Evidence map›Paper›PMID 37042139›Full record

ArticleBeijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences2023

[Pathologic features of paraspinal muscle biopsies in patients with adolescent idiopathic scoliosis].

D F Zheng, J Y Li, J X Li, Y S Zhang, Y F Zhong, M Yu

Open access · greenAbstract readEnglish Abstract
In one paragraph

Article in Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

D F ZhengDepartment of Pathology, School of Basic Medical Sciences Peking University/Peking University Third Hospital, Beijing 100191, China.
J Y LiDepartmant of Orthopaedics, Peking University Third Hospital, Beijing 100191, China.
J X LiSchool of Basic Medical Sciences, Peking University, Beijing 100191, China.
Y S ZhangDepartmant of Neurology, Peking University Third Hospital, Beijing 100191, China.
Y F ZhongDepartment of Pathology, School of Basic Medical Sciences Peking University/Peking University Third Hospital, Beijing 100191, China.
M YuDepartmant of Orthopaedics, Peking University Third Hospital, Beijing 100191, China.
Peking University Third Hospital · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo characterize the paraspinal muscles of adolescent idiopathic scoliosis (AIS) patients, and to further explore its etiology.

methodsClinical records and paraspinal muscle biopsies at the apex vertebra region during posterior scoliosis correction surgery of 18 AIS were collected from November 2018 to August 2019. Following standardized processing of fresh muscle tissue biopsy, serial sections with conventional hematoxylin-eosin (HE) and histochemical and immunohistochemical (IHC) with antibody Dystrophin-1 (R-domain), Dystrophin-2 (C-terminal), Dystrophin-3 (N-terminal), Dystrophin-total, Myosin (fast), major histocompatibility complex 1 (MHC-1), CD4, CD8, CD20, and CD68 staining were obtained. Biopsy samples were grouped according to the subjects' median Cobb angle (Cobb angle ≥ 55° as severe AIS group and Cobb angle < 55° as mild AIS group) and Nash-Moe's classification respectively, and the corresponding pathological changes were compared between the groups statistically.

resultsAmong the 18 AIS patients, 8 were in the severe AIS group (Cobb angle ≥55°) and 10 in the mild AIS group (Cobb angle < 55°). Both severe and mild AIS groups presented various of atrophy and degeneration of paraspinal muscles, varying degrees and staining patterns of immune-expression of Dystrophin-3 loss, especially Dystrophin-2 loss in severe AIS group with significant differences, as well as among the Nash-Moe classification subgroups. Besides, infiltration of CD4

conclusionThe histologic of paraspinal muscle biopsy in AIS had similar characteristic changes, the expression of Dystrophin protein was significantly reduced and correlated with the severity of scoliosis, suggesting that Dystrophin protein dysfunctions might contribute to the development of scoliosis. Meanwhile, the inflammatory changes of AIS were mainly manifested by T cell infiltration, and there seemed to be a certain correlation between inflammatory cell infiltration, MHC-1 expression and abnormal expression of Dystrophin. Further research along the lines of this result may open up new ideas for the diagnosis of scoliosis and the treatment of paraspinal myopathy.

Indexed as

KyphosisNon-alcoholic Fatty Liver DiseaseScoliosisAdolescentBiopsyDystrophinHumansParaspinal MusclesDystrophinAdolescentBiopsyDystrophin proteinParaspinal musclesScoliosis

Identifiers

PMID37042139
PMCPMC10091240
OpenAlexW4365135866

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.