Abstract
Introduction
Back pain, is still, one of the unrewarding problems to deal with in clinical medicine. Of the various forms of low back pain, only those syndromes associated with neurologic compression of the cauda equina or nerve roots, have reasonably well understood clinical presentation.
Nearly 80% of the population sustains an episode of low back pain (LBP) once during their lifetime[1]. LBP has high prevalence and significant contribution to disability. Within the vast differential of LBP, the most common source is intervertebral degeneration leading to degenerative disc disease and lumbar disc herniation [2]. Thus, an effective understanding of lumbar disc herniation (LDH), its origins, and how to appropriately treat LDH is of substantial importance.
Disc herniation is a greater threat in younger individuals between the ages of 30 and 50 years, in whom the nucleus material has good turgor, in contrast to older individuals in whom the nucleus is desiccated and fibrotic.
The intervertebral disc consists of an inner nucleus pulposus (NP) and an outer annulus fibrosus (AF). The central NP is a site of collagen secretion and contains numerous
proteoglycans (PG) 34. The NP is primarily composed of type II collagen. In contrast, the AF functions to maintain the NP within the center of the disc with low amount of PG and primarily concentric type I collagen fibers[3,5,6]. Several changes in the biology of the intervertebral disc are thought to contribute to LDH. These include reduced water retention in the NP [5,7,8], increased percent of type I collagen within the NP and inner AF[9], degradation of collagen and extracellular matrix (ECM) materials[10], and upregulation of systems of degradation such as apoptosis, matrix metalloproteinase (MMP) expression, and inflammatory pathways[11]
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Corresponding Author
Dr Rohit Raj
Junior Resident, Department of Orthopaedics, KMCH Katihar
DOI: https://dx.doi.org/10.18535/jmscr/v10i12.09
