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Imaging observation of
intervertebral disc degeneration in
patients with old thoracolumbar
fracture-related kyphotic deformity
Xi-long Cui1,3,4,5, Ao Ding2,5, Wen Yin1,4, Wan-mei Yang1,4, Wei Zhang1,4, Hao Wu1,4,
Ji-shi Jiang1,4, Yun-lei Zhai1,4, Zi-kai Hua3,4 & Hai-yang Yu1,4
Old thoracolumbar fracture with kyphosis (OTLFK) often results in low back pain, with intervertebral
disc degeneration being a signicant contributor. We hypothesized that patients with OTLFK
exhibit distinct patterns of disc degeneration compared to those with chronic low back pain without
kyphotic deformity. This study aimed to investigate the characteristics of disc degeneration in
OTLFK patients and explore its association with sagittal spinal parameters and endplate injury. A
retrospective analysis was conducted on 52 patients with OTLFK (observation group, OG) and 104
age-, gender-, and BMI-matched patients with chronic low back pain (control group, CG) treated at
our hospital between February 2017 and March 2023. Intervertebral disc degeneration from T11/12
to L5/S1 was assessed using MRI T2-weighted images and the Prrmann grading system. Sagittal
spinal parameters—including lumbar lordosis (LL), thoracic kyphosis (TK), local kyphosis Cobb angle
(LKCA), thoracolumbar kyphosis (TLK), pelvic tilt(PT), sacral slope(SS), and sagittal vertical axis
(SVA)—and endplate injury grades were measured in the OG. Dierences in disc degeneration between
the two groups were compared, and correlations between disc degeneration, sagittal parameters,
and endplate injury were analyzed. The OG exhibited signicantly higher overall disc degeneration
grades compared to the CG (p < 0.05), particularly at levels T11/12, T12/L1, L1/2, and L2/3. In the OG,
grade IV and V degenerations were predominantly found from T11/12 to L2/3, whereas in the CG,
they were mainly at L4/5 and L5/S1. Disc degeneration in the OG was signicantly correlated with
sagittal parameters and endplate injury grades (p < 0.05). Patients with OTLFK have higher grades of
disc degeneration in the thoracolumbar region compared to those with chronic low back pain without
kyphosis. Disc degeneration in OTLFK is associated with abnormal sagittal alignment and endplate
injury, suggesting that kyphotic deformity and altered spinal biomechanics contribute to accelerated
disc degeneration.
Keywords Old fracture, Kyphosis, Disc degeneration, Endplate injury, Sagittal parameters
Abbreviations
OTLFK old thoracolumbar fracture with kyphotic
OG observed group
CG control group
LL lumber lordosis
TK thoracic kyphosis
LKCA local kyphosis vertical cobb angle
TLK thoracolumbar kyphosis
SVA sagittal vertical axis
PT pelvic tilt
SS sacral slope
1Aliated Fuyang People’s Hospital of Anhui Medical University, Sanqing Road 501, Fuyang 236000, Anhui, China.
2Medical College, Hubei University for Nationalities, Enshi City, Hubei, China. 3School of Mechanical Engineering
and Automation, Shanghai University, Shanghai, China. 4Anhui Province Clinical Medical Research Center for
Spinal Deformities, Hefei, Anhui, China. 5Xi-long Cui and Ao Ding contributed equally to this work. email:
fy.yhy@163.com
OPEN
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Old thoracolumbar fracture with kyphosis (OTLFK) is characterized by a kyphotic deformity resulting from
improperly treated or delayed treatment of thoracolumbar fractures. e loss of anterior vertebral body height
leads to abnormal curvature of the spine1,2. Patients with OTLFK frequently experience low back pain, a common
complication associated with kyphotic deformities3. Causes of low back pain in these patients include spinal
stenosis, facet joint arthritis, and intervertebral disc degeneration4,5 with disc degeneration being a signicant
independent contributor6–8. Recent studies indicate that kyphotic deformities exacerbate abnormal mechanical
loading on the intervertebral discs, potentially accelerating degeneration9.
Intervertebral disc degeneration is inuenced by various factors such as abnormal mechanical stress10–12,
endplate injury13, and alterations in sagittal spinal alignment14,15. Specically, sagittal malalignment due to
kyphotic deformity has been shown to increase disc degeneration by changing load distributions along the spinal
column16. Previous studies have shown that individuals with scoliosis exhibit higher grades of disc degeneration
compared to healthy individuals, suggesting that spinal deformities can accelerate degenerative processes.
However, the patterns and mechanisms of disc degeneration in patients with OTLFK have not been thoroughly
investigated. However, the patterns and mechanisms of disc degeneration in patients with OTLFK have not been
thoroughly investigated, particularly in comparison to other spinal deformities like scoliosis17.
We hypothesized that patients with OTLFK have distinct characteristics of intervertebral disc degeneration
compared to patients with chronic low back pain without kyphotic deformity, and that this degeneration is
related to abnormal sagittal spinal-pelvis parameters and endplate injury resulting from the kyphotic deformity.
Understanding these relationships is crucial for developing targeted interventions to alleviate low back pain and
prevent further degeneration in these patients.
e purpose of this retrospective study was to compare the characteristics and distribution of intervertebral
disc degeneration between patients with OTLFK and matched controls with chronic low back pain. Additionally,
we aimed to identify factors associated with disc degeneration in OTLFK patients by analyzing the correlations
between disc degeneration grades, sagittal spinal parameters, and endplate injury grades.
Materials and methods
General information
All methods were performed in accordance with the relevant guidelines and regulations of the Ethics Committee
of the Aliated Fuyang People’s Hospital of Anhui Medical University. Signed informed consents were obtained
from all participants involved in the study.
Between February 2017 and March 2023, patients diagnosed with OTLFK at our hospital were retrospectively
enrolled in the observation group (OG). Inclusion criteria were: (1) MRI-conrmed old spinal fracture with
vertebral wedge deformity; (2) local kyphotic Cobb angle greater than 20°; (3) fracture duration of at least 6
months; and (4) complete imaging data, including MRI images of T11-S1 and full-length lateral radiographs
of the spine. Exclusion criteria were: (1) fresh fractures; (2) incomplete imaging data or unclear MRI images
of T11-S1; (3) history of spinal surgery; and (4) pathological fractures due to tumors or kyphotic deformities
caused by spinal inammation.
Based on these criteria, 52 patients (14 males and 38 females) with OTLFK were included. e patients’ ages
ranged from 53 to 77 years (mean age: 64.8 ± 6.4 years), and the duration of the condition ranged from 6 to 288
months (mean duration: 39.0 ± 59.5 months).
A control group (CG) of 104 patients (28 males and 76 females) with chronic low back pain was established by
matching patients according to age, gender, and body mass index (BMI) with those in the OG. Inclusion criteria
for the CG were: (1) matching the OG patients in gender, age (within 1-year dierence), and BMI (within 5%
dierence); (2) diagnosis of chronic low back pain according to established criteria18; and 3) complete MRI data
clearly showing the T11-S1 intervertebral discs. e main purpose of this study was to study disc degeneration
of kyphotic deformity in old spinal fractures, therefore, we selected patients with chronic low back pain who
may be caused by disc degeneration. Hence, we made exclusion criteria for the CG: (1) history of spinal surgery;
(2) low back pain caused by ankylosing spondylitis, rheumatoid arthritis, tumors, or other conditions; and (3)
spinal deformities.
Methods
Grade of intervertebral disc degeneration and endplate injury
Intervertebral disc degeneration from T11/12 to L5/S1 was evaluated using MRI T2-weighted images, applying the
Prrmann grading system19, which classies disc degeneration into grades I to V based on disc structure, signal
intensity, and distinction between nucleus pulposus and annulus brosus. (as shown in Fig.1). We evaluated disc
degeneration and endplate injury using a 1.5T MRI scanner (uMR 560, United Imaging, Shanghai, China ) with
a 24-channel spinal coil. All images of the lumbar spine were acquired in the sagittal plane using the following
parameters: eld of view = 330 × 320 cm, thickness = 4mm, number of slices = 12, and matrix = 352 × 60. A 2D
fast spin-echo T2-weighted sequence, echo time (TE) = 74.76ms, and repetition time (TR) = 2500 ms were used
for anatomical reference and IVD segmentation.
Endplate injury was assessed using the Rajasekaran grading as follows20: Grade 1, cartilaginous endplate was
normal in shape without cracks or defects; Grade 2, cartilage endplate is locally or globally thin, without cracks
or defects; Grade 3, nucleus and bone marrow contact, but the cartilage endplate outline is still present: Grade 4,
cartilage endplate injury area reaches 25%, usually accompanied by modic changes; Grade 5, cartilage endplate
injury area reaches 50%, accompanied by modic changes; and Grade 6, cartilage endplate suered extensive
damage until complete destruction disappeared.
e grade of intervertebral disc degeneration and endplate injury is rst judged by a doctor with 5 years
of experience in spinal surgery. A second doctor with 10 years of experience in spinal surgery does the same
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thing without knowing the judgment of the previous doctor. If there is a disagreement and no consensus can be
reached, the corresponding author, who has 30 years of experience in spinal surgery, makes the nal judgment.
Measurement of sagittal spinal and pelvic parameters
e spinal parameters were examined and recorded including oracic kyphosis (TK), Local kyphosis Cobb
angle (LKCA), Lumber lordosis (LL), oracolumbar kyphosis (TLK), Sagittal vertical axis (SVA), Pelvic tilt
(PT) and Sacral slope (SS)21.
Statistical analysis
Statistical analysis was performed using SPSS version 27.0 (IBM Corp., Armonk, NY, USA). Continuous variables
are presented as (
−
x
± s), and categorical variables are presented as frequencies or percentages. e rank-sum test
was performed to compare the dierences in disc degeneration grades at each level between the two groups, as
well as the distribution of dierent degeneration grades. Nonparametric tests for two independent samples and
correlation analyses were conducted to assess the relationships between disc degeneration grades, sagittal spinal
parameters, and endplate injury grades. A p-value < 0.05 was considered statistically signicant.
Results
Distribution of intervertebral disc degeneration grades
In the OG, the numbers of intervertebral discs with Prrmann grades I to V degeneration from T11-S1 were 0,
18, 148, 160, and 38 discs, respectively. In the CG, the corresponding numbers were 12, 166, 267, 270, and 13
discs, respectively. e overall disc degeneration grades were signicantly higher in the OG compared to the CG
(p < 0.05). e degeneration grades and their distribution are presented in Table1. At the T11/12, T12/L1, L1/2,
and L2/3 levels, the OG showed signicantly higher degeneration grades than the CG (p < 0.05). No signicant
dierences were observed between the two groups at L3/4, L4/5, and L5/S1 levels (p > 0.05). (Fig.2A). In the OG,
grade IV and V degenerations were predominantly concentrated from T11/12 to L2/3, whereas in the CG, they
were mainly at L4/5 and L5/S1 levels. e dierence in the distribution of high-grade degeneration between the
two groups was statistically signicant. However, there was no signicant dierence in the distribution of grades
II and III degeneration (p > 0.05) (Fig.2B).
Degeneration grade/
group
Segment, n (%)
T 11/12 T 12/L1 L 1/2 L 2/3 L 3/4 L 4/5 L 5/S1
IOG 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0)
CG 11 (91.7) 1 (8.3) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0) 0 (0.0)
II OG 5 (29.4) 7 (41.2) 5 (29.4) 0 (0.0) 0 (0.0) 1 (5.9) 0 (0.0)
CG 38 (22.9) 57 (34.3) 40 (24.1) 16 (9.6) 5 (3.0) 2 (1.2) 8 (4.8)
III OG 18 (12.2) 21 (14.2) 22 (14.9) 19 (12.8) 23 (15.5) 20 (13.5) 25 (16.9)
CG 26 (9.7) 28 (10.5) 31 (11.6) 49 (18.4) 51 (19.1) 40 (15.0) 42 (15.7)
IV OG 19 (11.9) 13 (8.1) 20 (12.5) 31 (19.3) 28 (17.5) 28 (17.5) 21 (13.1)
CG 28 (10.4) 16 (5.9) 33 (12.2) 36 (13.3) 48 (17.8) 59 (21.9) 50 (18.5)
VOG 10 (26.3) 11 (29.0) 5 (13.2) 2 (5.3) ) 1 (2.6) 3 (7.9) 6 (15.8)
CG 1 (7.7) 2 (15.4) 0 (0.0) 3 (23.1) 0 (0.0) 3 (23.1) 4 (30.8)
Signicance/P < 0.01 < 0.01 < 0.01 < 0.01 0.15 0.84 0.92
Tab le 1. Statistical table of intervertebral disc degeneration grades in the two groups.
Fig. 1. Disc degeneration Prrmann grade A to E are used for grades I to V, respectively.
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Correlation analysis of disc degeneration with sagittal parameters
e mean sagittal spinal parameters in the OG were as follows: TK,45.4 ± 20.1°; TLK,43.6 ± 17.7°; LKCA,
45.3 ± 17.0°; LL, 41.4 ± 17.2°; SS, 28.6 ± 9.5°; PT, 26.7 ± 8.2° and SVA, 4.9 ± 4.3cm. e results of the correlation
analysis are presented in Table2. Degeneration at the T11/12 intervertebral disc was positively correlated with
TLK and LL(p < 0.05). Degeneration at T12/L1 was also positively correlated with TK, TLK, LKCA, and LL
(p < 0.05). Degeneration at L1/2 was positively correlated with TLK and LKCA(p < 0.05). Degeneration at L2/3
was positively correlated with TLK and LKCA (p < 0.05)., and degeneration at L3/4 was positively correlated
with SVA (p < 0.05). Degeneration at L5/S1 was positively correlated with LL and SVA (p < 0.05). For pelvic
parameters, SS was negatively associated with T11 / 12, T12 / L1 and L1 / 2 disc degeneration grades, while PT
was positively associated with T11 / 12 and T12 / L1(p < 0.05).
Relationship between endplate injury distribution, sagittal parameters, and disc
degeneration
In the OG, the numbers endplate with Rajasekaran grades I–VI injury from T11-S1 were 12, 1, 51, 152, 60, and
108, respectively. High-grade endplate injuries were predominantly found from T11 to L3. e distribution of
endplate injuries is shown in Fig.3. Correlation analysis revealed a positive correlation between endplate injury
grades and disc degeneration grades (r = 0.46, p < 0.05). e incidence of Schmorl’s nodes was 12.8%, with 62.6%
occurring in the upper endplate and 37.4% in the lower endplate. Endplate injury grades were also correlated
with sagittal Spine and pelvic parameters. Endplate injury was correlated with sagittal parameters as shown in
Table3.
Discussion
is study demonstrated that patients with OTLFK have signicantly higher grades of intervertebral disc
degeneration in the thoracolumbar region compared to patients with chronic low back pain without kyphotic
Parameter
¯x
±s R/P
Segment
T 11/12 T 12/L1 L 1/2 L 2/3 L 3/4 L 4/5 L 5/S1
T K 45.4± 20.1° R 0.25 0.30 0.12 0.08 0.09 0.09 0.08
P 0.11 0.05* 0.45 0.61 0.57 0.56 0.62
T LK 43.6± 17.7° R 0.31 0.41 0.36 0.29 0.06 0.01 0.06
P 0.027* 0.003* 0.01* 0.038* 0.66 0.95 0.675
L KCA 45.3± 1 7.0° R 0.23 0.42 0.39 0.28 0.007 0.17 0.09
P 0.112 0.002* 0.005* 0.045 0.96 0.42 0.54
L L 41. 4± 17.2° R 0.3 0.3 0.23 0.009 0.17 0.12 0.39
P 0.036* 0.03* 0.11 0.95 0.22 0.4 0.005*
S VA 4. 9± 4.32
cm
R 0.01 0.004 0.15 0.055 0.3 0.18 0.32
P 0.5 0.7 0.3 0.7 0.049* 0.233 0.034*
SS 28.6 ± 9.5° R−0.92 −0.51 −0.28 0.02 0.11 0.12 0.11
P 0.01* 0.01* 0.05* 0.87 0.44 0.4 0.45
PT 26.7 ± 8.2° R 0.29 0.37 0.41 0.02 0.16 0.2 0.03
P 0.036* 0.007* 0.003* 0.9 0.27 0.15 0.84
Tab le 2. Correlation between disc degeneration and sagittal parameters. *Means P < 0.05, statistically
signicant.
Fig. 2. IDD grade, (A) the distribution of each disc degeneration grade; (B) the distribution of segments of the
same degeneration grade(*means P < 0.05, **means P < 0.01, ***means P < 0.001).
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deformity. Specically, high-grade degenerations were predominantly observed from T11/12 to L2/3 in
the OTLFK group, while in the control group, they were mainly at L4/5 and L5/S1 levels. Additionally, disc
degeneration in OTLFK patients was associated with abnormal sagittal spinal parameters and endplate injury.
Low back pain is a common symptom in patients with OTLFK3, and disc degeneration plays a signicant
role in its pathogenesis. In our study, grade IV–V disc degeneration accounted for 54.4% of cases in the
OTLFK group, compared to 38.9% in the control group. is higher incidence of severe disc degeneration may
contribute to the increased prevalence of low back pain in patients with kyphotic deformity resulting from old
spinal fractures. Disc degeneration leads to a loss of intervertebral height and induces inammatory responses5,8,
Parameter/group
Segment
T11/12 T12/L1 L1/2 L2/3 L3/4 L4/5 L5/S1
TK R 0.53 0.26 0.25 0.05 0.25 0.09 0.21
P 0.02* 0.09 0.1 0.75 0.1 0.57 0.16
TLK R 0.42 0.41 0.37 0.18 0.025 0.1 0.21
P 0.003* 0.003* 0.009* 0.21 0.86 0.47 0.15
LKCA R 0.4 0.38 0.29 0.2 0.06 0.13 0.22
P 0.004* 0.007* 0.039* 0.18 0.69 0.37 0.12
LL R 0.33 0.26 0.12 0.11 0.17 0.06 0.02
P 0.02* 0.07* 0.42 0.47 0.23 0.7 0.9
SVA R 0.19 0.26 0.13 0.2 0.2 0.19 0.04
P 0.22 0.09 0.42 0.2 0.17 0.22 0.98
SS R−0.31 −0.4 −0.17 0.16 0.07 0.05 −0.9
P 0.028* 0.004* 0.25* 0.28 0.62 0.97 0.54
PT R 0.17 0.3 0.01 0.015 0.2 0.12 0.2
P 0.24 0.03* 0.93 0.92 0.17 0.12 0.13
Tab le 3. Correlations between endplate injuries and sagittal parameters. *Means P < 0.05, statistically
signicant.
Fig. 3. Distribution of damage grades in each segments.
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ultimately causing low back pain. e mechanisms underlying disc degeneration are complex and multifactorial,
involving biomechanical changes, aging, genetic factors, cellular metabolic abnormalities, and the involvement
of inammatory cytokines8,22–25.
Abnormal mechanical stress is a critical factor in the development of disc degeneration. Increased stress can
directly damage the disc, disrupt intradiscal pressure balance, and cause structural alterations. is abnormal
load distribution further impairs the mechanical function of the disc, transferring excessive stress to the annulus
brosus, leading to its damage and contributing to pain6,26.
In patients with spinal deformities, such as idiopathic scoliosis and degenerative scoliosis, the apical vertebral
region experiences stress concentration, resulting in higher grades of disc degeneration compared to other
regions10,27. Yeung et al. reported that in adult patients with scoliosis, the nucleus pulposus deviates towards the
convex side of the curve, indicating uneven pressure distribution28. In cases of thoracolumbar disc herniation,
disc herniation is more likely to occur in the apical vertebral region and may be stress-related14.
In OTLFK, the kyphotic deformity alters the normal sagittal alignment of the spine, leading to abnormal
biomechanical forces on the intervertebral discs. e kyphotic angulation increases anterior shear forces
and compressive stresses on the anterior column of the spine, particularly at the apex of the deformity29,
conrming that kyphosis can cause disc stress abnormalities. is excessive stress on the anterior portions of the
intervertebral discs accelerates degenerative changes. Animal studies have shown that kyphotic deformities can
double the incidence of disc extrusion compared to normal spines30, conrming that kyphosis can cause stress
abnormalities that promote disc degeneration.
e thoracolumbar junction is a transitional zone between the thoracic kyphosis and lumbar lordosis,
making it susceptible to fractures and biomechanical stress concentration. In our study, 94% of OTLFK patients
had the apex of the kyphotic deformity located between T11 and L2. is localization corresponds to the area
where we observed the highest grades of disc degeneration. In contrast, in the control group, disc degeneration
was more prevalent at L4/5 and L5/S1 levels, which is consistent with previous studies indicating that these levels
are commonly aected by degenerative changes due to their high mobility and load-bearing functions31.
Interestingly, we found no signicant dierence in disc degeneration at L3/4, L4/5, and L5/S1 levels between
the two groups. is may be explained by compensatory mechanisms in patients with OTLFK, who oen exhibit
increased lumbar lordosis to maintain sagittal balance32. Increased lumbar lordosis may unload the anterior disc
and shi stress posteriorly towards the facet joints, potentially reducing disc degeneration at these levels15,32.
Additionally, the lower lumbar spine is farther from the apex of the kyphotic deformity and may be less aected
by the abnormal biomechanics associated with OTLFK28. Finally, Disc degeneration is associated with advancing
age33; hence, in both groups in this study, older patients had higher grades of degeneration.
Our ndings also highlight the relationship between sagittal spinal parameters and disc degeneration.
Abnormal sagittal alignment in OTLFK, characterized by decreased TK and increased TLK and LKCA, may
exacerbate shear and compressive forces on the intervertebral discs34. Larger TLK and LKCA indicate sharper
kyphotic deformities, which can increase anterior shear forces on the discs, promoting degeneration. Moreover,
sagittal imbalance, reected by increased SVA, shis the body’s center of gravity anteriorly, increasing the
load on the anterior column and contributing to disc degeneration35,36. However, in our study, the mean SVA
was 4.9cm, indicating that the patients did not have severe sagittal imbalance, which may explain the lack
of consistent correlation between SVA and disc degeneration at any levels. e compensatory mechanism of
kyphotic deformity in old spinal fractures is complex, and although we found a relationship between TK, TLK,
LACK, LL, and SVA and disc degeneration, none of the parameters was associated with disc degeneration at all
levels. erefore, large, stratied studies are required in the future.
In the sagittal parameters of the pelvis, Pelvic Incidence (PI), PT, and SS are commonly used indicators to
describe the anterior-posterior tilting state of the pelvis. e geometric relationship among these parameters is
dened as PI = PT + SS37. When assessing pelvic tilt, one can focus solely on the SS and PT parameters. In the
context of OTLFK, changes in pelvic tilt are observed, characterized by a retroversion of the pelvis, resulting in
a decrease in SS and an increase in PT32. is alteration occurs as a compensatory mechanism for thoracic and
lumbar kyphosis. Specically, an increase in TLK and LKCA, along with a decrease in SS and an increase in PT,
reects the adaptive adjustments of the pelvis during the restructuring of spinal morphology. Our results had
indicated a positive correlation between LKCA and TLK with the grade of intervertebral disc degeneration;
therefore, SS was negatively correlated with intervertebral disc degeneration, while PT showed a positive
correlation. Similar patterns had been observed in cases of endplate injury, further underscoring the signicance
of pelvic parameters in the pathological changes of the spine.
Endplate injury is closely associated with disc degeneration38. Damage to the endplate disrupts the nutritional
supply to the disc and alters the biomechanical environment, accelerating degenerative processes. In OTLFK
patients, endplate injuries were concentrated in the thoracolumbar region and were positively correlated with
disc degeneration grades. e kyphotic deformity and associated abnormal stress may lead to endplate fractures
and further exacerbate disc degeneration.
is study has several limitations. It was a retrospective analysis conducted at a single center with a relatively
small sample size, which may introduce selection bias. e cross-sectional design limits the ability to establish
causality between sagittal alignment, endplate injury, and disc degeneration. Longitudinal studies with larger
cohorts are needed to conrm these ndings. Additionally, biomechanical studies and in vitro experiments
could provide further insights into the mechanisms by which kyphotic deformity inuences disc degeneration.
Conclusion
Patients with OTLFK exhibit higher grades of intervertebral disc degeneration in the thoracolumbar region
compared to those with chronic low back pain without kyphosis. Disc degeneration in OTLFK is associated with
abnormal sagittal spine, pelvis alignment and endplate injury. ese ndings suggest that kyphotic deformity
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alters spinal biomechanics, leading to increased stress on the anterior column and accelerating disc degeneration.
Understanding these mechanisms is essential for developing targeted treatments to alleviate low back pain and
prevent further degeneration in patients with OTLFK.
Data availability
e patients’ data were collected in the Aiated Fuyang People’s Hospital of Anhui Medical University. e
datasets used and analyzed during the current study are available from the corresponding author on reasonable
request.
Received: 23 May 2024; Accepted: 9 December 2024
References
1. Seo, D. K. et al. Analysis of the risk factors for unfavorable radiologic outcomes aer Fusion surgery in oracolumbar Burst
fracture: what amount of postoperative thoracolumbar kyphosis correction is reasonable? J. Korean Neurosurg. S. 62 (1), 96–105
(2019).
2. Muratore, M., Ferrera, A., Masse, A. & Bistol, A. Osteoporotic vertebral fractures: predictive factors for conservative treatment
failure. A systematic review. Eur. Spine J. 27 (10), 2565–2576 (2018).
3. Schoenfeld, A. J. et al. Posttraumatic kyphosis: current state of diagnosis and treatment: results of a multinational survey of spine
trauma surgeons. J. Spinal Disord Tech. 23 (7), e1–e8 (2010).
4. Kuslich, S. D., Ulstrom, C. L. & Michael, C. J. e tissue origin of low back pain and sciatica: a report of pain response to tissue
stimulation during operations on the lumbar spine using local anesthesia. Orthop. Clin. N Am. 22 (2), 181–187 (1991).
5. Karunanayake, A. L., Pathmeswaran, A. & Wijayaratne, L. S. Chronic low back pain and its association with lumbar vertebrae and
intervertebral disc changes in adults. A case control study. Int. J. Rheum. Dis. 21 (3), 602–610 (2018).
6. Schwarzer, A. C. et al. e relative contributions of the disc and zygapophyseal joint in chronic low back pain. Spine 19 (7),
801–806 (1994).
7. Park, E. H. et al. Disc degeneration induces a mechano-sensitization of disc aerent nerve bers that associates with low back pain.
Osteoarthr. Cartil. 27 (11), 1608–1617 (2019).
8. Chepurin, D. et al. Bony stress in the lumbar spine is associated with intervertebral disc degeneration and low back pain: a
retrospective case-control MRI study of patients under 25 years of age. Eur. Spine J. 28 (11), 2470–2477 (2019).
9. Chen, X. et al. Relationship between lumbar disc herniation and roussouly classication in the sagittal alignment of the spine and
pelvis in young people. Quant. Imag. Med. Surg. 13 (7), 4687–4698 (2023).
10. Li, J. et al. Construction of the adjusted Scoliosis3D nite element model and Biomechanical Analysis under gravity. Orthop. Surg.
15 (2), 606–616 (2023).
11. Fan, W., Zhang, C., Zhang, D., Guo, L. & Zhang, M. Biomechanical responses of the human lumbar spine to vertical whole-body
vibration in normal and osteoporotic conditions. Clin. Biomech. 102, 105872 (2023).
12. Wang, H., Li, N., Huang, H., Xu, P. & Fan, Y. Biomechanical eect of intervertebral disc degeneration on the lower lumbar spine.
Comput. Method Biomec 1–9. (2022).
13. Subramanian, P. et al. Evaluation of disc and Endplate Degeneration in AO Type A fractures using magnetic resonance imaging
analysis. World Neurosurg. 178, e758–e765 (2023).
14. Gao, A., Wang, Y., Yu, M. & Liu, X. Analysis of sagittal prole and radiographic parameters in symptomatic thoracolumbar disc
herniation patients. Bmc Musculoskel Dis. 22(1). (2021).
15. Park, K. H. et al. e Association between Sagittal Plane Alignment and Disc Space narrowing of lumbar spine in Farmers. Annals
Rehabilitation Med. 45 (4), 294–303 (2021).
16. Kim, H. J. et al. e mid-term outcome of intervertebral disc Degeneration aer Direct Ver tebral Rotation in adolescent idiopathic
scoliosis. Spine 49 (23), 1661–1668 (2024).
17. Shang, Z. et al. e eect of global spinal alignment on cervical degeneration in patients with degenerative lumbar scoliosis. Worl d
Neurosurg. 190, e595–e603 (2024).
18. Kreiner, D. S. et al. Guideline summary review: an evidence-based clinical guideline for the diagnosis and treatment of low back
pain. Spine J. 20 (7), 998–1024 (2020).
19. Urrutia, J. et al. e Prrmann classication of lumbar intervertebral disc degeneration: an independent inter- and intra-observer
agreement assessment. Eur. Spine J. 25 (9), 2728–2733 (2016).
20. Rajasekaran, S., Venkatadass, K., Naresh Babu, J., Ganesh, K. & Shetty, A. P. Pharmacological enhancement of disc diusion and
dierentiation of healthy, ageing and degenerated discs. Eur. Spine J. 17 (5), 626–643 (2008).
21. Xilong, C. et al. Sagittal spinopelvic alignment in the Standing and Prone positions of patients with old traumatic thoracolumbar
kyphosis: relationship with immediately postoperative parameters. World Neurosurg. 176, e692–e696 (2023).
22. Yurube, T., Takeoka, Y., Kanda, Y., Kuroda, R. & Kakutani, K. Intervertebral disc cell fate during aging and degeneration: apoptosis,
senescence, and autophagy. North. Am. Spine Soc. J. (Nassj). 14, 100210 (2023).
23. Zhang, Q., Zhang, Y., Chon, T. E., Baker, J. S. & Gu, Y. Analysis of stress and stabilization in adolescent with osteoporotic idiopathic
scoliosis: nite element method. Comput. Method Biomec. 26 (1), 12–24 (2023).
24. Hiyama, A., Yokoyama, K., Nukaga, T., Sakai, D. & Mochida, J. A complex interaction between wnt signaling and TNF-alpha in
nucleus pulposus cells. Arthritis Res. er. 15 (6), R189 (2013).
25. Hiyama, A., Yokoyama, K., Nukaga, T., Sakai, D. & Mochida, J. Response to tumor necrosis factor-α mediated inammation
involving activation of prostaglandin E2 and wnt signaling in nucleus pulposus cells. J. Orthop. Res. 33 (12), 1756–1768 (2015).
26. Noguchi, M., Gooyers, C. E., Karakolis, T., Noguchi, K. & Callaghan, J. P. Is intervertebral disc pressure linked to herniation? An
in-vitro study using a porcine model. J. Biomech. 49 (9), 1824–1830 (2016).
27. Wang, L. et al. A Validated Finite Element Analysis of Facet Joint Stress in degenerative lumbar scoliosis. World Neurosurg. 95,
126–133 (2016).
28. Yeung, K. H. et al. Morphological changes of intervertebral disc detectable by T2-weighted MRI and its correlation with curve
severity in adolescent idiopathic scoliosis. Bmc Musculoskel Dis. ; 23(1). (2022).
29. Okamoto, Y. et al. e eect of kyphotic deformity because of vertebral fracture: a nite element analysis of a 10° and 20° wedge-
shaped vertebral fracture model. Spine J. 15 (4), 713–720 (2015).
30. De Inglez, M. C. C. M. et al. Evaluation of the inuence of kyphosis and scoliosis on intervertebral disc extrusion in French
bulldogs. Bmc Vet. Res. ; 14(1). (2018).
31. Torrie, P. A. G., Mckay, G., Byrne, R., Morris, S. A. C. & Harding, I. J. e inuence of lumbar spinal subtype on lumbar
intervertebral disc degeneration in Young and Middle-aged adults. Spine Deform. 3 (2), 172–179 (2015).
32. Lamartina, C. & Berjano, P. Classication of sagittal imbalance based on spinal alignment and compensatory mechanisms. Eur.
Spine J. 23 (6), 1177–1189 (2014).
Scientic Reports | 2024 14:31335 7
| https://doi.org/10.1038/s41598-024-82827-4
www.nature.com/scientificreports/
Content courtesy of Springer Nature, terms of use apply. Rights reserved
33. Machino, M. et al. Age-related degenerative changes and sex-specic dierences in osseous anatomy and intervertebral disc height
of the thoracolumbar spine. J. Clin. Neurosci. 90, 317–324 (2021).
34. Keorochana, G. et al. Eect of Sagittal Alignment on Kinematic Changes and Degree of Disc Degeneration in the lumbar spine.
Spine 36 (11), 893–898 (2011).
35. Moore, A. C., Holder, D. A. & Elliott, D. M. O-Axis Loading xture for spine biomechanics: Combined Compression and
bending. J. Biomech. Eng-T Asme 145(10). (2023).
36. Wei, X. et al. Correlations between the sagittal plane parameters of the spine and pelvis and lumbar disc degeneration. J. Orthop.
Surg. Res. ; 13(1). (2018).
37. Imai, N., Suzuki, H., Sakagami, A., Hirano, Y. & Endo, N. Correlation of the anatomical sacral slope with pelvic incidence in female
patients with developmental hip dysplasia: a retrospective cross-sectional study. J. Orthop. Surg. Res. ; 15(1). (2020).
38. Farshad-Amacker, N. A., Hughes, A., Herzog, R. J., Seifert, B. & Farshad, M. e intervertebral disc, the endplates and the vertebral
bone marrow as a unit in the process of degeneration. Eur. Radiol. 27 (6), 2507–2520 (2017).
Acknowledgements
No.
Author contributions
XLC, ZKH, and YHY designed the study. XLC and AD collected the data. WMY, AD, WY, WZ, and HW were
involved in manuscript writing, literature search, data interpretation, and data monitoring. AD, XLC, YHY, and
YLZ were responsible for data collection and analysis. All authors read and approved the nal manuscript.
Funding
is work was supported by Health Commission of Anhui Province (AHWJ2021b111), Health Commission of
Fuyang City (2021-1), and Anhui Medical University Fund Project (2021xkj210).
Declarations
Competing interests
e authors declare no competing interests.
Ethical approval and consent to participate
e current study was approved by the Ethics Committee of the Aliated Fuyang People’s Hospital of Anhui
Medical University before data collection and analysis (No.2021-19).
Additional information
Correspondence and requests for materials should be addressed to H.-y.Y.
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