Lumbar Spine Endplate Sclerosis is a Protective Factor for Cage Subsidence in Minimally Invasive Transforaminal Lumbar Interbody Fusion

Abstract

Study design

Retrospective single-center cohort study.

Objective

To investigate the predictive value of preoperative endplate Hounsfield unit (HU) measurements for cage subsidence (CS) following minimally invasive transforaminal lumbar interbody fusion (MI-TLIF), and to propose threshold values for risk stratification.

Methods

A total of 169 patients undergoing one- and two-level MI-TLIF with preoperative lumbar CT imaging were included. Endplate HU values were quantified within a 5-mm region of interest at the cage–endplate interface. Mild and severe CS was defined as 2-4 mm and ≥4 mm migration of the interbody cage into the adjacent vertebral endplate. Logistic regression analyses were employed to identify risk factors for CS.

Results

CS occurred in 39 of 464 endplates. Significantly lower L1 vertebral HU, reduced endplate HU at the surgical site, and obesity (BMI >25 kg/m²) were observed in the CS group. In multivariate analysis, obesity and endplate HU were independent predictor of CS (OR = 2.508; 95% CI, 1.135-5.546; OR = 0.989; 95% CI, 0.983-0.995). Among patients with L1 HU <117, those with endplate HU <221 had a significantly increased risk of CS (OR = 4.444; P = 0.0023). The area under the receiver operating characteristic curve for the combination of obesity (BMI >25 kg/m²) and endplate HU was 0.727 (95% CI 0.655-0.800).

Conclusions

Surgical site endplate sclerosis at the surgical site may be a protective factor against CS following MI-TLIF. Preoperative endplate HU assessment may assist in identifying patients at risk of CS following MI-TLIF.

Keywords

cage subsidence TLIF endplate bone mineral density CT

Introduction

Transforaminal lumbar interbody fusion (TLIF) is an effective and commonly used surgical technique for treating degenerative lumbar spine diseases. Since its introduction by Harms and Jeszenszky¹ in 1998, advancements in surgical techniques have led to the widespread adoption of minimally invasive TLIF (MI-TLIF), which has flourished over the past two decades. MI-TLIF has several advantages over the traditional open approach, including lesser blood loss, minimized soft tissue dissection, shorter hospital stays, faster rehabilitation, decreased need for analgesia and blood transfusion and decreased morbidity.^2-7 Additionally, reports indicate that both open- and MI-TLIF techniques result in significant postoperative improvements in functional outcomes,^6,7 with comparable fusion (55% and 98% at 6 months and 2 years, respectively)^2,7,8 and complication (5-8%) rates.⁵

Cage subsidence (CS) remains a common complication of progressive disc height narrowing, which may prevent successful fusion and result in pain and nonunion due to segmental instability.⁹ Reported CS rates vary between 4.8 and 45.9%, and various surgical influence subsidence risk, including cage type, more posterior cage position, and endplate violation during surgery.^10-13 Apart from surgical factors, patient-related factors, particularly decreased bone mineral density (BMD), have been identified as significant contributors to CS.^13-15 Although dual-energy X-ray absorptiometry (DXA) is a standard method for diagnosing osteoporosis, degenerative changes in the lumbar spine may result in the overestimation of BMD.¹⁶ Most patients undergoing lumbar surgery require computed tomography (CT) as part of their preoperative evaluation. L1 vertebral Hounsfield unit (HU) measurement is an alternative method to assess BMD and is correlated with CS.^17-19 Our previous study found that L1 HU < 117 significantly increased the likelihood of postoperative cage settling, with an estimated 4.1-fold elevated risk following MI-TLIF.²⁰ Site-specific CT-based HU is a surrogate marker for assessing BMD.^21,22 It has been reported that endplate volumetric BMD measured by quantitative CT is a reproducible measurement and appears more predictive for severe CS than trabecular volumetric BMD in patients with standalone lateral lumbar fusion.²³

However, to our knowledge, no studies have assessed the relationship between endplate HU measured using standard CT and the occurrence of CS in patients who undergo MI-TLIF. We aimed to assess (1) whether endplate HU and other potential risk factors can predict the occurrence of postoperative CS after MI-TLIF surgery and (2) whether there is a cutoff endplate HU for predicting postoperative CS in MI-TLIF patients.

Material and Methods

Patient Population

This retrospective study used a single-institution database from October 2016 to July 2019. This study was approved by the institutional review board of our hospital prior to data collection and analysis. The requirement for informed consent was waived because of the retrospective design of the study. Medical charts and preoperative and postoperative images were reviewed. The patient inclusion criteria were (1) age >18 years, (2) MI-TLIF involving one and two levels with bilateral pedicle screw fixation for lumbar degenerative disease, (3) preoperative spine CT within 6 months before surgery, and (4) a minimum follow-up of 1 year with radiographs. All levels were separated into CS and non-CS groups. We excluded patients with spine infection, spine tumor, spine trauma, history of spinal surgery, Schmorl’s node and metabolic bone disease other than osteopenia or osteoporosis; those lost to follow-up; and those who failed to complete the questionnaires or radiographic examinations. The Oswestry Disability Index (ODI) questionnaire and Visual Analog Scale (VAS) scores for back pain were collected preoperatively and at postoperative 6-month and 1-year to analyze patient-reported outcomes.

Surgical Technique

All procedures were performed by a single experienced spine surgeon following the standardized MI-TLIF technique. This approach involves percutaneous pedicle screw fixation combined with unilateral paramedian access, which enables bilateral neural decompression. Ipsilateral facetectomy was performed based on predominant radicular symptoms. Microscopic assistance was used for decompression, intervertebral disc removal, and cage insertion using a microendoscopic tubular retractor system. Endplate preparation was conducted using a combination of shavers, ring curettes, and angled curettes (A-SPINE, United Orthopedic Corporation, Taiwan) until the subchondral bony endplate was clearly exposed. Care was taken to completely remove the cartilaginous layer while preserving the integrity of the cortical endplate to avoid excessive weakening that could predispose to cage subsidence.

Fusion was achieved using locally harvested autologous bone combined with 1 mL demineralized bone matrix (OsteoSelect DBM Putty; Bacterin International, Belgrade, MT, USA). Synthetic bone grafts were not used in this study. A uniform banana-shaped PEEK cage (Rainboo1, A-SPINE, United Orthopedic Corporation, Taiwan) was used in all cases. The cage dimensions were consistent across all patients: height 7-14 mm, width 12 mm, and length 28 mm. Surgical drains were omitted, and the patients were advised to wear a spinal brace continuously for 3 months after surgery.

Medical Records (Data Collection) and Radiographic Measurement

Patient demographic data, such as age, sex, body mass index (BMI), diabetes mellitus, hypertension, rheumatoid arthritis, smoking status, number of surgical levels, and surgical levels were collected from medical records. All included patients completed follow-up assessments at 1, 3, 6, and 12 months postoperatively. Lumbar spine radiographs, including supine anteroposterior and lateral views, were obtained at each follow-up visit. Fusion status was evaluated using CT scans at 6 months postoperatively, while cage subsidence was assessed on plain radiographs at both 6 and 12 months. The Brantigan-Steffee-Fraser (BSF) classification was used to determine the success of interbody fusion after 3-mm slice CT. Only BSF-3 was considered radiographic union, whereas BSF-2 and BSF-1 were considered locked pseudarthrosis and nonunion, respectively. Cage subsidence (CS) was evaluated on lateral radiographs and defined as a migration of the cage >2 mm into the adjacent vertebral body, with mild and severe CS further classified as 2-4 mm and ≥4 mm of migration, respectively. Radiographic measurements were performed independently by two orthopedic residents. The mean values of the two assessments were used in the analysis. To ensure measurement consistency, intra- and inter-observer reliabilities were evaluated in a randomly selected subgroup of patients using Cronbach’s alpha coefficient, yielding values of 0.96 and 0.90, respectively.

To assess bone mineral density, HU values were calculated from lumbar spine CT scans using a picture archiving and communication system (PACS). The first lumbar vertebral HU was obtained by placing an elliptical region of interest (ROI) confined to the medullary space of three separate locations on the axial images: immediately inferior to the superior endplate, in the middle of the vertebral body, and superior to the inferior endplate (Figure 1). For each measurement, the largest possible elliptical region of interest was drawn, excluding the cortical margins, to prevent overestimation (Figure 2). HU values from the three axial cuts were averaged to obtain the mean HU value. Endplate HU was measured by drawing the largest possible elliptical ROI 5-mm beneath the cage contact surfaces.²³

Figure 1.

Illustration of vertebral (VB) HU measurements from three axial cuts confined by the largest elliptical region of interest (ROI). The HU values from the three axial cuts were averaged to obtain the mean HU values

Figure 2.

Illustration of endplate HU measurements from the superior and inferior endplates confined by the largest elliptical region of interest (ROI)

Statistical Analyses

Statistical analyses were performed using SPSS (version 24.0; IBM Corp., Armonk, NY, USA). The Shapiro–Wilk test was used to assess the normality of the data distribution, and all variables satisfied the assumption of normality (P > 0.05). Continuous data were analyzed using independent t-tests. Categorical data were compared using chi-squared or Fisher’s exact tests. Clinically relevant factors and those found to be significant in the univariate analysis were incorporated into the multivariate logistic regression analysis to identify independent risk factors for CS. Statistical significance was set at a two-tailed P-value <0.05. Possible risk factors were incorporated into the models, and the accuracy of individual prediction models was assessed using the area under the curve (AUC). A receiver operating characteristic (ROC) curve was used to determine the most appropriate threshold (cuff-off) value for models with higher sensitivity and specificity. The cutoff values of the validated continuous risk predictors were assessed by maximizing Youden’s J index.

Results

Study Population

Of the 343 patients who met the inclusion criteria, 169 with 464 endplates were included in this study. The reasons for exclusion included loss to follow-up (72 patients), missing data (30 patients), history of spinal surgery trauma, infection, or tumor (7 patients), Schmorl’s node (64 patients), and metabolic bone disorder (1 patient) (Figure 3). The mean patient age was 67.4 ± 11.8 years, 54 were men (32.0%), and the mean BMI was 26.6 ± 4.3 kg/m². One hundred and five patients underwent one-level surgery (62.1%) and 64 underwent two-level surgery (37.9%) (Table 1). By endplate analysis, the mean L1 vertebrae HU was 125.8 ± 49.3, and the mean endplate HU was 325.4 ± 89.8. There were 213 (45.9%) endplates with L1 vertebral HU < 117. CS was observed in 8.4% of the endplates. No statistically significant differences were noted between the CS and non-CS groups regarding baseline demographics, including age, sex, and comorbidities, such as hypertension, diabetes mellitus, and rheumatoid arthritis (Table 2). In contrast, obesity (BMI > 25 kg/m²) was significantly more frequent in the CS group (76.9 %) than in the non-CS group (59.8%) (P = 0.039). Additionally, both L1 vertebral body and endplate HU values were significantly lower in patients who developed subsidence (110.9 ± 44.2 vs 127.2 ± 50.0, P = 0.048; 272.5 ± 64.1 vs 330.3 ± 90.4, P < 0.0001, respectively). There were no significant differences between the groups in the number of surgical levels (one-, or two-level surgeries) or the contact site of the cage, whether at the superior or inferior endplate (Table 2).

Figure 3.

Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) flowchart

Table 1.

Demographic Data

Patient data	Results (n = 169)
Clinical parameters
Age, yrs	67.4 ± 11.8
Sex (male/female)	54/115
BMI, kg/m²	26.6 ± 4.3
Overweight (BMI >25)	100 (59.2%)
Diabetes mellitus	37 (21.9%)
Hypertension	76 (45.0%)
Rheumatoid arthritis	5 (3.0%)
Surgical parameters
Number of surgical levels
Two	64 (37.9%)
One	105 (62.1%)
Surgical level	Results (n = 232)
L2-3	2 (0.9%)
L3-4	48 (20.6%)
L4-5	141 (60.9%)
L5–S1	40 (17.2%)
Endplate data	Results (n = 464)
HU
Pre-op L1 HU	125.8 ± 49.3
Endplate HU	325.4 ± 89.8
Pre-op L1 HU <117	213 (45.9%)

Results are shown as mean ± standard deviation or the number of patients (%).BMI, body mass index; HU, Hounsfield unit

Table 2.

Association Between the Clinical Characteristics and Cage Subsidence

	No.	Cage subsidence		P-value
	No.	Yes	No	P-value
Clinical parameters
No. Of endplates		39	425
Age (years)	464	70.0 $\pm$ 10.2	67.7 $\pm$ 11.4	0.2387
BMI (kg/m²)	464	27.7 $\pm$ 4.4	26.7 $\pm$ 4.3	0.1609
Sex
Male	144	8 (20.5%)	136 (32.0%)	0.1519
Female	320	31 (79.5%)	289 (68.0%)
HU
L1 HU	464	110.9 $\pm$ 44.2	127.2 $\pm$ 50.0	0.0483^b
Endplate HU	464	272.5 $\pm$ 64.1	330.3 $\pm$ 90.4	<0.0001^b
Hypertension				0.7380
Yes	220	17 (43.6%)	203 (47.8%)
No	244	22 (56.4%)	222 (52.2%)
Rheumatoid arthritis				0.3321
Yes	14	2 (5.1%)	12 (2.8%)
No	450	37 (94.9%)	413 (97.2%)
Diabetes mellitus				0.6975
Yes	112	8 (20.5%)	104 (24.5%)
No	352	31 (79.5%)	321 (75.5%)
BMI >25 kg/m²				0.0394^b
Yes	284	30 (76.9%)	254 (59.8%)
No	180	9 (23.1%)	171 (40.2%)
Pre-op L1 HU <117				0.0951
Yes	213	23 (59.0%)	190 (44.7%)
No	251	16 (41.0%)	235 (55.3%)
Number of surgical levels
One	200	17 (43.6%)	183 (43.1%)	1.000
Two	264	22 (56.4%)	242 (56.9%)
Surgical level
L2-3	4	1 (2.6%)	3 (0.71%)	0.3913
L3-4	96	10 (25.6%)	86 (20.2%)
L4-5	284	22 (56.4%)	262 (61.6%)
L5–S1	80	6 (15.4%)	74 (17.4%)
Endplate
Superior	232	24 (61.5%)	208 (48.9%)	0.1801
Inferior	232	15 (38.5%)	217 (51.1%)

Data are presented as mean (standard deviation) or number (percentage).

^aP-values were calculated using the independent t-test for continuous variables and Fisher’s exact test for categorical variables.

^bSignificant result (P < 0.05).

BMI, body mass index.

The fusion rate at 6 months postoperatively was significantly higher in no CS and mild CS group(80.0%, no CS; 86.7%, mild CS; 0%, severe CS; P = 0.018) (Table 3). Notably, cage subsidence exceeding 4 mm was observed only in the non-fusion group (P = 0.0018). Although L1 HU did not differ significantly among the three groups, endplate HU values were markedly lower in both the mild and severe CS groups compared with the no-CS group. Nonetheless, the small sample size of the severe CS subgroup may limit the interpretability of this result (Table 4).

Table 3.

Fusion Status at 6-Month Postoperatively by Endplate (n = 464)

	N	Cage subsidence at 6 months			P
	N	No CS (<2 mm)	Mild CS (2-4 mm)	Severe CS (≥4 mm)	P
Non-fusion	94	86 (20.0%)	4 (13.3%)	4 (100%)	0.018*
Fusion	370	344 (80.0%)	26 (86.7%)	0 (0.0%)

Cage subsidence (CS) was categorized as no CS (<2 mm), mild CS (2-4 mm), and severe CS (≥4 mm)

*Significant result (P < 0.05).

Table 4.

Subsidence at 12-Month Postoperatively by Endplate (n = 464)

	Cage subsidence at 12 months			P
	No CS (<2 mm) n = 425	Mild CS (2-4 mm) n = 32	Severe CS (≥4 mm) n = 7	P
BMI (kg/m2)	26.7 ± 4.3	27.9 ± 4.7	26.6 ± 3.0	0.2853
L1 HU	127.2 ± 49.6	107.3 ± 38.2	127.2 ± 66.5	0.0891
Endplate HU	330.3 ± 90.4	271.7 ± 66.1	276.1 ± 58.5	0.0006*

*Significant result (P < 0.05).

Given the unique anatomical characteristics of the L5–S1 segment, a subgroup analysis was performed (Supplemental Table 1). Subsidence ≥4 mm occurred exclusively in the non-fusion group (P = 0.0338), indicating that substantial endplate collapse may be associated with an increased risk of non-fusion. Although endplate sclerosis appeared to have a protective effect against cage subsidence at L5–S1, subsidence ≥4 mm was occasionally observed even in sclerotic endplates, which may be attributed to intraoperative endplate injury during cage preparation (Supplemental Table 2).

The total number of complications did not differ between the two groups (P = 0.403). There was one case of wound infection, one case of nerve root injury, one case of screw loosening, one case of screw malposition, and two cases of anterior cage malposition in the non-CS group, whereas there were two cases of screw loosening and one case of nut loosening in the CS group. All complications were revised once the culprit was found, except in one case of an anteriorly placed cage that was asymptomatic. The revision rates were 3.8% and 8.3% in the non-CS and CS groups, respectively (Table 5).

Table 5.

Complications (n = 169)

Complications	CS group (n = 36)	Non-CS group (n = 133)	P-value
Perioperative
Dural tear	0	0	-
Wound problem/infection	0	1	-
Nerve root injury	0	1	-
Epidural hematoma	0	0	-
Implant-related
Screw loosening	2	1	-
Screw malposition	0	1	-
Cage malposition	0	2	-
Implant dislodgement	1	0	-
Total	3	6	0.403
Revision due to complication	3	5	-

Data are expressed as number of patients if not mentioned

The patient-reported outcomes between the CS and non-CS groups are summarized in Table 6. The mean preoperative VAS scores did not differ significantly between the two groups (non-CS, 6.2 ± 2.4; CS, 5.3 ± 2.6; P = 0.095). At both 6- and 12-month postoperative follow-ups, the VAS scores remained comparable (6 months: non-CS, 1.9 ± 1.7; CS, 1.8 ± 1.8; P = 0.983; 12 months: non-CS, 2.0 ± 1.3; CS, 2.3 ± 1.7; P = 0.273). The mean preoperative ODI scores were also not significantly different between the CS and non-CS groups (non-CS, 44.2 ± 19.5; CS, 41.8 ± 18.6; P = 0.573). Similarly, at 6- and 12-month follow-ups, the ODI scores were comparable (6 months: non-CS, 12.0 ± 12.3; CS, 14.7 ± 14.9; P = 0.314; 12 months: non-CS, 14.7 ± 8.8; CS, 16.9 ± 10.3; P = 0.205).

Table 6.

VAS and ODI Scores of CS and Non- CS Groups

Variables by endplate	n	CS group	n	Non-CS group	P
VAS (mean)
Pre-op	24	5.3 $\pm$ 2.6	292	6.2 $\pm$ 2.4	0.0948
6M VAS	26	1.8 $\pm$ 1.8	300	1.9 $\pm$ 1.7	0.9832
12M VAS	27	2.3 $\pm$ 1.7	314	2.0 $\pm$ 1.3	0.2730
ODI (mean)
Pre-op	23	41.8 $\pm$ 18.6	291	44.2 $\pm$ 19.5	0.5731
6M ODI	24	14.7 $\pm$ 14.9	294	12.0 $\pm$ 12.3	0.3137
12M ODI	29	16.9 $\pm$ 10.3	311	14.7 $\pm$ 8.8	0.2047

Results are shown as mean ± SDVAS, visual analog scale; ODI, Oswestry disability index; Δ, change.

*Significant result (P < 0.05)

The patient-reported outcomes between the fusion and non-fusion groups are summarized in Table 7. The preoperative VAS scores were not significantly different between the two groups (non-fusion, 5.9 ± 2.0; fusion, 6.1 ± 2.5; P = 0.372). At 6 and 12 months postoperatively, the VAS scores remained similar (6 months: non-fusion, 2.2 ± 1.8; fusion, 1.8 ± 1.6; P = 0.104; 12 months: non-fusion, 1.7 ± 1.2; fusion, 2.1 ± 1.3; P = 0.060). The mean preoperative and 6-month ODI scores were significantly lower in the fusion group than in the non-fusion group (preoperative: non-fusion, 48.8 ± 21.7; fusion, 42.9 ± 18.7; P = 0.033; 6 months: non-fusion, 15.1 ± 13.4; fusion, 11.4 ± 12.2; P = 0.036). At 12 months postoperatively, however, the ODI scores did not differ significantly between the two groups (non-fusion, 13.9 ± 7.1; fusion, 15.1 ± 9.3; P = 0.244).

Table 7.

VAS and ODI Scores of Non-fusion and Fusion Groups

Variables by endplate	n	Non-fusion group	n	Fusion group	P-value
VAS (mean)
Pre-op	60	5.9 $\pm$ 2.0	256	6.1 $\pm$ 2.5	0.3720
6M VAS	66	2.2 $\pm$ 1.8	260	1.8 $\pm$ 1.6	0.1035
12M VAS	62	1.7 $\pm$ 1.2	279	2.1 $\pm$ 1.3	0.0603
ODI (mean)
Pre-op	60	48.8 $\pm$ 21.7	254	42.9 $\pm$ 18.7	0.0328*
6M ODI	66	15.1 $\pm$ 13.4	252	11.4 $\pm$ 12.2	0.0360*
12M ODI	62	13.9 $\pm 7.1$	278	15.1 $\pm 9.3$	0.2443

Results are shown as mean ± SD VAS, visual analog scale; ODI, Oswestry disability index; Δ, change.

*Significant result (P < 0.05)

Predictive Factor and Cutoff Value for Subsidence Prediction

In multivariate logistic regression, obesity (BMI >25 kg/m²) and a lower endplate HU (odds ratio [OR] = 2.508, 95% confidence interval [CI] 1.135-5.546, P = 0.0231; odds ratio [OR] = 0.989, 95% confidence interval [CI] 0.983-0.995, P = 0.0004) (Table 8) were variables that significantly predicted subsidence. ROC curve analyses were performed, and the results demonstrated that the AUC (95% CI) of the endplate HU was 0.686 (0.601-0.770). The combined model, which included endplate HU and obesity (BMI >25), yielded an improved AUC (95% CI) of 0.727 (0.655-0.800) (Table 9, Figure 4). For patients with L1 HU <117, a higher endplate HU was identified as a significant protective factor against CS (non-CS, 295.2 ± 74.4; CS, 252.4 ± 55.8, P = 0.008) (Table 10). This result was similarly observed in patients who underwent single-level L4-5 MI-TLIF (non-CS, 284.1 ± 65.9; CS, 224.1 ± 48.6, P = 0.002) (Table 10). The cutoff endplate HU was determined to be 221 for patients with L1 HU <117, based on maximizing Youden’s J index. Patients with endplate HU <221 had an average subsidence rate of 27.3% (9 out of 33), whereas those with endplate HU ≥221 had an average subsidence rate of 7.8% (14 out of 180). After adjusting for age and BMI >25 kg/m2 and presence of RA, the odds of CS were 344% higher in patients with endplate HU <221 than in those with HU ≥221 (OR = 4.444, 95% CI 1.703-11.595, P = 0.0023) (Figure 5).

Table 8.

Multivariate Logistic Regression Analysis Using the Clinical Parameters of Cage Subsidence

Factor	Adjusted OR (95% CI)^a	P
BMI >25 kg/m²	2.508 (1.135-5.546)	0.0231*
Pre-op L1 HU	1.002 (0.991-1.013)	0.7523
Endplate HU	0.989 (0.983-0.995)	0.0004*

*Significant result (P < 0.05).

BMI, body mass index; OR, odds ratio.

Adjusted for age and presence of RA.

Table 9.

Area Under the Curve (AUC) for Endplate HU, Obesity, and Combined Models for Cage Subsidence

Risk predictor	Adjusted OR (95% CI)	P	AUC (95% CI)
Endplate HU	0.990 (0.984-0.995)	0.0002	0.686 (0.601-0.770)
BMI >25 kg/m²	2.244 (1.039-4.845)	0.0396	0.586 (0.515-0.657)
Combined model
Endplate HU & BMI >25 kg/m²			0.727 (0.655-0.800)

BMI, body mass index; OR, odds ratio.

Figure 4.

Receiver operating characteristic curve analysis of the model combining endplate HU and obesity for predicting cage subsidence

Table 10.

Subgroup Analysis of Cage Subsidence

Subgroup	No.	Cage subsidence		P
Subgroup	No.	Yes	No	P
Pre-op L1 HU <117	213	23	190
Endplate HU		252.4 $\pm$ 55.8	295.5 $\pm$ 74.4	0.0078*
At level L4-5 with pre-op L1 HU <117	130	13	117
Endplate HU		224.1 $\pm$ 48.6	284.1 $\pm$ 65.9	0.0018*

*Significant result (P < 0.05).

Figure 5.

The subsidence rate in osteoporotic patients (L1 HU < 117) was assessed using a cut-off value of 221 for endplate HU. Patients with endplate HU. Patients with endplate HU 25 kg/m2, and presence of RA, the odds of CS were 344% higher in patients with endplate H < 221 than in those with HU ≥ 221 (OR=4.444, 95% CI 1.703–11.595, P = 0.0023)

Discussion

We analyzed 464 endplates from 169 patients who underwent MI-TLIF and identified subsidence in 39 endplates. The preoperative lumbar spine endplate HU was used to assess the bone quality of the cage contact surface. Multivariate analysis revealed that obesity (BMI >25 kg/m²) and lower endplate HU values were significantly associated with increased subsidence rates. The findings indicated that the presence of two risk factors, obesity (BMI >25 kg/m²) and lower endplate HU, predicted CS, with an AUC of 0.727. In patients with L1 vertebral HU < 117, endplate HU < 221 was associated with a 3.44-fold higher risk of subsidence than endplate HU ≥ 221. This finding suggests that endplate sclerosis may serve as a protective factor against CS in patients with osteoporosis.

Because the endplate serves as the contact interface between the implants and vertebral bodies, pathological changes in the vertebral endplate, such as Modic changes (MCs), may influence load distribution and subsequently impact the occurrence of CS. Previous studies have suggested that endplate sclerosis can occur in endplates with MC types I, II, and III. The study by Liu et al²⁴ is consistent with our findings that these MCs are associated with endplate sclerosis and may serve as potential predictors for preventing CS in standalone OLIF procedures.²⁵ Additionally, MRI-based endplate bone quality (EBQ) scores have been proposed, with fatty infiltration-related MCs within the endplate leading to high EBQ scores. A high EBQ score was an independent predictor of CS in patients undergoing TLIF surgery.²⁶ Higher vertebral bone quality (VBQ) scores were first proposed by Soliman et al²⁷ to assist in identifying patients with osteoporosis at risk of CS after TLIF. Subsequent studies have demonstrated that EBQ scores provide greater accuracy than VBQ scores in predicting CS in patients with osteoporosis after TLIF.²⁸

The risk of CS is significantly associated with reduced BMD. Although BMD can be assessed preoperatively using DXA or quantitative CT (QCT), both methods have limitations. Both examinations involve radiation exposure, and neither modality is routinely performed in patients with degenerative lumbar disease. Additionally, BMD measurements may overestimate bone quality in patients with degenerative lumbar conditions or vascular calcification. QCT devices are not widely available in Taiwan and have limited accessibility. Therefore, not all patients underwent this examination before surgery. Although MRI is one of the most sensitive and specific modalities for evaluating the lumbar spine, CT is often the first imaging modality of choice because of its ability to efficiently provide detailed vertebral information. Lumbar spine CT^29-32 has been widely recognized as a crucial preoperative diagnostic tool for patients presenting with degenerative lumbar pathologies. Our study maximized the utility of lumbar spine CT to measure endplate HU and proposed an HU cutoff to predict the occurrence of CS following MI-TLIF.

CT-based vertebral HU values could be a more effective predictor of lumbar CS than the T-score of DXA in TLIF.¹⁹ Barbosa et al established a cut-off value of 135 at the L1 vertebrae using routine lumbar spine CT, and the result showed that HU <135 was an independent risk factor for CS after TLIF and PLIF (OR = 6, 95%CI = 1.95-34).¹⁷ Our previous study also identified a first lumbar vertebra HU <117 as a predictor of CS in patients who underwent MI-TLIF.²⁰ A meta-analysis and systematic review also reported that vertebral body HU is a protective factor CS following oblique lumbar interbody fusion (OR = 0.97, 95%CI = 0.95-1.00, P = 0.02).¹⁸ We drew inspiration from previous research suggesting that endplate HU provides better risk estimation for problems in implant-bone contact surfaces and predicts subsidence more effectively than vertebral HU. Our findings indicate that endplate sclerosis (HU ≥221) is a protective factor in patients with osteoporosis who are susceptible to CS.

The correlation between BMI and CS remains an area of ongoing debate. Our previous study found that an increased BMI was associated with higher subsidence rates following MI-TLIF.¹³ Behrbalk et al³³ also reported that a higher BMI increased risk in a stand-alone ALIF cohort. However, other studies did not identify obesity as a risk factor for CS in patients undergoing LLIF or ALIF.^34-36 Our findings suggest that obesity (BMI >25 kg/m²) does play a significant role in subsidence after MI-TLIF.

Since the threshold for developing clinical symptoms following CS has not been clearly established, we adopted the definition by Cho et al,³⁷ which considers ≥2 mm cage migration into the endplates, which represents a 20-30% reduction in disc height, as indicative of CS. To further evaluate the relationship between severity of CS and fusion, we classified the severity of subsidence into mild (2-4 mm) and severe (≥4 mm) categories. CS ≥ 4 mm was observed only in the non-fusion group, implying that substantial endplate collapse may compromise interbody stability and negatively affect the fusion process (Table 3, Supplemental table 1). Our results suggest that endplate HU may serve as a more reliable predictor of cage subsidence compared with L1 HU, highlighting the importance of local bone quality at the implant–endplate interface (Table 4, Supplemental table 2). Our findings suggest that endplate damage during preparation may increase the risk of CS, thereby reinforcing the protective effect of endplate sclerosis. This is consistent with previous work indicating that overzealous removal of the bony endplate can precipitate subsidence³⁸ and that the presence of sclerosis is associated with lower rates of intraoperative endplate injury and subsequent subsidence³⁹ Consequently, careful surgical technique aimed at preserving endplate integrity—not simply the presence of sclerosis—may reduce the risk of severe subsidence and thus decrease the possibility of non-fusion.

We further examined the correlation between functional outcomes and both CS (Table 6) and fusion status (Table 7). The results showed that CS greater than 2 mm at either 6 or 12 months postoperatively was not associated with poorer functional outcomes. However, patients who achieved fusion demonstrated significantly better ODI scores at 6 months compared with the non-fusion group, suggesting that successful fusion may contribute to improved early functional recovery.

Most studies have shown that the correlation between CS and patient-reported outcomes remains controversial, with clinical deterioration after PLIF and TLIF not being directly related to subsidence.^14,40 Some studies have reported that CS-related disc height reduction may lead to restenosis of the foramen regions or loss of segmental lumbar lordosis, resulting in unsatisfactory outcomes. Aoki et al⁴¹ reported that postoperative loss of lumbar lordosis is associated with greater residual low back pain in short-segment TLIF cohorts, which may explain the differences in the improvement of outcome scores.

The main limitations of this study are its small cohort and retrospective nature, which introduce observer-expectancy selection bias. These factors limit the generalizability of our findings to broader populations. Further multicenter prospective studies are warranted to validate these findings. Although rheumatoid arthritis did not show a significant difference between the CS and non-CS groups, the small number of RA patients in our cohort may have limited the power to detect a true association. Another limitation is that preoperative Modic changes were not evaluated. Although MCs are often discussed in relation to endplate pathology, the presence or stage of MCs does not necessarily correspond to endplate sclerosis. Liu et al²⁴ demonstrated that while sclerosis was more commonly observed in MC2 and MC3, many endplates with Modic changes did not exhibit sclerosis on CT or radiography. Because the primary objective of our study was to quantify endplate bone quality using CT-based HU rather than MRI findings, preoperative MC staging was not included in our dataset. Future studies incorporating both MRI-based MC classification and quantitative CT analysis may provide further insight into the interplay between Modic changes and endplate sclerosis. Due to the limited availability of preoperative DXA in our patients, we were unable to assess the correlation between DXA and endplate HU. Endplate destruction is a potential factor in CS; however, we did not investigate the relationship between CS and endplate injury during surgery. Nevertheless, experienced surgeons performed surgery on all patients using a consistent surgical technique.

Conclusion

This is the first study to use endplate HU values from standard lumbar spine CT to predict postoperative CS in patients undergoing MI-TLIF. Our results showed that obesity (BMI >25 kg/m²) and lower endplate HU were only independent predictor of CS after MI-TLIF. Surgical level endplate sclerosis may be screened preoperatively, as it is a protective factor for CS.

Supplemental Material

Supplemental Material - Lumbar Spine Endplate Sclerosis is a Protective Factor for Cage Subsidence in Minimally Invasive Transforaminal Lumbar Interbody Fusion

Supplemental Material for Trust in Lumbar Spine Endplate Sclerosis is a Protective Factor for Cage Subsidence in Minimally Invasive Transforaminal Lumbar Interbody Fusion by Hung-Kai Liao, Po-Chun, Liu, Hsi-Hsien Lin, Po-Hsin Chou, Shih-Tien Wang, Ming-Chau Chang, Chien-Lin Liu, Yu-Cheng Yao in Global Spine Journal.

Footnotes

ORCID iDs

Hung-Kai Liao

Hsi-Hsien Lin

Po-Hsin Chou

Shih-Tien Wang

Ming-Chau Chang

Yu-Cheng Yao

Ethical Considerations

The study protocol was approved by the IRB of Taipei Veterans General Hospital (IRB No.2022-04-009CC).

Consent to Participate

Written informed consent was obtained from all the participants. All procedures were performed in accordance with relevant guidelines.

Author Contribution

Concept, literature search and data collection: H-KL, Y-CY. Statistics, data analysis and interpretation: H-KL, P-CL. Drafting article: H-KL, P-CL, Y-CY. Critical revision of article: H-HL, P-HC, S-TW, M-CC, C-LL. All authors have read and approved the manuscript

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Declaration of Conflicting Interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data Availability Statement

The datasets generated and analyzed during the current study are available from the corresponding author upon reasonable request.*

Supplemental Material

Supplemental material for this article is available online.

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