Frictional keratosis, Smokeless keratosis, White sponge nevus, Coated tongue Similarities and differences of the clinical features.
FRICTIONAL KERATOSIS
Frictional keratosis is a white, keratotic lesion due to chronic mechanical irritation caused by sharp
edges of teeth or restorations, dental prosthesis, abrasive foods, vigorous tooth brushing, and playing
wind instruments. Alveolar ridge keratosis is a frictional keratosis located on the edentulous alveolar
ridge and/or retromolar pad. mucosae is a form of chronic oral frictional keratosis of the
nonkeratinized oral mucosa, usually located on the buccal mucosa or lips.
Frictional keratosis presents as diffuse, white plaques, pale-translucent to dense, white, and irregular.
White lesions are a group of pathological conditions affecting the oral mucosa giving clinically greyish or
white lesions.1,2 They are commonly encountered during clinical dental practice. Although some benign
physiologic entities may present as white lesions, systemic conditions, infections and malignancies may
also present as white oral lesions.3 The white lesions obtain their characteristics appearance from the
scattering of light through an altered mucosal surface. Such alterations may be the result of
hyperkeratosis (thickened layer of keratin/increased keratin production), acanthosis (abnormal but
benign thickening of stratum spinosum), intracellular edema of epithelial cells, reduced vascularity of
subjacent connective tissue, surface necrosis, fibrinous exudates covering an ulcer or fungal colonies .
White lesions were formerly called leukoplakia and believed often to be potentially malignant. The term
leukoplakia is now restricted to white lesions of unknown cause. Most white lesions are innocuous
keratoses caused by cheek biting, friction, or tobacco use, but other conditions must be excluded,
usually by biopsy. These include infections (such as candidiasis, syphilis, and hairy leucoplakia),
dermatoses (usually lichen planus), and neoplastic disorders (such as leucoplakias and carcinomas).
Chronic candidiasis may produce tough, adherent white patches (chronic hyperplastic candidiasis or
candida leucoplakias), which can have a malignant potential and may clinically be indistinguishable from
other leukoplakia’s, though they may be speckled.5 Frictional keratosis is a reactive white lesion caused
by prolonged mild irritation of the mucous membrane. It shows rough and frayed surface and upon
removal of the offending agent, the lesion resolves in 2 weeks. Biopsies should be performed on these
lesions that do not heal to rule out a dysplastic lesion.3,6,7 It is mostly caused by acute trauma which in
turn causes ulcers while long standing chronic trauma causes hyperkeratosis. The etiology for frictional
keratosis is habitual cheek biting, orthodontic appliance, ill-fitting denture, broken cusp, rough edges of
a carious tooth or maligned teeth. Clinical features are at first a patch which is pale translucent later it
becomes dense and white, mostly they occur in areas that are commonly traumatized like buccal
mucosa along the occlusal line, lips, lateral margins of tongue.
frictional hyperkeratosis is a benign abnormality of mucous membrane lining the inside of the mouth,
which generally occurs in adults. Typical symptoms are a white patch in the mouth, normally in the gums
or cheeks, often accompanied by a thickening of the skin in the affected area. This white patch can also
take the form of a horizontal white line.
This white discoloration indicates an overproduction of the fibrous protein, keratin. This is caused by
friction as two surfaces in the mouth rub against each other. The symptoms arise in the same way that
calluses form on the skin of hands and feet. The body reacts to the irritation by producing more cells, in
this case, keratin, giving the skin a different thickness and color.
Common causes of friction are: excessive tooth-brushing; repeated rubbing of the tongue against the
teeth; constant cheek or lip biting; broken or poorly fitted dentures and substandard fillings or caps or
jagged teeth.
The most effective way of treating oral frictional hyperkeratosis is to remove the cause of the friction by
correcting dentures, fillings, crowns, jagged teeth and any other sources of irritation.
COATED TONGUE
A coated tongue (also known as white tongue) is a symptom that causes your tongue to appear to have
a white coating. This typically occurs when bacteria, food matter, and other dead cells accumulate on
your tongue between its papillae (the features on the surface of your tongue that provide its distinctive
texture).
Causes of a Coated Tongue
Improper oral hygiene. Medications, including antibiotics. Alcohol, smoking, tobacco products, and
illegal drugs. Chronic health conditions like hypothyroidism, diabetes, and syphilis.
There are two important factors that cause this condition and they are often inter-connected. The first is
dehydration which can result in your saliva being stickier and less watery, so that the keratin on the
tongue papillae sticks together longer than they should rather than shedding. Tis is especially common
in patients who have been ill and have been on certain medications (such as antibiotics or
chemotherapy). Patients who are well and who smoke or use strong, alcohol-containing or dehydrating
mouth rinses may also develop oral dryness and hairy/coated tongue. Te second factor is lack of
activities that normally help the papillae to shed such as eating a sof diet or not eating much at all. Both
these factors are often present in patients who have been ill and have temporarily lost their appetite, or
have been unable to eat at all. Coated/hairy tongue is NOT infectious in nature and you cannot spread it
to family members or friends.
Coated/hairy tongue will usually go away once the underlying contributing factors have been eliminated
or corrected or when you fully recover from your illness. In most cases, drinking more water, cutting
back on caffeinated beverages, stopping the use of dehydrating mouth rinses and returning to a normal
balanced diet is all that is necessary. Gentle brushing of the tongue may encourage the top layers of
dead cells and keratin to come of and improve the tongue’s appearance.
Smokeless tobacco keratosis
Smokeless tobacco keratosis is a condition that causes thick white patches to form on skin in your
mouth. Your skin may also be wrinkled or look like leather. The patches form where you hold smokeless
tobacco in your mouth. Examples include your inner cheek and between your teeth and gums. Chewing
tobacco, snuff, and dipping tobacco (dip) can all cause this condition. Smokeless tobacco keratosis is also
called tobacco pouch keratosis or snuff dipper's lesion.
Apart from stopping the habit, no other treatment is indicated.] Long term follow-up is usually carried
out. Some recommend biopsy if the lesions persists more than 6 weeks after giving up smokeless
tobacco use or if the lesion undergoes a change in appearance (e.g. thickening, color changes, especially
to speckled white and red or entirely red). Surgical excision may be carried out if the lesion does not
resolve.
Smokeless tobacco keratosis results from chronic irritation from the placement of smokeless tobacco,
usually in the buccal vestibule. This irritation results in the deposition of excess fibrin-like material
throughout the submucosa and an increase in keratin production, which results in the characteristic
white corrugated appearance of the epithelium (the mucosa).
Leukoplakia and erythroplakia are clinically diagnostic terms. These lesions can be the result of multiple
pathophysiological processes that result in their appearance.
Verrucous carcinoma, a low-grade presentation of squamous cell carcinoma, has an increased keratin
production giving a verrucous, wart-like appearance. In addition, there is the thickening of the
epithelium (hyperplasia); however, very little if any dysplasia is seen within the epithelium.
Squamous cell carcinoma develops due to dysplastic changes throughout the epithelium, disrupting the
basement membrane and invasion into the connective tissue. These changes cause abnormal growth or
atrophy of epithelial tissue.
Smokeless tobacco keratosis may presents with a non-specific appearance, with hyperkeratotic and/or
acanthotic squamous epithelium. Intracellular edema and increased sub-epithelial vascularity may also
be noted. Of note, Para keratin chevrons above or within the superficial epithelial layers can generally
be visualized. Therefore, histologic examination of these lesions should evaluate for epithelial dysplasia.
Leukoplakia presents with hyperkeratosis, which is a thickened keratin layer, possible acanthosis, and a
thickened spinous layer. The diagnosis of leukoplakia is a clinical term only, and a biopsy is required to
determine a definitive diagnosis. The biopsy should be collected from the most severe site.
Over 90% of erythroplakia lesions present histopathologic ally with epithelial dysplasia, carcinoma in
situ, or superficially invasive squamous cell carcinoma. Keratin is typically not produced, and atrophy of
the epithelium is generally noted.
Verrucous carcinomas have a deceptively benign histopathologic presentation. These lesions exhibit
wide, elongated rete pegs that push into underlying connective tissue and have abundant Para keratin
clefts between surface projections. The epithelial cells are not generally dysplastic; however, an intense
inflammatory infiltrate is likely to be noted in the submucosa.
Squamous cell carcinoma arises from the dysplastic epithelium. Histologically it presents as cords or
islands of malignant epithelial cells penetrating/invading through the basement membrane into the
submucosa below. In
WHITE SPONGE NEVUS
White sponge nevus is a condition characterized by the formation of white patches of tissue called nevi
(singular: nevus) that appear as thickened, velvety, sponge-like tissue. The nevi are most commonly
found on the moist lining of the mouth (oral mucosa), especially on the inside of the cheeks (buccal
mucosa). Affected individuals usually develop multiple nevi. Rarely, white sponge nevi also occur on the
mucosae (singular: mucosa) of the nose, esophagus, genitals, or anus. The nevi are caused by a
noncancerous (benign) overgrowth of cells.
White sponge naevus presents as bilateral, sometimes symmetrical, soft white raised lesions of mucous
membranes. The surface may appear folded and it feels spongy, not hard. It cannot be detached. The
change may be quite subtle and localized or can involve the entire inside of the mouth.
It usually does not cause any symptoms, but patients may complain of roughness and of the
appearance.
The mouth is the commonest site affected and the insides of the cheeks the most common site within
the mouth. However the mucous membranes of inside the nose, the esophagus, the genitalia (vulva and
vagina) and anorectal sites can also be involved. Usually the mouth is the first site noticed.
No changes are noticed elsewhere on the skin, nails, hair or teeth. This is important when considering
other possible causes of the lesions.
There have been no reports of oral cancer developing in a white sponge naevus.
White sponge nevus can be present from birth but usually first appears during early childhood. The size
and location of the nevi can change over time. In the oral mucosa, both sides of the mouth are usually
affected. The nevi are generally painless, but the folds of extra tissue can promote bacterial growth,
which can lead to infection that may cause discomfort. The altered texture and appearance of the
affected tissue, especially the oral mucosa, can be bothersome for some affected individuals.
Mutations in the KRT4 or KRT13 gene cause white sponge nevus. These genes provide instructions for
making proteins called keratins. Keratins are a group of tough, fibrous proteins that form the structural
framework of epithelial cells, which are cells that line the surfaces and cavities of the body and make up
the different mucosae
References :
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Aghbali A, Pouralibaba F, Eslami H, Pakdel F, Jamali Z. White sponge nevus: a case report. J Dent
Res Dent Clin Dent Prospects. 2009 Spring;3(2):70-2. doi: 10.5681/joddd.2009.017. Epub 2009
Jun 5. Citation on PubMed or Free article on PubMed Central
Kimura M, Nagao T, Machida J, Warnakulasuriya S. Mutation of keratin 4 gene causing white
sponge nevus in a Japanese family. Int J Oral Maxillofac Surg. 2013 May;42(5):615-8. doi:
10.1016/j.ijom.2012.10.030. Epub 2012 Nov 24. Citation on PubMed
Marrelli M, Tatullo M, Dipalma G, Inchingolo F. Oral infection by Staphylococcus aureus in
patients affected by White Sponge Nevus: a description of two cases occurred in the same family.
Int J Med Sci. 2012;9(1):47-50. Epub 2011 Nov 18. Citation on PubMed or Free article on
PubMed Central
Martelli H Jr, Pereira SM, Rocha TM, Nogueira dos Santos PL, Batista de Paula AM, Bonan PR.
White sponge nevus: report of a three-generation family. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod. 2007 Jan;103(1):43-7. Epub 2006 Sep 1. Citation on PubMed
Nishizawa A, Nakajima R, Nakano H, Sawamura D, Takayama K, Satoh T, Yokozeki H. A de novo
missense mutation in the keratin 13 gene in oral white sponge naevus. Br J Dermatol. 2008
Sep;159(4):974-5. doi: 10.1111/j.1365-2133.2008.08716.x. Epub 2008 Jul 4. Citation on
PubMed
Rugg E, Magee G, Wilson N, Brandrup F, Hamburger J, Lane E. Identification of two novel
mutations in keratin 13 as the cause of white sponge naevus. Oral Dis. 1999 Oct;5(4):3214. Citation on PubMed