Foliate papillae appear as an area of vertical folds and grooves located on the extreme posterior-lateral surface of the tongue. Three patients were evaluated at . ·Foliate papilla and lingual tonsils Foliate papillae are slit-like structures found at the extreme posterior aspect of the lateral borders of the. Papillitis means inflammation of papillae of the tongue. Foliate Papillitis refers to inflammation of foliate papillae. They appear swollen and red.

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The tongue is an accessible organ that has been used for millennia as an indicator of health in both Western and Eastern medical philosophies. This article outlines the most common conditions affecting the tongue, from variations of normal to conditions affecting quality of life and potentially life-threatening lesions. Normally, posterior tongue anatomy is difficult to visualize by oneself; however, edentulous patients can often extend the tongue further than when dentate.

Hyperplasia secondary to upper respiratory tract infection or irritation from teeth makes these areas hyperplastic and uncomfortable and liable to further trauma.

Their round, raised shape can occasionally become prominent after folite. As these become more dilated and tortuous with age they can be more conspicuous. This can coliate prominent, especially when the diet is soft or even absent, such as during illness. Normal eating habits help to prevent the build-up of desquamated keratin squames on the surface of the tongue.

Enlarged Papillae: Causes, Symptoms & Treatment | Colgate® Oral Care

This condition has been associated with smoking, long-term use of mouthwashes and a soft diet, but it is not usually Candida related. Should simple reassurance as to its benign nature fail, treatment based on removal by gentle abrasion can be tried. Although also associated with chronic dry mouth, tongue fissuring can be a familial trait and is usually asymptomatic.

Although usually asymptomatic, some find the tongue sensitive and avoid spicy or salty foods. Some per cent of the population can be affected at some time.

Often familial, geographic tongue has also been found to be up to four times more prevalent in psoriasis-affected patients than in controls. Leukoplakia is a white lesion of the oral mucosa that cannot be characterized clinically or pathologically as any other disease. Despite the often-innocuous appearance, there may be underlying dysplasia, particularly, but not exclusively, if the leukoplakia affects the ventral surface of the tongue or floor of the mouth.

Such patients require referral to an oral medicine or oral and maxillofacial surgical unit for further assessment.

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It is rarely found in the mouth as pure erythroplakia and is more commonly found as part of speckled leukoplakia — a mixture of erythroplakia and leukoplakia. These lesions are more frequently found to show dysplasia on biopsy than pure leukoplakia and patients should be referred. With the advent of anti-retroviral therapy it is now less common in this group in the UK, but it can also be seen in patients immunosuppressed for medical reasons such as organ transplantation.

It presents with white, vertical corrugations on the lateral borders of the tongue and is linked to the Epstein-Barr virus. There may also be an element of tongue thrusting at these times, either in conjunction or as an isolated problem. This pressure and irritation from the teeth or dentures can produce a variety of symptoms varying from mild sensitivity to severe burning sensations.

The tongue often has indentations of the teeth contacted on the affected sites, predominantly the lateral borders and tip of the tongue. Trauma as a result of parafunction can also exacerbate underlying pathologies, in particular recurrent aphthous ulceration and geographic tongue. The classical description of the tongue in anemia, or iron, vitamin B12 and folate deficiency, is of a sore, smooth, reddened tongue. In practice, deficiency states are more commonly found before such appearances develop, such as when a patient complains of a burning tongue and the appearance of the tongue is relatively normal.


However, epidemiology in this area is hampered by a lack of agreed terminology. In some cases burning may simply be secondary to a mucosal disease such as lichen planus. A burning tongue in the absence of obvious mucosal disease can have local and systemic causes.

Local causes include candidiasis, xerostomia, poor denture design, esophageal reflux, and oral parafunctional habits. Systemic causes include anemia, haematinic deficiency, diabetes, drugs, and psychogenic factors such as cancerophobia, anxiety, and depression.

In some of these patients, psychosocial stressors, which preceded and possibly precipitated the syndrome, can be identified. Available data indicates that BMS affects predominantly females with an increased prevalence with age and following the menopause.

Diagnosis is made on the history, with the examination necessary to confirm the healthy mucosa and to look for any other causes of the complaint. Investigations are aimed at eliminating possible causal factors see table 1.

Management is initially based on reassurance and correction of all contributing factors. Should the problem persist, antidepressants can be used. Alternate strategies currently being explored include cognitive behavioral therapy and management along the lines of neuropathic pain. The main superficial mycosis affecting the oral mucosa is candidiasis.

Papillitiis albicans is the main Candida species causing such infections; however, it is also carried on the dorsum of the tongue in about 40 per cent of the normal foliats without problem. Oral carriage of Candida sp. Candidiasis of the tongue can show itself in several manifestations including pseudomembraneous candidiasis thrushacute atrophic candidiasis antibiotic sore tongue and chronic hyperplastic candidiasis candidal leukoplakia. Management includes control of predisposing causes and topical antifungal therapy with nystatin pastilles or amphotericin lozenges.

Miconazole oral gel is effective and well tolerated, but it should be remembered that the absorbed active ingredient can be sufficient to cause significant drug interactions, especially with warfarin. A particular variant of candidal infection on the tongue is median rhomboid glossitis see figure 1.

This is a rhomboid-shaped area of depapillation occurring in the midline on the tongue dorsum at the junction of the anterior two-thirds with the posterior one-third of the tongue. In this condition, and chronic hyperplastic candidiasis, systemic anti-fungal therapy with fluconazole or itraconazole is usually required.

The classical features are of bilateral, white striations on the buccal mucosa, but the tongue can be affected. Lichen planus on the tongue usually appears as white, plaque-like areas, although when active, ulceration can occur see figure 6.

Chronic lichen planus frequently leaves a depapillated, atrophic tongue mucosa. Diagnosis is based on a combination of clinical and histopathological findings. For active ulcerative lesions, treatment remains unsatisfactory. Topical steroid application in a variety of carrying agents papilltis the first-line treatment. The use of topical tacrolimus is currently being evaluated and offers hope for the future.

Oral lichen planus is potentially premalignant and oral lesions need re- biopsy if changes foliage of malignancy occur. To further prevent this development, it is advisable for such patients to avoid tobacco smoking and excessive use of alcohol. Lichenoid reactions have been known to occur as an adverse effect of various medications for many years. Over the last 20 years, however, it papllitis become increasingly apparent that oral lichenoid reactions may also occur as contact lesions against amalgam dental restorations.

On patch testing many such patients show positive reactions to ammoniated mercury. Once identified, such lesions can be cured by replacement of the amalgam restoration with an alternative restorative material.


Most cases commence in childhood and are mild flliate severity, but occasionally patients suffer persistent unrelenting ulceration, which significantly affects their quality of papillitid. These ulcers have a classical appearance of a round or oval well- defined shape, covered in fibrin, with a surrounding red halo. Non- keratinized mucosal surfaces such as the lateral border and ventral surface of the tongue are affected, rather than the keratinized tongue dorsum.

The ulcers usually resolve within two weeks. Genetic predisposition is thought to be the most common predisposing factor, although anemia or haematinic deficiency can precipitate ulceration in susceptible individuals.

The standard investigations for idiopathic recurrent aphthous ulceration includes a full blood count, serum ferritin, serum vitamin B12, red-cell folate and an antiendomysial or human antitissue transglutaminase antibody to detect silent coeliac disease.

Management is based on correction of underlying factors and symptomatic relief. A therapeutic ladder is frequently used from simple chlorhexidine and benzydamine mouthwashes initially, to topical steroids. Topical steroids such as hydrocortisone lozenges and triamcinolone dental paste are licensed for treating aphthous ulceration and are most effective when used as early as possible in the development of ulcers.

If systemic agents are needed, colchicine, corticosteroids, and thalidomide have been employed, although for many patients their side- effects will outweigh the benefits gained. Other causes of tongue ulceration include vesiculo-bullous disorders such as mucous membrane pemphigoid, pemphigus vulgaris, and linear IgA disease.

All of these are rare, can cause diagnostic confusion, and require referral for diagnosis and management. Tongue ulceration can also arise as a side effect of drug therapy. The potassium-channel activator nicorandil has recently been recognized as a new cause of persistent oral ulceration with a predilection for the tongue8 see figure 4. Withdrawal of the drug or dose reduction will resolve the ulcer.

Approximately new cases are diagnosed each year in the UK, most commonly in males over the age of 40, although an increasing incidence in young males has been noted recently. Smoking and alcohol are the most important risk factors with a synergistic effect reported.

The possible role of the human papilloma virus in the carcinogenesis of oral cancer is still under debate. The suspicion of the presence of oral cancer is mainly based on clinical factors. An ulcer persisting longer than three weeks or a change in texture of the oral mucosa papillitid worrying symptoms that require further assessment.

Rapid referral is warranted. Treatment is either by surgery or radiotherapy or a combination of both. Five-year survival rates have changed little for many years and remain at 50 per cent. Reconstruction of the surgical defect has greatly improved, however, with the development of microvascular techniques for free flaps to restore aesthetics and oral function.

The key factor in improving survival rates continues to be earlier presentation.

Foliate papillitis – Rooks Textbook of Dermatology

Oral lesions in patients with psoriasis: Cognitive therapy in the treatment of patients with resistant burning mouth syndrome: J Oral Path ; An open-label, dose-escalation pilot study of the effect of clonazepam in burning mouth syndrome. Derangement of warfarin anticoagulation by miconazole oral gel. Br Dent J ; Management of recalcitrant ulcerative oral lichen planus with topical tacrolimus.

J Am Acad Lapillitis ; Amalgam-contact hypersensitivity lesions and oral lichen planus. The diagnosis and management of recurrent aphthous stomatitis. Nicorandil can induce severe oral papllitis.

Human papillomavirus infection as a risk factor for squamous cell carcinoma of the head and neck. N Engl J Med ;

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