Introduction

 

Lichen Planus (LP) was first described by British physician Erasmus Wilson in 1896. (1) The lesions bear a resemblance to lichens, which are small plants often found growing on the rock face. The prevalence of lichen planus is unknown, but it is estimated to occur in  1-2 percent of the population. It most commonly affects middle-aged adults of both sexes, with a slight predominance in women. The World Health Organization recognizes seven different clinical forms of oral lichen planus

(OLP): reticular, papular, in plaques, atrophic, erosive, ulcerated, and bullous (3).  

 

The skin lesions are usually distributed symmetrically, most commonly on the flexor surfaces of the wrists, ankles, legs, trunk, oral and vaginal mucosa and in rare cases, the scalp and nails.  The oral mucosa is involved in about 50% of patients, often before or in the absence of cutaneous lesions. The buccal mucosa, tongue margins, and gingival mucosa show asymptomatic ill-defined, bluish white linear lesions that may initially be reticulated or lacy and may coalesce and increase in size. An erosive form may occur in which the patient complains of shallow, often painful, recurrent oral ulcers.  Patients with long-term oral mucosal lesions may have an increased risk of developing squamous cell carcinoma within the lesions (4). Chronic exacerbations and remissions are common. 

 

Aetiology

 

The aetiology of lichen planus is unknown, although many studies suggest an immunological pathogenesis. Lymphocytes, particularly T-cells, play a major role (2,5) . Other factors include antigen-presenting cells, adhesion molecules and inflammatory cytokines (6). While most cases of OLP are idiopathic, some are linked to medication use , hepatitis C virus infection, diabetes and lichenoid reactions to mercury and gold.  See Table 1  Other participating factors in OLP can be: stress, particular foods, dental plaque, systemic illness , candidaisis and poor oral hygiene.  

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Treatment

 

The treatment of patients with OLP is greatly individualized as patients vary  in severity of symptoms, extent of lesion involvement and response to treatment. Although many patients are asymptomatic and require no therapy, those who exhibit atrophic and erosive lesions are often a challenge to treat. A recent Cochrane Review has concluded that all therapies are palliative, and none appears to be  effective universally (7).  

 

Nutrition and Lifestyle

 

Research into the dietary and lifestyle factors involved in the incidence and progression of  OLP is scarce. There is some evidence that stress, smoking and alcohol intake is related to the incidence of OLP (8).Recent research has suggested that anxiety and depression may constitute risk factors that could influence the development of OLP (9). The level of anxiety and salivary cortisol of OLP patients has also been found to be high, prompting the researchers to conclude that this disease may be related to stress (10). Thus besides traditional treatment of OLP patients, it may be that psychological support is also needed.   

 

Most research concludes that nutrition has no direct influence in the aetiology of OLP. Increasingly more evidence in the field of nutritional medicine, however is being accumulated with regard to the effect of nutritional therapies in auto immune disorders and chronic inflammatory disease.  Whilst it is likely that OLP is not a nutritional deficiency disease, this article brings together the latest research in the field of nutrition medicine which may have implications in the management of OLP.  The aetiology of OLP is poorly understood and is believed to be multi factoral. Embracing a multi disciplinary approach in the management of this condition  may be of value.  

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Essential Fatty Acids

 

In recent years, researchers have become increasingly interested in the benefits of Omega-3 fatty acids and their ability to modulate the inflammatory process and production of prostaglandins and other cytokines. Fatty acid deficiencies often feature in auto immune disorders and chronic inflammatory conditions.  

 

Prostaglandins are potent mediators of the immuno-inflammatory pathways. The pro inflammatory prostaglandins (PGE2)  and other metabolites of Arachidonic Acid (AA) are released in response to tissue damage. Inhibition of prostaglandins by pharmacological agents has been demonstrated to enhance immunocompetence, and to suppress auto immune responses in animals and humans.   Adequate intake of the essential fatty acid precursors of the  anti inflammatory prostaglandins PGE1 and 3 can manipulate and oppose the excess production of PGE2 and other AA metabolites. Gammalionlenic acid (GLA)  works as an anti-inflammatory agent  in a similar way to steroid drugs, by blocking the mobilisation of AA, and the synthesis of certain leutrokines from AA (11).  Eicosapentaenoic acid (EPA) from fish oils and its metabolites also appears to compete with AA and prevent the synthesis of AA to inflammatory metabolites (12,13).  

 

Clinical studies have also reported that oral fish oil supplementation has beneficial effects in some auto immune disorders, supporting the idea that the omega three fatty acids in fish oil are anti-inflammatory (14). Vitamin E has also been shown to inhibit the production of pro inflammatory prostaglandins in human gingival fibroblasts and therefore suppress the activity of PGE2 (15).  

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Antioxidants

 

Oxidative stress is thought to make a significant contribution to all inflammatory diseases including those of the oral cavity (16). An increasing body of evidence is emerging to implicate free radical activity in the pathogenesis of the oral tissues (17).   The regeneration of the oral mucosa is zinc- and vitamin A-pathway dependent. Hyperkeratoses, a disturbed immune system and a higher incidence of oral malignancies have been reported in cases of deficiency . It has been reported that serum zinc and red cell folate  levels in OLP patients are lower, indicating a possible need for supplementation (18).  

 

Other research, however, has found no significant differences in carotenoid levels, except for a lower level of lycopene found in atrophic/erosive OLP cases. The researchers suggest that low serum retinol or carotenoid levels are not risk factors for occurrence of lichen planus, and any specific benefits of antioxidant micronutrients cannot be claimed for this inflammatory disorder (19).  

 

Serum concentrations of antioxidants, however do not always accurately reflect activity on a cellular level.  Serum concentrations of micronutrients may be good indicators of recent dietary intake, but it is the measurement of the metabolites of individual micronutrient pathways and target tissues which provide a more accurate picture of activity on a cellular level. For example white cell zinc concentrations are a more accurate determinant of zinc activity than serum concentration alone.   

 

It is also recognised that some individuals have an increased metabolic need for certain micronutrients, particularly where risk factors such as  age, poor nutrition, smoking, allergies, candidaisis or systemic diseases such as diabetes and thyroid disorders are present. In the OLP patient adequate antioxidant intake is, therefore of value.  

 

The antioxidant micronutrients are important not only for limiting oxidative damage and tissue damage, but also in preventing increased cytokine production, which is a  common feature in auto immune and chronic inflammatory disorders (20) .  The carotenoids are particularly useful in the maintenance and repair of mucus membranes and zinc has been shown as having a protective effect particularly where sodium lauryl sulphate sensitivity is present (21).  

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Food Sensitivities

 

Although food sensitivities are unlikely to be the cause of OLP, they have been implicated in exacerbating auto immune disorders and chronic inflammation, particularly where mucus membranes are involved.   Food allergies and food sensitivities are very different in aetiology. An allergic reaction produces an immediate response and is IgE mediated, an intolerance has delayed onset and is mostly IgG mediated. It has been hypothesized that serum levels of immunoglobulins may play a role in the pathogenesis of oral mucosal diseases, or reflect clinical changes in these conditions. Elevated levels of IgG1, IgG2, IgG3 and IgG4 have been determined by enzyme-linked immunosorbent assay (ELISA) in the resting whole saliva of patients with OLP (22).  Elevated IgG levels may be exacerbated by food  or chemical sensitivities.   

 

Inflammatory reactions to foods can manifest themselves in almost every organ or part of the body. They are capable of producing a huge array of symptoms depending on which organ or tissue is affected. In patients who exhibit other inflammatory conditions in addition to OLP, such as arthritis, asthma or eczema and frequent apthous ulceration, screening for food and chemical sensitivity may be indicated.  

 

 Laboratory tests for IgE and IgG mediated allergies include the RAST test (radioallergosorbent test). This is a blood test that determines the presence and level of  antibodies in the blood for specific foods and some food fractions.  Some laboratories have changed over to the ELISA and  FACT method of antibody detection which appears to be more sensitive and less expensive than RAST. The most common food sensitivities include wheat, milk and citrus fruits. 

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Sodium Lauryl Sulphate

 

Research into the direct effects of Sodium lauryl sulfate (SLS), on OLP is scarce. SLS, the most widely used detergent in toothpastes, however,  has been reported to cause adverse effects on oral mucus membrane (23). SLS in toothpastes has been shown to significantly increase the incidence of desquamation of the oral mucosa in sensitive patients.  It also appears that the  oral mucosa of pre-menopausal women is significantly more sensitive to SLS than oral mucosa of post-menopausal women (24). The avoidance of toothpastes or mouthwashes containing SLS, may be indicated for the OLP patient. Sensodyne Gel , for example is SLS free and there have been anecdotal reports of good results with the topical application of gels such as Aloe Vera,  Biotene and Gengigel mouthwashes and gel.    

 

Dietary Guidelines  

 

The following dietary advice may help in the management of OLP:

•  Avoid foods which are likely to irritate the mucus membranes such as acidic and sour foods such as  tomatoes, pineapple, citrus juices and fruits, vinegar, pickles and spicy foods such as chillies.  

• Avoid  crispy foods like toast and potato crisps as these can aggravate lichen planus especially if there are open sores in the mouth.  

• Avoid caffeinated drinks like coffee, chocolate and cola, as these can also irritate along with  strongly flavoured toothpastes. 

• Patients should be instructed to discontinue the use of chewing gum, boiled sweets, mints, toothpastes or mouth rinses that contain flavouring agents such as wintergreen, peppermint, spearmint and cinnamon.  

• Mouth rinses containing alcohol should be avoided in order to prevent patient discomfort and tissue irritation.  

• Prophy paste that is gritty or coarse should not be used because of irritation to the mucus membranes.   

 

Foods containing micronutrients useful in the protection and repair of mucus membrane are listed in Table 2.   

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Conclusion

 

One aspect we must remember when considering treatment protocols for erosive OLP is the chronic course of the disease and its recalcitrant nature. These factors mean that treatment has to be tolerated over long periods, and the onset of adverse side effects from long-term therapy must be taken into account. An holistic approach should also be considered when new management protocols are being considered for erosive OLP. For some patients, therefore, nutritional medicine may provide a valuable adjunctive therapy in the management of oral lichen planus.

 

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References

 

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2.Boyd AS, Neldner KH. Lichen planus. J Am Acad Dermatol 1991;25:593-619  

 

3 Silverman S, Bahl S. Oral lichen planus update: clinical characteristics, treatment responses and malignant transformation. Am J Dent. 1997;10:259-263.  

 

4 Silverman S, Gorsky M, Lozada-Nur F. A prospective follow-up study of 570 patients with oral lichen planus: persistence, remission, and malignant association. Oral Surg Oral Med Oral Pathol 1985;60:30-4.  

 

5 Porter SR, Kirby A, Olsen I, Barrett W. Immunologic aspects of dermal and oral lichen planus: a review. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997;83:358-66.  

 

6 Katta. R.,  American Family Physician, June 1, 2000, Baylor College of Medicine, 6560 Fannin, Suite 802, Houston, TX 77030  

 

7 Chan ES-Y, Thornhill M, Zakrzewska J. Interventions for treating oral lichen planus (Cochrane Review). In: The Cochrane Library, Issue 2 2003. Oxford: Update Software.  

 

8 Thorn JJ, Holmstrup P, Rindum J, et al. Course of various clinical forms of oral lichen planus. A prospective follow-up study of 611 patients. J Oral Pathol Med. 1988;17:213-218.  

 

9 Vallejo MJ, Huerta G, Cerero R, Seoane JM. Anxiety and depression as risk factors for oral lichen planus Dermatology. 2001;203(4):303-7  

 

10 Koray M, Dulger O, Ak G, Horasanli S, Ucok A, Tanyeri H, Badur S.The evaluation of anxiety and salivary cortisol levels in patients with oral lichen planus. Oral Dis. 2003 Nov;9(6):298-301  

 

11 Minkes,M., Stanford,N., Chi,M.M. et al : Cyclic adenosine monophosphate inhibits the availability of arachidonite to prostaglandin synthase in human platelet suspensions. J.Clin. Invest.59:449-54. 1977.  

 

12 Horrobin,D.F: The regulation of prostaglandin biosynthesis: negative feedback mechanisms and the selective control of formation 1 and 3 prostaglandin series: relevant to inflammation and immunity. Medical Hypothesis 6(7): 687-709. 1980.  

 

13 Lands,W.E., Byrnes,M.J.: The influence of ambient peroxides on the conversion of EPA  to prostaglandins. Progress in Lipid Research. 20:287-90. 1982.  

 

14 Calder PC: Dietary modification of inflammation with lipids: .Proc Nutr Soc. 2002 Aug;61(3):345-58.

 

15 el Attar TM, Lin HS:  Effect of vitamin C and vitamin E on prostaglandin synthesis by fibroblasts and squamous carcinoma cells.  Prostaglandins Leukot Essent Fatty Acids. 1992 Dec;47(4):253-7.  

 

16 Chapple I.L.C : Role of free radicals and antioxidants in the pathogenesis of the inflammatory periodontal diseases. J. Clin Pathol: Mol Pathol 1996; 49:247-255.  

 

17 Waddington R.J et al: Reactive oxygen species: a potential role in the pathogenesis of periodontal diseases. Oral Diseases 2000 ; 6:138-151.  

 

18 Thongprasom K, Youngnak P, Aneksuk V Folate and vitamin B12 levels in patients with oral lichen planus, stomatitis or glossitis. Southeast Asian J Trop Med Public Health. 2001 Sep;32(3):643-7  

 

19 Nagao T, Warnakulasuriya S, Ikeda N, Fukano H, Yamamoto S, Yano M, Miyazaki H, Ito Y. Serum antioxidant micronutrient levels in oral lichen planus. Oral Pathol Med. 2001 May;30(5):264-7.  

 

20 Schmidt. K.: Interaction of antioxidative micronutrients with host defence mechanisms. A critical review.  Int. J. for Vit. and Nutr. Res. 67(5):307-11. 1997.

 

21 Skaare AB, Rolla G, Barkvoll P The influence of triclosan, zinc or propylene glycol on oral mucosa exposed to sodium lauryl sulphate. Eur J Oral Sci. 1997 Oct;105(5 Pt 2):527-33.  

 

22 Sistig S, Vucicevic-Boras V, Lukac J, Kusic Z. Salivary IgA and IgG subclasses in oral mucosal diseases. Oral Dis. 2002 Nov;8(6):282-6.  

 

23 Herlofson BB, Barkvoll P. Oral mucosal desquamation caused by two toothpaste detergents in an experimental model. Eur J Oral Sci. 1996 Feb;104(1):21-6.  

 

24 Herlofson BB, Barkvoll P. Oral mucosal desquamation of pre- and post-menopausal women. A comparison of response to sodium lauryl sulphate in toothpastes. J Clin Periodontol. 1996 Jun;23(6):567-71