Cause of Idiopathic Scoliosis (original) (raw)
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Etiology of Idiopathic Scoliosis: Current Trends in Research*
The Journal of Bone and Joint Surgery-American Volume, 2000
Current population studies characterize idiopathic scoliosis as a single-gene disorder that follows the patterns of mendelian genetics, including variable penetrance and heterogeneity. The role of melatonin and calmodulin in the development of idiopathic scoliosis is likely secondary, with indirect effects on growth mechanisms. Reported abnormalities of connective tissue, skeletal muscle, platelets, the spinal column, and the rib cage are all thought to be secondary to the deformity itself. Although no consistent neurological abnormalities have been identified in patients with idiopathic scoliosis, it is possible that a defect in processing by the central nervous system affects the growing spine. The true etiology of idiopathic scoliosis remains unknown; however, it appears to be multifactorial. *No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study. †Woodridge Orthopaedic and Spine Center,
European Spine Journal, 2004
There is no generally accepted scientific theory for the etiology of idiopathic scoliosis. As part of its mission to widen understanding of scoliosis etiology, the International Federated Body on Scoliosis Etiology (IBSE) introduced the electronic focus group (EFG) as a means of increasing debate of extant knowledge on important topics. This has been designated as an on-line Delphi discussion. The text for this EFG was written by Professor Thomas G Lowe MD and drawn from research carried out by himself and his coworkers on platelet calmodulin levels in patients with adolescent idiopathic scoliosis. To explain the relationship of platelet calmodulin levels to scoliosis curve changes in AIS brought about spontaneously, by brace treatment, or surgery Dr Lowe attributes the platelet calmodulin changes to paraspinous muscle activity and suggests that the calmodulin acts as a systemic mediator of tissues having a contractile system (actin and myosin). Controversy includes: 1) the lack of normal data and the large variability in baseline levels of platelet calmodulin, necessitating the use of the AIS subjects as their own controls; 2) calmodulin is not usually used as a marker of platelet activation; 3) whether the platelet calmodulin changes which appear to reflect an abnormality of a portion of the spine are related to local and/or regional changes in muscles, nervous system, or immature vertebrae. What is not controversial is the need for more research on platelets and the immature deforming skeleton in relation to etiology and prognosis.
European Spine Journal, 2012
Objective The purpose of this review is to elucidate the metabolic processes involved in the pathogenesis of adolescent idiopathic scoliosis (AIS) in light of research by the present authors as well as current literature. Methods Pathogenetic mechanisms involved in AIS were modeled as (a) a form of neuromuscular scoliosis (in conjunction with an adverse mechanical environment such as bipedality), in which hormonal and other chemical factors act as regulators of skeletal muscle tone and function; (b) as a consequence of an abnormality in growth of the spinal column (in conjunction with an adverse mechanical environment such as bipedality), in which hormones and other chemical factors act as regulators of growth; and (c) as a mechanical failure of one side of the vertebral column due to a defect in trabecular formation or mineralization (in conjunction with an adverse mechanical environment such as bipedality); in which hormonal and other chemical factors act as regulators of bone formation, mineralization and/or resorption. Results and conclusion Current evidence supporting these models individually or in combination is discussed. Keywords Adolescent idiopathic scoliosis Á Melatonin Á Calmodulin Á Estrogen Á Bipedality The etiology of adolescent ''idiopathic'' scoliosis remains unresolved Idiopathic scoliosis is a deformity of the torso that involves all three planes of the body and is associated with lateral deviation and axial rotation of the involved segments as well as substantial lordosis if located in the thoracic spine. Infantile and juvenile/adolescent idiopathic scoliosis (AIS) need to be distinguished, because they are likely to be distinct entities. Henceforward, the term 'idiopathic'' scoliosis is going to be used to define specifically AIS. The search for an etiology of AIS may sound like an oxymoron. However, to the best of our knowledge, idiopathic scoliosis is probably not as ''idiopathic'' as previously considered. Starting in the late 1960s, substantial research efforts have been directed to investigate possible mechanisms, none of which explain all the different facets of this complex disease. A detailed overview of this E. Acaroglu (&)
Etiology and pathogenesis of adolescent idiopathic scoliosis
Seminars in Spine Surgery, 2015
Despite many years of dedicated research into the etio-pathogenesis, not one single cause for adolescent idiopathic scoliosis has been identified. The purpose of this review is to give a comprehensive overview of the current evidence and main etiological theories. Intrinsic causal mechanisms are found in the alignment of the upright human spino-pelvic complex and growth patterns of the immature spine. Studies on potential extrinsic mechanisms are mainly focused on neuromuscular, metabolic and genetic etiological pathways. We can conclude that scoliosis is the spine's preconditioned response to a multitude of offenses that lead to a disturbance of the delicate human rotational spino-pelvic balance during growth.
Pathogenesis of Idiopathic Scoliosis
Spine, 1999
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Scoliosis, 2013
This paper aims to integrate into current understanding of AIS causation, etiopathogenetic information presented at two Meetings during 2012 namely, the International Research Society of Spinal Deformities (IRSSD) and the Scoliosis Research Society (SRS). The ultimate hope is to prevent the occurrence or progression of the spinal deformity of AIS with non-invasive treatment, possibly medical. This might be attained by personalised polymechanistic preventive therapy targeting the appropriate etiology and/or etiopathogenetic pathways, to avoid fusion and maintain spinal mobility. Although considerable progress had been made in the past two decades in understanding the etiopathogenesis of adolescent idiopathic scoliosis (AIS), it still lacks an agreed theory of etiopathogenesis. One problem may be that AIS results not from one cause, but several that interact with various genetic predisposing factors. There is a view there are two other pathogenic processes for idiopathic scoliosis namely, initiating (or inducing), and those that cause curve progression. Twin studies and observations of family aggregation have revealed significant genetic contributions to idiopathic scoliosis, that place AIS among other common disease or complex traits with a high heritability interpreted by the genetic variant hypothesis of disease. We summarize etiopathogenetic knowledge of AIS as theories of pathogenesis including recent multiple concepts, and blood tests for AIS based on predictive biomarkers and genetic variants that signify disease risk. There is increasing evidence for the possibility of an underlying neurological disorder for AIS, research which holds promise. Like brain research, most AIS workers focus on their own corner and there is a need for greater integration of research effort. Epigenetics, a relatively recent field, evaluates factors concerned with gene expression in relation to environment, disease, normal development and aging, with a complex regulation across the genome during the first decade of life. Research on the role of environmental factors, epigenetics and chronic non-communicable diseases (NCDs) including adiposity, after a slow start, has exploded in the last decade. Not so for AIS research and the environment where, except for monozygotic twin studies, there are only sporadic reports to suggest that environmental factors are at work in etiology. Here, we examine epigenetic concepts as they may relate to human development, normal life history phases and AIS pathogenesis. Although AIS is not regarded as an NCD, like them, it is associated with whole organism metabolic phenomena, including lower body mass index, lower circulating leptin levels and other systemic disorders. Some epigenetic research applied to Silver-Russell syndrome and adiposity is examined, from which suggestions are made for consideration of AIS epigenetic research, cross-sectional and longitudinal. The word scoliogeny is suggested to include etiology, pathogenesis and pathomechanism.
Etiological Theories of Adolescent Idiopathic Scoliosis: Past and Present
The open orthopaedics journal, 2017
Adolescent idiopathic scoliosis is one of the most common spinal deformities, yet its cause is unknown. Various theories look to biomechanical, neuromuscular, genetic, and environmental origins, yet our understanding of scoliosis etiology is still limited. Determining the cause of a disease is crucial to developing the most effective treatment. Associations made with scoliosis do not necessarily point to causality, and it is difficult to determine whether said associations are primary (playing a role in development) or secondary (develop as a result of scoliosis). Scoliosis is a complex condition with highly variable expression, even among family members, and likely has many causes. These causes could be similar among homogenous groups of AIS patients, or they could be individual. Here, we review the most prevalent theories of scoliosis etiology and recent trends in research.