Ossification of the Posterior Longitudinal Ligament (OPLL)

What it is. The posterior longitudinal ligament undergoes progressive ectopic endochondral ossification, producing a mass that encroaches on the spinal canal, narrows it and compresses the cord. OPLL is the most common cause of cervical compressive myelopathy in East Asian populations and is increasingly recognised worldwide as imaging advances. Most of it is asymptomatic and discovered incidentally; once symptomatic myelopathy develops, timely surgical decompression is essential to prevent irreversible cord damage.

Who. Prevalence in Japanese adults on CT or radiograph screening is 1.9-4.3 percent, with comparable figures in Korea and China; Caucasian populations sit at 0.1-0.3 percent, 10-20 times lower. Men are affected about 2:1, onset is typically at 40-60 years, and the course is slowly progressive. Symptomatic myelopathy develops in 5-15 percent of those with OPLL.

Where. The C3-C5 levels are most commonly affected, but the ossification can extend from C2 into the thoracic spine. Ossification of the ligamentum flavum (OLF) or yellow ligament (OYL) coexists in 5-10 percent.

Natural history. The ossification grows slowly over years, and cervical myelopathy is the most common symptomatic presentation. Minor trauma can precipitate acute myelopathy on a canal that pre-existing OPLL has already narrowed, a scenario dealt with under Clinical Assessment.

The ligament. The PLL runs along the posterior surface of the vertebral bodies from C2 to the sacrum and forms the anterior boundary of the spinal canal. In OPLL it is progressively replaced by mature lamellar bone through endochondral ossification, mediated by osteogenic differentiation of ligamentous mesenchymal stem cells; the staged sequence from ligament hypertrophy through chondroid metaplasia to ossification is set out below. The mass grows anterior to the dura and can eventually incorporate or replace the ventral dural layer, which is the origin of the surgical problem of dural ossification.

Molecular drivers. The key drivers are the bone morphogenetic proteins BMP-2, BMP-4 and BMP-7, osteocalcin, Runx2 (osteoblast differentiation) and Sox9 (chondrogenesis), with TGF-beta as a profibrotic signal. The strongest genetic association is a polymorphism of COL6A1 (collagen type VI alpha 1, rs6919606); R-Spondin 2 in the Wnt pathway and N-cadherin are also implicated. OPLL shares pathogenic pathways with diffuse idiopathic skeletal hyperostosis (DISH) and ossification of the ligamentum flavum (OLF).

Risk factors and associations. Beyond East Asian heritage (Japanese, Korean, Chinese), the associations are genetic, metabolic, endocrine, skeletal, dietary and mechanical:

• A family history of OPLL increases the risk 5-10 times
• Diabetes mellitus, impaired glucose tolerance, hyperinsulinaemia and the metabolic syndrome
• Hypoparathyroidism, the classical endocrine association
• DISH (Forestier disease), which coexists in 25-40 percent of OPLL patients
• A high-salt, low-animal-protein diet, proposed on epidemiological correlation
• Repeated micro-trauma to the PLL, cervical repetitive stress and occupational neck loading, which may trigger an osteogenic response

The CT classification. The Japanese Investigation Committee classification (1994) is the standard system, defining four types by the morphological pattern of ossification on sagittal CT reformats. The type carries a surgical implication, tabulated alongside its morphology and frequency.

The canal occupancy ratio. OPLL thickness divided by the anteroposterior canal diameter on axial CT quantifies severity: less than 30 percent is mild, 30-60 percent moderate, and greater than 60 percent severe. Surgical decompression is generally recommended when the ratio exceeds 60 percent or progressive myelopathy is present.

The K-line (kyphosis line). Fujiyoshi et al. proposed the K-line as a practical radiographic tool for selecting the approach. On a lateral cervical radiograph, or a sagittal CT, draw a straight line joining the midpoints of the spinal canal at C2 and C7, that is, the midpoint of the canal's anteroposterior diameter at each level. The OPLL is K-line positive when the mass does not cross or extend posterior to the line, and K-line negative when it does.

Why it predicts the outcome. Posterior decompression works by allowing the cord to drift posteriorly, away from the ossified mass. In a K-line positive patient the cord can shift back behind the OPLL, posterior laminoplasty is appropriate, and good neurological recovery is expected. If the mass is so large, or the alignment so kyphotic, that the OPLL crosses the line, the cord cannot shift past it; posterior decompression alone is insufficient and an anterior or combined approach is needed.

The dynamic K-line. Fujiyoshi's original description is a static measurement on a neutral lateral, and that is its main practical weakness: cervical alignment changes with posture, so a patient who is K-line positive in neutral can become K-line negative in flexion, and the cord is compressed in the position the neck actually adopts rather than the one the radiographer asked for. Later work therefore groups patients by whether the line stays positive across neutral and flexion films, and a patient who converts is a poor candidate for laminoplasty alone despite a reassuring neutral film. Obtain neutral and flexion laterals before committing to a posterior-only decompression; see cervical myelopathy for the dynamic K-line groups illustrated on paired films.

Dural ossification. Where the ossified ligament has incorporated or replaced the ventral dura, resecting the OPLL leaves a dural defect. It is present in approximately 5.7 percent of surgical cases, becomes more probable when the canal occupancy ratio is greater than 60 percent, and predicts intraoperative CSF leak. The axial CT is read for two signs before any anterior resection:

When either sign is present, anterior OPLL resection will almost certainly create a dural defect. The surgeon either plans for CSF management or chooses the floating method, in which the OPLL is thinned and allowed to float anteriorly without complete resection; both are set out under Management.

Thoracic OPLL. Rarer than cervical disease and more dangerous. The thoracic spine is kyphotic, so the cord already lies draped against the anterior ossified mass and posterior decompression alone allows little posterior cord drift; the K-line logic that works in the lordotic cervical spine often fails here, decompression may be inadequate and the cord can even be injured. The thoracic cord has a watershed blood supply, especially in the mid-thoracic region, so it is vulnerable to ischaemic injury during decompression and manipulation. T-OPLL is often of the continuous type, the thoracic canal is narrow, and it frequently coexists with ossification of the ligamentum flavum posteriorly, producing front-and-back ("pincer") compression that a single-sided decompression cannot relieve.

Thoracic strategy. The options are posterior decompression with instrumented fusion, often with some kyphosis correction (dekyphosis); posterolateral or anterior transthoracic decompression for a focal anterior beak; or a circumferential procedure for combined OPLL and OLF. Intra-operative neuromonitoring with MEP and SSEP is essential given the high cord-injury risk, and patients must be counselled that transient or permanent neurological worsening is more common than after cervical surgery.

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History. Onset is insidious: slowly progressive clumsiness of the hands and gait disturbance over months to years. Loss of hand dexterity (difficulty with buttons, chopsticks, writing) is an early sign; the gait becomes stiff-legged and spastic with frequent falls; urinary hesitancy, urgency and incontinence appear in advanced cases. Neck pain may be present but is often minimal relative to the degree of myelopathy. A history of minor trauma (whiplash, a fall) matters, because it can precipitate acute deterioration.

Examination. The signs to elicit:

• Motor: upper limb weakness, particularly of the intrinsic hand muscles, and spastic lower limb weakness
• Reflexes: hyperreflexia, a positive Hoffmann sign, a positive Babinski sign
• Sensory: variable sensory loss below the level of compression
• Gait: spastic, broad-based, with decreased proprioception
• Neck range of motion may be limited; examine cautiously to avoid precipitating myelopathy
• Lhermitte sign, an electric-shock sensation on neck flexion, is non-specific

Grading. The modified Japanese Orthopaedic Association (mJOA) score, 0-18, is the standard clinical tool for severity, and the mJOA recovery rate is used to quantify post-operative improvement:

• Mild, mJOA 15-17: subtle hand dysfunction, no gait disturbance
• Moderate, mJOA 12-14: obvious hand dysfunction, mild gait disturbance
• Severe, mJOA less than 12: marked gait disturbance, possible bowel and bladder dysfunction

Surgical decompression is generally recommended for moderate and severe myelopathy (mJOA less than 15) and for progressive mild myelopathy.

OPLL or spondylotic myelopathy. The distinction matters because OPLL carries additional surgical risks, dural ossification and CSF leak among them, and may require different operative strategies. OPLL is confirmed by demonstrating ossification of the PLL on CT, not just disc protrusion or osteophytes, so always obtain CT in addition to MRI when OPLL is suspected: MRI may not clearly distinguish OPLL from disc material and osteophytes, although the signal characteristics described under Investigations help.

Minor trauma on an OPLL canal. A canal already narrowed by OPLL has no reserve space for the cord. A relatively trivial hyperextension injury (a fall onto the face, a low-speed motor vehicle collision, even a fall from standing in an older patient) momentarily buckles the ligamentum flavum and pinches the cord between it and the anterior OPLL, often producing a spinal cord injury without any fracture or dislocation, the SCIWORA-type pattern in adults with stenosis. The classic syndrome is acute central cord syndrome, the most common incomplete cord injury: upper-limb weakness disproportionately worse than the legs, hands worst, variable bladder dysfunction and sacral sparing, reflecting the central (medial) location of the cervical hand fibres.

Managing the acute injury. Urgent MRI defines cord compression and signal change. Maintain spinal cord perfusion by supporting mean arterial pressure, often to a MAP target of around 85 to 90 mmHg, and avoid hypotension and hyperextension; high-dose steroids are not routinely recommended. For a patient with ongoing cord compression, early surgical decompression, increasingly favoured and often within about 24 hours, gives better neurological recovery than delayed surgery, though a purely central cord injury with minimal residual compression may initially be managed expectantly. This is exactly why an asymptomatic OPLL patient must be counselled about trauma risk, and why a pre-existing stenotic OPLL lowers the threshold for considering decompression.

Radiographs. The first-line films are AP, lateral and flexion-extension views of the cervical spine. Look for a radiodense band posterior to the vertebral bodies, the cervical alignment (lordosis or kyphosis) and the flowing anterior osteophytes of DISH. Radiographs may miss early or small OPLL, CT is more sensitive, and the lateral view serves the K-line but is not sufficient for diagnosis.

Dynamic views. Flexion-extension films assess cervical instability or a mobile OPLL. Segmental mobility matters if posterior surgery is planned, because instability may necessitate fusion; perform them cautiously in a myelopathic patient to avoid cord injury.

CT with sagittal reformats. The gold standard for diagnosis and classification. On sagittal reformats the ossification appears as a hyperdense strip along the posterior vertebral body margin, distinct from the vertebral cortex, and this is the view on which the type is assigned. Axial cuts give the canal occupancy ratio (OPLL thickness divided by the sagittal canal diameter) and the double-layer and single-layer signs of dural ossification.

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MRI. The ossified mass is low signal on both T1 and T2, whereas disc material is typically T2 hyperintense, which is what lets MRI help separate OPLL from disc. T2 sagittal and axial sequences show the cord compression at the OPLL levels, and T2 hyperintensity within the cord indicates myelomalacia. That signal change carries prognostic weight: pre-operative T2 cord signal correlates with post-operative recovery, and multi-level high signal predicts a poorer outcome.

CT myelography. For the patient in whom MRI is contraindicated (pacemaker, cochlear implant). Contrast outlines the thecal sac and shows the relationship between the OPLL mass and the cord, and it can confirm dural ossification when the CT signs are equivocal.

The minimum workup for suspected OPLL myelopathy is CT plus MRI: CT classifies the OPLL and evaluates dural ossification, MRI assesses cord compression and signal change. Report the OPLL type, the canal occupancy ratio, the K-line status and the presence or absence of dural ossification signs.

The decision. Most OPLL is asymptomatic and does not require surgery; the operation is for myelopathy. Once decompression is indicated, the choice between anterior and posterior surgery rests on the OPLL type, the canal occupancy ratio, the K-line status, the number of levels involved, the cervical alignment and the presence of dural ossification. Anterior surgery removes the mass directly at the price of a high dural injury risk; posterior surgery decompresses indirectly through posterior cord shift. Mixed and continuous types often require multi-level surgery.

ACAF, anterior controllable antedisplacement and fusion. The most important recent addition to OPLL surgery, designed to solve the exact problem that makes anterior corpectomy dangerous: peeling a dura-adherent ossified mass off the cord. A conventional corpectomy removes the vertebral bodies and then tries to resect the OPLL, risking a massive and unrepairable dural tear. ACAF instead moves the whole vertebral-body-plus-OPLL complex forward as a single unit and never removes the ossified mass at all:

1. The anterior plate and screws are positioned first, with screws set to the intended new, more anterior position
2. The vertebral bodies bearing the OPLL are isolated by bilateral longitudinal osteotomies at the body-pedicle junction, with the discs above and below released, freeing a "bone-OPLL complex"
3. That freed complex is lifted anteriorly (ante-displaced) and held forward by tightening it onto the pre-contoured plate

Why it matters. Because the OPLL is never separated from the dura, the cord being decompressed by translating the whole anterior wall forward, the dreaded step of stripping ossified dura is avoided. That is the rationale for ACAF's lower CSF-leak profile in difficult, dura-adherent disease, precisely the population in which the double-layer sign and a high canal occupancy ratio make corpectomy most hazardous.

CSF leak, the signature complication. It is the most feared and characteristic complication of anterior OPLL surgery, and it tracks dural ossification: the incidence runs from 5 percent when no dural signs are present to over 30 percent when the double-layer or single-layer sign is identified on pre-operative CT. Prevention rests on identifying those signs before the operation, using the floating method instead of OPLL resection, and having dural repair materials available. When a leak occurs, it is managed with the repair, lumbar drainage and monitoring set out under Anterior Decompression.

C5 palsy. Weakness of deltoid and biceps is the most common neurological complication after posterior cervical decompression for OPLL. It typically manifests 1-7 days post-operatively and is thought to result from traction on the C5 nerve root during posterior cord shift; most recover, but the weakness can be distressing for patients. The risk may be reduced by a foraminotomy at C4-C5 at the time of laminoplasty.

What predicts a good result. Segmental type, K-line positive status, an mJOA greater than 12, myelopathy of less than 12 months' duration, no T2 cord signal change on MRI, and age less than 65 years.

What predicts a poor one. Continuous or mixed type, K-line negative status, an mJOA less than 10, long-standing myelopathy of greater than 2 years, multi-level T2 cord hyperintensity, and age greater than 70 years.

The modifiable factor. Duration of myelopathy is the most important prognostic factor the surgeon can influence: earlier decompression yields better outcomes, so do not delay surgery in progressive myelopathy.