The current concept that the hypertrophic variety of spondylitis (spondylitis osteoarthritica) is not an arthritis but a spondylosis arising as a reaction to changes primary in the intervertebral disks is based on the views promulgated by Schmorl and his followers.1 The intervertebral disks, through the effect of age and of continuous functional stress, pass through stages of fibrillation, dehydration, fissuring and "brown degeneration." Defects in the cartilage plates, which may be congenital, traumatic or infectious in origin, permit extrusion of disk material into the vertebral bodies and penetration of vessels from the spongiosa into the normally avascular intervertebral disks, which may become calcified or ossified. The thinning of the disks and the loss of their normal buffer effect are attended by sclerosis of the adjacent vertebral borders and by marginal proliferation which may proceed to bony ankylosis. This progressive series of events has been duplicated experimentally.2
HORWITZ T. DEGENERATIVE LESIONS IN THE CERVICAL PORTION OF THE SPINE. Arch Intern Med (Chic). 1940;65(6):1178–1191. doi:10.1001/archinte.1940.00190120095008
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