Group+1

= = =__**SKIN AND ORAL MUCOSA** __ =

// **e-facilitator: Sophie** //
//**Learning Outcomes:**// //The skin is described as an organ that covers a very large surface area. It is also susceptible to many diseases and disorders. Skin is also very closely related to the oral mucosa. Verify this through the following learning outcomes a. Describe the histological structure of skin and relate this to its function. b. Discuss the factors that contribute to skin colour and outline how exposure to UV radiation affects the skin. c. Design and present a poster on a skin condition that affects the oral mucosa and identify the implications this has to oral health.//

//Epidermis//

 * ======//cells//======
 * ======//layers//======

**5. UV Radiation**

 * ======//How exposure to ultraviolet (UV) radiation affects the skin//======

**6. Skin Condition: //Oral Lichen Planus//**

 * ======//Histology//======
 * //Diagnosis//
 * //Clinical features//
 * //Implications to oral health//
 * //Management//

__THE INTEGUMENTARY SYSTEM- SKIN__
"Would you be enticed by a coat that is waterproof, stretchable and washable that invisibly repairs small cuts, rips and burns and that is guaranteed to last a lifetime with reasonable care? Sounds too good to be true? Well you already have such a coat- its your **skin**- //cutaneous membrane//" (Marieb et al 2007, p. 152).

Skin (being the largest organ) the //epithelial membrane// that covers the body surface along with sweat, oil glands, hair and nails are all part of the **Integumentary system** (also called the //integument//). Integument which means' covering' keeps water and other molecules in the body along with keeping water and bacteria out. Without our skin we would quickly fall prey to bacterial infection and perish from water and heat loss (Marieb 2009). Immunologically, skin along with mucous membranes and secretions from skin (//**sebum**- contains chemicals that are toxic to bacteria)// form the //first line// of defence for our innate (non-specific) immune response of our immune system.

__FUNCTION OF SKIN__
The main functions of Skin are all //protective// as it insulates and cushions the deeper body organs and protects the entire body from; mechanical damage (cuts), chemical damage (acids and bases), thermal damage (heat and cold), ultraviolet radiation (in sunlight) and bacteria (Marieb 2009). //These are specified in table 1.//



Keratin (fibrous structural protein) is an important component of skin as it is the uppermost layer which makes the skin tough and helps prevent water loss from the body surface. Along with keratin the skin's rich capillary network and sweat glands, both controlled by the nervous system play an important role in regulating heat loss from the body surface. This occurs because the skin acts as a 'mini-excretory system' as urea, salts and water are all lost when we sweat.

Skin also acts a manufacturing unit as it synthesis several proteins important in immunity and also Vitamin D (Modified cholesterol molecules located in the skin are converted to vitamin D by sunlight).

Cutaneous sensory receptors are located in the skin that include touch,pressure, temperature and pain receptors all part of the nervous system. They are extremely important as they keep the nervous system / brain aware of the body's external environment. They act as a go-between (intercom) to our nervous system as they pick up hard bumps and pressure and even the slights breeze of air running through hair.

__HISTOLOGICAL STRUCTURE OF SKIN__
The skin is structurally composed of two kinds of tissue: the outer **epidermis** and the underlying **dermis** that are firmly connected. The epidermis is made up of stratified squamous epithelium and like all other epithelial tissues it is avascular. It can also become keratinised. The dermis is made up of mostly dense connective tissue. Deep to the dermis is the **subcutaneous tissue** or //**hypodermis**// which is essentially adipose tissue. Subcutaneous tissues serve as shock absorbers and insulate the deeper tissues from extreme temperature changes occurring outside the body.

**//Cells//**
The cells that are present in the epidermis are //keratinocytes//, //melanocytes//, //Merkel cells// and //Langerhans cells//.


 * //Keratinocytes//** are the most predominate cell in the epidermis. Their main function is to produce keratin, the fibrous protein that helps give the epidermis its protective properties (Marieb et al 2007). They arise in the deepest part of the epidermis from a layer of cells; the //stratum basale// //(figure 1)//, that undergo constant mitotic division. Keratinocytes are tightly connected to each other by desmosomes.


 * //Melanocytes//** (spider-shaped epithelial cells) synthesis the pigment melanin and are found in the deepest layer of the epidermis //stratum// //Basale// //(figure 1)//. As melanin is made, it is accumulated in the membrane-bound granules called //melanosomes// that are moved along the actin filaments by motor proteins to the ends of the melanocyte's processes (spider-arms) from where they are taken up by nearby keratinocyte //(figure 2)//. The melanin granules accumulate on the superficial side of the keratinocyte nucleus forming a pigment shield that protects the nucleus from the damaging effects of ultraviolet (UV) radiation in the sunlight (Marieb et al 2007).

//**Langerhans cells**// (star-shaped //dendritic// cells) arise from bone marrow and migrate to the epidermis. Langerhans cells are phagocytes that ingest foreign substances and help activate our immune system.

//**Merkel cells**// (shaped like a spiky hemisphere) are present at the epidermal-dermal junction.They are associated with a 'disc-like' sensory nerve ending; therefore having a sensory receptor function associated with touch.

//**Layers**//

The epidermis consists of five layers, from deep to superficial; //stratum basale, stratum spinosum, stratum granulosum//, //stratum lucidum// and //stratum corneum (figure 2).//

//**Stratum Basale (basal layer)**// is the deepest epidermal layer and is attached to the underlying dermis. It consists of a single row of cells which is continually renewed due to the many mitotic nuclei. It also contains the youngest keratinocytes. 10-25% of the cells in the stratum basale are melanocytes which extend among the surrounding cells reaching well into the next superficial layer; stratum spinosum (Marieb et al 2007). Merkel cells are also present in this layer of stratum.

//**Stratum Spinosum (prickly layer)**// is several layers thick.The cells are a web-like system of intermediate filaments (mainly tension-resisting bundles of pre-keratin filaments) which elongate their cytosol to attach to desmosomes //(figure 2)//. The keratinocytes in this layer are particularly irregular in shape (spiky) therefore known as prickle cells. Found amongst the keratinocytes are melanin granules and Langerhans cells which are most abundant in this stratum.

//**Stratum Granulosum (granular layer)**// the thin granular layer consist of three to five cell layers in which keratinocytes appearance changes //(figure 2)//. They flatten their nuclei and organelles begin to disintegrate resulting into two types of granules: The //keratinohyaline granules// that help form keratin in the more superficial layers and //lamellated granules// which contain a waterproofing glycolipid that is disbursed into the extracellular space and is a major factor in slowing water across the epidermis (Marieb et al 2007). this is all part of the keratinocytes 'toughening up' to make the outer strata the strongest skin region.

The epidermis relies on capillaries from its underlying connective tissue (the dermis) for its nutrients. Above the stratum granulosum the epidermal cells are too far from the dermal capillaries and so they die. this is a normal occurrence.

//**Stratum Lucidum (clear layer)**// visible only on thick skin that covers the palms, fingertips and soles of feet appears as a thin translucent band just superior to the stratum granulosum. It consists of a few rows of clear, flat, dead keratinocytes with indistinct boundaries. Here or in the superficial stratum corneum the gummy substance of the keratohyaline granules cling to the keratin filaments in the cells causing them to aggregate in parallel arrays.

//**Stratum Corneum (Cornified Layer)**// the outer most layer is a zone of 20 to 30 cell layers thick. Keratin and thickened plasma membranes of cells in this stratum protect the skin against abrasion and penetration. The glycolipids between the cells also waterproofs this layer. The Stratum Corneum provides a protective 'overcoat' for the body. The shingle-like cells of the stratum corneum are referred to as cornified cells. they are the dandruff shed from the scalp and flakes that remove dry skin.

Dermis
The dermis is a dense (fibrous) connective tissue and contains cells typically of those found in any connective tissue proper: fibroblasts, macrophages, mast cells, white blood cells and its semi fluid matrix which is embedded with fibers.The dermis binds the entire body together and is richly supplied with nerve fibers, blood vessels and lymphatic vessels. Although hair follicles, oil and sweat glands are derived from the epidermal tissue they reside in the dermis.

The dermis has two layer: the //papillary and reticular// layers //(figure 3)//. The **papillary layer** is thin and superficial to the reticular layer and is areolar connective tissue in which the collagen and elastin fibers form a loosely woven mat that is heavily filled with blood vessels. The **reticular layer** accounts for approximately 80% of the thickness of the dermis and is a dense irregular connective tissue (Marieb et al 2007). A network of blood vessels, the //cutaneous plexus// that nourishes this layer lies between the reticular layer and the hypodermis //(figure 3//).

The collagen fibers of the dermis gives skin strength and resiliency that prevents most jabs and scrapes from penetrating the dermis. Collagen binds water and helps keep the skin hydrated. Elastin fibers provide the stretch-recoil properties of skin.

__**FACTORS THAT CONTRIBUTE TO SKIN COLOUR**__
Human skin colour can range from almost black (due to very high concentrations of the dark brown pigment melanin) to nearly colorless (appearing pinkish white due to the blood vessels under the skin) in different people. Skin colour is determined primarily by the amount and type of melanin, otherwise referred to as the pigment in the skin. There is huge variation in skin color in human beings and this is largely due to genetics. As a general pattern people with ancestors from tropical regions and higher altitudes (hence greater UV light exposure) have darker skin than people with ancestors from subtropical regions.

Melanin itself is an organic polymer and comes in two types, a cysteine rich red/yellow form known as pheomelanin and a less soluble black/brown form known as eumelanin. Both amount and type are determined by four to six genes which operate under incomplete dominance. One copy of each of those genes is inherited from each parent. Each gene comes in several alleles, resulting in the great variety of different skin tones. Measurement of human skin colour is often based on subjective categories, e.g., moderate brown, rarely burns, tans very easily, burns easily, sometimes burns, usually tans etc (Barsh 2003).

The characteristic phenotype of fair skin, freckling and red hair is associated with large amounts of pheomelanin and small amounts of eumelanin and is caused by a loss of functional alleles in a single gene (Barsh 2003).

Even though light and dark skinned individuals have similar numbers of melanocytes on the same body positions, the melanin containing organelles called melanosomes, are larger, more numerous, and more pigmented in dark compared to light skin (Barsh 2003).

__**HOW EXPOSURE TO ULTRAVIOLET (UV) RADIATION AFFECTS THE SKIN**__
Ultraviolet radiation is a form of radiation given out by the sun. It has many damaging effects, and can cause sunburn, skin cancer and photo-ageing symptoms such as wrinkles. It is particularly dangerous because like other forms of solar radiation such as heat and light, UVR cannot be seen or felt (Primary & Ambulatory Care Division 2008).

There are 3 different types of ultraviolet (UV) radiation – UVA, UVB and UVC (Primary & Ambulatory Care Division 2008). • UVA (longer wavelength) causes premature aging and wrinkling of the skin and is a cause of skin cancer • UVB (medium wavelength) is more dangerous than UVA and is the major cause of skin cancers, sunburning and cataracts • UVC (shorter wavelength) is extremely dangerous but does not reach the earth's surface due to absorption in the atmosphere from the Ozone layer

Follow link for an animation on how UV light damages the skin: http://www.mydr.com.au/skin-hair/animation-uv-radiation-damages-your-skin

Biosperical Instruments (2001) states that UV rays also have there positive effects as they are necessary for our body to produce vitamin D, a substance that helps strengthen bones and safeguards against diseases such as Rickets. Some scientists have shown that Vitamin D lowers the risk of getting some kinds of internal cancer, like colon cancer.

UV light is also used as a therapy for psoriasis, a condition in which the skin sheds its cells too quickly, resulting in itchy, scaly patches on various parts of the body. When exposed to ultraviolet rays, the growth of the skin cells is slowed, relieving the symptoms.

1) Texture Changes caused by the sun (Figure 4) -UV exposure causes thickening and thinning of the skin. Thick skin is found in coarse wrinkles especially on the back of the neck that do not disappear when the skin is stretched. A condition called solar elastosis is seen as thickened, coarse wrinkling and yellow discoloration of the skin. A common effect of UV exposure is thinning of the skin causing fine wrinkles, easy bruising, and skin tearing (Brannon 2007).

Figure 4: Texture changes caused by skin (ADAM 2005)

2) Blood Vessel Changes caused by the sun -UV radiation causes the walls of blood vessels to become thinner leading to bruising with only minor trauma in sun-exposed areas. For example, most of the bruising that occurs on sun-damaged skin occurs on the backs of the hands and forearms not on the inside of the upper arm or even the inside of the forearm. The sun also causes the appearance of telangiectasias (figure 5), tiny blood vessels, in the skin especially on the face (Brannon 2007).

Figure 5:Telangiectasias on the leg (ADAM 2005)

3) Pigmentation Changes -The most noticeable sun-induced pigment change is a freckle or solar lentigo. Light-skinned people tend to freckle more noticeably. A freckle is caused when the melanin-producing cell, or melanocyte, is damaged causing it to get bigger. Large freckles, also known as age spots or liver spots, can be seen on the backs of the hands, chest, shoulders, arms (figure 7), and upper back (figure 6). These are not actually age related but sun-damage related. UV exposure can also cause white spots especially on the legs, but also on the backs of the hands and arms, as melanocytes are destroyed (Brannon 2007).

Figure 6:Solar Lentigo on back (ADAM 2005) Figure 7: Solar Lentigo on arm (ADAM 2005)

4) Skin Bumps (Actinic/Seborrheic Keratosis) -UV radiation causes an increased number of moles in sun-exposed areas. Sun exposure also causes precancerous lesions called actinic keratoses (figure 9) that develop especially on the face, ears, and backs of the hands (figure 8). The are small crusty bumps that can often be felt better than they can be seen. Actinic keratoses are felt to be premalignant lesions because 1 in 100 cases per year will develop into squamous cell carcinoma. UV exposure also causes seborrheic keratoses, which are warty looking lesions that appear on the skin. In contrast to actinic keratoses, seborrheic keratoses do not become cancerous (Brannon 2007).

Figure 8: Actinic Keratoses-arm (ADAM 2005) Figure 9:Actinic Keratoses -close up (ADAM 2005)

5) Skin Cancers (Basal Cell Carcinoma, Squamous Cell Carcinoma and Melanoma) -The ability of the sun to cause skin cancer is a well-known fact. The 3 main skin cancers are melanoma, basal cell carcinoma (figure 10), and squamous cell carcinoma (figure 11). Melanoma is the most deadly skin cancer because it metastasizes more readily than the other skin cancers. It is believed that the amount of exposure of the skin to the sun before the age of 20 is actually the determining risk factor for melanoma. Basal cell carcinoma is the most common skin cancer and tends to spread locally, not metastasize. Squamous cell carcinoma is the second most common skin cancer, and it can metastasize although not as commonly as melanoma. The risk of getting basal cell carcinoma or squamous cell carcinoma is determined by a person's lifetime exposure to UV radiation and the person's pigment protection (Brannon 2007).

Figure 10:Basal Cell Carcinoma (ADAM 2005) Figure 11: Squamous Cell Carcinoma (ADAM 2005)

Malignant melanoma (figure 12) is the most dangerous form of skin cancer. Fortunately, it is not as common as the other types of sun-related skin cancers, known as basal cell carcinoma and squamous cell carcinoma. While exposure to UV light increases your risk of melanoma, it is also possible for melanomas to appear on areas of skin that are not typically exposed to the sun (myDr 2004).

Figure 12:Melanoma (ADAM 2005)

UV radiation also stimulates specialised skin cells called melanocytes to produce melanin, a brown-black skin pigment. Melanin can help to protect your skin against further exposure to the sun by filtering out some of the UV rays, and gives your skin a tanned appearance. However, even a light tan is a sign that you have been exposed to too much sun. Although the process of tanning is your body’s natural way of providing the lower levels of skin with protection from further sun damage, the level of protection is minimal. In fact, a tan usually provides no more protection than an SPF 2 sunscreen (myDr 2004).

__**SKIN CONDITION THAT AFFECTS THE ORAL MUCOSA: ORAL LICHEN PLANUS**__
Lichen Planus is a skin condition what may affect the oral mucosa. According to Mollaoglu (2000), approximately half of the patients with cutaneous lichen planus have oral involvement, in the case of oral involvement it is known as Oral Lichen Planus. Oral Lichen Planus (OLP) is a chronic inflammatory disease of the oral mucosa with its aetiology unknown due to poorly understood aetiopathogenesis. It is the most common non-infectious oral mucosal disease in patients referred to oral medicine and oral pathology clinics (Sugerman & Savage, 2004). It has a prevalence of approximately 1% (Waal, 2009). Sugerman & Savage reported that Oral Lichen Planus is prevalent in female adult patients over forty years of age, with younger adults and children of both sexes also possibly being affected. Although the aetiology is unknown, there are known triggers that are said to cause the symptoms of oral lichen planus. OLP is characteristically associated with eclinical course and resistance to most conventional treatments (Cheng, 2002).



Histology
Tyldesley argues that the most characteristic changes found in all clinical variants of the disease are found in the dermis as a well defined band of inflammatory cells, predominantly lymphocytes, lies below, but separated from the dermal-epidermal junction. These inflammatory cells seen within the epithelium are greater in number in contrast to normal mucosa. Oral Lichen Planus is characterized by a dense sub-epithelial lympho-hystiocytic infiltrate, increased numbers or intra-epithelial lymphocytes and degeneration of basal keratinocytes (Sugerman & Savage, 2002).

Colloid (hyaline, cytoid, civatte) bodies which appear as homogenous eosinophillic globules are formed by the degenerating basal keratinocytes. The formation of the colloid bodies propose that the degenerating basal keratinocytes are apoptotic. The basal keratinocytes have disrupted anchoring elements (hemidesmosomes, filaments, fibrils) due to its degeneration. Along with the anchoring elements, the epithelial basement membrane of the oral mucosa is disturbed, causing breaks, branches and duplications to occur. The disrupted anchoring elements in conjunction with the disturbed basement membrane and degeneration of basal keratinocytes form histological clefts and clinical blistering as a result of weakness at the epithelial-connective tissue interface (Sugerman & Savage, 2002).

Tyldesley explains that the histology of a papule suggests that it's formation may be due to the building up of a band of inflammatory cells in the dermis resulting in the displacement of the epithelium outwards to form the papule. Tyldesley also suggests that the epithelium overlying the papule may show a variety of reactions varying from atrophy to acanthosis and from parakeratosis to hyperorthokeratosis.

Diagnosis
Oral Lichen Planus in many cases may be diagnosed clinically. However, specialist referral is required for thorough patient investigation, management and review. Sugerman and Savage suggest a complete history and physical examination by a multidisciplinary group of health care providers may be required to investigate oral, skin, nail, scalp, genital, oesophageal, laryngeal and conjunctival invovlement.

In the absence of typical reticular oral lichen planus manifestations elsewhere in the mouth, Waal states that the non-reticular types may be difficult to diagnose clinically with confidence, as a result he suggests the event of the taking of a biospy to be considered to allow for accurate diagnosis.

Direct immunofluorescence can help distinguish erosive, ulcerative or the very rare bullous form of oral lichen planus from pemphigus vulgaris, benign mucous membrane pemphigoid, dermatitis herpetiformis and linear IgA bullous dermatitis (Sugerman & Savage, 2002).

Although, Oral LIchen Planus can be diagnosed clinically in most instances (Waal, 2009). It's diagnosis however, may be difficult as lesions of the oral mucosa may show similar characterisitics on clinical observation although having different morphology. Lesions may also have similar morphology but with a different clinical appearance, hence making to process of diagnosis intricate. These associated lesions are commonly referred to as oral lichenoid reactions or oral lichenoid lesions (OLLs) (Waal, 2009).

Oral lichen planus may associate with other immune-mediated diseases including alopecia areata, dermatomyositis, morphea and ulcerative colitis. OLP is also reported to be associated with hepatitis C infection and chronic active hepatitis C. However, Sugerman & Savage explain associations between oral lichen planus and systemic diseases may be co-incidental as oral lich planus is relatively common as it predominately occurs in many adults. Multiple drugs used to treat these systemic diseases also brings about a trigger for oral lichenoid lesions as a side effect.

Patients with OLP may have co-incident skin lesions that present frequently as pruritic flat-topped violaceous papules and plaques, predominately on the flexor aspects of the wrists or ankles, extensor aspects of the lower legs, the skin of the lower central back and the natal cleft (Sugerman & Savage, 2002). Hence, questioning the patient about other existing skin conditions may provide further information for diagnosis.

Lichen planus is a T-cell mediated autoimmune damage to basal keratinocytes. Chen explains that suspected aetiological factors include drugs, food, oral candidiasis, hepatitis C, cigarette smoking, contact allergic factors such as amalgam or gold dental restorative material and trauma from periodontal prosthesis. Therefore, obtaining an honest and detailed medical and social history is a vital contribution which will aid in correctly diagnosing a patient.

**Clinical Features**
Clinically, Sugerman & Savage identify Oral lichen planus existing as white striations, white papules, whites plaques, erythema, erosions or blisters on the mucosa. These distinct white striations are known as Wickham's striae, which were named after Louis-Fédéric Wickham. Oral lichen planus predominately affects the buccal mucosa, gingival and the tongue, with Waal reporting the involvment of the palate and the lips being quite rare, while the palate and even more so the floor of the mouth rarely affected.



The clinical presentation is nearly always in a bilateral, more or less symmetrical pattern of arious morphologies (Waal, 2009). The two most common types of OLP being the erythematous, plaque type and ulcerative type. And the atrophic and bullous types being rare. Although Waal states that the various types may co-exist in a patient and may change over time.

Oral lichen planus usually persists for many years with periods of exacerbation and quiescence (Sugerman & Savage, 2002). Sugerman & Savage attempt to explain that during the periods of exacerbation in OLP there is an increase in erythema or ulceration, in turn increasing the levels of pain and sensitivity being felt by the patient. They also continue to go on to explain that during the periods of quiescence, a decrease is present in the extent of erythema or ulceration for the patient, with levels of pain and sensitivity being experienced lowering during the period. Below is a table which lists the various clinical types of oral lichen planus in the two catergories; asymptomatic and symptomatic, and provides a summary of characteristics for each individual form along side the listed clnical types.

//Table 2. Clinical features of oral lichen planus (Cheng, 2002)//
 * **Symptom** || **Clinical types** || **Description** ||
 * Asymptomatic || Reticular || Wickham's striae with discrete erythematous border ||
 * || Plaque-like || Resemble leukoplakia, common in smokers ||
 * || Papules || Small white pinpoint papules ||
 * Symptomatic || Atrophic || Diffuse red patch, peripheral radiating white striae, chronic desquamative gingivitis ||
 * || Erosive || Irregular erosion covered with a pseudomembrane ||
 * || Bullous || Small bullae or vesicles that rupture easily ||

**Implications to Oral Health**
Severe cases may invovle painful sores and ulcers of the mouth as Sugerman & Savage describe that the symptoms vary from mucosal sensitivity to continuous debilitating pain. Such ulcers and painful sores may cause discomfort during maintaining oral hygiene; teeth brushing. Thus, making it difficult for the patient to efficiently clean their teeth and gums. And as a consequence, issues regarding the patients oral health may arise, such as periodontal diseases and other oral diseases e.g caries.

In addition to other implications to a patient's oral health; as a result of pain and sensitivity, performing an oral examination may be uncomfortable for the patient, in turn not only causing problems for the patient but also causing difficulties for the operator due to a restless patient. The undesirable experience may trigger a bevaviour response and change a patient's feelings towards dental appointments. This may lead to the patient avoiding any future dental visits.

Below is an image of ulcerative oral lichen planus on the surface of the tongue, which causes discomfort during maintaining oral hygiene.



As there is ongoing concern that oral lichen planus may be premalignant, malignant transformation data is currently under review and further prospective studies are still required (Sugerman & Savage, 2002).

According to Sugerman & Savage in 2002, Oral lichen planus on clinical and/or histological grounds were probably epithelial dysplasias (lichenoid dysplasias) that progressed subsequently to overt squamous cell carcinoma (SCC). It has been reported in 'Oral lichen planus: causes, diagnosis and management' that approximately 0.2 percent of oral lichen planus patients develop oral squamous cell carcinoma each year. In comparison to that, another study by Scully et al. showed 5 percent of oral lichen planus patients who do not use tobacco products develop SCC, most frequently in atrophic, erosive and plaque lesions. It is therefore unlikely that oral lichen planus is inherently premalignant. The cause of increased oral cancer risk in oral lichen planus patients is unknown, although Sugerman & Savage suggest the oral mucosa affected by OLP may be compromised to the extent of being more sensitive to exogenous mutagens in tobacco, alcohol, betel quid and //Candida albicans.//

Therefore, very severe cases of oral lichen planus of the mouth can slightly increase the risk of oral cancer (Fransiscus, 2009). For this reason it is important to manage and control the disease with medications, good oral hygiene and regular physical exams to monitor changes in the disease.

**Management**
Alcohol, tobacco, spicy foods, peppermint, cinnamon, citrus type foods and stressful situations trigger the symptoms and shoud be avoided if possible (Fransiscus, 2009). Maintaining good personal oral hygiene will improve the symptoms, thus ensuring the patient is instructed with thorough oral hygiene instructions is highly important in managing OLP. Exacerbation of oral lichen planus has been linked to periods of psychological stress and anxiety, Sugerman & Savage argue it being a predictable correlation with any condition that is related to an immune system imbalance. Within reason, avoiding stressful events or participating in activites which have the ability to reduce stress levels contribute to managing oral lichen planus.

Cheng reports that non-erosive oral lichen planus is asymptomatic and treatment is often unnecessary, however, he also goes on to explain that symptomatic patients with an apparent contact dental factor may require a patch test to be conducted with replacement of the amalgam or gold restorative material. This is suggested in those who are sensitized to these metals.

Waal suggests that in a case of more of less proven oral lichen planus, treatment can only be symptomatic. Topical ointments or mouth rinses of corticosteriods suffice, although Waal questions the efficency of these treatments as it has been expressed that there has not been sufficient evidence to support this. Only in severe cases systemic medication may be considered and surgical treatment or laser treatment is also an option for management and treatment for persistent, painful lesions.

According to Tyldesley, the skin lesions are usually relatively slow in onset and generally last no longer than nine months, even the most protracted cases rarely exceeding two years of duration. When lesions subside, there often remains a pigmented patch which may then take a very much longer time to fade.

__REFERENCE LIST__
//**Texts**//

Burket, L. W., Greenberg, M. S., Glick, M., (2003). //Burket's oral medicine: diagnosis & treatment,// 10th ed, BC Decker Inc, Spain, pp. 107-114. Cheng, S. Y., (2002). "Oral Lichen Planus", //Hong Kong Dermatology & Venerology Bulletin//, vol. 10, no. 4, pp. 170-173.

Fransiscus, A., (2009), "Hcv- extrahepatic manifestations: lichen planus", //HCSP fact sheet//, accessed 21/09/09

Johnson, H., SOldano, A.C., Kovich, O., et al., (2008), "Oral lichen planus", Dermatology Online Journal, vol.14, no.5.

Marieb E 2009, '//Essentials of Human Anatomy and Physiology ' ninth edition//, Pearson Benjamin Cummings, San Francisco  Marieb E & hoehn K 2007, //'Human Anatomy & Physiology' seventh edition//, Pearson Benjamin Cummings, San Francisco

Mollaoglu, N., (2000), "Oral lichen planus: a review", Br J Oral Maxillofac Surg, vol. 38, pp. 370-377.

Scully C., Beyli M., Ferreiro M. C., et al., (1998), "Update on oral lichen planus; etiopathogenesis and management", //Crit Rev Oral Biol M//ed, vol. 9, pp. 86-122.

Seoane, J., Romero, M. A., Varela-Centelles, P., Diz-Dios, P. & Garcia-Pola, M. J., (2004), "Oral lichen planus: a clinical and morphometris strudy of oral lesions in relaion to clinical presentation", //Brazillian Dental Journal//, vol. 15, no. 1, pp. 9-12.

Sugerman, P. B., Savage, N. W., (2004), "Oral lichen planus: Causes,diagnosis and management", //Australian Dental Journal//, vol. 47, no. 4, pp. 290-297.

Tyldesley, W. R., (1974), "Oral lichen planus", //British Journal of Oral Surgery//, vol. 11, pp. 187-206.

Waal, I. V. D., (2009), "Oral lichen planus and oral lichenoid lesions; a critical appraisal with emphasis on the diagnostic aspects", //Med Oral Patol Oral Cir Bucal//, vol, 14, no. 7, pp. E310-E314.

//**Web**//

Brannon, H 2007, Effects of sun on the skin: Visible skin changes caused by UV Radiation, About.com: Dermatology, viewed 29/08/09, 

Primary & Ambulatory Care Division, 2008, Ultraviolet Radiation (UVR) and the UV Index, Australian Government: Department of Health and Ageing, viewed 15/08/09, 

myDr, 2004, Animation: UV Radiation damages your skin, CMP Medical Australia, viewed 10/08/09 

Bioshperical Instruments, 2001, Effects of UV Radiation on you, NSF Polar Programs UV Monitoring Network, viewed 10/08/09 

Barsh GS, 2003, What controls variation in Human Skin Colour? PLOS Biology, viewed 10/08/09 

//**Images**//

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