Introduction:
Chronic low back pain (CLBP) is one of the biggest medical and social problems in the world today1,2. The cost to the United States is estimated to be $100 billion annually 3, 4. A large number of studies have shown that intervertebral disc can be the main origin of low back pain. Discogenic low back pain (DLBP) originating from intervertebral disc degeneration is considered to be one of the major causes of CLBP 5. In addition, CLBP is one of the major causes of disability and thus has a major socioeconomic impact.
The manuscript’s aim was to comprehensively review the pathophysiological factors of DLBP. Additionally, it also addressed its diagnostic methods and management.
Methods:
A search through PubMed and Cochrane Library …show more content…
Discogenic pain originates from the development of fissures in the annulus fibrosus with consequent vascularization of growing granulation tissue and growth of nociceptive nerve fibers along the tear area6. With age, intervertebral disc undergoes significant changes including loss of water content from nucleus pulposus, disc thinning, decreased levels ofhyaluronic acid, keratinized sulfate, with increase in low molecular weight glycoprotein , fibril degeneration and collagen fibers deposition. These changes lead to loss of elasticity of the nucleus pulposus, disc structure relaxation, cartilage cystic change, and thus the fibrous ring …show more content…
Nucleus pulposus tissue is wrapped by the annulus and isolated from peripheral blood circulation. Studies have found that degeneration of the intervertebral disc tissue showed a high concentration of a variety of cytokines. When the annulus fibrosus ruptures, the nucleus pulposus is identified by the autoimmune system after exposure, which induces an autoimmune reaction and produces proinflammatory substances such as interleukin and tumor necrosis factor. Among them, interleukin -1 (interleukin-1, IL-1) can stimulate prostaglandin E2 (prostaglandin, E2, PGE2) and 5- serotonin (5-hydroxytryptamine, 5-HT) synthesis, and can improve the body's sensitivity to pain . IL-6 can stimulate local inflammatory cell aggregation, activation and inflammatory mediator
Chronic low back pain (CLBP) is one of the biggest medical and social problems in the world today1,2. The cost to the United States is estimated to be $100 billion annually 3, 4. A large number of studies have shown that intervertebral disc can be the main origin of low back pain. Discogenic low back pain (DLBP) originating from intervertebral disc degeneration is considered to be one of the major causes of CLBP 5. In addition, CLBP is one of the major causes of disability and thus has a major socioeconomic impact.
The manuscript’s aim was to comprehensively review the pathophysiological factors of DLBP. Additionally, it also addressed its diagnostic methods and management.
Methods:
A search through PubMed and Cochrane Library …show more content…
Discogenic pain originates from the development of fissures in the annulus fibrosus with consequent vascularization of growing granulation tissue and growth of nociceptive nerve fibers along the tear area6. With age, intervertebral disc undergoes significant changes including loss of water content from nucleus pulposus, disc thinning, decreased levels ofhyaluronic acid, keratinized sulfate, with increase in low molecular weight glycoprotein , fibril degeneration and collagen fibers deposition. These changes lead to loss of elasticity of the nucleus pulposus, disc structure relaxation, cartilage cystic change, and thus the fibrous ring …show more content…
Nucleus pulposus tissue is wrapped by the annulus and isolated from peripheral blood circulation. Studies have found that degeneration of the intervertebral disc tissue showed a high concentration of a variety of cytokines. When the annulus fibrosus ruptures, the nucleus pulposus is identified by the autoimmune system after exposure, which induces an autoimmune reaction and produces proinflammatory substances such as interleukin and tumor necrosis factor. Among them, interleukin -1 (interleukin-1, IL-1) can stimulate prostaglandin E2 (prostaglandin, E2, PGE2) and 5- serotonin (5-hydroxytryptamine, 5-HT) synthesis, and can improve the body's sensitivity to pain . IL-6 can stimulate local inflammatory cell aggregation, activation and inflammatory mediator