Study Design, The herniated portion of the lumbar disc was analyzed immunoh
istochemically for inflammatory infiltrates to determine their immunophenot
ype.
Objective. To investigate the pathomechanism behind spontaneous regression
of herniated discs.
Summary of Background Data. Spontaneous regression of herniated interverteb
ral discs has been increasingly reported. The inflammatory response of the
host has been suggested as a factor in this phenomenon. However, whether th
e inflammation is induced from direct chemical irritation of the nucleus pu
lposus material or whether it is secondary to an autoimmune response to the
nucleus pulposus remains controversial.
Methods. The herniated portion of the disc was collected from 38 patients w
ho underwent surgery for lumbar disc herniation, Thin cryostat sections wer
e made, and the extent to which inflammatory cells had infiltrated the disc
specimen was defined. Then the immunophenotype of cellular infiltrates in
the herniated disc specimens was assessed by immunostaining using a series
of antibodies for lymphocyte, monocyte, macrophage, and dendritic cell mark
ers.
Results. The inflammatory infiltrates in 14 of the 38 herniated discs were
subjected to immunohistochemical analysis, None of them expressed the immun
ophenotypic markers of the lymphocyte (CD20, CD45RO, CD4, CD8, TCR gamma de
lta), mature monocyte (CD33), or dendritic cell (CD1a, CD80, CD86, S100), A
bundant infiltration of CD68-positive cells that lacked CD33 but had a vari
able amount of CD11b, CD11c, and CD40 likely represents a process of differ
entiation from monocytes to macrophages.
Conclusions, These findings are consistent with an immunophenotype of infla
mmatory responses to tissue injury or chemical irritation Father than antig
en-specific immune responses. Therefore, understanding the mechanism of tis
sue repair is fundamentally important in the management of patients with di
sc herniations.