Pathophysiology of Spondylosis
Spondylosis is fundamentally a degenerative cascade initiated by intervertebral disc degeneration, which triggers secondary facet joint arthropathy, osteophyte formation, and ligamentous changes that collectively narrow the spinal canal and neural foramina, potentially causing mechanical compression and ischemic injury to neural structures. 1
Primary Degenerative Process
The pathophysiological sequence begins with disc degeneration as the primary initiating event, though facet joint degeneration can also serve as an alternative starting point 2, 1. The disc loses hydration and structural integrity, leading to decreased disc height and altered biomechanical load distribution across the motion segment 1.
The Three-Phase Degenerative Model
The progression follows a well-established pattern described by Kirkaldy-Willis 2:
Dysfunction Phase: Early disc and facet degeneration begins, with initial biomechanical changes. Radiographically, this manifests as facet vacuum formation without considerable arthropathy 2.
Instability Phase: As degeneration advances, the vertebral segment becomes increasingly dynamic and unstable. Fluid accumulates within facet joint spaces (facet effusion), and progressive facet arthropathy develops alongside worsening degenerative disc disease 2. The posterior ligamentous complex begins to show pathological changes 2.
Restabilization Phase: Eventually, the segment undergoes autofusion at the facets and endplates. Facet effusion is replaced by vacuum phenomena in severe osteoarthritis, and intervertebral disc vacuum continues to accumulate with cleft formation 2.
Secondary Structural Changes and Compression Mechanisms
Osteophyte Formation and Canal Stenosis
Osteophytes form at the disc-vertebral body junction and facet joints as a response to abnormal mechanical stress, progressively encroaching on the spinal canal and neural foramina 1. In cervical spondylosis specifically, the hypertrophic disc-osteophyte complex anteriorly and buckled ligamentum flavum posteriorly create a pincer mechanism that compresses the spinal cord 3.
Congenital Factors
Congenital spinal stenosis significantly amplifies the clinical impact of degenerative changes 4. Patients with developmentally narrow canals are far more likely to develop neurologic symptoms from the same degree of spondylotic changes compared to those with normal canal dimensions 1.
Neural Injury Mechanisms
Direct Mechanical Compression
The narrowed canal produces direct mechanical pressure on the spinal cord or nerve roots, which can cause immediate neurological dysfunction 1. The severity correlates with the degree of compression: gray matter flattening and mild demyelination occur at 40-44% of normal anteroposterior diameter, while extensive gray matter necrosis with white matter gliosis develops at 12-19% 5.
Ischemic Injury
Intermittent ischemic injury represents a critical pathophysiological mechanism, particularly in cervical spondylotic myelopathy 5. Each episode of hypoperfusion produces focal infarction and cavitation in gray matter, followed by progressive white matter demyelination 5. This explains the characteristic stepwise decline pattern seen in approximately 75% of cervical spondylotic myelopathy patients, where discrete neurological deteriorations occur separated by periods of relative stability 5.
Age-Related and Genetic Factors
Spondylosis is fundamentally an age-related degenerative process, with spondylotic changes appearing commonly in patients over 30 years of age 6. However, the correlation between imaging findings and symptoms is poor—a 10-year longitudinal MRI study demonstrated that cervical disc degeneration progressed in 85% of patients, yet symptoms developed in only 34% 6.
Genetic predisposition plays a significant role in determining who develops clinically significant disease 7. Familial clustering has been documented, with genetics determining spinal shape and similar spines tending to degenerate in similar patterns 7.
Clinical Implications of Pathophysiology
The multifactorial etiology means that not all spondylotic changes produce symptoms 8. When symptoms do occur, they range from localized discomfort to radiculopathy (from foraminal stenosis and nerve root compression) to myelopathy (from central canal stenosis and cord compression) 8, 1.
The ischemic component of cord injury means that prolonged compression can cause irreversible damage even if decompression is eventually performed 5. This is why approximately 20% of patients initially managed conservatively ultimately require surgery, and why untreated severe cervicomedullary compression carries a 16% mortality rate 5.