RT Journal
A1 Lotz, Jeffrey C.
A1 Ulrich, Jill A.
T1 Innervation, Inflammation, and Hypermobility May Characterize Pathologic Disc Degeneration: Review of Animal Model Data
JF The Journal of Bone & Joint Surgery
JO The Journal of Bone & Joint Surgery
YR 2006
FD April 1
VO 88
IS suppl_2
SP 76
OP 82
DO 10.2106/JBJS.E.01448
UL http://dx.doi.org/10.2106/JBJS.E.01448
AB Animal models provide important clues to the pathomechanisms of human
intervertebral disc degeneration. Previous reviews on this topic have
highlighted the fact that loss of nuclear volume (and, consequently, pressure)
is a common trigger for tissue-remodeling and anatomic change consistent with
degeneration in humans. Unfortunately, a large gap still exists in the medical
knowledge base that serves to distinguish symptomatic from asymptomatic
degeneration. Because disc degeneration per se is not a basis for clinical
intervention, identification of specific features underlying discogenic pain
is of the utmost importance to advance the current level of care and identify
novel therapeutic targets. This article presents animal-model evidence that
pathologic, or painful, degeneration is characterized by ineffective
injury-healing of peripheral tissue. Because the disc is only vascularized at
the vertebral end plate and the outer part of the anulus, these are the likely
sites for focal damage, inflammation, neoinnervation, and nociceptor
sensitization. Consequently, while nuclear insufficiency is likely the root of
degenerative change, the end plate and peripheral part of the anulus are more
likely the source of patient discomfort.