Aims

CRP is an acute-phase protein that is used as a biomarker to follow severity and progression in infectious and inflammatory diseases. Its pathophysiological mechanisms of action are still poorly defined. CRP in its pentameric form exhibits weak anti-inflammatory activity. The monomeric isoform (mCRP) exerts potent proinflammatory properties in chondrocytes, endothelial cells, and leucocytes. No data exist regarding mCRP effects in human intervertebral disc (IVD) cells. This work aimed to verify the pathophysiological relevance of mCRP in the aetiology and/or progression of IVD degeneration.

The belief that an intervertebral disc must degenerate before it can herniate has clinical and medicolegal significance, but lacks scientific validity. We hypothesised that tissue changes in herniated discs differ from those in discs that degenerate without herniation. Tissues were obtained at surgery from 21 herniated discs and 11 non-herniated discs of similar degeneration as assessed by the Pfirrmann grade. Thin sections were graded histologically, and certain features were quantified using immunofluorescence combined with confocal microscopy and image analysis. Herniated and degenerated tissues were compared separately for each tissue type: nucleus, inner annulus and outer annulus. Herniated tissues showed significantly greater proteoglycan loss (outer annulus), neovascularisation (annulus), innervation (annulus), cellularity/inflammation (annulus) and expression of matrix-degrading enzymes (inner annulus) than degenerated discs. No significant differences were seen in the nucleus tissue from herniated and degenerated discs. Degenerative changes start in the nucleus, so it seems unlikely that advanced degeneration caused herniation in 21 of these 32 discs. On the contrary, specific changes in the annulus can be interpreted as the consequences of herniation, when disruption allows local swelling, proteoglycan loss, and the ingrowth of blood vessels, nerves and inflammatory cells. In conclusion, it should not be assumed that degenerative changes always precede disc herniation. Cite this article: Bone Joint J 2013;95-B:1127–33

Aims. To investigate metallosis in patients with magnetically controlled growing rods (MCGRs) and characterize the metal particle profile of the tissues surrounding the rod. Methods. This was a prospective observational study of patients with early onset scoliosis (EOS) treated with MCGRs and undergoing rod exchange who were consecutively recruited between February 2019 and January 2020. Ten patients were recruited (mean age 12 years (SD 1.3); 2 M:8 F). The configurations of the MCGR were studied to reveal the distraction mechanisms, with crucial rod parts being the distractable piston rod and the magnetically driven rotor inside the barrel of the MCGR. Metal-on-metal contact in the form of ring-like wear marks on the piston was found on the distracted portion of the piston immediately outside the barrel opening (BO) through which the piston rod distracts. Biopsies of paraspinal muscles and control tissue samples were taken over and away from the wear marks, respectively. Spectral analyses of the rod alloy and biopsies were performed to reveal the metal constituents and concentrations. Histological analyses of the biopsies were performed with haematoxylin and eosin staining. Results. Titanium (Ti), vanadium (V), and neodymium (Nd) concentrations in the biopsies taken near the wear marks were found to be significantly higher than those in the control tissue samples. Significantly increased Nd concentrations were also found in the tissues near the barrel of the MCGR. Chronic inflammation was revealed by the histological studies with fibrosis and macrophage infiltration. Black particles were present within the macrophages in the fibrotic tissues. Conclusion. Ti and V were generated mainly at the BO due to metal-on-metal contact, whereas the Nd from the rotor of the MCGR is likely released from the BO during distraction sessions. Phagocytotic immune cells with black particles inside raise concern regarding the long-term implications of metallosis. Cite this article: Bone Joint J 2020;102-B(10):1375–1383

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To investigate the correlations among cytokines and regulatory T cells (T-regs) in ankylosing spondylitis (AS) patients, and their changes after anti-tumour necrosis factor-α (TNF-α) treatment.

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Implant-related postoperative spondylodiscitis (IPOS) is a severe complication in spine surgery and is associated with high morbidity and mortality. With growing knowledge in the field of periprosthetic joint infection (PJI), equivalent investigations towards the management of implant-related infections of the spine are indispensable. To our knowledge, this study provides the largest description of cases of IPOS to date.

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This study was performed to explore the effect of melatonin on pyroptosis in nucleus pulposus cells (NPCs) and the underlying mechanism of that effect.

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A variety of surgical methods and strategies have been demonstrated for Andersson lesion (AL) therapy. In 2011, we proposed and identified the feasibility of stabilizing the spine without curettaging the vertebral or discovertebral lesion to cure non-kyphotic AL. Additionally, due to the excellent reunion ability of ankylosing spondylitis, we further came up with minimally invasive spinal surgery (MIS) to avoid the need for both bone graft and lesion curettage in AL surgery. However, there is a paucity of research into the comparison between open spinal fusion (OSF) and early MIS in the treatment of AL. The purpose of this study was to investigate and compare the clinical outcomes and radiological evaluation of our early MIS approach and OSF for AL.

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Degenerative cervical spondylosis (DCS) is a common musculoskeletal disease that encompasses a wide range of progressive degenerative changes and affects all components of the cervical spine. DCS imposes very large social and economic burdens. However, its genetic basis remains elusive.

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Gram-negative infections are associated with comorbid patients, but outcomes are less well understood. This study reviewed diagnosis, management, and treatment for a cohort treated in a tertiary spinal centre.

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Traumatic central cord syndrome (CCS) typically follows a hyperextension injury and results in motor impairment affecting the upper limbs more than the lower, with occasional sensory impairment and urinary retention. Current evidence on mortality and long-term outcomes is limited. The primary aim of this study was to assess the five-year mortality of CCS, and to determine any difference in mortality between management groups or age.

This review provides a concise outline of the advances made in the care of patients and to the quality of life after a traumatic spinal cord injury (SCI) over the last century. Despite these improvements reversal of the neurological injury is not yet possible. Instead, current treatment is limited to providing symptomatic relief, avoiding secondary insults and preventing additional sequelae. However, with an ever-advancing technology and deeper understanding of the damaged spinal cord, this appears increasingly conceivable. A brief synopsis of the most prominent challenges facing both clinicians and research scientists in developing functional treatments for a progressively complex injury are presented. Moreover, the multiple mechanisms by which damage propagates many months after the original injury requires a multifaceted approach to ameliorate the human spinal cord. We discuss potential methods to protect the spinal cord from damage, and to manipulate the inherent inhibition of the spinal cord to regeneration and repair. Although acute and chronic SCI share common final pathways resulting in cell death and neurological deficits, the underlying putative mechanisms of chronic SCI and the treatments are not covered in this review.

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Non-coding microRNA (miRNA) in extracellular vesicles (EVs) derived from mesenchymal stem cells (MSCs) may promote neuronal repair after spinal cord injury (SCI). In this paper we report on the effects of MSC-EV-microRNA-381 (miR-381) in a rodent model of SCI.

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Inflammatory response plays a pivotal role in the pathophysiological process of intervertebral disc degeneration (IDD). A20 (also known as tumour necrosis factor alpha-induced protein 3 (TNFAIP3)) is a ubiquitin-editing enzyme that restricts nuclear factor-kappa B (NF-κB) signalling. A20 prevents the occurrence of multiple inflammatory diseases. However, the role of A20 in the initiation of IDD has not been elucidated. The aim of the study was to investigate the effect of A20 in senescence of TNF alpha (TNF-α)-induced nucleus pulposus cells (NPCs).

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To study the associations of lumbar developmental spinal stenosis (DSS) with low back pain (LBP), radicular leg pain, and disability.

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To evaluate the histopathological examination of peri-implant tissue samples as a technique in the diagnosis of postoperative spinal implant infection (PSII).

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The aim of this study was to determine the diagnostic utility of histological analysis in spinal biopsies for spondylodiscitis (SD).

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Cervical spondylosis is often accompanied by dizziness. It has recently been shown that the ingrowth of Ruffini corpuscles into diseased cervical discs may be related to cervicogenic dizziness. In order to evaluate whether cervicogenic dizziness stems from the diseased cervical disc, we performed a prospective cohort study to assess the effectiveness of anterior cervical discectomy and fusion on the relief of dizziness.

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We present a case series of five patients who had revision surgery following magnetic controlled growing rods (MGCR) for early onset scoliosis. Metallosis was found during revision in four out of five patients and we postulated a mechanism for rod failure based on retrieval analysis.

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The aim of this study was to evaluate the time course of changes in parameters of diffusion tensor imaging (DTI) such as fractional anisotropy (FA) and apparent diffusion coefficient (ADC) in patients with symptomatic lumbar disc herniation. We also investigated the correlation between the severity of neurological symptoms and these parameters.

Dysphagia is a common complication of anterior surgery of the cervical spine. The incidence of post-operative dysphagia may be as high as 71% within the first two weeks after surgery, but gradually decreases during the following months. However, 12% to 14% of patients may have some persistent dysphagia one year after the procedure. It has been shown that female gender, advanced age, multilevel surgery, longer operating time and severe pre-operative neck pain may be risk factors. Although the aetiology remains unclear and is probably multifactorial, proposed causes include oesophageal retraction, prominence of the cervical plate and prevertebral swelling. Recently, pre-operative tracheal traction exercises and the use of retropharyngeal steroids have been proposed as methods of reducing post-operative dysphagia.

We performed a systematic review to assess the incidence, aetiology, risk factors, methods of assessment and management of dysphagia following anterior cervical spinal surgery.

Cite this article: Bone Joint J 2013;95-B:868–73.

A number of causes have been advanced to explain the destructive discovertebral (Andersson) lesions that occur in ankylosing spondylitis, and various treatments have been proposed, depending on the presumed cause. The purpose of this study was to identify the causes of these lesions by defining their clinical and radiological characteristics.

We retrospectively reviewed 622 patients with ankylosing spondylitis. In all, 33 patients (5.3%) had these lesions, affecting 100 spinal segments. Inflammatory lesions were found in 91 segments of 24 patients (3.9%) and traumatic lesions in nine segments of nine patients (1.4%). The inflammatory lesions were associated with recent-onset disease; a low modified Stoke ankylosing spondylitis spine score (mSASSS) due to incomplete bony ankylosis between vertebral bodies; multiple lesions; inflammatory changes on MRI; reversal of the inflammatory changes and central bony ankylosis at follow-up; and a good response to anti-inflammatory drugs. Traumatic lesions were associated with prolonged disease duration; a high mSASSS due to complete bony ankylosis between vertebral bodies; a previous history of trauma; single lesions; nonunion of fractures of the posterior column; acute kyphoscoliotic deformity with the lesion at the apex; instability, and the need for operative treatment due to that instability.

It is essential to distinguish between inflammatory and traumatic Andersson lesions, as the former respond to medical treatment whereas the latter require surgery.

The post-operative changes in the serum levels of CRP and serum amyloid A (SAA) were investigated prospectively in 106 patients after posterior lumbar interbody fusion. In 96 patients who did not have complications related to infection within the first year after operation, the median levels of CRP before operation and on days 3, 7 and 13 after were 0.02 (0.01 to 0.03), 9.12 (2.36 to 19.82), 1.64 (0.19 to 6.10) and 0.53 (0.05 to 2.94) mg/dl, respectively and for SAA, 2.6 (2.0 to 3.8), 1312.1 (58.0 to 3579.8), 77.3 (1.8 to 478.4), 14.1 (0.5 to 71.9) μg/ml, respectively. The levels on day 3 were the highest for both CRP and SAA and significantly decreased (p < 0.01) by day 7 and day 13.

In regard to CRP, no patient had less than the reference level (0.1 mg/dl) on day 7. In only three had the level decreased to the reference level, while in 93 it was above this on day 13. However, for SAA, the levels became normal on day 7 in 10 cases and on day 13 in 34 cases. The ratios relative to the levels on day 3 were significantly lower for SAA compared with CRP on day 7 and day 13. Of the ten patients with infection in the early stages, the level of CRP decreased slightly but an increase in SAA was observed in six.

We concluded that SAA is better than CRP as a post-operative inflammatory marker.

There have been few reports regarding the efficacy of posterior instrumentation alone as surgical treatment for patients with pyogenic spondylitis, thus avoiding the morbidity of anterior surgery. We report the clinical outcomes of six patients with pyogenic spondylitis treated effectively with a single-stage posterior fusion without anterior debridement at a mean follow-up of 2.8 years (2 to 5). Haematological data, including white cell count and level of C-reactive protein, returned to normal in all patients at a mean of 8.2 weeks (7 to 9) after the posterior fusion. Rigid bony fusion between the infected vertebrae was observed in five patients at a mean of 6.3 months (4.5 to 8) post-operatively, with the remaining patient having partial union. Severe back pain was immediately reduced following surgery and the activities of daily living showed a marked improvement. Methicillin-resistant Staphylococcus aureus was detected as the causative organism in four patients.

Single-stage posterior fusion may be effective in patients with pyogenic spondylitis who have relatively minor bony destruction.

No previous studies have examined the physical characteristics of patients with cauda equina syndrome (CES). We compared the anthropometric features of patients who developed CES after a disc prolapse with those who did not but who had symptoms that required elective surgery. We recorded the age, gender, height, weight and body mass index (BMI) of 92 consecutive patients who underwent elective lumbar discectomy and 40 consecutive patients who underwent discectomy for CES. On univariate analysis, the mean BMI of the elective discectomy cohort (26.5 kg/m² (16.6 to 41.7) was very similar to that of the age-matched national mean (27.6 kg/m², p = 1.0). However, the mean BMI of the CES cohort (31.1 kg/m² (21.0 to 54.9)) was significantly higher than both that of the elective group (p < 0.001) and the age-matched national mean (p < 0.001). A similar pattern was seen with the weight of the groups. Multivariate logistic regression analysis was performed, adjusted for age, gender, height, weight and BMI. Increasing BMI and weight were strongly associated with an increased risk of CES (odds ratio (OR) 1.17, p < 0.001; and OR 1.06, p <  0.001, respectively). However, increasing height was linked with a reduced risk of CES (OR 0.9, p < 0.01). The odds of developing CES were 3.7 times higher (95% confidence interval (CI) 1.2 to 7.8, p = 0.016) in the overweight and obese (as defined by the World Health Organization: BMI ≥ 25 kg/m²) than in those of ideal weight. Those with very large discs (obstructing > 75% of the spinal canal) had a larger BMI than those with small discs (obstructing < 25% of the canal; p < 0.01). We therefore conclude that increasing BMI is associated with CES.

We conducted a prospective follow-up MRI study of originally asymptomatic healthy subjects to clarify the development of Modic changes in the cervical spine over a ten-year period and to identify related factors. Previously, 497 asymptomatic healthy volunteers with no history of cervical trauma or surgery underwent MRI. Of these, 223 underwent a second MRI at a mean follow-up of 11.6 years (10 to 12.7). These 223 subjects comprised 133 men and 100 women with a mean age at second MRI of 50.5 years (23 to 83). Modic changes were classified as not present and types 1 to 3. Changes in Modic types over time and relationships between Modic changes and progression of degeneration of the disc or clinical symptoms were evaluated. A total of 31 subjects (13.9%) showed Modic changes at follow-up: type 1 in nine, type 2 in 18, type 3 in two, and types 1 and 2 in two. Modic changes at follow-up were significantly associated with numbness or pain in the arm, but not with neck pain or shoulder stiffness. Age (≥ 40 years), gender (male), and pre-existing disc degeneration were significantly associated with newly developed Modic changes.

In the cervical spine over a ten-year period, type 2 Modic changes developed most frequently. Newly developed Modic changes were significantly associated with age, gender, and pre-existing disc degeneration.

We reviewed seven children with torticollis due to refractory atlanto-axial rotatory fixation who were treated in a halo vest. Pre-operative three-dimensional CT and sagittal CT imaging showed deformity of the superior articular process of C2 in all patients. The mean duration of halo vest treatment was 67 days (46 to 91). The mean follow-up was 34 months (8 to 73); at the latest review six patients demonstrated remodelling of the deformed articular process. The other child, who had a more severe deformity, required C1-2 fusion.

We suggest that patients with atlanto-axial rotatory fixation who do not respond to conservative treatment and who have deformity of the superior articular process of C2 should undergo manipulative reduction and halo-vest fixation for two to three months to induce remodelling of the deformed superior articular process before C1-2 fusion is considered.

There have been very few reports in the literature of gout and pseudogout of the spine. We describe six patients who presented with acute sciatica attributable to spinal stenosis with cyst formation in the facet joints. Cytopathological studies confirmed the diagnosis of crystal arthropathy in each case.

Specific formation of a synovial cyst was identified pre-operatively by MRI in five patients. In the sixth, the diagnosis was made incidentally during decompressive surgery. Surgical decompression alone was undertaken in four patients. In one with an associated degenerative spondylolisthesis, an additional intertransverse fusion was performed. Another patient had previously undergone a spinal fusion adjacent to the involved spinal segment, and spinal stabilisation was undertaken as well as a decompression.

In addition to standard histological examination material was sent for examination under polarised light which revealed deposition of urate or calcium pyrophosphate dihydrate crystals in all cases.

It is not possible to diagnose gout and pseudogout of the spine by standard examination of a fixed specimen. However, examining dry specimens under polarised light suggests that crystal arthropathy is a significant aetiological factor in the development of symptomatic spinal stenosis associated with cyst formation in a facet joint.

We have treated 175 patients with a chordoma over a ten-year period. Only two had a family history of the condition and we describe these in this paper. In one patient the tumour was at the craniocervical junction and in the other the lesion affected the sacrum. We have undertaken a literature review of familial chordoma and have identified chromosomal abnormalities associated with the condition.

There are few reports on the treatment of pyogenic lumbar spondylodiscitis through the posterior approach using a single incision. Between October 1999 and March 2003 we operated on 18 patients with pyogenic lumbar spondylodiscitis. All underwent posterior lumbar interbody fusion using an autogenous bone graft from the iliac crest and pedicle screws via a posterior approach. The clinical outcome was assessed using the Frankel neurological classification and the criteria of Kirkaldy-Willis. Under the Frankel classification, two patients improved by two grades (C to E), 11 by one grade, and five showed no change. The Kirkaldy-Willis functional outcome was excellent in five patients, good in ten and fair in three. Bony union was confirmed six months after surgery in 17 patients, but in one patient this was not achieved until two years after operation. The mean lordotic angle before operation was 20° (−2° to 42°) and the mean lordotic angle at the final follow-up was 32.5° (17° to 44°). Two patients had a superficial wound infection and two a transient root injury. Posterior lumbar interbody fusion with an autogenous iliac crest bone graft and pedicle screw fixation via a posterior approach can provide satisfactory results in pyogenic spondylodiscitis.

Discogenic low back pain is a common cause of disability, but its pathogenesis is poorly understood. We collected 19 specimens of lumbar intervertebral discs from 17 patients with discogenic low back pain during posterior lumbar interbody fusion, 12 from physiologically ageing discs and ten from normal control discs. We investigated the histological features and assessed the immunoreactive activity of neurofilament (NF200) and neuropeptides such as substance P (SP) and vasoactive-intestinal peptide (VIP) in the nerve fibres.

The distinct histological characteristic of the painful disc was the formation of a zone of vascularised granulation tissue from the nucleus pulposus to the outer part of the annulus fibrosus along the edges of the fissures. SP-, NF- and VIP-immunoreactive nerve fibres in the painful discs were more extensive than in the control discs. Growth of nerves deep into the annulus fibrosus and nucleus pulposus was observed mainly along the zone of granulation tissue in the painful discs. This suggests that the zone of granulation tissue with extensive innervation along the tears in the posterior part of the painful disc may be responsible for causing the pain of discography and of discogenic low back pain.