Abstract:syndrome. In the current study, 105 patients with pSS and 93 healthy controls were tested for VDR gene polymorphisms (BsmI, ApaI, TaqI and FokI) genotypes. There were no statistical differences in the distribution of BsmI, TaqI, ApaI and FokI genotypes and the common haplotypes between pSS patients and healthy controls. We hypothesized that the TaqI, BsmI, ApaI, and FokI polymorphisms of the VDR gene are not associated with the development of primary Sjögren's syndrome in the Hungarian population studied.
“…Similarly, in two other studies comparing patients with SS and healthy controls, no difference in vitamin D levels was noted . Also, one study could not find any associations between vitamin D receptor gene polymorphisms/haplotypes and SS . With regard to disease manifestations, one study reported low levels of vitamin D in patients with SS presenting with peripheral neuropathy or with lymphoma compared to patients without these manifestations .…”
“…Similarly, in two other studies comparing patients with SS and healthy controls, no difference in vitamin D levels was noted . Also, one study could not find any associations between vitamin D receptor gene polymorphisms/haplotypes and SS . With regard to disease manifestations, one study reported low levels of vitamin D in patients with SS presenting with peripheral neuropathy or with lymphoma compared to patients without these manifestations .…”
“…It is known that the VDR gene is situated on chromosome 12 (12q12-q14). It has numerous single nucleotide polymorphisms (SNPs) (gene polymorphisms sites) and expresses a ligand-activated transcription factor [33,34]. Some of these SNPs play critical roles in the modification of 1,25-dihydroxyvitamin D uptake [17] and can promote vitamin D function and metabolism [33].…”
Section: Vitamin D and Genetic Variancesmentioning
Background and aims. Vitamin D is synthesized in the skin with the aid of ultraviolet-B radiation, playing a variety of roles in the body. Temporomandibular disorders (TMDs) are a group of pathological conditions involving the temporomandibular joints as well as the masticatory muscles and othersurrounding tissues. In the present narrative review, we investigated the potential role of vitamin D in the etiology of temporomandibular disorders in order todetermine whether the current knowledge supports 25-hidroxyvitamin D (25-OHD) supplementation in temporomandibular disorders associated with insufficient or deficient levels of vitamin D. Methods. A literature research was performed in PubMed, Scopus, Science Direct, and Google Scholar databases, and a total of 10 articles were included for analysis. Results.Among the observational studies published to date, investigating the role for vitamin D in the etiology of TMDs, six of them suggest that there is a connection between the two aspects. In this context, patients suffering from TMD, with deficient levels of vitamin D (<30 ng/mL), are most likely to benefit from supplementation, whereas individuals with vitamin D level >50ng/mL probably have little benefit from supplementation.Conclusion.Vitamin D might be a safe, simple, and potentially beneficial way to prevent TMDs or to reduce pain; however, more randomized and placebo-controlled trials are required before any firm conclusions can be drawn.
“…In contrast, Agmon-Levin et al [61] found no difference in serum 25(OH)D between SS patients and controls, although levels were lower in patients with peripheral neuropathy (18.6 vs 22.6 ng/ml) or lymphoma (13.2 vs 22.0 ng/ml). Furthermore, there is no evidence that genetic polymorphisms in the vitamin D pathway associate with the prevalence or severity of SS [62]. No studies have investigated the effect of vitamin D treatment in SS.…”
The prevalence of vitamin D deficiency is increased among patients with CTDs. The active form of vitamin D (calcitriol) is a potent regulator of the immune system and may suppress inflammatory responses. This has led to claims that vitamin D may be a safe treatment, or a treatment adjunct, to reduce systemic inflammation in this patient population. It is important to note, however, that there is insufficient evidence from robust clinical trials to support these novel uses for vitamin D. In this review we examine the potential role of vitamin D as a treatment adjunct for CTDs. We will discuss how vitamin D may modulate the immune response and review the current evidence for using vitamin D to treat CTDs and their associated co-morbidities. We conclude that while there is much excitement about vitamin D in this context, further well-designed trials are needed to demonstrate its efficacy in the treatment of patients with CTDs.
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