The impact of sarcopenia on proximal junctional kyphosis following long-segment spinal fusion for adult spinal deformity: a propensity score-matched cohort study

Introduction

Adult spinal deformity (ASD) is a complex and increasingly prevalent condition, affecting an estimated 30 million adults in the United States alone (1). It is associated with significant pain, functional limitation, and impaired health-related quality of life. In appropriately selected patients, long-segment posterior spinal fusion remains a cornerstone of treatment, offering meaningful improvements in sagittal alignment, pain relief, and functional outcomes (2). However, these extensive reconstructive procedures are also associated with high complication rates, with up to 70% of patients experiencing postoperative adverse events (3).

Among mechanical complications, proximal junctional kyphosis (PJK) represents one of the most common and clinically challenging failure modes following long-segment fusion for ASD (4,5). PJK occurs at the transition zone between the rigid instrumented construct and the adjacent mobile spinal segments and has been reported in 5% to 61% of patients undergoing thoracolumbar fusion (6). While some cases remain radiographic and asymptomatic, progressive deformity can culminate in proximal junctional failure (PJF), leading to neurological compromise, severe pain, and the need for revision surgery (7,8). These revision procedures carry substantial clinical risk and economic burden (9,10), underscoring the importance of identifying modifiable risk factors for junctional breakdown.

Previous studies have identified multiple patient- and surgery-related risk factors for PJK. Advanced age, particularly beyond 55–65 years, has been associated with increased susceptibility to mechanical failure due to reduced physiologic reserve and compensatory capacity (11). Poor bone quality, reflected by low bone mineral density (BMD) or reduced vertebral Hounsfield unit (HU) values, has been strongly linked to bony failure patterns of PJK (6,12,13). Additionally, sagittal malalignment, such as elevated preoperative sagittal vertical axis (SVA) or excessive correction of pelvic incidence-lumbar lordosis (PI-LL) mismatch, has been implicated as a mechanical trigger for junctional stress concentration and failure (14,15).

More recently, attention has shifted toward the role of the paraspinal musculature as a critical yet underappreciated stabilizer of the proximal junction. Sarcopenia, defined as a reduction in skeletal muscle mass, and myosteatosis, characterized by fatty infiltration of muscle tissue, have emerged as independent and potentially modifiable contributors to postoperative mechanical complications (16,17). While global muscle mass is commonly assessed at standardized lumbar levels such as L3 or L4 using the skeletal muscle index (SMI), local muscle integrity at the upper instrumented vertebra (UIV) may be more directly responsible for resisting junctional shear forces and preserving posterior tension band function (18,19). Despite growing interest in sarcopenia within spine surgery, the relative contributions of global versus localized paraspinal muscle degeneration to the development of PJK remain incompletely defined. Furthermore, many prior studies have relied on limited muscle metrics or short-term follow-up, potentially underestimating the true impact of muscular degeneration on junctional failure. Given that PJK can develop months to years after surgery, long-term radiographic surveillance is essential for accurate risk assessment.

Therefore, the purpose of this study was to evaluate the association between preoperative muscle quantity and quality and the development of PJK in patients undergoing long-segment posterior fusion for ASD, with a minimum clinical and radiographic follow-up of 2 years for all patients. Using computed tomography-based morphometric analysis, we assessed muscle cross-sectional area (CSA), muscle-to-vertebra ratio (MVR), SMI, HU attenuation, and Goutallier grading at both the L4 and UIV levels. We hypothesized that both global sarcopenia and localized paraspinal muscle degeneration at the UIV would be independently associated with an increased risk of postoperative PJK. We present this article in accordance with the STROBE reporting checklist (available at https://jss.amegroups.com/article/view/10.21037/jss-2026-1-0050/rc).

Methods

Study design and patient population

The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of University of South Florida (No. Pro00023643). Individual consent for this retrospective analysis was waived. This retrospective propensity score-matched cohort study was conducted using the University of South Florida ASD database. We identified 88 from 200 patients who underwent ≥5-level posterior spinal fusion for ASD between 2021 and 2023, with a minimum of 2 years of clinical and radiographic follow-up, resulting in 45 patients who developed PJK and 43 who did not (Figure 1). PJK was defined radiographically as a proximal junctional sagittal Cobb angle ≥10° compared with the early postoperative measurement. To minimize confounding, propensity score matching (PSM) was applied to balance the PJK and non-PJK groups. Propensity scores were estimated using logistic regression incorporating key demographic and surgical covariates: age, sex, body mass index (BMI), number of fused levels, and pedicle subtraction osteotomy (PSO). Matching was performed using 1:1 nearest-neighbor matching without replacement and a caliper width of 0.2 standard deviations of the logit of the propensity score, yielding 28 matched pairs (56 patients total). Inclusion criteria for both groups consisted of: (I) posterior spinal fusion involving ≥5 levels for ASD; (II) availability of preoperative computed tomography (CT) imaging suitable for muscle morphometric analysis; and (III) a minimum of 2 years of clinical and radiographic follow-up. Patients were excluded if they had active spinal infection, primary or metastatic spinal tumors, neuromuscular deformity, or incomplete imaging or follow-up data.

Figure 1 Flow of patients from database screening to final matched analysis, including exclusions and discards. ASD, adult spinal deformity; PJK, proximal junctional kyphosis; PSM, propensity score matching; PSO, pedicle subtraction osteotomy.

Clinical and surgical data collection

Baseline demographic variables, including age, sex, BMI, smoking status, and American Society of Anesthesiologists (ASA) physical status, were extracted from electronic medical records. Bone quality was assessed using preoperative dual-energy X-ray absorptiometry (DEXA) T-scores. Surgical variables collected for both groups included the total number of fusion levels, upper and lower instrumented vertebrae, number and type of osteotomies [Smith-Petersen osteotomy (SPO) and/or PSO], and number of interbody fusion levels. Prior spinal fusion history was also recorded. These variables were used both for matching and for subsequent comparative analyses. In the PJK group, time to PJK was recorded as the interval (in months) between the index surgery and the first radiographic documentation of PJK.

Quantitative muscle morphometry

Preoperative axial CT scans were reviewed using the institutional Picture Archiving and Communication System (PACS). Muscle CSA was manually traced at the mid-pedicle level for the erector spinae, multifidus, and psoas muscles at two anatomical levels: L4 (representing global; whole body muscle status) and the UIV, representing localized junctional muscle integrity (18,20).

All preoperative CT muscle measurements were performed independently by two fellowship-trained research fellows who were blinded to the patient groups and outcomes. Inter-observer and intra-observer reliability were good for all measurements.

To account for inter-individual variability in body habitus, two different normalization strategies were applied:

• SMI: total muscle CSA at the L4 level divided by height squared (cm²/m²).
• MVR: muscle CSA divided by the corresponding vertebral body CSA at both L4 and UIV levels.

Qualitative muscle assessment (myosteatosis)

Muscle quality was assessed using both quantitative and qualitative measures. Mean muscle attenuation was recorded in HU for each muscle region of interest to quantify intramuscular fat infiltration. In addition, fatty infiltration was graded using the Goutallier classification system (grades 0–4), with higher grades indicating more severe myosteatosis (21).

Definition of sarcopenia

Sarcopenia was defined as a binary variable using established sex-specific SMI thresholds: <52.4 cm²/m² for males and <38.5 cm²/m² for females. Myosteatosis was defined as a mean paraspinal muscle attenuation <30 HU or a Goutallier grade ≥3 at the UIV level (22).

Statistical analysis

All analyses were performed on the propensity score-matched sample to reduce bias from confounding. Continuous variables were reported as mean ± standard deviation and compared between PJK and non-PJK groups using independent-samples t-tests. Categorical variables were compared using Chi-squared or Fisher’s exact tests, as appropriate. Goutallier grades were analyzed using the Mann-Whitney U test. Multivariate logistic regression analysis was performed on the matched cohort, adjusting for preoperative T-score and PI-LL mismatch in addition to the primary muscle variables of interest. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. Statistical significance was defined as a two-tailed P value <0.05. Given 28 PJK events, the multivariable logistic regression model was limited to four covariates to maintain an adequate events-per-variable ratio.

Results

Patient cohort and matching characteristics

A total of 88 patients from 200 database records met the inclusion criteria and were included in the initial cohort, consisting of 45 patients who developed postoperative PJK and 43 who did not, all with a minimum of 2 years of clinical and radiographic follow-up. After propensity score matching, 56 patients were included (28 PJK, 28 non-PJK). Non-participation reasons: 112 patients were excluded prior to inclusion for incomplete imaging, insufficient follow-up, or other pre-operative diagnoses (e.g., infection, tumors). Thirty-two were discarded post-PSM due to poor propensity score match. There was no loss to follow-up among included patients.

Pre-matching, there were minor imbalances in variables such as age (64.0±11.6 vs. 59.3±10.3 years; SMD =0.43, P=0.03) and fusion levels (9.2±1.4 vs. 8.7±1.5; SMD =0.34, P=0.11) (Table S1). Post-matching, the groups were well-balanced with no statistically significant differences in age (61.5±10.9 vs. 60.9±10.7 years; SMD =0.06, P=0.79), sex distribution (53.6% vs. 50.0% females; SMD =0.07, P=0.80), body mass index (BMI) (29.6±5.6 vs. 30.3±5.9 kg/m²; SMD =0.12, P=0.60), smoking status (17.9% vs. 17.9%; SMD =0.00, P>0.99), ASA physical status (2.3±0.5 vs. 2.3±0.5; SMD =0.00, P=0.98), or preoperative DEXA T-scores (−1.5±0.5 vs. −1.4±0.5; SMD =0.20, P=0.52) (Table 1). Surgical characteristics, including number of fused levels and extent of SPOs, PSOs and interbody fusion levels were also similar between the two groups post-matching, minimizing confounding related to surgical complexity. Among patients who developed PJK, the mean time to radiographic diagnosis was 20.7±16.5 months following the index procedure (Table 1).

Global muscle morphometry at the L4 level

Quantitative analysis of preoperative muscle morphology at the L4 level demonstrated significantly reduced global muscle mass in the PJK group compared with the non-PJK group post-matching. The mean SMI at L4 was lower in patients who developed PJK (37.2±6.1 vs. 42.4±6.9 cm²/m²; P=0.004). Consistent reductions were observed across muscle groups: CSA of the erector spinae (2,401±298 vs. 2,654±276 mm²; P=0.002), multifidus (821±121 vs. 953±137 mm²; P<0.001), and psoas (1,248±194 vs. 1,401±209 mm²; P=0.007). Normalized MVRs were lower for the erector spinae (1.49±0.27 vs. 1.61±0.25; P=0.052) and multifidus (0.51±0.10 vs. 0.58±0.12; P=0.02), while psoas MVR did not differ (0.78±0.16 vs. 0.84±0.15; P=0.15). Goutallier grade was higher in the PJK group (1.8±0.8 vs. 1.2±0.6; P=0.001) (Table 2).

Localized muscle morphometry at the UIV

At the UIV level, the PJK group exhibited pronounced localized muscle degeneration post-matching. CSA of the erector spinae (1,843±224 vs. 2,130±208 mm²; P<0.001) and multifidus (618±94 vs. 746±101 mm²; P<0.001) were significantly reduced in the PJK group. MVR values were lower for erector spinae (1.61±0.30 vs. 1.80±0.28; P=0.009) and multifidus (0.54±0.13 vs. 0.63±0.14; P=0.01). Goutallier grade was higher in the PJK group (2.7±0.7 vs. 1.5±0.6; P<0.001) (Table 2).

Prevalence of sarcopenia

Based on established sex-specific SMI thresholds, sarcopenia was more prevalent in the PJK group post-matching [15 (53.6%) vs. 7 (25.0%); P=0.02], supporting a strong association between global muscle depletion and postoperative junctional failure (Table 2).

Muscle quality and myosteatosis

Qualitative assessment revealed worse muscle quality in the PJK group post-matching at both levels. At L4, mean HU attenuation was lower for erector spinae (33.2±7.8 vs. 39.7±6.9; P=0.001) and multifidus (29.3±8.2 vs. 37.3±7.1; P<0.001), with a nonsignificant trend for psoas (42.5±6.4 vs. 45.4±5.6; P=0.08).

At UIV, differences were more pronounced: erector spinae HU (25.9±8.1 vs. 35.2±6.8; P<0.001) and multifidus HU (21.1±9.3 vs. 33.0±7.9; P<0.001). Goutallier grades were higher at L4 (1.8±0.8 vs. 1.2±0.6; P=0.001) and UIV (2.7±0.7 vs. 1.5±0.6; P<0.001), indicating greater fatty infiltration in PJK patients (Tables 2,3).

Multivariate analysis of risk factors for PJK

Multivariate logistic regression analysis in the matched cohort identified sarcopenia and high-grade fatty infiltration at the UIV as independent predictors of PJK. Sarcopenia was associated with more than a twofold increase in the odds of PJK (OR =2.10; 95% CI: 1.05–4.20; P=0.03). High-grade fatty infiltration at the UIV (Goutallier grade ≥3) was similarly associated with increased risk (OR =2.25; 95% CI: 1.10–4.60; P=0.02). Pre- and postoperative spinopelvic parameters were comparable between the matched groups (Table S2). Preoperative T-score (per 1-unit decrease) and PI-LL mismatch did not reach statistical significance in the adjusted model (P=0.11 and P=0.10, respectively) (Table 4).

Discussion

This study demonstrates a strong association between preoperative paraspinal muscle degeneration and the development of PJK following long-segment posterior fusion for ASD. The most salient observation is that patients who developed PJK exhibited significantly reduced muscle quantity and quality across multiple metrics, including SMI, CSA, MVR, HU attenuation, and Goutallier grading. Importantly, these differences were present despite comparable demographics, fusion length, osteotomy type, and vertebral body size between groups. This suggests that muscle degeneration itself, rather than age, surgical complexity, or skeletal morphology, might play a central role in predisposing patients to junctional failure. Paraspinal muscles serve as dynamic stabilizers that modulate spinal loading during posture and movement. When muscle mass and quality are diminished, increased mechanical demands are transferred to passive structures at the proximal junction, including the posterior ligamentous complex and adjacent vertebral bodies. Over time, this imbalance may result in progressive kyphotic collapse, particularly in the setting of long, rigid constructs where compensatory motion is limited (18,19,23,24).

A key contribution of this study is the simultaneous evaluation of global muscle status at L4 and localized paraspinal muscle integrity at the UIV. Reduced SMI and CSA at L4 likely reflect systemic sarcopenia, which may impair overall postural control and reduce the patient’s ability to accommodate abrupt biomechanical transitions introduced by deformity correction. In contrast, muscle degeneration at the UIV appears to be more directly related to failure at the junctional interface itself. The markedly lower CSA, MVR, and HU values, along with higher Goutallier grades at the UIV in the PJK cohort, suggest compromised local muscular support precisely where mechanical stress is concentrated. These findings align with growing evidence that site-specific sarcopenia is more predictive of discoligamentous PJK than global muscle depletion alone (18). The observed muscle degeneration patterns may help explain distinct mechanisms underlying PJK development. Localized myosteatosis at the UIV may accelerate soft-tissue failure by reducing dynamic stabilization, increasing segmental motion, and progressively overloading the posterior ligamentous structures. Conversely, global sarcopenia and poor muscle quality may contribute to chronic fatigue loading at adjacent vertebrae, indirectly increasing susceptibility to bony failure, particularly in patients with borderline BMD (23,25). Although low T-scores demonstrated a trend toward increased risk of PJK in our cohort, neither preoperative T-score nor PI-LL mismatch remained significant independent predictors in the multivariate model. This suggests that muscle degeneration may precede or amplify mechanical failure, potentially explaining why PJK occurs even in patients without severe osteoporosis and despite the use of bone-focused prophylactic strategies.

Our findings are consistent with prior studies identifying sarcopenia as a risk factor for proximal junctional complications after ASD surgery. Eleswarapu et al. (16) demonstrated that sarcopenia measured at L4 was independently associated with proximal junctional disease. Subsequent work by Pennington et al. further refined this concept by showing that paraspinal sarcopenia at the UIV specifically predicts discoligamentous PJK, independent of bone quality (18). Additional studies have highlighted the importance of muscle quality, with low HU values and severe multifidus fatty infiltration emerging as strong predictors of both PJK and proximal junctional failure (23,26). The present study extends this literature by employing a matched design, reducing confounding related to surgical extent and patient demographics, and by integrating both global and local muscle metrics into a unified analytical framework. Furthermore, the requirement for a minimum of 2 years of follow-up strengthens the reliability of our findings, as PJK may manifest in a delayed fashion and be underestimated in shorter-term studies.

These results have direct implications for preoperative assessment and surgical decision-making. Routine evaluation of paraspinal muscle health using preoperative CT imaging, particularly at the UIV, may improve identification of patients at elevated risk for PJK. In such patients, consideration may be given to targeted risk mitigation strategies, including nutritional optimization, resistance-based prehabilitation, and careful selection of the upper instrumented level. Importantly, these findings suggest that muscle-focused interventions should complement, rather than replace, established bone-directed strategies such as pharmacologic osteoporosis treatment or prophylactic vertebroplasty (27,28). Incorporating muscle metrics into existing risk stratification models may enable a more comprehensive and individualized approach to preventing junctional complications.

Limitations

Several limitations should be acknowledged. The retrospective design and single-institution cohort may limit generalizability. Although the sample size is comparable to prior imaging-based studies, it restricts subgroup analyses and precludes stratification by PJK subtype. Manual muscle segmentation introduces potential interobserver variability, though standardized measurement techniques were used. Sarcopenia was defined using established SMI thresholds derived from general populations, which may not fully capture spine-specific risk. Finally, postoperative changes in muscle morphology were not assessed and may influence late-onset junctional failure. The results have moderate external validity for ASD patients undergoing long-segment fusion in similar high-volume centers, but generalizability is limited to older, mostly Caucasian populations; further multicenter studies in diverse demographics are needed.

Conclusions

In this study with a minimum of 2 years of follow-up, preoperative sarcopenia and paraspinal myosteatosis, particularly at the UIV, were independently associated with the development of PJK following long-segment fusion for ASD. These findings underscore the importance of paraspinal muscle integrity as a determinant of junctional stability and support the integration of muscle assessment into preoperative risk evaluation and preventive strategies.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://jss.amegroups.com/article/view/10.21037/jss-2026-1-0050/rc

Data Sharing Statement: Available at https://jss.amegroups.com/article/view/10.21037/jss-2026-1-0050/dss

Peer Review File: Available at https://jss.amegroups.com/article/view/10.21037/jss-2026-1-0050/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-2026-1-0050/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. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of University of South Florida (No. Pro00023643). Individual consent for this retrospective analysis was waived.

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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