Systemic review of nutritional supplements dimethyl sulfoxide (DMSO) and methylsulfonylmethane (MSM) in the treatment of osteoarthritis

Department of Primary Care, University of Southampton, UK.
Osteoarthritis and Cartilage (Impact Factor: 4.17). 05/2008; 16(11):1277-88. DOI: 10.1016/j.joca.2008.03.002
Source: PubMed

ABSTRACT Conventional treatment of osteoarthritis (OA) with non-steroidal anti-inflammatory drugs is associated with serious gastrointestinal side effects and in view of the recent withdrawal of some cyclo-oxygenase-2 inhibitors, identifying safer alternative treatment options is needed. The objective of this systematic review is to evaluate the existing evidence from randomised controlled trials of two chemically related nutritional supplements, dimethyl sulfoxide (DMSO) and methylsulfonylmethane (MSM) in the treatment of OA to determine their efficacy and safety profile.

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    • "It shows radioprotective (Goddu et al. 1996) and antioxidant properties (Repine et al. 1981; Mobarok 1998; Dkhar and Sharma 2010), antitumor activity (Fahim et al. 2003), and inhibits necrosis of the cells (Camici et al. 2006; Iida et al. 2007). Medical doctors prescribe it for a variety of ailments including pain, inflammation, scleroderma, interstitial cystitis and arthritis, and elevated intracranial pressure (Goodnough et al. 1980; Karaca et al. 1991; McGee et al. 1991; Brien et al. 2008; Kim et al. 2011). For the variety of its positive effects it is considered to be the aspirin of our era. "
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    ABSTRACT: Dimethyl sulfoxide (DMSO), a by-product of the pulping industry, is widely used in biological research, cryobiology and medicine. On cellular level DMSO was shown to suppress NMDA-AMPA channels activation, blocks Na+ channel activation and attenuates Ca2+ influx (Lu and Mattson 2001). In the present study we explored the whole-cell patch-clamp to examine the acute effect of high concentrations of DMSO (0.1-2 mol/l) on cation channels activity in human erythrocytes. Acute application of DMSO (0.1-2 mol/l) dissolved in Cl--containing saline buffer solution significantly inhibited cation conductance in human erythrocytes. Inhibition was concentration-dependent and had an exponential decay profile. DMSO (2 mol/l) induced cation inhibition in Cl-- containing saline solutions of: 40.3 ± 3.9% for K+, 35.4 ± 3.1% for Ca2+ and 47.4 ± 1.9% for NMDG+. Substitution of Cl- with gluconate- increased the inhibitory effect of DMSO on the Na+ current. Inhibitory effect of DMSO was neither due to high permeability of erythrocytes to DMSO nor to an increased tonicity of the bath media since no effect was observed in 2 mol/l glycerol solution. In conclusion, we have shown that high concentrations of DMSO inhibit the non-selective cation channels in human erythrocytes and thus protect the cells against Na+ and Ca2+ overload. Possible mechanisms of DMSO effect on cation conductance are discussed.
    General Physiology and Biophysics 03/2013; 32(1):23-32. DOI:10.4149/gpb_2013004 · 1.17 Impact Factor
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    • "Methylsulfonylmethane (MSM) is a very simple organic sulfur-containing compound that occurs naturally in a variety of fruits, vegetables, grains, and animals including humans [15]. MSM is a normal oxidative metabolite product of dimethyl sulfoxide (DMSO) that reduces peripheral pain, inflammation and arthritis, and might inhibit the degenerative changes occurring in osteoarthritis [16]. Furthermore, we recently reported that MSM suppresses breast cancer growth by down-regulating STAT3 and STAT5b pathways [17]. "
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    ABSTRACT: Methylsulfonylmethane (MSM) is a naturally occurring sulfur compound with well-known anti-oxidant properties and anti-inflammatory activities. But, its effects on bone are unknown. Growth hormone (GH) is regulator of bone growth and bone metabolism. GH activates several signaling pathways such as the Janus kinase (Jak)/signal transducers and activators of transcription (STAT) pathway, thereby regulating expression of genes including insulin-like growth factor (IGF)-1. GH exerts effects both directly and via IGF-1, which signals by activating the IGF-1 receptor (IGF-1R). In this study, we investigated the effects of MSM on the GH signaling via the Jak/STAT pathway in osteoblasts and the differentiation of primary bone marrow mesenchymal stem cells (MSCs). MSM was not toxic to osteoblastic cells and MSCs. MSM increased the expression of GH-related proteins including IGF-1R, p-IGF-1R, STAT5b, p-STAT5b, and Jak2 in osteoblastic cells and MSCs. MSM increased IGF-1R and GHR mRNA expression in osteoblastic cells. The expression of MSM-induced IGF-1R and GHR was inhibited by AG490, a Jak2 kinase inhibitor. MSM induced binding of STAT5 to the IGF-1R and increased IGF-1 and IGF-1R promoter activities. Analysis of cell extracts by immunoprecipitation and Western blot showed that MSM enhanced GH-induced activation of Jak2/STAT5b. We found that MSM and GH, separately or in combination, activated GH signaling via the Jak2/STAT5b pathway in UMR-106 cells. Using siRNA analysis, we found that STAT5b plays an essential role in GH signaling activation in C3H10T1/2 cells. Osteogenic marker genes (ALP, ON, OCN, BSP, OSX, and Runx2) were activated by MSM, and siRNA-mediated STAT5b knockdown inhibited MSM-induced expression of osteogenic markers. Furthermore, MSM increased ALP activity and the mineralization of MSCs. Taken together, these results indicated that MSM can promote osteogenic differentiation of MSCs through activation of STAT5b.
    PLoS ONE 10/2012; 7(10):e47477. DOI:10.1371/journal.pone.0047477 · 3.23 Impact Factor
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    • "Our current study therefore strongly indicates that oxidative damage does not play a major role in the age-related etiology of cartilage damage and OA. In this respect, the role of antioxidant treatment (either taken as supplements or via enriched dietary intake) may not be effective, and although in the last decades a number of randomized clinical trials have been performed which tested the use of supplements as treatment for OA, antioxidant supplementation so far has not shown clear efficacy (Wluka et al. 2002; Canter et al. 2007; Brien et al. 2008). Subsequent direct proof that oxidative damage is not involved in OA should be provided by genetic studies and agerelated cartilage-specific interference in metabolism, ROS production and cartilage degradation. "
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    ABSTRACT: The increasing average age in developed societies is paralleled by an increase in the prevalence of many age-related diseases such as osteoarthritis (OA), which is characterized by deformation of the joint due to cartilage damage and increased turnover of subchondral bone. Consequently, deficiency in DNA repair, often associated with premature aging, may lead to increased pathology of these two tissues. To examine this possibility, we analyzed the bone and cartilage phenotype of male and female knee joints derived from 52- to 104-week-old WT C57Bl/6 and trichothiodystrophy (TTD) mice, who carry a defect in the nucleotide excision repair pathway and display many features of premature aging. Using micro-CT, we found bone loss in all groups of 104-week-old compared to 52-week-old mice. Cartilage damage was mild to moderate in all mice. Surprisingly, female TTD mice had less cartilage damage, proteoglycan depletion, and osteophytosis compared to WT controls. OA severity in males did not significantly differ between genotypes, although TTD males had less osteophytosis. These results indicate that in premature aging TTD mice age-related changes in cartilage were not more severe compared to WT mice, in striking contrast with bone and many other tissues. This segmental aging character may be explained by a difference in vasculature and thereby oxygen load in cartilage and bone. Alternatively, a difference in impact of an anti-aging response, previously found to be triggered by accumulation of DNA damage, might help explain why female mice were protected from cartilage damage. These findings underline the exceptional segmental nature of progeroid conditions and provide an explanation for pro- and anti-aging features occurring in the same individual.
    Age 09/2011; 33(3):247-60. DOI:10.1007/s11357-010-9175-3 · 3.45 Impact Factor
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