Superior displacement of the inflexion point does not predict proximal junctional kyphosis after fusion for adult spinal deformity

Introduction

Despite increasing utilization and demonstrated improvements in clinical outcomes (1), adult spinal deformity (ASD) surgery remains associated with high complication rates, with proximal junctional kyphosis (PJK) representing one of the most prevalent modes of failure (2-4). PJK is characterized by progressive structural deterioration immediately proximal to the upper instrumented vertebra (UIV) and typically develops within months to years following the index procedure. Its onset frequently necessitates revision surgery with extension of the fusion construct, exposing patients to greater operative risk, prolonged recovery, and increased psychological burden (5).

Extensive work has examined radiographic and procedural contributors to PJK, including screw trajectory (6), construct length (7), and degree of correction (8). Yet a key determinant of postoperative sagittal mechanics remains insufficiently explored: the sagittal balance inflection point. The inflection point, marking the transition between lumbar lordosis and thoracic kyphosis, represents a mechanically sensitive region where bending moments redistribute to maintain global alignment (9). After deformity correction and long-segment fusion, distal rigidity limits compensatory motion, often producing a relative superior migration of this transition as proximal segments assume greater balance demands. Superior displacement may shift moment transfer toward proximal junctional levels, increasing angular and ligamentous stresses in the proximal thoracic spine, a region with limited adaptive capacity. This stress concentration provides a plausible biomechanical pathway for junctional failure and the development of PJK. Although inflection point displacement has been associated with altered postoperative force distribution (10,11), its mechanistic role in PJK pathogenesis remains insufficiently defined (11). From a biomechanical perspective, superior displacement of the inflection point may shift loads proximally, increasing mechanical stress at adjacent segments and predisposing them to accelerated degeneration (9). Viewed through this framework, the inflection point represents a potentially modifiable risk factor for PJK.

Accordingly, the objective of this study is to determine whether superior displacement of the sagittal balance inflection point is associated with increased incidence of PJK in patients with ASD undergoing posterior instrumented fusion from L2 or above to the pelvis. Establishing this relationship may introduce a new alignment parameter for operative planning. If inflection point displacement contributes to PJK risk, strategies to preserve transition architecture may reduce revision rates, improve long-term outcomes, and lower the clinical and economic burden associated with ASD surgery. We present this article in accordance with the STROBE reporting checklist (available at https://jss.amegroups.com/article/view/10.21037/jss-2026-1-0010/rc).

Methods

Study design and patient selection

This study was conducted as a single-center retrospective cohort analysis at a large academic institution. Patients were recruited from the Brain and Spine Neurosurgery Department at the University of South Florida and Tampa General Hospital. All consecutive patients who underwent posterior spinal fusion for ASD between 2017 and 2024 were screened for inclusion. Eligible patients were required to have undergone fusion extending from L2 or above to the pelvis for ASD correction, including both patients with and without prior spinal instrumentation. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the Institutional Review Board at the University of South Florida (No. Pro00023643). The requirement for informed consent was waived due to the retrospective nature of the study and use of de-identified data.

Inclusion required the availability of complete standing preoperative and postoperative full-length scoliosis radiographs and a minimum radiographic follow-up of 12 months. Patients were excluded if postoperative imaging was incomplete, unavailable, or did not meet the minimum follow-up requirement. Only patients with sufficient radiographic data to assess postoperative junctional changes were included in the final analysis. Of the patients initially identified, 85 were excluded due to incomplete data or lost to follow-up.

The diagnosis of PJK was determined radiographically, and the minimum 12-month follow-up period was calculated from the time of the index surgery. Patients who underwent revision or other reoperation prior to the 12-month time point were not excluded from the analysis. The diagnosis of PJK was determined according to the follow-up interval measured from the index surgery, and the occurrence of revision did not reset the timeline for PJK assessment. Revision events were recorded and are reported in Table 1. Preoperative and postoperative standing scoliosis radiographs were reviewed to identify the thoracolumbar inflection point and to measure spinopelvic parameters, including pelvic incidence (PI), pelvic incidence-lumbar lordosis mismatch (PI-LL), sagittal vertical axis (SVA), pelvic tilt (PT), sacral slope (SS), and lumbar lordosis (LL), using Surgimap (version 20; Nemaris Inc., New York, NY).

Data collection and variable definitions

Data were extracted from electronic medical records, operative reports, and follow-up documentation. To reduce selection bias, consecutive patients meeting predefined inclusion and exclusion criteria during the study period were included. Standardized radiographic definitions and measurement protocols were applied to minimize measurement variability. Prior fusion was defined as any previous spine surgery requiring instrumentation at a thoracic or lumbar segment.

PJK was assessed radiographically at follow-up visits occurring ≥12 months postoperatively and was defined as a postoperative increase of >10° in the Cobb angle measured between the UIV and UIV + 1, consistent with established criteria (12). The definition was based solely on radiographic findings and did not incorporate clinical symptoms. Patients were classified into PJK and non-PJK groups based on this definition.

The thoracolumbar inflection point was defined in Surgimap as the vertebral level at which sagittal curvature transitions from thoracic kyphosis to lumbar lordosis on standing lateral radiographs, identified by a change in the direction of the segmental Cobb angle (i.e., reversal from kyphotic to lordotic alignment) (Figure 1).

Figure 1 Thoracolumbar inflection point on standing lateral radiograph. The thoracolumbar inflection point (green) marks the transition between thoracic kyphosis (yellow) and lumbar lordosis (blue), representing the vertebral level where sagittal curvature changes direction. L, lumbar; T, thoracic.

Superior displacement was defined as a postoperative cranial shift of ≥1 vertebral level of the thoracolumbar inflection point relative to its preoperative location. For analytic purposes, displacement was categorized as 0–3+ vertebral levels and further grouped as 1-level and >1-level shifts.

Radiographic variables included apex displacement >1 level and spinopelvic parameters (PI, PT, PI-LL mismatch, SVA, LL, and SS). Pre-post changes (Δ) in these parameters were calculated. Baseline radiographic parameters were analyzed as continuous variables (per-unit increase) in regression models. PI was stratified a priori using a clinically established threshold of 55°, categorizing patients as low PI (<55°) or high PI (≥55°) based on preoperative measurements (12,13).

Apex displacement was defined as a postoperative cranial shift of the sagittal apex by greater than one vertebral level relative to its preoperative position and was analyzed as a binary variable (>1-level vs. ≤1-level).

Clinical covariates included age, sex, body mass index (BMI), frailty score, and prior fusion. Frailty was assessed using the Modified Frailty Index-11 (MFI-11) (14). Comorbidities included congestive heart failure (CHF), chronic obstructive pulmonary disease (COPD), diabetes mellitus, hypertension, myocardial infarction, peripheral vascular disease, cerebrovascular disease (including transient ischemic attack or stroke without residual deficit), impaired sensorium, and osteoporosis.

Statistical analysis

The association between superior displacement of the thoracolumbar inflection point and PJK was evaluated using logistic regression, with PJK specified as a binary outcome.

Superior inflection-point displacement was evaluated both categorically (>1 vertebral level) and continuously (per vertebral level increase) to assess potential dose-response effects. Univariable logistic regression models were first performed to estimate crude associations across subgroups and patient factors. Additional univariable logistic regression models evaluated individual clinical covariates (age, sex, BMI, osteoporosis, frailty, and prior fusion) to estimate their associations with PJK.

Multivariable logistic regression modeling was performed using a staged approach: (I) a clinical-only model (age, sex, BMI, osteoporosis, frailty score, prior fusion) was first constructed; (II) an expanded comorbidity-adjusted model retained superior displacement and all variables from the clinical-only model and additionally incorporated patient comorbidities; (III) a combined clinical-mechanical model incorporated superior inflection displacement (>1 level) and apex displacement (>1 level) with clinical covariates; (IV) a fully adjusted comprehensive model included superior displacement, radiographic change parameters (ΔSS, ΔLL, ΔPI-LL), and a prespecified reduced clinical covariate set (age, sex, BMI, diabetes mellitus, CHF, myocardial infarction, frailty, osteoporosis, and prior fusion) to limit overparameterization given the available number of outcome events. Odds ratios (ORs) with 95% confidence intervals (CIs) and regression coefficients (β) were reported.

Interaction terms were formally tested to evaluate potential effect modification between superior displacement and (I) prior fusion status; (II) UIV region (upper, middle, and lower thoracic spine); (III) whether the inflection point was located within versus outside the instrumented construct; and (IV) age. Stratified subgroup analyses were performed accordingly. A secondary analysis was performed in a restricted cohort of patients who developed radiographic PJK at follow-up, as defined by the prespecified radiographic criteria, to evaluate associations within this subset. When significant interactions were identified, stratified analyses were performed and regression coefficients (β) were reported to describe the directionality of the effect. Stratified analyses were also performed within predefined low- and high-PI cohorts to evaluate the association between superior displacement and PJK across pelvic morphology strata. Model discrimination was assessed using the area under the curve (AUC), and calibration was evaluated using the Brier score. The incremental predictive contribution of superior displacement beyond clinical covariates was assessed by the change in discrimination (ΔAUC) and calibration (Brier score) relative to the base clinical model. Variance inflation factors (VIFs) were calculated to assess multicollinearity, and events-per-variable (EPV) were computed to evaluate model stability.

Missing covariate data were handled using complete-case analysis at the model level; no imputation was performed. As a result, sample size and event counts varied across models depending on covariate availability. Statistical significance was defined as P<0.05. All analyses were conducted using Python (version 3.12).

Results

Patient characteristics

The cohort comprised 250 adult patients undergoing corrective spinal surgery (Table 1).

Incidence of PJK

Incidence of PJK was comparable between patients with versus without superior inflection point displacement >1 level (35.8% vs. 34.5%). Patients with prior fusion demonstrated significantly higher rates of PJK compared with fusion-naïve individuals (42.1% vs. 30.3%, P=0.04).

Association between superior displacement and PJK

Superior inflection-point displacement greater than one vertebral level was not significantly associated with PJK (OR =1.22, P=0.55). Similar null findings were observed when alternative categorical definitions of displacement were evaluated. Apex displacement greater than one vertebral level likewise demonstrated no significant association with postoperative PJK, and simultaneous inclusion of superior and apex displacement demonstrated no combined effect.

Radiographic parameters and radiographic change (Δ) analyses

In univariable logistic regression analyses of baseline radiographic parameters, baseline PT (P=0.62), PI (P=0.07), LL (P=0.48), PI-LL mismatch (P=0.28), and SVA (P=0.69) were not significantly associated with PJK, while baseline SS showed a statistically significant association (P=0.03). In univariable change-parameter models, ΔLL (P=0.02), ΔSS (P=0.02), and ΔPI-LL mismatch (P=0.005) were significantly associated with PJK, whereas ΔPT (P=0.12), ΔPI (P=0.52), and ΔSVA (P=0.83) were not. However, after multivariable adjustment, none of the radiographic change parameters remained independently associated with PJK (all P>0.05) (Table 2).

Subgroup and interaction analyses

Subgroup analyses evaluated the association between superior displacement and PJK across prior fusion status, upper versus mid versus lower thoracic UIV regions, and inflection point location relative to the construct. Across all strata, superior displacement was not significantly associated with PJK. Formal interaction testing between strata revealed no statistically significant interaction terms (all P>0.05, Table 3, Figure 2).

Figure 2 Stratified analysis of the association between superior inflection-point displacement and PJK across prior fusion status, UIV region, and inflection-point location. PJK, proximal junctional kyphosis; UIV, upper instrumented vertebra.

An age-by-displacement interaction was statistically significant (P=0.03), indicating that the association between displacement and PJK varied with advancing age. Stratified analyses by prior fusion status demonstrated opposing trends, with a positive association in previously fused patients (β=+0.44) and a negative association in fusion-naïve patients (β=−0.55), although neither reached statistical significance (Figure 3).

Figure 3 Predicted probability of PJK according to age and frailty across levels of superior inflection-point displacement. (A) Predicted probability of PJK across age stratified by displacement status, adjusted for frailty. (B) Predicted probability of PJK across frailty score stratified by displacement status, adjusted for age. PJK, proximal junctional kyphosis.

When stratified by PI using the predefined 55° threshold, superior displacement remained non-significant in both groups. In the low-PI cohort (<55°), the odds of PJK were similar between patients with and without inflection point displacement (OR =1.18). In the high-PI cohort (≥55°), inflection point displacement likewise was not associated with increased PJK risk (OR =1.05).

Multivariable modeling

Univariable logistic regression analyses were performed to evaluate associations between clinical and radiographic variables and the development of postoperative PJK. Frailty score and prior fusion demonstrated significant crude associations with PJK, whereas age, sex, BMI, and baseline radiographic parameters were not significantly associated.

In the clinical-only model, frailty score remained independently associated with PJK (β=+0.20, OR =1.22, P=0.04), while prior fusion also demonstrated a significant association (β=−0.63, OR =0.54, P=0.04). Age, sex, and BMI were not significantly associated with PJK in this model.

Superior thoracolumbar inflection-point displacement was modeled continuously (per vertebral level increase), no significant association with postoperative PJK was observed (OR =1.12, 95% CI: 0.66–1.89, P=0.67), providing no evidence of a linear dose–response relationship. In the corresponding categorical analysis (>1 vertebral level), superior displacement likewise demonstrated no significant association with PJK (OR =1.00, 95% CI: 0.53–1.91, P=0.99).

In the combined clinical-mechanical model, superior displacement greater than one level (P=0.54) and apex displacement greater than one level (P=0.79) were not significantly associated with PJK. Frailty (P=0.03) and prior fusion (P=0.02) remained independently associated with PJK in this model.

The fully adjusted comprehensive model incorporated superior displacement, radiographic change parameters (ΔSS, ΔLL, ΔPI-LL), and a reduced set of clinical covariates. In this model, superior displacement was not independently associated with PJK (OR =1.286, 95% CI: 0.657–2.516, P=0.46). No covariate retained statistical significance after full adjustment, including frailty and prior fusion (Table 4).

A forest plot illustrating the adjusted ORs and confidence intervals for predictors in the fully adjusted model is shown in Figure 4.

Figure 4 Adjusted predictors of PJK. Forest plot of adjusted odds ratios for predictors of PJK in the expanded covariate multivariable logistic regression model. Points indicate adjusted odds ratios and horizontal bars indicate 95% confidence intervals. BMI, body mass index; CHF, congestive heart failure; COPD, chronic obstructive pulmonary disease; CVA, cerebrovascular accident; PJK, proximal junctional kyphosis; TIA, transient ischemic attack.

Model performance and diagnostics

Fully adjusted model demonstrated modest discriminative ability, with an area under the receiver operating characteristic curve of 0.691 and a Brier score of 0.205. Adding superior displacement to the base clinical model resulted in a negligible increase in discrimination (AUC increase of 0.003) and minimal change in calibration, indicating no meaningful incremental predictive value (Figure 5).

Figure 5 Predictive performance of clinical and inflection-point displacement models for PJK. Model performance with and without superior inflection-point displacement. (A) ROC curves comparing discrimination of the base clinical model, the extended model including displacement, and the fully adjusted model. (B) Calibration curves showing agreement between predicted and observed probabilities for each model. (C) NRI evaluating the incremental predictive contribution of displacement to the base clinical model. AUC, area under the curve; NRI, net reclassification improvement; PJK, proximal junctional kyphosis; ROC, receiver operating characteristic.

VIFs ranged from approximately 1.0 to 2.3, demonstrating no evidence of substantial multicollinearity. The complete-case fully adjusted model included 66 PJK events and 15 predictors, yielding an EPV ratio of 4.1, below conventional recommendations for logistic regression modeling and suggestive of potential model instability.

Discussion

The sagittal balance inflection point has been proposed as a moderator of postoperative load redistribution (15-17). Biomechanical models suggest that superior translation of this point after fusion may shift gravitational and muscular demands proximally, intensifying stress on the motion segments immediately above a long construct (18,19). Building on this premise, we hypothesized that superior displacement of the inflection point would be associated with the development of PJK.

This hypothesis was not supported. Superior inflection-point displacement was not significantly associated with PJK across any analytic framework. Incidence rates were similar between patients with and without displacement, and the association remained non-significant when displacement was modeled as a continuous variable, across subgroup analyses, and in interaction testing. Furthermore, adding displacement to multivariable models did not meaningfully change model discrimination or calibration. Taken together, these findings indicate that superior translation of the inflection point, as measured on static standing radiographs, does not appear to influence the occurrence of PJK in this cohort.

Alignment parameters demonstrated a similar pattern. ΔSS, ΔLL, and ΔPI-LL were associated with PJK in univariable analyses, but these relationships did not persist after multivariable adjustment. Baseline parameters were likewise not associated with PJK. While these alignment parameters may reflect aspects of postoperative sagittal correction, the present findings suggest that their independent association with junctional failure is limited once broader clinical and comorbidity factors are considered.

Subgroup and interaction analyses further reinforced the absence of a consistent relationship between inflection-point displacement and PJK. No meaningful interactions were identified between displacement and prior fusion status, UIV region, or inflection-point location relative to the construct. Although an age-by-displacement interaction reached statistical significance, stratified analyses did not demonstrate significant associations within age groups. As a result, this interaction likely reflects statistical variability rather than a reproducible biological relationship and should be interpreted cautiously.

Prior work has suggested that perturbation of sagittal transition architecture may influence postoperative mechanics and increase PJK incidence (11,20). The present analysis did not identify a stable independent association between inflection-point displacement and PJK after multivariable adjustment. These findings suggest that while sagittal transition geometry may influence postoperative biomechanics, superior displacement of the inflection point alone is insufficient to explain junctional failure.

Clinical covariates provided additional context. Frailty and prior fusion were associated with PJK in clinical-only and partially adjusted models, although these associations attenuated after full adjustment. Frailty increases with advancing age (21), and this substrate offers a plausible explanation for the age-dependent signal observed in the interaction analysis. Older or physiologically vulnerable patients may have reduced capacity to accommodate altered mechanical loading at the proximal junction following long-segment fusion. Prior fusion may exert a similar effect by limiting the number of remaining mobile segments available to absorb redistributed forces. However, because these associations did not persist in the fully adjusted model, these observations should be interpreted cautiously and likely reflect the broader multifactorial nature of junctional failure rather than isolated independent effects.

From a biomechanical perspective, the absence of an association with static inflection-point displacement does not necessarily exclude a role for sagittal transition mechanics in junctional failure. Spinal motion is governed by coupled, segment-dependent mechanics in which adjacent vertebrae collectively accommodate rotational and translational demands. Instrumented fusion alters this mechanical environment by constraining motion within the construct and redistributing load to adjacent mobile segments (22). As a result, the proximal junction may experience increased bending moments and shear stresses rather than isolated translational effects, mechanisms that have been implicated in models of junctional failure (23,24). Static radiographic measurements of inflection-point position may therefore incompletely capture the mechanical environment that ultimately contributes to PJK.

Future investigations may benefit from focusing on segmental and dynamic mechanics around the proximal junction rather than static positional metrics alone. Characterizing adjacent-segment rotation, motion patterns, or load-sharing behavior may provide a more comprehensive understanding of how sagittal transition architecture interacts with postoperative biomechanics to influence junctional stability.

Limitations

The retrospective, single-center design limits the generalizability of these findings, and the modest number of patients who developed PJK may have reduced the power to detect additional associations related to displacement. PJK outcomes were derived from institutional radiographic follow-up and therefore may not capture events that occurred outside the system. Larger multicenter prospective studies are needed to validate the relationship between inflection-point displacement and PJK and to determine if and how this parameter can be incorporated into operative planning.

Conclusions

In this retrospective cohort of patients undergoing long-segment fusion to the pelvis for ASD, superior displacement of the thoracolumbar inflection point was not associated with radiographic PJK. This finding remained consistent across categorical analyses, subgroup stratification, and multivariable models. Although frailty and prior fusion were associated with PJK in partially adjusted models, no covariate remained independently significant after full adjustment. These results suggest that static superior displacement of the thoracolumbar inflection point alone does not independently contribute to postoperative PJK, highlighting the multifactorial nature of junctional failure following ASD surgery.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://jss.amegroups.com/article/view/10.21037/jss-2026-1-0010/rc

Data Sharing Statement: Available at https://jss.amegroups.com/article/view/10.21037/jss-2026-1-0010/dss

Peer Review File: Available at https://jss.amegroups.com/article/view/10.21037/jss-2026-1-0010/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jss.amegroups.com/article/view/10.21037/jss-2026-1-0010/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the Institutional Review Board at the University of South Florida (No. Pro00023643). The requirement for informed consent was waived due to the retrospective nature of the study and use of de-identified data.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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