Introduction
Proximal junctional kyphosis (PJK) remains a prevalent and challenging complication following long-segment spinal fusion for adult spinal deformity, with reported incidence rates varying widely from 5% to 46% across the literature [1, 2]. This heterogeneity in reported prevalence is largely attributed to variations in diagnostic definitions, patient demographics, and radiographic protocols. Clinically, PJK can lead to significant patient morbidity, ranging from localized pain and sagittal malalignment to proximal junctional failure (PJF) and neurological deficits in severe cases, necessitating revision surgery [3, 4]. 
The etiology of PJK is multifactorial, resulting from an intricate interplay between patient-specific characteristics, surgical techniques (e.g. upper instrumented vertebra selection and sagittal alignment restoration), and postoperative biomechanical forces [2, 5]. Among patient-related risk factors, body mass index (BMI) has garnered significant attention in recent years. High BMI is associated with increased mechanical load on the spinal construct and technical intraoperative challenges, which may predispose patients to junctional complications [5, 6]. However, the association between BMI and the development of PJK remains a matter of ongoing controversy. While some studies have identified high BMI as an independent risk factor, others have reported no significant correlation [1, 7]. This inconsistency likely arises from methodological differences, including differences in PJK classification, the inclusion of confounding variables such as bone mineral density and sarcopenia, and heterogeneous follow-up durations [2]. Given these conflicting findings, further investigation into the predictive value of BMI is warranted. Therefore, the purpose of this study is to evaluate the relationship between BMI and the prevalence of PJK in patients undergoing long spinal fusion for degenerative canal stenosis. Furthermore, this study provides a detailed analysis of the prevalence of PJK across temporal phases—specifically early and late onset—to elucidate whether BMI exerts a differential influence on the timing of this complication

Methods
Study design and patient population 
This retrospective study was conducted at ShafaYahyaeian Hospital, Tehran, Iran, between January 2018 and December 2021. The study included patients who underwent long spinal fusion for degenerative canal stenosis with a minimum 24-month follow-up. Long spinal fusion was defined as fusion involving ≥5 moving segments or fusion extending to the pelvis with iliac fixation (iliac or S2 alar-iliac screws). 

Inclusion and exclusion criteria 
Patients were included if they
1) Underwent long spinal fusion for degenerative canal stenosis; 2) Had a minimum 24-month follow-up; 3) Had available preoperative and follow-up radiographic images.

Patients were excluded if they had
1) Preoperative kyphotic deformity at the proximal junctional region; 2) Significant BMI change (>5 units) during follow-up; 3) Previous spinal surgery at fused levels; 4) Primary spinal deformity as a surgical indication; 5) Incomplete medical records or radiographic data.
Initially, 129 patients were identified; 35 were excluded due to BMI changes, leaving 94 patients. Of these, 76 completed a minimum 24-month follow-up and were included in the final analysis. 

Data collection 
Demographic data, including age, sex, weight, and height, were collected from medical records. BMI was calculated as weight (kg) divided by height (m²). 

Radiographic assessment 
All radiographic measurements were performed on standing full-spine lateral radiographs by two independent observers blinded to clinical outcomes. PJK was defined as an increase in Cobb angle between the UIV inferior endplate and the UIV+2 superior endplate of >10° compared to the preoperative measurement [8]. 
1) Early PJK: Developing within 6 months postoperatively; 2) Late PJK: Developing after 6 months postoperatively

Statistical analysis 
Descriptive statistics were expressed as Mean±SD for continuous variables and frequencies (percentages) for categorical variables. Comparisons between groups were performed using independent-samples t tests or the Mann-Whitney U test for continuous variables, and the chi-square test for categorical variables. Logistic regression was performed for multivariate analysis. Statistical significance was set at P<0.05. 

Results 
Patient demographics: The study included 76 patients (52 women, 24 men) with a mean age of 60.2 years (range: 43-78 years). The mean follow-up duration was 38.4 months (range: 24-51 months). The mean BMI was 27.6 kg/m² (range: 18.3-34.8 kg/m²) (Table 1); PJK prevalence: PJK occurred in 34 patients (44.7%) overall.


Early PJK occurred in 26 patients (34.2%) and late PJK in 18 patients (23.7%); BMI and PJK: In early PJK, mean BMI was significantly higher in the PJK group (29.6 vs 23.4 kg/m², P<0.001) (Table 2).


No significant difference was found for late PJK; BMI categories and PJK risk (Table 3); Multivariate analysis (Table 4); Surgical intervention: Among early PJK patients, 16(61.5%) required surgical intervention.





Mean BMI was significantly higher in surgically treated patients (30.8 vs 28.4 kg/m², P=0.023). 

Discussion
This study identifies a significant association between higher BMI and the development of PJK following long-segment spinal fusion for degenerative lumbar disease. Patients with early PJK had a significantly higher mean BMI than those without PJK, and multivariate analysis identified BMI as an independent predictor of early PJK (odds ratio: 1.32 per 1 kg/m² increase) [8, 9].
The overall PJK prevalence in our study (44.7%) is consistent with what is reported in the literature for long fusions, which ranges from 5-46% depending on the definition and patient cohort [1, 8] . This high rate in our study may be attributed to strict radiographic monitoring and the inclusion of patients with advanced degenerative pathology requiring long-segment constructs. Crucially, the rate of early PJK (occurring within 6 months postoperatively; 34.2%) exceeded that of late PJK (23.7%). This temporal pattern supports prior findings indicating that the majority of PJK cases develop in the early postoperative period, primarily driven by immediate mechanical failure or junctional segment overload rather than long-term degenerative changes [10, 11].
The strong association between elevated BMI and early PJK observed in this study is consistent with several clinical cohorts [8, 9, 12]. Biomechanically, a higher BMI contributes to increased mechanical loading on the upper instrumented vertebra (UIV) and adjacent segments through several interconnected pathways. Obesity increases the axial load and gravity-line displacement, causing greater rotational bending moments at the transition zone between the rigid instrumented construct and the upper segments [12, 13]. Second, patients with obesity often exhibit postural compensations, such as an anteriorly shifted sagittal vertical axis, which increases the mechanical demand on the posterior ligamentous complex [13, 14]. The technical challenge of surgical exposure in patients with high BMI may lead to unintended damage to the posterior tension band (interspinous ligaments and facet capsules) at the UIV level, compromising structural integrity [15]. Obesity-related systemic inflammation and impaired microvascular circulation have been shown to delay bone healing and ligamentous recovery, increasing susceptibility to early mechanical failure [16].
In our sample, 61.5% of patients who developed early PJK required revision surgery, and these patients had a significantly higher mean BMI than those managed conservatively. This implies that a higher BMI not only increases the risk of developing PJK but also predisposes patients to severe or symptomatic forms such as PJF that necessitate surgical reoperation [9, 1].
While many studies agree that obesity is a risk factor for mechanical failure, some review studies have reported conflicting results regarding the direct correlation between BMI and PJK. This inconsistency is likely due to heterogeneity in surgical techniques, different definitions of PJK, and varying follow-up periods across cohorts [1, 12]. However, when focusing specifically on early mechanical complications rather than late degenerative progression, the impact of body weight becomes more pronounced, as demonstrated in our findings.
Based on the findings, we propose several clinical strategies to mitigate the risk of early PJK in patients with high BMI:
• Preoperative optimization: Whenever clinically feasible, weight reduction and physical conditioning should be encouraged prior to elective surgery to reduce early mechanical demands on the constructs [12, 16].
• Surgical construct adjustments: In patients with high BMI, surgeons should consider preventive strategies such as soft-tissue preservation at the UIV, prophylactic vertebral augmentation (cementing the UIV/UIV+1), or using transition rods (tapered rods) to graduate the stiffness at the junction [11, 15].
• Sagittal alignment planning: Avoiding overcorrection of lumbar lordosis in obese patients is critical, as matching their natural, slightly more kyphotic or compensated alignment can lower junctional stress [13, 14].
• Postoperative monitoring: Patients with a BMI >25 kg/m² should undergo more frequent and careful radiographic follow-up during the first 6 months to detect early junctional changes before they progress to catastrophic failure.

Conclusion 
High BMI is an independent predictor of early PJK (≤6 months) following long spinal fusion, with every unit increase in BMI raising the risk by 32%. High BMI is also associated with a greater likelihood of requiring surgical revision for early PJK. In contrast, BMI does not significantly influence late-onset PJK (>6 months). Preoperative weight optimization and tailored protective surgical strategies at the UIV level are recommended to mitigate the risk of early mechanical failure in patients with high BMI.

Strengths and limitation
Our study had several strengths. First, we specifically focused on patients undergoing long spinal fusion (≥5levels or pelvic fixation) for degenerative canal stenosis, which is a well-defined population. Second, we distinguished between early and late PJK, which allowed us to identify the time-dependent relationship between BMI and PJK. Third, we analyzed the relationship between BMI and the need for surgical intervention, which provided additional information beyond the presence of radiographic PJK. Fourth, we used standardized definitions for PJK and long spinal fusion. However, our study had some limitations. First, the retrospective design introduced potential biases as noted by O’Neill et al. [17]. Second, our sample size (76 patients) may have been insufficient to detect smaller differences in subgroup analyses. Third, the study was conducted at a single center, which may limit generalizability. Fourth, we excluded patients with >5 unit change in BMI during follow-up, which may have removed some informative patients. Fifth, we did not collect data on bone mineral density, a known risk factor for PJK, as discussed by Line et al. (2020). Sixth, interobserver and intraobserver reliability for radiographic measurements as not formally assessed. 

Future research
Future studies should focus on several areas. First, prospective studies with larger sample sizes are needed to confirm our findings, as recommended by Cho et al. [18]. Second, biomechanical studies using finite element analysis could help elucidate the mechanisms by which increased BMI leads to PJK. Third, intervention studies evaluating the effect of preoperative weight loss on PJK rates would be valuable. Fourth, multi-centerstudies would increase sample sizes and improve generalizability. Fifth, longer follow-up studies (5-10 years) would help determine if the relationship between BMI and PJK persists over time. BMI is an independent predictor of early PJK (OR=1.32, 95% CI, 1.18%, 1.48%, P<0.001) Higher BMI is significantly associated with increased prevalence of early PJK following long spinal fusion. Overweight patients have a substantially higher risk and should be counseled preoperatively. Weight optimization and modified surgical techniques should be considered in high-risk patients.

Ethical Considerations
Compliance with ethical guidelines
The ethical principles observed in the article, such as the informed consent of the participants, the confidentiality of information, the permission of the participants to cancel their participation in the research.

Funding
This research did not receive any grant from funding agencies in the public, commercial, or non-profit sectors.

Authors' contributions
Conceptualization and supervision: Ebrahim Ameri and Hassan Ghandhari; Methodology: Farshad Nikoii and Ehsan Ghavidel; Formal analysis: Ehsan Ghavidel and Javad Moeini; Data curation and Data collection: Javad Moeini, Mohammad Reza Shakeri, and Ehsan Ghavidel; Data analysis: Ehsan Ghavidel and Mohammad Reza Chehrasan; Project administration: Ebrahim Ameri, Hassan Ghandhari, and Farshad Nikoii; Investigation and writing: All authors.

Conflict of interest
The authors declared no conflict of interest.



References

1. Lau D, Clark AJ, Scheer JK, Daubs MD, Coe JD, Paonessa KJ, et al. Proximal junctional kyphosis and failure after spinal deformity surgery: a systematic review of the literature as a background to classification development. Spine (Phila Pa 1976). 2014; 39(25):2093-102. [DOI:10.1097/brs.0000000000000627] [PMID]
2. Lee BJ, Bae SS, Choi HY, Park JH, Hyun SJ, Jo DJ, et al. Proximal junctional kyphosis or failure after adult spinal deformity surgery - review of risk factors and its prevention. neurospine. 2023; 20(3):863-75. [DOI:10.14245/ns.2346476.238] [PMID]
3. Hostin R, McCarthy I, O-rien M, Bess S, Line B, Boachie-Adjei O, et al. Incidence, mode, and location of acute proximal junctional failures after multi-segment posterior spinal fusion for adult spinal deformity. Spine. 2013; 38(12):1008-15. [DOI:10.1097/brs.0b013e318271319c] [PMID]
4. Sebaaly A, Sylvestre C, El Quehtani Y, Riouallon G, Larrieu D, Boissiere L, et al. Incidence and risk factors for proximal junctional kyphosis: results of a multicentric study of adult scoliosis. Clin Spine Surg. 2018; 31(3):E178-83. [DOI:10.1097/bsd.0000000000000630] [PMID]
5. Safaee MM, Tenorio A, Osorio JA, Choy W, Amara D, Lai L, et al. The impact of obesity on perioperative complications in patients undergoing anterior lumbar interbody fusion. J Neurosurg Spine. 2020; 33(3):332-41. [DOI:10.3171/2020.2.spine191418] [PMID]
6. Yagi M, Yamanouchi K, Fujita N, Funao H, Ebata S. Proximal junctional failure in adult spinal deformity surgery: an in-depth review. Neurospine. 2023; 20(3):876-89. [DOI:10.14245/ns.2346566.283] [PMID]
7. Kim HJ, Bridwell KH, Lenke LG, Park MS, Ahmad A, Song KS, et al. Proximal junctional kyphosis results in inferior SRS pain subscores in adult deformity patients. Spine (Phila Pa 1976). 2013; 38(11):896-901. [DOI:10.1097/brs.0b013e3182815b42] [PMID]
8. Glattes RC, Bridwell KH, Lenke LG, Kim YJ, Rinella A, Edwards C 2nd. Proximal junctional kyphosis in adult spinal deformity following long instrumented posterior spinal fusion: incidence, outcomes, and risk factor analysis. Spine (Phila Pa 1976). 2005; 30(14):1643–9. [DOI:10.1097/01.brs.0000169451.76359.49] [PMID]
9. Hart RA, McCarthy I, Ames CP, Shaffrey CI, Hamilton DK, Hostin R. Proximal junctional kyphosis and proximal junctional failure. Neurosurg Clin N Am. 2013; 24(2):213-8. [DOI:10.1016/j.nec.2013.01.001] [PMID]
10. Yagi M, Akilah KB, Boachie-Adjei O. Incidence, risk factors and classification of proximal junctional kyphosis: Surgical outcomes review of adult idiopathic scoliosis. Spine (Phila Pa 1976). 2011; 36(1):E60-8. [DOI:10.1097/brs.0b013e3181eeaee2] [PMID]
11. Lafage V, Mohamed A, Katchis C, Daniels A, Diebo B, Ames C, et al. Beyond kyphosis: modes of failure at the proximal junction in adult spinal deformity. Spine (Phila Pa 1976). 2026; 51(5):360-7. [DOI:10.1097/brs.0000000000005509] [PMID]
12. Pajak A, Dekhne M, Lui ATH, Akosman I, Cunningham ME, Kim HJ, et al. The impact of obesity on radiographic and clinical outcomes following adult spinal deformity surgery-a systematic review and meta-analysis. Spine J. 2026; 26(1):147-57. [DOI:10.1016/j.spinee.2025.07.004] [PMID]
13. Soroceanu A, Burton DC, Diebo BG, Smith JS, Hostin R, Shaffrey CI, et al. Impact of obesity on complications, infection, and patient-reported outcomes in adult spinal deformity surgery. J Neurosurg Spine. 2015; 23(5):656-64. [DOI:10.3171/2015.3.spine14743] [PMID]
14. Klineberg E, Schwab F, Ames C, Hostin R, Bess S, Smith JS, et al. Acute reciprocal changes distant from the site of spinal osteotomies affect global postoperative alignment. Adv Orthop. 2011; 2011:415946. [DOI:10.4061/2011/415946] [PMID]
15. Feeley A, McDonnell J, Feeley I, Butler J. Obesity: An independent risk factor for complications in anterior lumbar interbody fusion? A systematic review. Global Spine J. 2022; 12(8):1894-903. [PMID]
16. Bagherifard A, Hemmatyar A, Khosravi K, Rouzbahani A, Mokhtari K, Yahyazedeh H, et al. The impact of obesity on bone health: molecular pathways, metabolic interactions, and associated pathologies. Int J Obes (Lond). 2026; 50(1):87-115. [DOI:10.1038/s41366-025-01907-1] [PMID]
17. Oʼneill KR, Lenke LG, Bridwell KH, Hyun SJ, Neuman B, Dorward I, et al. Clinical and radiographic outcomes after 3-column osteotomies with 5-year follow-up. Spine (Phila Pa 1976). 2014; 39(5):424-32. [DOI:10.1097/brs.0000000000000156] [PMID]
18. Cho SK, Shin JI, Kim YJ. Proximal junctional kyphosis following adult spinal deformity surgery. Eur Spine J. 2014; 23(12):2726-36. [DOI:10.1007/s00586-014-3531-4] [PMID]