Assessment of status of end plate and diffusion in degenerative disc disease

Abstract

Although multi-factorial, alterations in nutrition are considered to be the final common pathway for DDD [24]. Along with intact nutritional pathways, a stable mechanical environment that will maintain the normal hydrostatic pressure is also important to maintain the health of the disc. The end plate (EP) plays a crucial role in maintaining the mechanical environment and the intact nutritional pathways and thus, plays a crucial role in both the health and disease of the lumbar discs. However, it is reduced to a thin layer of cartilaginous tissue early in life and is susceptible to mechanical failure [25]. Autopsy studies have demonstrated microcracks and progressive failure of the EP even in the first decade of life. Corresponding physiological changes in diffusion have also been demonstrated by serial post-contrast magnetic resonance imaging (MRI) studies [26, 27]. These damages increase in frequency and severity over the age, but the healing potential of the EP is not clear. EP damage can precipitate DDD in a variety of ways including altered nutrition [28], leakage of protein macro-molecules and loss of hydrostatic pressure, altered matrix synthesis [21-23, 29, 30], secondary annular damage and vascularization of the nucleus pulposus without auto immune changes [31, 32]. It is now well accepted that structural failure of the EP may be the crucial factor in initiating the progress of DDD [11, 21, 26, 30, 33, 34]. © 2010 Springer-Verlag Berlin Heidelberg.