A Systematic Review of the Efficacy of Topical Skin Application of Dimethyl Sulfoxide on Wound Healing and as an Anti-Inflammato

IGP Duimel-Peeters, MSc;[1] RH Houwing, MD;[2] CP Teunissen, MSc;[3] MPF Berger, PhD;[4] LHEH Snoeckx, PhD;[5] RJG Halfens, PhD[1]


Pressure ulcers, also commonly referred to as bedsores, pressure sores, decubitus ulcers, or simply decubitus, can develop when sustained load, friction, or shear is applied to localized areas of the body, leading to degeneration of the skin and underlying soft tissues. As in other countries, pressure ulcers form a major problem in Dutch institutions for healthcare services.[1] There are various theories that explain the etiology of pressure ulcers, with most experts adhering to the theory that pressure ulcers result from chronic occlusion of capillary blood flow, leading to alternating periods of ischemia and reperfusion. This process is associated with repetitive formation of reactive oxygen species (ROS) and concomitant tissue necrosis.[2] Recently, pilot studies have revealed that rubbing the intact skin with a dimethyl sulfoxide (DMSO)-containing cream during the first stage of pressure ulcers according to the four grade system of the European Pressure Ulcer Advisory Panel (EPUAP) leads to a decrease in pressure ulcer occurrence among high-risk patients.[3,4]

DMSO [(CH3)2 S-O] is a water-white to straw-yellow-colored organic liquid. It is an oily substance with a smell of sulfur and a slightly bitter taste. In topical application, this simple, highly polar chemical compound has been found to alleviate ischemic damage in several experimental animal models.[5,6] In addition to an analgesic effect, the most important property of DMSO is the enhancement of percutaneous penetration.[7] When used in combination with other substances, DMSO facilitates diffusion through the stratum corneum of the skin, triggers the formation of deposits in the deeper layers of the subcutaneous tissue, and promotes transport into the local blood vessels.[8] Hence, dermatologists use it as a vehicle for other medications.

In pressure ulcer tissue, like any tissue in which inflammation occurs, repetitive ischemia-reperfusion episodes lead to the local formation of ROS. The main representatives of these radicals are the superoxide anion (O?2-), hydrogen peroxide (H2O2), and the hydroxyl radical (OH-). Since DMSO is known to be a hydroxyl-inactivating compound, it can be assumed that its beneficial effects on pressure ulcers are based upon this activity.
The purpose of this review was to evaluate the literature on the efficacy of DMSO in various concentrations on wound healing and as an anti-inflammatory drug administered by topical application to the skin.


A MEDLINE literature research was carried out covering the last 36 years (starting in 1966). At first, the search focused on studies involving DMSO by one specific disorder, e.g., pressure ulcers. However, this did not yield enough articles, so the domain was expanded. The following keywords were used: dimethyl sulfoxide, clinical dermatology, pharmacology and toxicology, bio-penetrator, the skin, hydroxyl radicals, ROS, scavengers, treatment of ulcers, and inflammation. In addition, the references of all articles retrieved were further examined. The same search was done in PUBMED and EMBASE-Excerpta Medica. A last extensive search strategy was used in the Cochrane Library by means of the Cochrane Controlled Trial Register and the Cochrane Database of Clinical Reviews. Finally, the Cochrane Skin Group and the Cochrane Wounds Group were explored. Abstracts were not selected. One unpublished study was selected because of its relevance to the topic of the present review.[4] Studies were only included if DMSO was applied locally on the diseased skin in conditions involving wound healing and/or inflammation or on healthy skin in order to determine its sensitivity to various DMSO concentrations. Research using experimental animals was excluded.

Table 1 lists the criteria used, which were weighed by three independent reviewers with different backgrounds (dermatology, pharmacy, and physiotherapy and movement sciences).



1. Bours GJJW, Halfens RJG, Huijer Abu-Saad H, Grol RTPM. Prevalence, prevention, and treatment of pressure ulcers: A descriptive study in 89 institutions in the Netherlands. Research in Nursing and Health 2002;25(2):99–110.
2. Houwing R, Overgoor M, Kon M, et al. Pressure-induced skin lesions in pigs: Reperfusion injury and the effects of vitamin C. J Wound Care 2000;9(1):36–40.
3. Four-Grade System. Presented at the European Pressure Ulcer Advisory Panel (EPUAP). Oxford, UK, September 20–22, 1998.
4. Van Rossum JP. Behandeling en preventie van decubitus met dimethylsulfoxide—verslag van een pilot studie (Treatment and prevention of decubitus with dimethyl sulfoxide—a report of a pilot-study). Unpublished report, personal communication, 1997.
5. Lishner M, Lang R, Kedar I, Ravid M. Treatment of diabetic perforating ulcers (mal perforant) with local dimethyl sulfoxide. J Am Geriatr Soc 1985;33:41–3.
6. Kedar I, Jacob E, Ravid M. Dimethylsulfoxide in acute ischaemia of the kidney: Experimental models in the rat and in the dog. Ann NY Acad Sci 1983;411:131.
7. Sulzberger MB, Cortese TA, Fishman L. Some effects of DMSO on human skin in vivo. Ann NY Acad Sci 1967;141(1):437–50.
8. Kappert A. Experimental and clinical evaluation of topical dimethyl sulfoxide in venous disorders of the extremities. Ann NY Acad Sci 1975;243:403–7.
9. Feinstein AR. Clinical Epidemiology: The Architecture of Clinical Research. Philadelphia, PA: WB Saunders, 1985.
10. Bouter LM, van Dongen MCJM. Epidemiologisch onderzoek: Opzet en Interpretatie [Epidemiologic Research: Principles and Methods] [Dutch]. Houtem/Diegem: Bohn Stafleu Van Loghum, 1995:183–6.
11. Assendelft WJJ, Scholten RJPM, van Eijk JTM, Bouter LM. De praktijk van systematische reviews III. Methodologische beoordeling van onderzoeken (The practice of systematic reviews. A methodological assessment of research). Ned Tijdschr Geneeskd 1999;143(14):714–8.
12. Scherbel AL, McCormack LJ, Layle JK. Further observations on the effect of dimethyl sulfoxide in patients with generalized scleroderma (progressive systemic sclerosis). Ann NY Acad Sci 1967;141(1):613–29.
13. Alberts DS, Dorr RT. Case report: Topical DMSO for mitomycin-c-induced skin ulceration. Oncol Nurs Forum 1991;18:693–5.
14. Engel MF. Indications and contraindications for the use of DMSO in clinical dermatology. Ann NY Acad Sci 1967;141(1):638–45.
15. Engel MF. Dimethyl sulfoxide (DMSO) in clinical dermatology. South Med J 1966;59(10):1318–20.
16. Agner T, Serup J. Quantification of the DMSO-response, a test for assessment of sensitive skin. Clin Exp Dermatol 1989;14:214–7.
17. Goris RJA, Dongen LMV, Winters HAH. Are toxic oxygen radicals involved in the pathogenesis of reflex sympathetic dystrophy? Free Radic Res 1986;3(1–5):13–8.
18. Geertzen JHB, de Bruijn H, de Bruijn-Kofman AT, Arendzen JH. Reflex sympathetic dystrophy: Early treatment and psychological aspects. Arch Phys Med Rehabil 1994;75:442–5.
19. Langendijk PNJ, Zuurmond WWA, Van Apeldoorn HAC, Van Loenen AC, De Lange JJ. Goede resultaten van behandeling van acute reflectoir-sympathische dystrofie met een 50%-dimethylsulfoxide-crème (Good results of the treatment of acute reflex sympathetic dystrophy by using a 50%-dimethyl sulfoxide cream). Ned Tijdschr Geneeskd 1993;137(10):500–3.
20. Salim AS. Role of free radical scavengers in the management of refractory duodenal ulceration. J Surg Res 1994;56:45–52.
21. Frosch PJ, Duncan S, Kligman AM. Cutaneous biometrics I. The response of human skin to dimethyl sulfoxide. Br J Dermatol 1980;102:263–73.
22. Binnick SA, Shore SS, Corman A, Fleishmajer R. Failure of dimethyl sulfoxide in the treatment of scleroderma. Arch Dermatol Res 1977;113:1398–1402.

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