Recent advances in the aetiology of adolescent idiopathic scoliosis

Cheung, Kenneth M.C.; Wang, Tao; Qiu, Guixing; Luk, Keith D. K.

doi:10.1007/s00264-007-0393-y

Cited by 61 publications

(49 citation statements)

References 57 publications

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“…Another prerequisite for the progression of adolescent idiopathic scoliosis is the presence of an adolescent growth spurt (Lowe et al, 2000;Cheung et al, 2008), but it is disputed whether Homo erectus already evolved this distinctive human growth pattern (Smith, 1993;Tardieu, 1998;Smith, 2004;Zihlman et al, 2004;Graves et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Revisiting scoliosis in the KNM-WT 15000 Homo erectus skeleton

Schiess¹,

Boeni²,

Rühli³

et al. 2014

Journal of Human Evolution

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Owing to its completeness, the 1.5 million year old Nariokotome boy skeleton KNM-WT 15000 is central for understanding skeletal biology of Homo erectus. Nevertheless, since Latimer and Ohman (2001, Axial dysplasia in Homo erectus. J Hum Evol 40:A12) reported on asymmetries and distortions of Nariokotome boy's axial skeleton suggesting adolescent idiopathic scoliosis, possibly associated with congenital skeletal dysplasia, it is questionable whether it still can be used as reference for Homo erectus. Recently, however, the presence of skeletal dysplasia has been refuted. Here, we present a morphologic and morphometric reanalysis of the assertion of idiopathic scoliosis. We demonstrate that unarticulated vertebral columns of non-scoliotic and scoliotic individuals can be distinguished based on the lateral deviation of the spinous process, lateral and sagittal wedging, vertebral body torsion, pedicle thickness asymmetry and asymmetry of the superior and inferior articular facet area. A principal component analysis of the overall asymmetry of all seven vertebral shape variables groups KNM-WT 15000 within non-scoliotic modern humans. An anomaly of vertebrae T1-T2 is compatible with a short left convex curve at the uppermost thoracic region, possibly due to injury or local growth dysbalance. Asymmetries of the facet joints L3-L5 suggest a local right convex curve in the lower lumbar region that probably resulted from juvenile traumatic disc herniation. This pattern is incompatible with adolescent idiopathic scoliosis or other types of scoliosis, including congenital, neuromuscular or syndromic scoliosis. It is, however, consistent with a recent reanalysis of the rib cage that did not reveal any asymmetry. Except for these possibly trauma-related anomalies, the Nariokotome boy fossil therefore seems to belong to a normal Homo erectus youth without evidence for adolescent idiopathic scoliosis or other severe pathologies of the axial skeleton. AbstractOwing to its completeness, the 1.5 million year old Nariokotome boy skeleton KNM-WT 15000 is central for understanding skeletal biology of Homo erectus. Nevertheless, since Latimer and Ohman (2001, Axial dysplasia in Homo erectus. J Hum Evol 40:A12) reported on asymmetries and distortions of Nariokotome boy's axial skeleton suggesting adolescent idiopathic scoliosis, possibly associated with congenital skeletal dysplasia, it is questionable whether it still can be used as reference for Homo erectus. Recently, however, the presence of skeletal dysplasia has been refuted. Here, we present a morphologic and morphometric reanalysis of the assertion of idiopathic scoliosis. We demonstrate that unarticulated vertebral columns of non-scoliotic and scoliotic individuals can be distinguished based on the lateral deviation of the spinous process, lateral and sagittal wedging, vertebral body torsion, pedicle thickness asymmetry and asymmetry of the superior and inferior articular facet area. A principal component analysis of the overall asymmetry of all seven vertebral shap...

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Section: Discussionmentioning

confidence: 99%

Revisiting scoliosis in the KNM-WT 15000 Homo erectus skeleton

Schiess¹,

Boeni²,

Rühli³

et al. 2014

Journal of Human Evolution

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“…Importantly, there is now increasing evidence to support a role for abnormal spinal bone tissue as a primary intrinsic driver of AIS pathogenesis and a key determinant of curve progression [12,15]. It is has previously been reported that AIS patients exhibit lower lumbar spine bone mineral density (LSBMD) [9,10,55] and altered vertebral growth [9,10,29], resulting in disparity between the growth of anterior and posterior vertebrae, resulting in rotational lordosis.…”

Section: Intrinsic Factors Of the Ais Spinal Musculoskeletal System Smentioning

confidence: 99%

“…The consensus is therefore that AIS is a multifactorial disease [12], with increasing evidence from genetic studies for the central role of intrinsic factors in contributing to its pathology and progression. Ultimately, clarifying the molecular basis for these pathogenic drivers will facilitate the development of pharmacological therapeutics.…”

Section: Introductionmentioning

confidence: 99%

Adolescent idiopathic scoliosis: evidence for intrinsic factors driving aetiology and progression

Ede

Jones

2016

International Orthopaedics (SICOT)

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Adolescent idiopathic scoliosis (AIS) is now considered to be a multifactorial heterogeneous disease, with recent genomic studies supporting the role of intrinsic factors in contributing to the onset of disease pathology and curve progression. Understanding the key molecular signalling pathways by which these intrinsic factors mediate AIS pathology may facilitate the development of pharmacological therapeutics and the identification of predictive markers of progression. The heterogenic nature of AIS has implicated multiple tissue types in the disease pathophysiology, including spinal bone, intervertebral disc and paraspinal muscles. In this review, we highlight some of the mechanisms and intrinsic molecular regulators within these different tissue types and review the evidence for their involvement in AIS pathology.

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“…However, the etiopathogeny is still unclear, largely due to its multifactorial origin (Weinstein et al, 2008). While a clear genetic basis is lacking so far (Miller, 2007), AIS is correlated in part with abnormal levels of tyrosine, sex and growth hormones, dysfunction of the melatonin-signaling pathway, and calcium-binding receptor protein calmodulin (Ahn et al, 2002;Moreau et al, 2004;Azeddine et al, 2007;Cheung et al, 2008). These biochemical abnormalities, however, might be more related to the progression rather than the origin of AIS (Kindsfater et al, 1994;Machida et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Vestibular Asymmetry as the Cause of Idiopathic Scoliosis: A Possible Answer fromXenopus

Lambert¹,

Malinvaud²,

Glaunès

et al. 2009

J. Neurosci.

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Human idiopathic scoliosis is characterized by severe deformations of the spine and skeleton. The occurrence of vestibular-related deficits in these patients is well established but it is unclear whether a vestibular pathology is the common cause for the scoliotic syndrome and the gaze/posture deficits or if the latter behavioral deficits are a consequence of the scoliotic deformations. A possible vestibular origin was tested in the frog Xenopus laevis by unilateral removal of the labyrinthine endorgans at larval stages. After metamorphosis into young adult frogs, X-ray images and three-dimensional reconstructed micro-computer tomographic scans of the skeleton showed deformations similar to those of scoliotic patients. The skeletal distortions consisted of a curvature of the spine in the frontal and sagittal plane, a transverse rotation along the body axis and substantial deformations of all vertebrae. In terrestrial vertebrates, the initial postural syndrome after unilateral labyrinthectomy recovers over time and requires body weight-supporting limb proprioceptive information. In an aquatic environment, however, this information is absent. Hence, the lesion-induced asymmetric activity in descending spinal pathways and the resulting asymmetric muscular tonus persists. As a consequence the mostly cartilaginous skeleton of the frog tadpoles progressively deforms. Lack of limb proprioceptive signals in an aquatic environment is thus the element, which links the Xenopus model with human scoliosis because a comparable situation occurs during gestation in utero. A permanently imbalanced activity in descending locomotor/posture control pathways might be the common origin for the observed structural and behavioral deficits in humans as in the different animal models of scoliosis.

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Recent advances in the aetiology of adolescent idiopathic scoliosis

Cited by 61 publications

References 57 publications

Revisiting scoliosis in the KNM-WT 15000 Homo erectus skeleton

Revisiting scoliosis in the KNM-WT 15000 Homo erectus skeleton

Adolescent idiopathic scoliosis: evidence for intrinsic factors driving aetiology and progression

Vestibular Asymmetry as the Cause of Idiopathic Scoliosis: A Possible Answer fromXenopus

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