Model of Osteopathy Lumbar Degenerative Disk

Question: Describe about the Model of Osteopathy for Lumbar Degenerative Disk. Answer: Introduction The intervertebral disc is a cartilaginous arrangement. Various factors have been found to trigger the degeneration of the intervertebraldisc. The main contributing aspects are found to be aging, genetics, nutrition, metabolic, infection and mechanical factors. Degeneration of the intervertebraldisc is clinically important because back pain is intensely connected with it. The major triggering factors The major triggering influences individually or collectively cause intervertebraldisc degeneration. Ageing The density of cells in the disc deteriorates with aging due to the degraded production of the matrix. The collagen IX and I) and non-collagen protein content increases and the synthesis rate and concentrationof proteoglycans (Aggrecan) decreases in the nucleus. These events progressively makes the nucleus more fibrous, dry, solid and granular and can cause cracks to appear (Kepler et al., 2013). Genetic influences Vitamin D receptor gene variants Fok I and Taq I have been found to be involved in disc degeneration. Decaying of mRNA gets increased by Taq I which damages the glycosaminoglycan sulphation by vitamin D. polymorphism in these variants can also accelerate degenerative. The alleles of the interleukin-1 gene are allied with disc bulging (Kepler et al., 2013). Nutrition According to Boubriak et al. (2013), reduction in the transportation of nutrients in the disc is a cause of degeneration. A declined stream of vital nutrients leads to an amplification of oxidative stress indicators. A lower level of oxygen and an acidic pH from the anaerobic metabolism cause a drop in the synthesis of proteoglycan and protein. A reduction in nutrient quantity can also decrease the amount of viable cells of the disc. Metabolic factors Metabolic disorders like diabetes mellitus and alkaptonuria can facilitate disc deterioration either by meddling with the usual biochemistry of matrix production or by depositing foreign ingredients inside the disc. A significant decrease in hexosamine content increased the activity of carbohydrate metabolism enzymes and amplified hydroxyproline in diabetes patients which causes a deficiency in the incorporation of S-sulphate in the disk. Alkaptonuria patients suffer disc degeneration due to the deposition of black intradiscal pigments (Nerlich Boos, 2016). Low-grade infection The systematic review of Urquhart et al. (2015), recognized reasonable information to specify low virulent bacteria have a role in low back pain with disc degeneration. This evidence suggests an association between low-grade infection and Modic Type 1 alteration related to disc herniation (Urquhart et al., 2015). Mechanical factors Vibration adversely affects metabolism and nutrition of the disc. Torsional movements produce tension in the collagen fibers in the annulus and torsion injury may lead to disc degeneration. Vertebral endplate fails due to fracturing when subjected to a severe compression load (Gawri et al., 2014). Process by which intervertebraldisc becomes a source of pain The intervertebraldisc serves to sustain compression load and can be a source of pain. The annulus fibrosus may get damaged due to these factors and can become a significant source of pain if the annulus extends to the external part and the nerves become sensitized. If the nucleus pulposus leaks out of the disc and interacts with nerve roots, it can cause inflammation and create pain (Gawri et al., 2014). Conclusion The evidence suggests that disc degeneration is an age-dependent, genetic and cell-mediated molecular degradation progression which is facilitated by inflectional, metabolic, mechanical and nutritional factors. The evidence established these factors cause fissures and cracks in the disc matrix, thickens the vertebral endplate, disrupts the biomechanical functioning of the discand cause tears in the annulus. References Boubriak, O., Watson, N., Sivan, S., Stubbens, N., Urban, J. P. (2013). Factors regulating viable cell density in the intervertebral disc: blood supply in relation to disc height.Journal of anatomy,222(3), 341-348. Gawri, R., Rosenzweig, D. H., Krock, E., Ouellet, J. A., Stone, L. S., Quinn, T. M., Haglund, L. (2014). High mechanical strain of primary intervertebral disc cells promotes secretion of inflammatory factors associated with disc degeneration and pain.Arthritis research therapy,16(1), 1. Kepler, C. K., Ponnappan, R. K., Tannoury, C. A., Risbud, M. V., Anderson, D. G. (2013). The molecular basis of intervertebral disc degeneration.The Spine Journal,13(3), 318-330. Nerlich, A. G., Boos, N. (2016). Advances in Lumbar Degenerative Disk Disease Pathophysiology Comprehension. InAdvanced Concepts in Lumbar Degenerative Disk Disease(pp. 41-59). Springer Berlin Heidelberg. Urquhart, D. M., Zheng, Y., Cheng, A. C., Rosenfeld, J. V., Chan, P., Liew, S., Cicuttini, F. M. (2015). Could low grade bacterial infection contribute to low back pain? A systematic review.BMC medicine,13(1), 1.