BMP7 Recombinant Adenovirus Therapy Of Degenerative Disc Disease

Low back pain is one of the major causes of disability and, thus, has a major socioeconomic impact. The lifetime prevalence of low back pain is 75% to 80% of the population. Many of these spinal impairments are the direct or indirect result of degenerative disc disease (DDD). Current treatment options, including both conservative and surgical measures, target the clinical symptoms of intervertebral disc degeneration, as opposed to addressing the pathologic processes occurring early in the course of degeneration. However, recent advances in molecular biology may allow for the development of treatments focusing on the cellular changes that occur in this disease.The precise etiology and pathophysiology of DDD remains to be clearly delineated. It is known that the matrix of a healthy nucleus pulposus is rich in proteoglycans and type II collagen, whereas the annulus fibrosus is rich in type I collagen. The progressive decline in proteoglycan of the nucleus pulposus is known to be a significant and characteristic factor of the early stages of DDD. At the biochemical level, the diminished proteoglycan content reflects an imbalance in the normal anabolic and catabolic functions of the nucleus pulposus cells. With reductions in proteoglycan content of the intervertebral matrix, the nucleus pulposus dehydrates, decreasing disc height and altering its load-bearing capacity. This in turn may directly affect overall spinal biomechanical function. Although disc degeneration most probably evolves in response to a complex interplay of multiple biochemical and biomechanical factors, the ability to restore proteoglycan content may have therapeutic benefit by increasing disc hydration and potentially improving biomechanics. In 1991,Thompson et al reported that human recombinant insulin-like growth factor-1 (IGF-1), epidermal growth factor (EGF), fibroblast...