Molecular biology of cervical myelopathy and spinal cord injury: role of oligodendrocyte apoptosis.
BACKGROUND
Rational design of treatment strategies for cervical myelopathy and spinal cord injury requires a working knowledge of the molecular biology underlying these pathological processes. The cellular process of apoptosis is an important component of tissue and organ development as well as the natural response to disease and injury. Recent studies have convincingly demonstrated that apoptosis also plays a pivotal role in numerous pathological processes, contributing to the adverse effects of various diseases and traumatic conditions. A growing body of evidence has implicated apoptosis as a key determinant of the extent of neurological damage and dysfunction after acute spinal cord injury and in chronic cervical myelopathy.


OBJECTIVE
To provide clinicians and research investigators interested in spinal cord injury and myelopathy with a practical and up-to-date basic science review of cellular apoptosis in the context of spinal cord pathology.


METHODS
A review of recently published or presented data from molecular biological, animal model and human clinical studies.


METHODS
A computer-based comprehensive review of the English-language scientific and medical literature was performed in order to identify relevant publications with emphasis given to more recent studies.


RESULTS
Investigation into the role of apoptosis in spinal cord injury and myelopathy has drawn the interest of an increasing number of researchers and has yielded a substantial amount of new information.


CONCLUSIONS
Apoptosis is a fundamental biological process that contributes to preservation of health as well as development of disease. There is now strong evidence to support a significant role for apoptosis in secondary injury mechanisms after acute spinal cord injury as well in the progressive neurological deficits observed in such conditions as spondylotic cervical myelopathy.
Kim
David H
DH
The Boston Spine Group, New England Baptist Hospital, Boston, MA 02120, USA.
Vaccaro
Alexander R
AR
Henderson
Fraser C
FC
Benzel
Edward C
EC
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002574:Cervical Vertebrae; D006801:Humans; D008967:Molecular Biology; D009836:Oligodendroglia / Q000502:physiology*; D011379:Prognosis; D013118:Spinal Cord Diseases / Q000473:pathology*; D013119:Spinal Cord Injuries / Q000473:pathology*