Background: There is growing interest in identifying predictors of large scoliosis curves at initial presentation, but few data to guide such preventive efforts. The association of neighborhood socioeconomic deprivation with curve magnitude in this context has not been previously evaluated. The purpose of our study was to determine the correlation of socioeconomic deprivation with scoliosis curve magnitude at initial presentation. Secondarily, we assessed the correlation of body mass index (BMI) with curve severity. Methods: We retrospectively identified 202 patients presenting with adolescent idiopathic scoliosis to a single tertiary care center in Massachusetts from January 2015 to August 2018. The Area Deprivation Index (ADI), a validated composite measure of neighborhood socioeconomic deprivation, was calculated for each patient. Curve magnitude, age, sex, BMI, race, and insurance status were recorded. Pearson correlation was used to determine the association of the ADI and BMI with scoliosis severity.Results: There was no correlation between the ADI and the magnitude of scoliosis at presentation (r = 0.055; P = 0.43). Greater BMI was moderately correlated with increased scoliosis curve magnitude (r = 0.28; P < 0.001). There was no association between curve magnitude and patient age, sex, race, or insurance status. Conclusions: The finding that neighborhood socioeconomic deprivation did not correlate with greater scoliosis severity at presentation may be suggestive of equitable access to specialized scoliosis care. Future research should determine whether this reassuring finding is unique to Massachusetts--a state with high rates of health insurance coverage--or generalizable to other US states. In addition, our study further corroborates the notion that greater BMI is associated with larger scoliosis curves, and calls for targeted interventions to facilitate early scoliosis detection in the growing childhood obese population. Level of Evidence: Level II-prognostic study and retrospective study.

Post natal bone repair elicits a regenerative mechanism that restores the injured tissue to its pre-injury cellular composition and structure and is believed to recapitulate the embryological processes of bone formation. Prior studies showed that Nanog, a central epigenetic regulator associated with the maintenance of embryonic stem cells (ESC) was transiently expressed during fracture healing, Bais et al., 2009 [1]. In this study, we show that murine bone marrow stromal cells (MSCs) before they are induced to undergo osteogenic differentiation express ~50× the background levels of Nanog seen in murine embryonic fibroblasts (MEFs) and the W20-17 murine marrow stromal cell line stably expresses Nanog at ~80× the MEF levels. Nanog expression in this cell line was inhibited by BMP7 treatment and Nanog lentivrial shRNA knockdown induced the expression of the terminal osteogenic gene osteocalcin. Lentivrial shRNA knockdown or lentiviral overexpression of Nanog in bone MSCs had inverse effects on proliferation, with knockdown decreasing and overexpression increasing MSC cell proliferation. Surgical marrow ablation of mouse tibia by medullary reaming led to a ~3 fold increase in Nanog that preceded osteogenic differentiation during intramembranous bone formation. Lentiviral shRNA knockdown of Nanog after surgical ablation led to an initial overexpression of osteogenic gene expression with no initial effect on bone formation but during subsequent remodeling of the newly formed bone a ~50% decrease was seen in the expression of terminal osteogenic gene expression and ã50% loss in trabecular bone mass. This loss of bone mass was accompanied by an increased ~2–5 fold adipogenic gene expression and observed increase of fat cells in the marrow space. In summary these data show that Nanog is expressed during surgically induced marrow bone formation and is functionally involved in post natal marrow stromal cell maintenance and differentiation.

Therapeutic Level IV. See Instructions for Authors for a complete description of levels of evidence.