Pathophysiology of Canine Intervertebral Disc Disease: From Degeneration to Hansen Type I Extrusion

Intervertebral disc disease (IVDD) is the most common spinal cord disorder in dogs and a major cause of pain and neurological dysfunction¹. The disease originates from progressive degeneration of the intervertebral disc (IVD), ultimately leading to disc extrusion and spinal cord compression, most commonly seen in Hansen Type I herniation. 

Structure and Functional Biology of the Intervertebral Disc 

The intervertebral disc consists of two primary components. The nucleus pulposus forms a gelatinous, proteoglycan-rich core responsible for absorbing compressive forces, while the annulus fibrosus is composed of concentric collagen lamellae that provide structural integrity and resistance to deformation¹. 

Progressive degeneration of these structures disrupts spinal biomechanics and predisposes to herniation. 

Degenerative Cascade and Chondroid Metaplasia 

IVD degeneration is defined by chondroid metaplasia of the nucleus pulposus, a process observed in both chondrodystrophic and non-chondrodystrophic dogs. However, degeneration is significantly accelerated in chondrodystrophic breeds due to the expression of fibroblast growth factor 4 (FGF4) retrogene on chromosome 12^1,3,4. 

During this process, notochordal cells are gradually replaced by chondrocyte-like cells, and the extracellular matrix undergoes transformation toward a cartilage-like structure with disorganized collagen deposition. Concurrently, glycosaminoglycan content decreases while collagen proportion increases, leading to loss of hydration and elasticity. 

Traditionally, degeneration has been categorized into: 

• Chondroid metaplasia, associated with Hansen Type I disc extrusion  

• Fibroid metaplasia, more commonly linked to Hansen Type II protrusion  

This review focuses on chondroid metaplasia due to its central role in acute disc extrusion. 

Progression to Disc Extrusion 

As degeneration advances, mineralization of the nucleus pulposus occurs. This weakens the annulus fibrosus, leading to rupture and sudden extrusion of disc material into the vertebral canal. This process defines Hansen Type I intervertebral disc herniation^1,4. 

Once extruded, disc material causes spinal cord compression and nerve root injury. Additionally, exposure of nucleus pulposus to the epidural space triggers an inflammatory response characterized by lymphocytic and macrophage infiltration⁵. 

Inflammation and Secondary Injury Mechanisms 

Inflammation plays a significant role in worsening neurological damage. Epidural edema may exacerbate spinal cord compression, while cytokine-mediated injury contributes to secondary neural damage. In severe cases, disruption of the dura may allow inflammatory mediators to directly affect the spinal cord¹. 

However, no consistent correlation has been established between the amount of extruded disc material and severity of neurological deficits, although some evidence suggests a weak association with extrusion volume¹. 

Limitations of Current Classification Systems 

Existing histological and imaging-based classification systems, including those proposed by Bergknut et al., Kranenburg et al., and Pfirrmann-based MRI grading, primarily evaluate structural degeneration^1,6. However, they do not fully capture functional injury mechanisms such as hemorrhage, neural compression severity, or inflammatory burden. 

Conclusion 

IVDD represents a progressive degenerative cascade driven by genetic predisposition and biochemical matrix alterations. The transition from chondroid metaplasia to acute disc extrusion is central to Hansen Type I pathology and forms the basis for clinical neurological disease in dogs. 

Reference 

1. Gómez Álvarez I, Verdes García JM, Espino López L. Intervertebral disc disease in dogs. InPets 2025 Jun 20 (Vol. 2, No. 3, p. 26). MDPI. https://www.mdpi.com/2813-9372/2/3/26 

2. Brown EA, Dickinson PJ, Mansour T, Sturges BK, Aguilar M, Young AE, Korff C, Lind J, Ettinger CL, Varon S, Pollard R. FGF4 retrogene on CFA12 is responsible for chondrodystrophy and intervertebral disc disease in dogs. Proceedings of the National Academy of Sciences. 2017 Oct 24;114(43):11476-81. https://www.pnas.org/doi/pdf/10.1073/pnas.1709082114 

3. Dickinson PJ, Bannasch DL. Current understanding of the genetics of intervertebral disc degeneration. Frontiers in veterinary science. 2020 Jul 24;7:431. https://www.frontiersin.org/journals/veterinary-science/articles/10.3389/fvets.2020.00431/pdf 

4. Fenn J, Olby NJ, Canine Spinal Cord Injury Consortium (CANSORT-SCI). Classification of intervertebral disc disease. Frontiers in veterinary science. 2020 Oct 6;7:579025. https://www.frontiersin.org/journals/veterinary-science/articles/10.3389/fvets.2020.579025/full 

5. Willems N, Tellegen AR, Bergknut N, Creemers LB, Wolfswinkel J, Freudigmann C, Benz K, Grinwis GC, Tryfonidou MA, Meij BP. Inflammatory profiles in canine intervertebral disc degeneration. BMC veterinary research. 2016 Jan 13;12(1):10. https://link.springer.com/content/pdf/10.1186/s12917-016-0635-6.pdf 

6. Niemeyer F, Galbusera F, Beukers M, Jonas R, Tao Y, Fusellier M, Tryfonidou MA, Neidlinger‐Wilke C, Kienle A, Wilke HJ. Automatic grading of intervertebral disc degeneration in lumbar dog spines. JOR spine. 2024 Jun;7(2):e1326. https://onlinelibrary.wiley.com/doi/pdf/10.1002/jsp2.1326