In 2010, research established a link between vitamin D insufficiency and a variety of nonspecific bone pain. Apart from its mood and immunity-boosting properties, taking vitamin D on a regular basis may help reduce unpleasant bone-related diseases, such as back pain.
Furthermore, in 2014, Ali Haghnegahdar from Shiraz University of Medical Sciences issued a study protocoll for a randomized controlled trial on the role of vitamin D3 in the treatment of lumbar disc herniation concerning pain and sensory aspects.
These is his abstract (Source: researchgate.net):
Background Vitamin D receptors have been found in the spinal cord, nerve roots, dorsal root ganglia, and glial cells, and a connection between vitamin D’s genetic polymorphism and the development of lumbar disc degeneration and herniation has been shown. The metabolic effects of active vitamin D metabolites have been investigated in nucleus pulposus and annulus fibrosus cells. Lumbar disc herniation is a process involving immunological and inflammatory cells and processes that are targets of vitamin D’s immune-regulating properties as a neurosteroid hormone. Apart from its immunological modulatory effects, vitamin D has been shown to have receptors in skeletal muscle. Additionally, it has an effect on sensory neurons, modulating pain. We intend to investigate the function of vitamin D3 in discogenic pain and associated sensory impairments in this study. Additionally, we will discuss the effect of post-treatment 25-hydroxy vitamin D3 levels on the intensity of pain and sensory impairments.
Additionally, the cut-off value for serum 25-hydroxy vitamin D3 that is effective in resolving pain and sensory impairments associated with lumbar disc herniation will be investigated. Methods/Design We will undertake a double-blind, randomized, placebo-controlled clinical study. Our research sample will consist of 380 patients with unilateral lumbar disc herniation and a discogenic pain duration of less than 8 weeks. Individuals without contraindications will be split into three groups according to their blood 25-hydroxy vitamin D3 level, and each group will be randomly assigned to receive either a single-dose 300,000-IU intramuscular vitamin D3 injection or a placebo. All patients will be treated conservatively. The McGill Pain Questionnaire and a visual analogue scale will be used to examine patients pre- and post-treatment. Throughout the 15-day period of this study, questions will be completed every three days during telephone interviews (a total of five times). Interviews for the early and final stages will take place at our clinic. Serum 25-hydroxy vitamin D3 levels will be determined after 15 days in those who have received vitamin D3 (190 individuals).
In 2019, another study conducted through a partnership of several pharmacy departments of universities and hospitals in Fujian, China revealed that Vitamin D inhibits NF-κB signaling pathways and reduces the level of inflammation and oxidative stress in the intervertebral disc, delays cell aging, and inhibits apoptosis. Therefore, the researchers confirmed that vitamin D can greatly improve intervertebral disc degeneration.
This is their research astract (Source: pubmed):
To ascertain the effectiveness and mechanism of action of vitamin D in the treatment of intervertebral disc degeneration. Three-month-old mice were used to construct the intervertebral disc degeneration model. Additionally, intervertebral disc degeneration was identified one month later in the vitamin D group and the control group using X-ray, Western blotting, quantitative real-time polymerase chain reaction (qRT-PCR), and enzyme-linked immunosorbent assay (ELISA), et al. Additionally, we cultivated mouse intervertebral disc nucleus pulposus cells in vitro to confirm and analyze the effect of vitamin D on nucleus pulposus cells. In vivo, mice in the vitamin D group demonstrated dose-dependent inhibition of intervertebral disc degeneration in terms of decreasing inflammatory responses, oxidative stress, blocking apoptosis, and delaying cell aging when compared to the control group. Collagen II was raised and collagen X was decreased in mice treated with vitamin D in vitro, compared to the control group. In vivo and in vitro tests, the vitamin D treatment group’s intervertebral disc tissue or nucleus pulposus cells expressed less p65 and IB kinase and more inhibitor of NF-B, showing that vitamin D can suppress the NF-B pathway. Vitamin D slowed intervertebral disc degeneration by blocking the NF-B pathway, which may alleviate inflammatory responses, protect cells from oxidative stress, prevent apoptosis, and postpone cell senescence.