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      Research progress on the etiology and pathogenesis of adolescent idiopathic scoliosis

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          Abstract

          Etiology of adolescent idiopathic scoliosis (AIS), a complicated three-dimensional spinal deformity with early-onset, receives continuous attention but remains unclear. To gain an insight into AIS pathogenesis, this review searched PubMed database up to June 2019, using key words or medical subject headings terms including “adolescent idiopathic scoliosis,” “scoliosis,” “pathogenesis,” “etiology,” “genetics,” “mesenchymal stem cells,” and their combinations, summarized existing literatures and categorized the theories or hypothesis into nine aspects. These aspects include bone marrow mesenchymal stem cell studies, genetic studies, tissue analysis, spine biomechanics measurements, neurologic analysis, hormone studies, biochemical analysis, environmental factor analysis, and lifestyle explorations. These categories could be a guidance for further etiology or treatment researches to gain inspiration.

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          Epidemiology of adolescent idiopathic scoliosis.

          Markus Rafael Konieczny, Hüsseyin Senyurt, Rüdiger Krauspe (2013)
          Adolescent idiopathic scoliosis is a common disease with an overall prevalence of 0.47-5.2 % in the current literature. The female to male ratio ranges from 1.5:1 to 3:1 and increases substantially with increasing age. In particular, the prevalence of curves with higher Cobb angles is substantially higher in girls than in boys: The female to male ratio rises from 1.4:1 in curves from 10° to 20° up to 7.2:1 in curves >40°. Curve pattern and prevalence of scoliosis is not only influenced by gender, but also by genetic factors and age of onset. These data obtained from school screening programs have to be interpreted with caution, since methods and cohorts of the different studies are not comparable as age groups of the cohorts and diagnostic criteria differ substantially. We do need data from studies with clear standards of diagnostic criteria and study protocols that are comparable to each other.
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            Mechanisms for fiber-type specificity of skeletal muscle atrophy.

            Jeffrey E. Pessin, Yichen Wang (2013)
            There are a variety of pathophysiologic conditions that are known to induce skeletal muscle atrophy. However, muscle wasting can occur through multiple distinct signaling pathways with differential sensitivity between selective skeletal muscle fiber subtypes. This review summarizes some of the underlying molecular mechanisms responsible for fiber-specific muscle mass regulation. Peroxisome proliferator-activated receptor gamma coactivator 1-alpha protects slow-twitch oxidative fibers from denervation/immobilization (disuse)-induced muscle atrophies. Nutrient-related muscle atrophies, such as those induced by cancer cachexia, sepsis, chronic heart failure, or diabetes, are largely restricted to fast-twitch glycolytic fibers, of which the underlying mechanism is usually related to abnormality of protein degradation, including proteasomal and lysosomal pathways. In contrast, nuclear factor kappaB activation apparently serves a dual function by inducing both fast-twitch fiber atrophy and slow-twitch fiber degeneration. Fast-twitch glycolytic fibers are more vulnerable than slow-twitch oxidative fibers under a variety of atrophic conditions related to signaling transduction of Forkhead box O family, autophagy inhibition, transforming growth factor beta family, and nuclear factor-kappaB. The resistance of oxidative fibers may result from the protection of peroxisome proliferator-activated receptor gamma coactivator 1-alpha.
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              The effects of endurance, strength, and power training on muscle fiber type shifting.

              James R M Wilson, Michael C. Zourdos, Jeong Kim … (2012)
              Muscle fibers are generally fractionated into type I, IIA, and IIX fibers. Type I fibers specialize in long duration contractile activities and are found in abundance in elite endurance athletes. Conversely type IIA and IIX fibers facilitate short-duration anaerobic activities and are proportionally higher in elite strength and power athletes. A central area of interest concerns the capacity of training to increase or decrease fiber types to enhance high-performance activities. Although interconversions between type IIA and IIX are well recognized in the literature, there are conflicting studies regarding the capacity of type I and II fibers to interconvert. Therefore, the purpose of this article is to analyze the effects of various forms of exercise on type I and type II interconversions. Possible variables that may increase type II fibers and decrease type I fibers are discussed, and these include high velocity isokinetic contractions; ballistic movements such as bench press throws and sprints. Conversely, a shift from type II to type I fibers may occur under longer duration, higher volume endurance type events. Special care is taken to provide practical applications for both the scientist and the athlete.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Chin Med J (Engl)
                Journal ID (iso-abbrev): Chin. Med. J
                Journal ID (publisher-id): CM9
                Title: Chinese Medical Journal
                Publisher: Wolters Kluwer Health
                ISSN (Print): 0366-6999
                ISSN (Electronic): 2542-5641
                Publication date (Print): 20 February 2020
                Publication date (Electronic): 20 February 2020
                Volume: 133
                Issue: 4
                Pages: 483-493
                Affiliations
                Department of Orthopedics, Peking Union Medical College Hospital, Beijing 100730, China.
                Author notes
                Correspondence to: Dr. Qian-Yu Zhuang, Peking Union Medical College Hospital, 1 Shuai Fu Yuan, Beijing 100730, ChinaE-Mail: zhuangqianyu@ 123456126.com
                Article
                Publisher ID: CMJ-2019-1250
                DOI: 10.1097/CM9.0000000000000652
                PMC ID: 7046244
                PubMed ID: 31972723
                SO-VID: 9af13f03-a629-4065-a966-d5d086d0e952
                Copyright © Copyright © 2020 The Chinese Medical Association, produced by Wolters Kluwer, Inc. under the CC-BY-NC-ND license.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0

                History
                Date received : 04 August 2019
                Categories
                Subject: Review Articles
                Custom metadata
                OPEN-ACCESS TRUE

                Keywords: scoliosis,pathogenesis,etiology,mesenchymal stem cells
                Data availability:
                Keywords: scoliosis, pathogenesis, etiology, mesenchymal stem cells

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