Proximal Junctional Kyphosis

What is proximal junctional kyphosis (PJK)?

It refers to an increase in kyphosis in the segment of the spine immediately above the upper end of an instrumented spinal fusion.

Simply put: imagine a long construct (rods and screws) correcting scoliosis or kyphosis. At the point where this “rigid” segment ends and the “mobile” spine begins, excessive forward angulation (kyphosis) may gradually develop, due to:

• degeneration of the disc and supporting ligaments,
• compression fracture of the uppermost instrumented vertebra or the adjacent vertebra above,
• instability or subluxation of the adjacent facet joint.

Radiographically, PJK is commonly defined as a kyphotic angle > 10° measured between the inferior endplate of the upper instrumented vertebra and the superior endplate of the second vertebra above the fusion, or an increase of ≥ 10° compared with preoperative measurements.

How common is it after spinal fusion?

PJK is a frequent radiographic finding after long posterior spinal fusions.

Data from international clinical series indicate that:

• In adults undergoing surgery for degenerative spinal deformity, PJK occurs in approximately 17–40% of patients.
• In adolescents treated for idiopathic scoliosis or Scheuermann kyphosis, similar rates are reported, with some series demonstrating even higher prevalence.
• In older patients with advanced degeneration and osteoporosis, the likelihood of radiographic PJK is even greater.

Importantly, not all patients develop symptoms. In many cases, PJK is a radiographic finding that requires only routine surveillance.

What are the main risk factors?

The development of PJK is multifactorial, related to spinal anatomy, patient-specific factors, and surgical variables (fusion length, technique, and instrumentation).

Patient-related factors

• Advanced age at the time of surgery.
• Low bone mineral density / osteoporosis.
• Pre-existing disc and facet degeneration at the proximal junction.
• Marked preoperative kyphosis or regional kyphosis immediately above the upper instrumented level.

Surgery-related factors

• Extensive fusion constructs involving many spinal levels.
• Fusion to the sacrum/pelvis, increasing stiffness of the caudal spinal segment.
• Very rigid constructs (thicker rods, full fixation without a “transition zone”).
• Extensive soft-tissue dissection and disruption of the supraspinous/interspinous ligaments at the upper end of the fusion.
• Inappropriate selection of the upper instrumented vertebra (ending the fusion in a transitional or kyphotic segment).
• Injury to the facet joints at the upper end of the fusion.

How is it related to sagittal balance & spinopelvic parameters?

PJK is closely related to overall posture in space—sagittal balance—and parameters such as pelvic incidence (PI), lumbar lordosis (LL), thoracic kyphosis (TK), and sagittal vertical axis (SVA).

When deformity correction is overly aggressive (large changes in lordosis or abrupt correction of kyphosis), a pronounced stiff transition zone is created between the fused and the mobile spine. This can lead to:

• increased mechanical stress at the proximal junction,
• accelerated disc and ligament degeneration,
• microinstability or fracture of the upper instrumented or adjacent vertebra.

Examples of high-risk scenarios include:

• Large corrections of lumbar lordosis (> 30°) relative to pelvic incidence (PI).
• Marked preoperative or postoperative thoracic kyphosis.
• High pelvic incidence (> 55°), often necessitating long and extensive corrective fusions.

Contemporary deformity planning emphasizes alignment targets that achieve optimal balance without overcorrection, which would otherwise transfer excessive stress to the proximal junction.

When does PJK usually appear after surgery?

PJK is typically an early to mid-term complication, although it may also develop later.

• Many patients demonstrate early kyphotic changes within the first 3–6 months after fusion.
• Approximately 60–70% of the total kyphotic progression occurs within the first postoperative year.
• However, delayed progression beyond 2 years has been reported, particularly in patients with advanced degeneration or osteoporosis.

This is why systematic postoperative follow-up with clinical assessment and radiographic surveillance is essential.

How and why does it develop – what is the pathophysiology?

PJK results from a combination of mechanical loading, tissue degeneration, and surgical factors affecting the proximal spinal segment.

Key mechanisms include:

• Extensive muscle and ligament disruption at the upper end of the fusion, leading to loss of the posterior tension band (supraspinous/interspinous ligaments, facet capsules).
• Intervertebral disc collapse and accelerated degeneration immediately above the fusion.
• Compression fracture of the adjacent vertebra, particularly in osteoporotic bone.
• Stress concentration due to the transition from rigid to mobile segments.
• Suboptimal selection of fusion levels, such as terminating the construct in a transitional spinal region.

In younger patients, failure is more often disc–ligamentous, whereas in older patients with osteoporosis, osseous failure (fracture at or above the upper instrumented level) predominates.

What are the symptoms & when is it dangerous?

Many cases of PJK remain a radiographic finding without clinical symptoms. However, a subset of patients eventually become symptomatic.

Possible symptoms

• Upper back or neck pain, often worse in the upright position.
• Sensation of forward imbalance, postural change, or visible deformity.
• Difficulty walking, early fatigue, or need for support.
• In severe cases: paresthesia, weakness, or gait instability due to neural compression (nerve roots or spinal cord).
• Rarely: dysphagia or voice changes when deformity significantly affects the cervical region.

PJK is considered clinically significant when associated with neurological deficit, rapid progression of deformity, severe pain, or functional impairment. In such cases, it represents a pathologic condition that often requires surgical intervention.

How is PJK diagnosed and measured (radiographic criteria)?

Diagnosis relies on clinical evaluation and specialized imaging, primarily standing full-spine radiographs.

Standard diagnostic criteria include:

• Kyphotic angle > 10° measured between:
  • the inferior endplate of the upper instrumented vertebra, and
  • the superior endplate of the second vertebra above the fusion,
• and/or an increase ≥ 10° compared with preoperative measurements.

Adjunctive tools:

• Standing lateral full-spine radiographs to assess sagittal balance (SVA, LL, etc.).
• CT or MRI when fracture, implant failure, pseudarthrosis, or neural compression is suspected.
• Clinical assessment of posture, balance, pain, and neurological function.

Is there a classification system? What does it mean in practice?

Several classification systems have been proposed to distinguish mild from severe PJK and to identify the underlying failure mechanism.

Based on kyphotic angle (Proximal Junctional Angle – PJA)

• Mild PJK: PJA increase ~10–14°.
• Moderate PJK: PJA increase ~15–19°.
• Severe PJK: PJA ≥ 20°, often associated with postural deterioration or neurological symptoms.

Based on failure type

• Type 1 – disc–ligamentous failure (disc degeneration, ligamentous laxity, subluxation).
• Type 2 – osseous failure (fracture at the upper instrumented vertebra or adjacent level).
• Type 3 – implant–bone interface failure (screw pullout, loosening).

In practice, this classification helps determine whether observation is sufficient or whether revision surgery with extension of fusion, osteotomies, or structural reinforcement is required.

How is it treated – conservative & surgical?

Not all forms of PJK require surgery. Management is individualized based on symptoms, progression, radiographic findings, and overall patient health.

Conservative management

• Close clinical and radiographic monitoring in mild, stable cases.
• Analgesic therapy for pain control.
• Physical therapy focusing on paraspinal muscle strengthening, posture, and balance.
• Treatment of osteoporosis (bisphosphonates, vitamin D, calcium, or anabolic therapy when indicated).

Surgical management (revision)

Considered when there is:

• severe pain refractory to conservative care,
• progressive deformity with functional decline,
• neurological deterioration (myelopathy, radiculopathy),
• inability to maintain sagittal balance.

Revision procedures often include:

• Extension of the fusion to higher spinal levels.
• Corrective osteotomies (Smith–Petersen, Pedicle Subtraction Osteotomy/PSO) to restore global sagittal alignment.
• Interbody fusion at selected levels.
• Structural bone augmentation (e.g., cement-augmented pedicle screws in osteoporotic bone).

These are technically demanding revision procedures that should be performed in specialized deformity centers such as Neuroknife.

How does it affect functional outcome & quality of life?

The clinical spectrum of PJK ranges from an incidental radiographic finding to a major cause of persistent postoperative pain and disability.

Current evidence indicates that:

• In mild cases, many patients do not report significant deterioration in quality-of-life scores (SRS, ODI), aside from possible cosmetic concerns.
• In more severe cases (PJA ≥ 20°), patients often experience greater pain, particularly in the upper back or neck, with less improvement in pain-related outcome measures.
• When neurological compromise occurs, PJK may lead to substantial loss of daily function (walking, activities of daily living) and necessitate revision surgery.

At Neuroknife, our objective is to identify early which cases are likely to remain stable and which are prone to progression, allowing timely intervention with the least possible burden to the patient.