosis (-3.2%), similar to non-scoliotic controls (-3.4%), as well as AIS (-2.5%) and NM scoliosis (-4.5%; p=1.000). However, the disc AP% showed a lordosis (+24.3%), which sharply contrasts to the kyphotic discs of controls (-1.5%; p<0.001), but was similar to AIS (+17.5%) and NM scoliosis (+20.5%). The results demonstrate that anterior lengthening is part of the three-dimensional deformity in different types of scoliosis and is exclusively located in the intervertebral discs. The bony vertebral bodies maintain their kyphotic shape, which indicates that there is no active bony overgrowth. Anterior lengthening appears to be a passive result of any scoliotic deformity, rather than being related to the specific cause of AIS.

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