Diseases of the lips and tongue in children. Independent and symptomatic cheilitis. Causes, symptoms, diagnosis, treatment.
The oral mucous is the mucous membrane that covers all oral structures except the clinical crowns of the teeth. It is composed of two layers: (1) the stratified squamous epithelium and (2) supporting connective tissue, called the lamina propria. The epithelium may be keratinized, parakeratinized, or nonkeratinized depending upon its location. The lamina propria varies in thickness and supports the epithelium. It may be attached to the periosteum of the alveolar bone, or it may be interposed over the submucosa, which may vary in different regions of the mouth (e.g., the floor of the mouth, the soft palate). The submucosa, consisting of connective tissues varying in density and thickness, attaches the mucous membrane to the underlying bony structures. The submucosa contains glands, blood vessels, nerves, and adipose tissue.
The oral mucosa may be divided into three major functional types:
(1) masticatory mucosa;
(2) lining or reflective mucosa;
(3) specialized mucosa;
The masticatory mucosa is composed of the free and attached gingiva the mucosa of the hard palate. The epithelium of these tissues is keratinized, and the lamina propria is a dense, thick, firm connective tissue containing collagenous fibers. The hard palate has a distinct submucosa except for a few narrow specific zones. The dense lamina propria of the attached gingiva is connected to the cementum and the periosteum of the bony alveolar process.
The lining or reflective mucosa covers the inside of the lips, cheek, vestibule, lateral surfaces of the alveolar process (except the mucosa of the hard palate), floor of the mouth, soft palate, and inferior surface of the tongue. Lining mucosa is a thin, movable tissue with a relatively thick, nonkeratinized epithelium and a thin lamina propria. The submucosa is composed mostly of thin, loose connective tissue with muscle and collagenous and elastic fibers, with different areas varying from one another in their structure. The junction of lining mucosa with masticatory mucosa is the mucogingival junction, located at the apical border of the attached gingiva facially and lingually in the mandibular arch and facially in the maxillary arch. The specializedmucosa covers the dorsum of the tongue and the taste buds. The epithelium is nonkeratinized except for the covering of the dermal filiform papillae.
Cheilitis is inflammation of the lips. This inflammation may include the perioral skin (the skin around the mouth), the vermilion border and/or the labial mucosa. The skin and the vermilion border are more commonly involved, as the mucosa is less affected by inflammatory and allergic reactions. It is a general term, and there are many recognized types and different causes.
Cheilitis is a general term that refers to an inflammation of the vermilion border of the lips. The vermilion zone is the junction between the skin and the mucosa. This zone has a thick squamous epithelium and an abundant capillary supply within the interdigitating rete ridges and dermal papillae. The capillary supply makes the zone red. Cheilitis, aside from being cosmetically disfiguring, can compromise daily activities like eating and speaking. Cheilitis is classified into various types: angular cheilitis, actinic cheilitis, contact cheilitis, plasma cell cheilitis, cheilitis glandularis, cheilitis granulomatosa, exfoliative cheilitis and factitious chelitis. Lip lesions can be manifestations of systemic diseases, a localized expression of dermatologic diseases or a localized condition of the lips. In most cases, a good history, thorough clinical examination and relevant investigations will help the clinician arrive at a diagnosis.
Actinic, or solar, cheilitis represents accelerated tissue degeneration of the vermilion of the lips, especially the lower lip, secondary to chronic exposure to sunlight. This condition occurs almost exclusively in whites and is especially prevalent in those with fair skin.
Etiology and Pathogenesis.
The wavelengths of light most bresponsible for actinic cheilitis and, in general, other degenerative actinically related skin conditions are usually considered to be those between 2900 and 3200 nm (ultraviolet B [UVB]). This radiant energyaffects not only the epithelium but also the supporting connective tissue.
The affected vermilion of the lips takes on an atrophic, pale to silvery gray, glossy appearance, often with fissuring and wrinkling at right angles to the cutaneous-vermilion junction. Slightly firm, bilateral swelling of the lower lip is also common. In advanced cases the junction is irregular or totally effaced, with a degree of epidermization of the vermilion. Mottled areas of hyperpigmentation and keratosis are often noted, as well as superficial scaling, cracking, erosion, ulceration, and crusting .
The overlying epithelium is typically atrophic and hyperkeratotic. Basophilic change of submucosa (elastin replacement of collagen) and telangiectasia are also seen. Treatment. Because of the positive relationship between
exposure to UV light and carcinoma, lip protection is indicated. The use of lip balm containing the sunscreen
agent para-aminobenzoic acid (PABA) or its derivatives is indicated during periods of sun exposure in
high-risk patients. Sun-blocking opaque agents also boost the effectiveness of the balm. Chronic sun damage mandates periodic examination and a biopsy if ulceration persists or if there is induration. If atypical changes are noted within the epithelium, a vermilionectomy may be performed in association with mucosal advancement to replace the damaged vermilion. This operation is associated with some morbidity, primarily in relation to lip pares thesia, therefore prompting some to advocate wedge excision for suspicious lesions. Acceptable results are also
obtainable with the use of laser surgery or cryosurgery, as well as with topical 5-fluorouracil.
Exfoliative cheilitis, a rare, localized condition, is a chronic superficial inflammatory condition that is characterized by regular peeling of a superficial excessive layer of keratin. Bleeding may occur, resulting in hemorrhagic crusts. People with this condition may have some degree of pain and difficulty speaking, eating or smiling. Because of their unpleasant appearance, people with exfoliative cheilitis may avoid socializing, seek periods of seclusion and be subject to clinical depression. This paper reports the case of a patient with exfoliative cheilitis and provides a photographic record of the changes that occurred over a period of 10 days.
Malay male was referred from the department of dermatology to the dental clinic
of Hospital Universiti Sains
When the patient was referred to the dental clinic, he had been taking 30 mg prednisolone regularly for 2 months, as prescribed by the dermatologist. He had also completed a course of cloxacillin and metronidazole. Results of a previous oral swab of the lesion revealed normal oral flora. He had no symptoms of gastrointestinal disturbances or other relevant medical conditions. No member of his family had a similar condition. He reported occasional lip biting, and no use of new creams, toothpaste or cosmetic items around the lips before the problem began.
The results of a general
examination revealed a thin young man who weighed
The results of a battery of tests, including complete blood work and liver function tests, a Mantoux test and chest radiograph showed no abnormalities. Results of a lip swab taken forCandida were negative. A wedge biopsy of the lower lip was done under local anesthesia after removal of the superficial crust. Histopathological exam ination revealed parakeratosis and slight acanthosis of the epithelium, a mild-to-moderate lymphoplasmacytic infiltration of the lamina propria, and some degree of vascular dilatation and engorgement in the submucosa. Inflammatory bowel conditions were also ruled out after consultation with a gastroenterologist. The overall findings suggested a diagnosis of exfoliative cheilitis.
The development of the lesion was observed over a period of days after the removal of the superficial yellowish white crust and the subsequent biopsy of the lip. The patient was asked to admit himself to the ward so that he could be closely observed for any factitious activity and the development of the lesion. During the first 2 days, a few vesicular eruptions appeared at the junction of the vermilion border of the lip and labial mucosa lining the vestibule (Fig. 2). The erythema seemed to decrease by the third day (Fig. 3), and a thin layer of keratin formed over the lip (Fig. 4). It progressively thickened by the eighth day (Fig. 5) and was firmly adherent to the underlying mucosa. Fig. 6 shows the lesion as it appeared on the tenth day.
The patient was prescribed a topical antifungal agent (clotrimazole 2% cream), which did not improve his condition. Since a psychiatric evaluation revealed significant depression, the patient was prescribed antidepressants (fluvoxamine 50 mg once daily). These improved his condition somewhat, but did not resolve it completely. At the same time, he underwent thorough prophylaxis and instruction in oral hygiene, followed by extraction of the badly decayed teeth and restoration of the other teeth. However, subsequent dental appointments revealed that the patient was unable to maintain good oral hygiene.
Currently, the patient uses petroleum jelly for relief and continues to spend his time at home because of his condition. Exfoliative cheilitis reportedly occurs more commonly in females.However, Taniguchi and Kono, in a review of the reported cases in the literature about exfoliative cheilitis, showed that females are affected only margin-ally more often than males. Including our case and the one reported by Leyland and Field, an equal number of males and females have been reported in the literature so far. Reichart and others, however, reported that AIDS patients with exfoliative cheilitis were pre-dominantly male. The majority (62%) of patients affected were younger than 30 years of age, many of whom were younger than 20 years of age.Clinicians’ knowledge of the clinical course of this disease is important for accurate diagnosis. Exfoliative cheilitis is an infrequently mentioned condition; details given about the course of this disease are inadequate. This report records in detail the clinical progress of the disease over a period of 10 days. The preoperative image (Fig. 1) shows a thick yellowish white coating on the lower lip and some loose adherent bilateral fragments of keratin on the upper lip. The mid portion of the upper lip seems to have a thin coating of keratin and appears almost normal. On day 1 (Fig. 2), the lower lip is erythematous after removal of the loosely adherent keratin coat; the upper lip was untouched. Since a biopsy of the lower lip was done after removal of the keratin layer, all subsequent images show the biopsy wound in the mid portion of the lower lip. However, the subsequent normal changes that occurred are visible on either side of the biopsy wound. The vesicular lesions seen at the junction of the vermilion border and labial mucosa may be due to the trauma induced by the removal of the plaque if the plaque was adherent in those areas when it was being removed; the presence of acanthosis in the epithelium would be a contributing factor. Over a period of the next 9 days (Figs. 3–6), the erythema seems to decrease gradually as the keratin layer seems to thicken. A comparison of the lower and upper lip shows that on day 1, the upper lip keratin layer had already begun to form and that toward day 10, the keratin layer of the upper lip seemed thicker than that of the lower lip. This observation suggests that the cycle proceeds differently for the upper and lower lip; certain areas of the lip may be peeling while others may be just forming the keratin layer, giving an impression of continuously peeling lips. Daley and Gupta and Brooke reported a similar cyclical pattern of disease activity. Brooke8 mentioned a 5-day period for completion of the whole cycle. Our patient claimed that the hyperkeratotic plaque developed and became loose over a period of 2 weeks and that he regularly peeled the plaque when it became loose because of the associated discomfort. The build-up then recurred over time. Other signs and symptoms associated with this con-dition reported in the literature include a tingling sensa-tion, pain, soreness of the mouth and throat, an itchy sensation, a feeling of dryness, ulceration, fissuring of the lips and bleeding. Our patient had pain and bleeding, but no other symptoms. In most reported cases, like our patient’s, the lower lip was affected more severely than the upper lip. The cause of exfoliative cheilitis is unknown, although many reports suggest factitious activity; others re-port exfoliative cheilitis without factitious activity. Our patient had no factitious activity, as confirmed from observation during his 10-day admission to the hos-pital. In fact, he took particular care to avoid pain and bleeding when moving his lips. However, the possibility of Munchausen’s syndrome cannot be ruled out in those cases in which the patient does not give any indication of factitious activity when questioned or observed. The onset of the condition is often associated with a stressful period in a person’s life, as was the case with our patient. Personality disorders associated with depression have been implicated in cases of exfoliative cheilitis, and antidepressants have been found to decrease the severity of the disease. However, most patients treated with antidepressants showed improvement in, but no complete remission of the disease. Our patient’s condition improved when he was on antidepressants, but he, too, had no complete relief. Raede and others14 discussed the possibility of cheilocandidosis. It involves compromised immunity or the presence of other obvious predisposing factors that cause candidal infection of the lips. The authors achieved successful resolution of such lesions with antifungal therapy. However, for people who have no specific predisposing factors, such as our patient and others, Candida could not be isolated from the lesion nor did the condition respond to antifungal therapy.
Oral sepsis has also been implicated as a cause of exfoliative cheilitis because it has resolved after implementation of good oral hygiene. Our patient had very poor oral hygiene, but even after oral rehabilitation, he had difficulty maintaining good oral hygiene. His condition may be the result of multifactorial causes such as oral sepsis, associated with and aggravated by stress that resulted in clinical depression.
Exfoliative cheilitis may resolve spontaneously, but if persistent, it is usually refractory to treatment and difficult to manage. Our patient did not respond to systemic steroids. Other unsuccessful treatment options attempted by others are cryosurgery and keratinolytic agents.
Exfoliative cheilitis predominantly affects both sexes under 30 years of age and typically follows a cyclical course characterized by normal or erythematous lips at one stage, which progressively thickens because of a steady, excessive formation of keratin until the lips flake or crust. The cycle completes with the sloughing of the keratin layer from the surface of the lips and occurs at different days on different portions of the lips. Lips with the thick keratin layer exposed to water tend to take up water and seem to have a thick yellowish white coating. The duration of the cycle may vary amongst patients.
No appropriate treatment has been identified for this condition because the cause remains unclear.
Figure 1: Preoperative presentation of the lips.
Figure 2: Erythematous appearance of lower lip after removal of the keratin layer (day 1).
Figure 3: A decrease in erythema is evident; the biopsy wound is seen in the centre (day 3).
Figure 4: Further reduction in ery-thema; formation of keratin layer is evident (day 4).
Figure 5: Marked thickening of the keratin layer (day 8).
Figure 6: The keratin layer of the upper lip seemingly thicker than that of the lower lip (day 10).
Angular cheilitis is inflammation of one, or more commonly both, of the corners of the mouth. Angular cheilitis often represents an opportunistic infection of fungi and/or bacteria, with multiple local and systemic predisposing factors being involved in the initiation and persistence of the lesion. Such factors include nutritional deficiencies, overclosure of the mouth, dry mouth, a lip-licking habit, drooling, immunosuppression, and others. Treatment for angular cheilitis varies based on the exact causes of the condition in each case, but often an antifungal cream is used among other measures. It is a fairly common problem, and is more prevalent in people without any natural teeth who wear dentures, and in elderly people, although it may also occur in children.
Angular cheilitis is a fairly non specific term which describes the presence of a lesion in a specific anatomic site (i.e. the corner of the mouth). As there are different possible causes and contributing factors from one person to the next, the appearance of the lesion is somewhat variable. The lesions are more commonly symmetrically present on both sides of the mouth, but sometimes only one side may be affected. In some cases, the lesion may be confined to the mucosa of the lips, and in other cases the lesion may extend past the vermilion border (the edge where the lining on the lips becomes the skin on the face) onto the facial skin. Initially, the corners of the mouth develop a gray-white thickening and adjacent erythema (redness). Later, the usual appearance is a roughly triangular area of erythema, edema (swelling) and maceration at either corner of the mouth.
The mucosa of the lip may become fissured (cracked), crusted, ulcerated oratrophied. There is not usually any bleeding. Where the skin is involved, there may be radiating rhagades (linear fissures) from the corner of the mouth. Infrequently, the dermatitis (which may resemble eczema) can extend from the corner of the mouth to the skin of the cheek or chin. If Staphylococcus aureus is involved, the lesion may show golden yellow crusts. In chronic angular cheilitis, there may be suppuration (pus formation), exfoliation (scaling) and formation of granulation tissue.
Sometimes contributing factors can be readily seen, such as loss of lower face height from poorly made or worn dentures, which results in mandibular overclosure ("collapse of jaws"). If there is a nutritional deficiency underlying the condition, various other signs and symptoms such as glossitis (swollen tongue) may be present. In people with angular cheilitis who wear dentures, often there may be erythematous mucosa underneath the denture (normally the upper denture), an appearance consistent with denture-related stomatitis. Typically the lesions give symptoms of soreness, pain, pruritus (itching) or burning or a raw feeling.
Angular cheilitis is thought to be multifactorial disorder of infectious origin, with many local and systemic predisposing factors are known to be involved. The sores in angular cheilitis are often infected with fungi (yeasts), or sometimes bacteria, or a combination. This may represent a secondary, opportunistic infectionby these pathogens, and some studies have linked the initial onset of angular cheilitis with nutritional deficiencies, especially of the B vitamins and iron (which causesiron deficiency anemia). which in turn may be evidence of malnutrition or malabsorption. Angular cheilitis can be a manifestation of contact dermatitis, which is considered in two groups; irritational and allergic.
The involved organisms are:
Candida can be detected in 93% of angular cheilitis lesions. This organism is found in in the mouths of about 40% of healthy individuals, and it is considered by some to be normal commensal component of the oral microbiota. However, Candida shows dimorphism, namely a yeast form which is thought to be relatively harmless and a pathogenic hyphal form which is associated with invasion of host tissues. Potassium hydroxide preparation is recommended by some to help distinguish between the harmless and the pathogenic forms, and thereby highlight which cases of angular cheilitis are truly caused by Candida. The mouth may act as a reservoir of Candida that reinfects the sores at the corners of the mouth and prevents the sores from healing.
A lesion caused by recurrence of a latent herpes simplex infection can occur in the corner of the mouth. Really this is herpes labialis (a cold sore), and is sometimes termed "angular herpes simplex". A cold sore at the corner of the mouth behaves similarly to elsewhere on the lips, and follows a pattern of vesicle (blister) formation followed by rupture leaving a crusted sore which resolves in about 7–10 days, and recurs in the same spot periodically, especially during periods of stress. Rather than utilizing antifungal creams, angular herpes simplex is treated in the same way as a cold sore, with topical antiviral drugs such as aciclovir.
22% of cases of angular cheilitis are due to irritants. Saliva contains digestive enzymes, which may have a degree of digestive action on tissues if they are left in contact. The corner of the mouth is normally exposed to saliva more than any other part of the lips. Reduced lower facial height (vertical dimension or facial support) is usually caused by edentulism (tooth loss), or wearing worn down, old dentures or ones which are not designed optimally. This results in overclosure of the mandible (collapse of the jaws), which extenuates the angular skin folds at the corners of the mouth, in effect creating an intertriginous skin crease. The tendency of saliva to pool in these areas is increased, constantly wetting the area, which may cause tissue maceration and favors the development of a yeast infection. As such, angular cheilitis is more commonly seen in edentulous people (people without any teeth). It is by contrast uncommon in persons who retain their natural teeth. Angular cheilitis is also commonly seen in denture wearers. Angular cheilitis is present in about 30% of people with denture-related stomatitis. It is thought that reduced vertical dimension of the lower face may be a contributing factor in up to 11% of elderly persons with angular cheilitis and in up to 18% of denture wearers who have angular cheilitis. Reduced vertical dimension can also be caused by tooth migration, wearing orthodontic appliances, and elastic tissue damage caused by ultraviolet light exposure and smoking.
Habits or conditions that keep the corners of the mouth moist might include chronic lip licking, thumb sucking (or sucking on other objects such as pens, pipes, lollipops), dental cleaning (e.g. flossing), chewing gum, hypersalivation, drooling and mouth breathing. Some consider habitual lip licking or picking to be a form of nervous tic, and do not consider this to be true angular cheilitis, instead calling it perl?che (derived from the French word pourl?cher meaning "to lick one’s lips"), or "factitious cheilitis" is applied to this habit. The term "cheilocandidiasis" describes exfoliative (flaking) lesions of the lips and the skin around the lips, and is caused by a superficial candidal infection due to chronic lip licking. Less severe cases occur during cold, dry weather, and is a form of chapped lips. Individuals may lick their lips in an attempt to provide a temporary moment of relief, only serving to worsen the condition.
The sunscreen in some types of lip balm degrades over time into an irritant. Using expired lipbalm can initiate mild angular cheilitis, and when the person applies more lipbalm to alleviate the cracking, it only aggravates it. Because of the delayed onset of contact dermatitis and the recovery period lasting days to weeks, people typically do not make the connection between the causative agent and the symptoms.
Several different nutritional deficiency states of vitamins or minerals have been linked to AC. It is thought that in about 25% of people with AC, iron deficiencyor deficiency of B vitamins are involved. Nutritional deficiencies may be a more common cause of AC in third world countries. Chronic iron deficiency may also cause koilonychia (spoon shaped deformity of the fingernails) and glossitis (inflammation of the tongue). It is not completely understood how iron deficiency causes AC, but it is known that it causes a degree of immunocompromise (decreased efficiency of the immune system) which may in turn allow an opportunistic infection of candida. Vitamin B2 deficiency (ariboflavinosis) may also cause AC, and other conditions such as redness of mucous membranes, magenta colored glossitis (pink inflammation of the tongue). Vitamin B5 deficiency may also cause AC, along with glossitis, and skin changes similar to seborrhoeic dermatitisaround the eyes, nose and mouth. Vitamin B12 deficiency is sometimes responsible for AC, and commonly occurs together with folate deficiency (a lack of folic acid), which also causes glossitis and megaloblastic anemia. Vitamin B3 deficiency (pellagra) is another possible cause, and in which other association conditions such as dermatitis, diarrhea, dementia and glossitis can occur. Biotin (vitamin B7) deficiency has also been reported to cause AC, along with alopecia (hair loss) and dry eyes. Zinc deficiency is known to cause AC. Other symptoms may include diarrhea, alopecia and dermatitis. Acrodermatitis enteropathica is an autosomal recessive genetic disorder causing impaired absorption of zinc, and is associated with AC.
In general, these nutritional disorders may be caused by malnutrition, such as ma in strict vegan diets, or by malabsorption secondary to gastrointestinal disorders (e.g. Celiac disease or chronic pancreatitis) or gastrointestinal surgeries (e.g. pernicious anemia caused by ileal resection in crohn's disease).
Some systemic disorders are involved in angular cheilitis by virtue of their association with malabsorption and the creation of nutritional deficiencies described above. Such examples include people with anorexia nervosa. Other disorders may cause lip enlargement (e.g. orofacial granulomatosis), which alters the local anatomy and extenuates the skin folds at the corners of the mouth. More still may be involved because they affect the immune system, allowing normally harmless organisms like Candida to become pathogenic and cause an infection. Xerostomia (dry mouth) is thought to account for about 5% of cases of AC. Xerostomia itself has many possible causes, but commonly the cause may be side effects of medications. Conversely, conditions which cause drooling or sialorrhoea (excessive salivation) can cause angular cheilitis by creating a constant wet environment in the corners of the mouth. About 25% of people with Down syndrome appear to have AC. Other possible oral manifestations of down syndrome include macroglossia (a large tongue), which may protrude from the mouth constantly. Inflammatory bowel diseases (such as Crohn's disease or ulcerative colitis) can be associated with angular cheilitis. In Crohn's it is likely the result of malabsorption and immunosuppressive therapy which gives rise to the sores at the corner of the mouth. Glucagonomas are rarepancreatic endocrine tumors which secrete glucagon, and cause a syndrome of dermatitis, glucose intolerance, weight loss and anemia. AC is a common feature of glucagonoma syndrome. Infrequently, angular cheilitis may be one of the manifestations of chronic mucocutaneous candidiasis, and sometimes cases of oropharyngeal or esophageal candidiasis may accompany angular cheilitis. Angular cheilitis may be present in human immunodeficiency virus infection, neutropenia, or diabetes. Angular cheilitis is more common in people with eczema because their skin is more sensitive to irritants. Other conditions possibly associated include plasma cell gingivitis, Melkersson-Rosenthal syndrome, or sideropenic dysphagia (also called Plummer-Vinson syndrome or Paterson-Brown-Kelly syndrome).
Several drugs may cause AC as a side effect, by various mechanisms, such as creating drug induced xerostomia. Various examples include isotretinoin, indinavirand sorafenib. Isotretinoin (Accutane), an analog of vitamin A, is a medication which dries the skin. Less commonly, angular cheilitis is associated with primaryhypervitaminosis A, which can occur when large amounts of liver (including cod liver oil and other fish oils) are regularly consumed or as a result from an excess intake of vitamin A in the form of vitamin supplements. Recreational drug users may develop AC. Examples include cocaine, methamphetamines, heroin and hallucinogens.
Angular chielitis is normally a diagnosis made clinically. If the sore is unilateral rather than bilateral, this suggests a local factor (e.g. trauma) or a split syphilitic papule. Angular cheilitis caused by mandibular overclosure, drooling and other irritants is usually bilateral.
The lesions are normally swabbed to detect if Candida or pathogenic bacterial species may be present. Persons with angular cheilitis who wear dentures often also will have their denture swabbed in addition. A complete blood count (full blood count) may be indicated, including assessment of the levels of iron, ferritin, vitamin B12 (and possibly other B vitamins), and folate.
There are 4 aspects to the treatment of angular chieltis. Firstly, potential reservoirs of infection inside the mouth are identified and treated. Oral candidiasis, especially denture-related stomatitis is often found to be present where there is angular cheilitis, and if it is not treated, the sores at the corners of the mouth may often recur. This involves having dentures properly fitted and disinfected. Commercial preparations are marketed for this purpose, or simply the dentures are left in dilute (1:10 concentration) household bleach overnight, but only if they are plastic and do not contain any metal parts, and with rinsing under clean water before use. Improved denture hygiene is often required thereafter, including not wearing the denture during sleep and cleaning it daily.
Secondly, there may be a need to increase the vertical dimension of the lower face to prevent overclosure of the mouth and formation of deep skin folds. This may require the construction of a new denture with an adjusted bite. Rarely, in cases resistant to normal treatments, surgical procedures such as collagen injections (or other facial fillers such as autologous fat or crosslinked hyaluronic acid) are used in an attempt to restore the normal facial contour. Other measures which seek to reverse the local factors that may be contributing to the condition include improving oral hygiene, stopping smoking or other tobacco habits and use of a barrier cream (e.g. zinc oxide paste) at night.
Thirdly, treatment of the infection and inflammation of the lesion themselves is addressed. This is usually with topical antifungal medication, such asclotrimazole, amphotericin B ketoconazole, or nystatin cream. Some antifungal creams are combined with corticosteroids such as hydrocortisone or triamcinolone to reduce inflammation, and some antifungals such as miconazole cream also have some antibacterial action. Diiodohydroxyquinoline is another topical therapy for angular cheilitis. If Staphylococcus aureus infection is demonstrated by microbiological culture to be responsible (or suspected), the treatment may be changed to fusidic acid cream, an antibiotic which is effective against this type of bacteria. Aside from fusidic acid, neomycin, mupirocin, metronidazole, and chlorhexidine, are alternative options for this scenario.
Finally, if the condition appears resistant to treatment, investigations for underlying causes such as anemia or nutrient deficiencies or HIV infection. Identification of the underlying cause is essential for treating chronic cases. The lesions may resolve when the underlying disease is treated, e.g. with a course of oral iron or B vitamin supplements. Patch testing is recommended by some in cases which are resistant to treatment and where allergic contact dermatitis is suspected.
Allergic Contact Cheilitis
Contact cheilitis is a term used to describe inflammation of the lips, most often caused by either irritant contact cheilitis (ICC) or allergic contact cheilitis (ACC). This inflammation can cause a variety of signs and symptoms, such as dryness, scaling, crusting, fissuring, erythema, edema and/or angular cheilitis, as well as burning or itching.
Contact allergy of the oral mucosa, allergic contact stomatitis (ACS), is less common than contact allergy of skin of the lips. A potential explanation regarding this phenomenon involves saliva’s cleansing effect, washing away antigens that are presented to the mucosa, where antigen-presenting cells may also be less prevalent. The vascularity of the buccal mucosa also aids in the dispersal of antigens; however, despite this, the mucosa can become sensitized, with a subsequent inflammatory reaction, most often to dental materials and appliances, such as metals, acrylics fillings, crowns and dentures. Cheilitis and circumoral dermatitis usually accompany primary allergic stomatitis, although stomatitis does not necessarily always accompany primary allergic cheilitis. Of interest, early allergen exposure to the oral mucosa may actually be a means to creating tolerance. For example, it is well documented that wearing metal dental braces prior to nickel exposure (ear piercing) confers a lower risk of developing nickel allergy than the reverse of first piercing then being braced.
Eczematous cheilitis is inflammation of the lips presenting as redness with dryness and scaling. It may also be called lip dermatitis. The lips may be divided into three zones – the outer zone comprising the skin next to the lips, the vermilion margin and the mucosal aspect. The first two areas are the most commonly affected. The major causes of eczematous cheilitis are atopic dermatitis and irritant or allergic contact reactions.
Eczematous cheilitis can be divided into two major groups based on the cause:
Often a combination of factors is present.
Rarely contact urticaria may present as a cheilitis when the allergen is used in small amount frequently, such as the flavouring in a toothpaste.
Sometimes no cause can be identified.
The chronic form of eczematous cheilitis presents with redness, dryness, scaling and fissuring. The angle of the mouth is often also involved (angular cheilitis).
The perioral skin and vermilion margin (where the red mucosa meets the skin) are the most commonly affected parts of the lips.
It is important to look for and note skin and mucosal lesions elsewhere as these may give a clue as to the cause.
Treatment will depend on the cause. Where an exogenous cause has been identified, this should be avoided if possible. If this does not result in improvement, consider another factor such as a second allergen, irritant or endogenous cause.
The tongue is a muscular organ in the mouth. The tongue is covered with moist, pink tissue called mucosa. Tiny bumps called papillae give the tongue its rough texture. Thousands of taste buds cover the surfaces of the papillae. Taste buds are collections of nerve-like cells that connect to nerves running into the brain.
The tongue is anchored to the mouth by webs of tough tissue and mucosa. The tether holding down the front of the tongue is called the frenum. In the back of the mouth, the tongue is anchored into the hyoid bone. The tongue is vital for chewing and swallowing food, as well as for speech.
The four common tastes are sweet, sour, bitter, and salty. A fifth taste, called umami, results from tasting glutamate (present in MSG). The tongue has many nerves that help detect and transmit taste signals to the brain. Because of this, all parts of the tongue can detect these four common tastes; the commonly described “taste map” of the tongue doesn’t really exist.
Glossitis can mean soreness of the tongue, or more usually inflammation with depapillation of the dorsal surface of the tongue (loss of the lingual papillae), leaving a smooth and erythematous (reddened) surface, (sometimes specifically termed atrophic glossitis). In a wider sense, glossitis can mean inflammation of the tongue generally. Glossitis is often caused by nutritional deficiencies and may be painless or cause discomfort. Glossitis usually responds well to treatment if the cause is identified and corrected. Tongue soreness caused by glossitis is differentiated from burning mouth syndrome, where there is no identifiable change in the appearance of the tongue, and there are no identifiable causes.
Glossitis may occur as a primary condition ñauses may include:
– Bacterial / Viral Infections
– Mechanical Irritation from teeth, dentures etc.
– Tobacco, Hot Food, Alcohol
– Allergy to toothpaste, mouthwash, etc.
Median rhomboid glossitis
Median rhomboid glossitis (MRG, also known as central papillary atrophy, or glossal central papillary atrophy) is a condition characterized by an area of redness and loss of lingual papillae, situated on the dorsum of the tongue in the midline immediately in front of the circumvallate papillae. Median rhomboid glossitis is thought to be created by a chronic fungal infection, and usually is a type of oral candidiasis.
Rarely is any soreness associated
with the condition. Apart from the appearance of the lesion, there are usually
no other signs or symptoms. The typical appearance of the lesion is an oval or
rhomboid shaped area located in the midline of the dorsal surface of the
tongue, just anterior (in front) of the sulcus terminalis. The lesion is
usually symmetric, well demarcated, erythematous and depapillated, which has a
smooth, shiny surface. Less typically, the lesion may be hyperplastic or
lobulated and exophytic. There may be candidal lesions at other sites in the
mouth, which may lead to a diagnosis of chronic multifocal oral candidiasis.
Sometimes an approximating erythematous lesion is present on the palate (a
"kissing lesion"). The lesion is typically 2 –
Predisposing factors include smoking, denture wearing, use of corticosteroid sprays or inhalers and human immunodeficiency virus (HIV) infection. Candida species even in healthy people mainly colonizes the posterior dorsal tongue. Median rhombiod glossitis is thought to be a type of chronic atrophic (or erythematous) candidiasis. Microbiological culture of the lesion usually shows Candida mixed with bacteria.
The diagnosis is usually made on the clinical appearance, and tissue biopsy is not usually needed. The histologic picture is one of superficial candidal hyphal infiltration and a polymorphonuclear leukocytic inflammatory infiltrate present in the epithelium. The rete ridges are elongated and hyperplastic (pseudoepitheliomatous hyperplasia, which may be mistaken for carcinoma).
Treatment may involve smoking cessation and prescription of topical or systemic antifungal medication. Usually the mucosal changes resolve with antifungal therapy, but sometimes the lesion is resistant to complete resolution.
Figure 1. This well-demarcated erythematous area on the posterior tongue represents a partial loss of the filiform papillae.
Figure 2. Remarkable pseudoepitheliomatous hyperplasia of the squamous epithelium is seen on intermediate magnification. Parakeratosis is noted, and mixed inflammation is predominant in the stroma of this H&E-stained material.
Median rhomboid glossitis—also known as central papillary atrophy and posterior midline atrophic candidiasis—is a type of erythematous candidiasis unique to the midline posterior tongue. It occurs in as many as 1% of adults.
This condition was once thought to represent a developmental defect. The embryonic tongue is formed when the lateral processes meet in the midline and fuse over the tuberculum impar. In some cases, the posterior dorsal point of fusion is abnormal, resulting in the development of an area of smooth, erythematous mucosa lacking papillae. This area is more susceptible to recurring, chronic atrophic candidiasis. Today, however, most authors do not subscribe to the embryogenesis theory. Instead, they believe that median rhomboid glossitis is related to an infection of Candida albicans, which is the most common fungal organism of the oral cavity. Candidiasis is exceedingly common. C albicans is a component of the oral flora in up to 50% of the population; most of these individuals show no clinical evidence of disease. Symptomatic candidiasis is associated with numerous conditions, including nutritional deficiencies, diabetes, xerostomia, and immune deficiencies and disorders. Symptomatic candidiasis may occur in healthy individuals who have no predisposing factors. Men are affected more often than women (3:1), and adults more often than children. Clinically, median rhomboid glossitis manifests as a well-delineated erythematous area located along the midline posterior dorsal tongue just anterior to the circumvallate papillae (figure 1). This area represents a zone of atrophic filiform papillae. Its rhomboid shape usually “points” in an anteroposterior direction. Additionally, it is not unusual in median rhomboid glossitis to have a “kissing lesion,” or area of roughness, most commonly in the area of the hard and soft palate where the tongue generally rests against the palate.
Fissured tongue can be defined as tongue with cracks and grooves. Medically, fissured tongue is described as multiple small furrows or grooves on the dorsal surface of the tongue. The grooves or fissures could be deep or shallow, one or more and may occur on any side of the tongue. Nevertheless, most of the fissures occur on the middle 1/3rd of the organ.
The ailment of fissured tongue affects approximately 5% of the US population. The condition is less common in children but as we grow, the chances of having this increases. Men are affected a bit more as compared to their counterpart, the women.
Fissured tongue is also known as
· Scrotal tongue
· Plicated tongue
· Lingua plicata
· Furrowed tongue
Below mentioned are the characteristics of fissured tongue.
· The fissures or grooves affect only tongue and no other structure in the oral cavity
· Pain and burning sensation in the tongue
· Cracks, grooves or clefts happen on the top and sides of the tongue
· The grooves may be shallow or deep as
· The fissures may connect with each other making the tongue appearing like divided in lobes or sections
· Redness of the tongue
· Difficulty in eating and swallowing
· Severe burning when food or water put on it
Picture : Fissured Tongue
Picture : Fissured Tongue (right side of tongue)
Picture : Fissured Tongue (cracks and groves)
Though the perfect etiology of fissured tongue is not known, here are some predicted causative factors that may give rise to fissured tongue:-
· Polygenic mode of inheritance is likely to cause fissured tongue
· Melkersson-Rosenthal syndrome
· Injury to oral cavity or tongue (maybe direct injury or through teeth grinding, tongue biting)
· Severe alcohol consumption
· Severe tobacco chewing
· Eating hard food (such as betel nut) that may injure tongue
· Down syndrome
· As in association with benign migratory glossitis (geographic tongue)
· As in association with granulomatous disease
· Allergic reaction or oral thrush
· Injury to the tongue while brushing the teeth or gums
· Unusual dryness of mouth (as in Sjogren’s Syndrome)
· Some drug reaction
· Over body heat
The diagnose is done mainly based on oral examination. The fissured or grooved tongue is easy to identify. The condition is further confirmed as a doctor observes the signs and symptoms and asks the history to the patient. In some rare case, the health care provider may ask for the biopsy taking tongue’s tissue to check the malignancy.
Nearly 2-5% of the US population is affected by this ailment. Though sure cause factors for fissured tongue are unknown there are some conditions associated with this ailment. They are mentioned below
Downs syndrome: Almost 8 out of 10 children with chromosomal disorder (trisomy) have fissured tongue. Down syndrome is one of the commonest condition associated with tongue problems.
Geographic tongue: This condition is also referred to as BMG (Benign Migratory Glossitis). Although there are no symptoms other than burning and pain in the tongue while eating spicy and hot foods.
Melkersson-Rosenthal Syndrome: Quite rare condition though, Melkersson-Rosenthal syndrome is another condition associated with fissured tongue. Nevertheless, this may also show the symptoms of swelling in lips and face and Bell’s Palsy (paralysis of the face-partially or completely)
The treatment of fissured tongue depends on the causative factors. If it is due to infection or injury, healing is done by prescribing antibiotics and topical soothing creams. Keeping oral hygiene is must to cure fissured tongue. Removal of debris from the fissures and grooves is must to prevent further worsening of the condition.
Hydration of the tongue is important to cure fissured tongue. Plain water drinking is the best remedy for fissured tongue. About other treatments for this ailment, it is observed that while some prefer spearmint, natural healers advise keeping baking soda gargling to heal the wounds faster. Cleaning the tongue with soft brush or gently swiping of tongue-cleaner is advised.
The name black hairy tongue may sound scary, but the condition is harmless. Black hairy tongue is caused by bacteria or fungi in the mouth, which make the tongue appear black and hairy. It's easily remedied by good old-fashioned oral hygiene.
Black discoloration on the dorsal surface of the tongue. Black hairy tongue is characterized by a hairy and discolored tongue.
Hairy tongue (lingua villosa) refers to a marked accumulation of keratin on the filiform papillae on the dorsal surface of the tongue, giving a hair-like appearance. Black tongue (lingua nigra) refers to a black discoloration of the tongue, which may or may not be associated with hairy tongue. However, the elongated papillae of hairy tongue usually develop discoloration due to growth of pigment producing bacteria and staining from food. Hence the term black hairy tongue, although hairy tongue may also be discolored yellow or brown. Transient, surface discoloration that is not associated with hairy tongue can be brushed off. Drug induced black hairy tongue specifically refers to BHT that develops because of medication.
Black hairy tongue is caused by too much bacteria or yeast growth in the mouth. The bacteria build up on tiny rounded projections called papillae. These lie along the surface of the tongue. Instead of shedding as they normally do, the papillae start to grow and lengthen, creating hair-like projections. They can grow to 15 times their normal length.
Normally, the papillae are pinkish-white. But as they grow, pigments from food, drinks, and possibly the bacteria or yeast themselves get caught in the papillae, dyeing the tongue a color. Most often that color is black, hence the name. But the tongue can also turn brown, yellow, green, or a variety of other colors.
Certain lifestyle habits and conditions can make people more likely to develop black hairy tongue. They include:
· poor oral hygiene
· smoking tobacco
· drinking a lot of coffee or tea
· using antibiotics (which may disrupt the normal balance of bacteria in the mouth)
· being dehydrated
· taking medications that contain the chemical bismuth (such as Pepto-Bismol for upset stomach)
· not producing enough saliva
· regularly using mouthwash that contains peroxide, witch hazel, or menthol
· getting radiation therapy to the head and neck
Black hairy tongue is more common in men, people who use intravenous drugs, and those who are HIV-positive.
Other than the appearance of the tongue, most people with black hairy tongue don't have any symptoms or feel any discomfort. The exception is when there is too much growth of the yeast Candida albicans, which can cause a burning sensation on the tongue. This burning sensation is called glossopyrosis.
Some people complain of a tickling feeling in the back of the roof of the mouth, a metallic taste in their mouth, or nausea. In more severe cases, the condition may lead to a gagging feeling. Sometimes, food getting caught inside the extra-long papillae can cause bad breath.
Diagnosis is usually made on the clinical appearance without the need for a tissue biopsy. However, when biopsies have been taken, the histologic appearance is one of marked elongation and hyperparakeratosis of the filiform papillae and numerous bacteria growing on the epithelial surface.
Hairy tongue may be confused with hairy leukoplakia, however the latter usually occurs on the sides of the tongue and is associated with an opportunistic infection with Epstein-Barr virus on a background immunocompromise (almost always human immunodeficiency virus infection but rarely other conditions which suppress the immune system).
Practicing good oral hygiene is the best way to treat black hairy tongue. Gently brush your teeth twice a day with a soft toothbrush. Also, brush your tongue. You can use a tongue scraper to make sure you're thoroughly cleaning the area. Drink plenty of water throughout the day to help keep your mouth clean.
Other tips include:
· If you smoke, quit.
· Add more roughage to your diet. Soft foods won't clean off the tongue effectively
Geographic tongue (also known as benign migratory glossitis, BMG, erythema migrans, erythema migrans lingualis, glossitis areata exfoliativa, glossitis areata migrans, lingua geographica, stomatitis areata migrans, wandering rash of the tongue, and transitory benign plaques of the tongue), is an inflammatory condition of the mucous membrane of the tongue, usually on the dorsal surface. It is a common condition, affecting approximately 2-3% of the general population. It is characterized by areas of smooth, red depapillation (loss of lingual papillae) which migrate over time. The name comes from the map-like appearance of the tongue, with the patches resembling the islands of an archipelago. The cause is unknown, but the condition is entirely benign (importantly, it does not represent oral cancer), and there is no curative treatment. Uncommonly, geographic tongue may cause a burning sensation on the tongue, for which various treatments have been described with little formal evidence of efficacy.
Signs and symptoms
The appearance of geographic tongue is variable from one person to the next and changes over time. The bottom image shows fissured tongue combined with geographic tongue more posteriorly. It is common for these two conditions to coexist.
In health, the dorsal surface of the tongue is covered in tuft like projections called lingual papillae (some of which are associated with taste buds), which give the tongue an irregular surface texture and a white-pink color. Geographic tongue is characterized by areas of atrophy and depapillation (loss of papillae), leaving an erythematous (darker red) and smoother surface than the unaffected areas. The depapillated areas are usually well demarcated, and bordered by a slightly raised, white, yellow or grey, serpingious (snaking) peripheral zone. A lesion of geographic tongue may start as a white patch before the depapillation occurs. Sometimes there may be only one lesion, but this is uncommon, and more usually the lesions may start at multiple different locations on the tongue, and then over time the areas coalesce to form the typical map-like appearance. The lesions usually change in shape, size and migrate to other areas, sometimes within hours. The condition may affect only part of the tongue, with a predilection for the tip and the sides of the tongue, or the entire dorsal surface at any one time. The condition goes through periods of remission and relapse. Loss of the white peripheral zone is thought to signify periods of mucosal healing.
There are usually no symptoms, but in some cases persons may experience pain or burning e.g. when eating hot, acidic, spicy or other kinds of foods (e.g. cheese, tomatoes, fruit). Where there is a burning symptom, other causes of a burning sensation on the tongue are considered, such as oral candidiasis.
The cause is unknown. Geographic tongue does not usually cause any symptoms, and in those cases where there are symptoms, an oral parafunctional habit may be a contributory factor. Persons with parafunctional habits related to the tongue may show scalloping on the sides of the tongue. Some suggest that hormonal factors may be involved, because one reported case in a female appeared to vary in severity in correlation with oral contraceptive use. People with geographic tongue frequently claim that their condition worsens during periods of psychologic stress. Geographic tongue is inversely associated with smoking and tobacco use. Sometimes geographic tongue is said to run in families, and it is reported to be associated with several different genes, though studies show family association may also be caused by similar diets. Some have reported links with various human leukocyte antigens, such as increased incidence of HLA-DR5, HLA-DRW6 and HLA-Cw6 and decreased incidence in HLA-B51. Vitamin B2 deficiency (ariboflavinosis) can cause several signs in the mouth, possibly including geographic tongue, although other sources state that geographic tongue is not related to nutritional deficiency. Fissured tongue often occurs simultaneously with geographic tongue, and some consider fissured tongue to be an end stage of geographic tongue.
In the past, some research suggested that geographic tongue was associated with diabetes, seborrheic dermatitis and atopy, however more modern research does not corroborate these findings. Some studies have reported a link between geographic tongue and psoriasis, although 90% of children who are diagnosed with geographic tongue do not contract psoriasis. Again however, modern research studies do not support any link between psoriasis and geographic tongue. Lesions that are histologically indistinguishable from geographic tongue may also be diagnosed in Reiter's syndrome (arthritis, uveitis/conjunctivitis and urethritis).
he differential diagnosis includes oral lichen planus, erythematous candidiasis, leukoplakia, lupus erythematosus, glossitis, and chemicl burns. Atrophic glossitis is usually distinguished from benign migratory glossitis on the basis of the migrating pattern of the lesions and the presence of a whitish border, features which are not present in atrophic glossitis, which instead shows lesions which enlarge rather than migrate. Rarely, blood tests may be required to distinguish from glossitis associated with anemia or other nutritional deficiencies. Since the appearance and the history of the condition (i.e. migrating areas of depapillation) are so striking, there is rarely any need for biopsy. When biopsy is taken, the histopathologic appearance is quite similar to psoriasis one of:
Subepithelial T lymphocyte inflammatory infiltrate.
Migration of neutrophilic granulocytes into the epithelial layer, which may create superficial microabscesses, similar to the Munro's microabscesses described in pustular psoriasis.
Since most cases cause no symptoms, reassuring the person affected that the condition is entirely benign is usually the only treatment.
When symptoms are present, topical anesthetics can be used to provide temporary relief. Other drugs that have been used to manage the symptoms include antihistamines, corticosteroids or anxiolytics, but these drugs have not been formally assessed for efficacy in geographic tongue. If some foodstuffs exacerbate or trigger the symptoms, then cutting these foods out of the diet may benefit. One uncontrolled trial has shown some benefit in controlling the symptoms of geographic tongue.
The condition may disappear over time, but it is impossible to predict if or when this may happen.
Geographic tongue is the name of a condition that gets its name from its map-like appearance on the upper surface and sides of the tongue. It may occur in other areas of mouth, as well.
Geographic tongue is a harmless, benign condition that isn't linked to any infection or cancer. Two other names for geographic tongue are benign migratory glossitis and erythema migrans.
Affecting about 1% to 3% of people, geographic tongue can show up at any age. However, it tends to affect middle-aged or older adults more often. And it appears to be more common in women than in men.
The telltale signs of geographic tongue are irregular, smooth, red patches on parts of the tongue. These patches may:
· Have a white or light-colored border
· Vary in size, shape, and color
· Appear one area, and then move to another area
· Come and go or change very quickly in days, weeks, or months
· Last up to a year
You may be unaware that you have geographic tongue until your dentist or other health care provider diagnoses it during an oral exam.
About one in 10 people with geographic tongue may have mild discomfort or a burning or painful sensation. This is often from sensitivity to substances such as:
· Hot, spicy, or acidic foods
· Cigarette smoke
Geographic tongue occurs when parts of the tongue are missing layers of small bumps called papillae. They normally cover the entire upper layer of your tongue. Geographic tongue has also been seen more frequently in people with psoriasis and in those with fissured tongue. In fissured tongue, cracks and grooves appear on the tops and sides of the tongue.
Diet then certainly plays some role in the problem. Someone with geographic tongue might benefit from having their blood tested for vitamin B deficiency and then increasing their consumption of the vitamin if one is fond. Zinc supplementation has also been found to be effective and others get relief from chewing on mint and sucking mint candies during and after a flare up.
While it is not a treatment, one way to prevent the problem is to avoid exacerbating foods. These can vary but commonly include:
• Spicy food
• Strong cheese
• Sour food
• Mouth washes
There is no known cure for geographic tongue and management normally consists of switching to the recommended diet. However other temporary treatments can include the topical application of steroid ointment which can treat the symptoms temporarily. Where there is pain, antihistamines have been shown to be effective in reducing burning (perhaps implicating allergic reaction?). In most cases however the condition is asymptomatic and manageable without treatment.
· Over-the-counter pain relievers
· Mouth rinses with anesthetic
· Corticosteroids applied directly on the tongue
· Zinc supplements
If you're wondering about steps you can take to hasten the relief of symptoms, try limiting these substances or avoid them altogether:
· Hot, spicy, or acidic foods or dried, salty nuts
Geographic tongue is a harmless, benign condition that isn't linked to any infection or cancer. Two other names for geographic tongue are benign migratory glossitis and erythema migrans.
rophic glossitis, also known as bald tongue, smooth tongue, Hunter glossitis, Moeller glossitis, or M?ller-Hunter glossitis, is a condition characterized by a smooth glossy tongue that is often tender/painful, caused by complete atrophy of the lingual papillae (depapillation). The dorsal tongue surface may be affected totally, or in patches, and may be associated with a burning sensation, pain and/or erythema. Atrophic glossitis is a non-specific finding, and has a great many causes, usually related to various nutritional deficiencies or other factors such as xerostomia (dry mouth) or anemia. Although the terms M?ller and Hunter glossitis were originally used to refer to sepcifically the glossitis that occurs in vitamin B12 deficiency secondary to pernicious anemia, they are now used as synonyms for atrohpic glossitis generally.
Candidiasis may be a concurrent finding or an alternative cause of erythema, burning, and atrophy.
Geometric glossitis, also termed herpetic geometric glossitis, is a term used by some to refer to a chronic lesion associated with herpes simplex virus (HSV) type I infection, in which there is a deep fissure in the midline of the tongue and gives off multiple branches. The lesion is usually very painful, and there may be erosions present in the depths of the fissures. Similar fissured lesions which are not associated with HSV, as may occur in fissured tongue, do not tend to be painful. The name comes from the geometric pattern of the fissures which are longitudinal, crossed or branched. It is described as occurring in immunocompromized persons, e.g. who have leukemia. However, the association between herpes simplex and geometric glossitis is disputed by some due to a lack of gold standard techniques for diagnosis of intraoral herpetic lesions, and the high prevalence of asymptomatic viral shedding in immunocompromized individuals. Treatment is with systemic aciclovir.
Melkersson–Rosenthal syndrome is a rare neurological disorder characterized by recurring facial paralysis, swelling of the face and lips (usually the upper lip), and the development of folds and furrows in the tongue. Onset is in childhood or early adolescence. After recurrent attacks (ranging from days to years in between), swelling may persist and increase, eventually becoming permanent. The lip may become hard, cracked, and fissured with a reddish-brown discoloration. The cause of Melkersson–Rosenthal syndrome is unknown, but there may be a genetic predisposition. It can be symptomatic of Crohn's disease or sarcoidosis.
Treatment is symptomatic and may include nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids to reduce swelling, antibiotics and immunosuppressants. Surgery may be indicated to relieve pressure on the facial nerves and reduce swelling, but its efficacy is uncertain. Massage and electrical stimulation may also be prescribed.