The word \"chondrodystrophoid\" literally means faulty development or nutrition of cartilage. In humans, chondrodystrophoism is recognized physically (phenotypically) as dwarfism, where individuals are smaller than normal and whose parts (especially limbs) are disproportionate. Certain breeds of dogs, such as dachshunds, show their chondrodystrophism by having disproportionately short and angulated limbs. However, phenotypic characteristics alone can not be used to identify chondrodystrophoid dogs. Other breeds, such as miniature poodles and beagles, have been histochemically identified to have chondrodystrophoid disks and yet do not appear outwardly to be chondrodystrophoid.
...Biochemical differences between chondrodystrophoid and nonchondrodystrophoid disks are apparent shortly after birth and explain the differences in the types of degeneration that occur. The degeneration that occurs in chondrodystrophoid disks is called chondroid metaplasia because the nucleus pulposus is gradually replaced with cartilage. Degeneration takes place rapidly and begins as early as 6 months of age starting at the periphery of the nucleus pulposus and progressing centrally. A dramatic and rapid increase in collagen content, as much as 30-40% by dry weight, is seen between 6 and 12 months of age. In addition, total glucosaminoglycan content will be 30 to 50% lower than age matched nonchondrodystrophoid dogs within the first 3 years resulting in a great loss of water content in the nucleus. When this happens, the nucleus loses its elasticity and no longer acts as an efficient shock absorber. Eventually the hyaline cartilage which forms calcifies, leading to almost complete lose of elasticity intervertebral the nucleus pulposus. The overall result is that of placing more of the \"workload\" on the annulus fibrosus while it is simultaneously undergoing degeneration. Disruption of the annulus fibrosus eventually occurs, especially at its weakest point, the thinner dorsal area lying just below the spinal canal. This allows nuclear material to escape, usually dorsally into the spinal canal or dorsolaterally to impinge on the nerve roots exiting the intervertebral foramina.
In comparison, nonchondrodystrophoid disks degenerate by fibroid metaplasia with the process becoming clinically significant at 8 to 10 years of age. Fibroid degeneration involves a gradual process of dehydration, and therefore loss of elasticity, of the nucleus pulposus with the incorporation of increasing amounts of collagen and polysaccharides (chondroitin sulfate and keratin sulfate). This causes a gradual diminishing of the border between the annulus fibrosus and the nucleus pulposus, and thus a weakening of the disk's overall biomechanical abilities. Partial rupture of the annulus fibrosus may result allowing the nucleus pulposus to bulge into the annulus and possibly the spinal canal.