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Updated: Jun 14, 2026

Cell-based Assay Protocol for the Prognostic Prediction of Idiopathic Scoliosis Using Cellular Dielectric Spectroscopy
Published on: October 16, 2013
Exploring the potential relationships between idiopathic scoliosis and various multifactorial diseases: a systematic
Kenney Ki Lee Lau1, Karlen Ka Pui Law2, Owen O Man Kam3
1Department of Orthopaedics and Traumatology, The University of Hong Kong, Pok Fu Lam, Hong Kong. kenneykl@connect.hku.hk.
Background:
Although the etiology of adolescent idiopathic scoliosis (AIS) remains largely elusive, it is widely recognized as a multifactorial condition shaped by both genetic predispositions and environmental influences. This review seeks to explore the intricate relationships between idiopathic scoliosis and its associated comorbidities, with the goal of advancing our understanding of this multifaceted disorder.
Methods:
Primary studies involving human subjects diagnosed with idiopathic scoliosis and presenting comorbid conditions were included. Six online databases (AMED, CENTRAL, CINAHL, EMBASE, MEDLINE, and WOS) were systematically searched. Two reviewers independently screened citations and extracted data. Studies were categorized based on commonly examined diagnoses, and outcome measures were descriptively reported.
Results:
Our search yielded 1185 citations, with 9 studies meeting the eligibility after screening. These studies examined comorbidities involving conditions like malocclusion, central precocious puberty (CPP), gingival diseases, malignant hematopoietic neoplasms (MHN), temporomandibular joint disorders (TMD), and functional gastrointestinal disorders (FGD). Significant associations were found between AIS and these multifactorial disorders, including dental anomalies (i.e., asymmetrical canine, midline deviations, crossbites, overbite, multiple malocclusion, gingivitis, distocclusion, asymmetric molar occlusion, maxillary overjet, crowding, and reverse chewing cycles), digestive issues (i.e., FGD), endocrine disruptions (i.e., CPP), musculoskeletal imbalances (i.e., reduced masseter muscle volume, higher Fonseca Anamnestic Index score, and greater Helkimo Clinical Dysfunction Index score), and oncological conditions (i.e., MHN).
Conclusion:
We have presented the multifactorial and potential systemic nature of AIS by revealing its associations with comorbid conditions. These relationships may indicate shared genetic, hormonal, neuromuscular, and immunological pathways.
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