Benign Mucosal Lesions of the Oral Cavity

The word "stomatitis" literally means inflammation of the mouth.

Inflammation

of the mucous lining of any of the structures in the mouth May involve the cheeks, gums, tongue, lips and roof or floor of the mouth.

The inflammation can be caused by conditions in the mouth itself, such as poor oral hygiene, poorly fitted dentures, mouth burns from hot food or drinks conditions that affect the entire body, such as medications, allergic reactions, or infections.

Stomatitis

is usually a painful condition, associated with redness, swelling, and occasional bleeding from the affected area. Bad breath (halitosis) may also accompany the condition. Stomatitis affects all age groups, from the infant to the elderly.

number of factors can cause stomatitis. Poorly fitted oral appliances, cheek biting, or jagged teeth can persistently irritate the oral structures. Chronic mouth breathing due to plugged nasal airways can cause dryness of the mouth tissues, which in turn leads to irritation.

 Drinking

beverages that are too hot can burn the mouth, leading to irritation and pain. Diseases, such as herpetic infections (the common cold sore), gonorrhea, measles, leukemia, AIDS, and lack of vitamin C can present with oral signs.

 Other

systemic diseases associated with stomatitis include inflammatory bowel disease (IBD) an inflammatory multisystem disorder of unknown cause eg SLE.

 Aphthous

stomatitis, also known as recurrent aphthous ulcers (RAU) or canker sores, is a specific type of stomatitis that presents with shallow, painful ulcers that are usually located on the lips, cheeks, gums, or roof or floor of the mouth. These ulcers can range from pinpoint size to up to 1 in (2.5 cm) or more in diameter

 Though

the causes of canker sores are unknown, nutritional deficiencies, especially of vitamin B12, folate, or iron is suspected. Generalized or contact stomatitis can result from excessive use of alcohol, spices, hot food, or tobacco products. Sensitivity to mouthwashes, toothpastes, and lipstick can irritate the lining of the mouth.

 Exposure

to heavy metals, such as mercury, lead, or bismuth can cause stomatitis. Thrush, a fungal infection, is a type of stomatitis.

 Diagnosis

of stomatitis can be difficult. A patient's history may disclose a dietary deficiency, a systemic disease, or contact with materials causing an allergic reaction. A physical examination is done to evaluate the oral lesions and other skin problems.

 Blood

tests may be done to determine if any infection is present. Scrapings of the lining of the mouth may be sent to the laboratory for microscopic evaluation, or cultures of the mouth may be done to determine if an infectious agent may be the cause of the problem.

 The

treatment of stomatitis is based on the problem causing it. Local cleansing and good oral hygiene are fundamental. Sharp-edged foods such as peanuts, and potato chips should be avoided. A soft toothbrush should be used, and the teeth and gums should be brushed carefully.

 Local

factors, such as ill-fitting dental appliances or sharp teeth, can be corrected by a dentist. An infectious cause can usually be treated with medication. Systemic problems, such as AIDS, leukemia, and anemia are treated by the appropriate medicine.

 Minor

mouth burns from hot beverages or hot foods will usually resolve on their own in a week or so. Chronic problems with aphthous stomatitis are treated by first correcting any vitamin B12, iron, or folate deficiencies.

 If

those therapies are unsuccessful, medication can be prescribed which can be applied to each aphthous ulcer with a cotton-tipped applicator. This therapy is successful with a limited number of patients. More recently, low-power treatment with a carbon dioxide laser has been found to relieve the discomfort of recurrent aphthae.

 Major

outbreaks of aphthous stomatitis can be treated with tetracycline antibiotics or corticosteroids. Valacyclovir has been shown to be effective in treating stomatitis caused by herpesviruses.

 Patients

may also be given topical anesthetics (usually a 2% lidocaine gel) to relieve pain and a protective paste (Orabase) or a coating agent to protect eroded areas from further irritation from dentures, braces, or teeth.

 Alternate

treatment of stomatitis mainly involves prevention of the problem. Patients wth such dental appliances as dentures should visit their dentist on a regular basis. Patients with systemic diseases or chronic medical problems need to ask their health care provider what types of oral problems they can expect from their particular disease.

 Botanical

medicine can assist in resolving stomatitis. One herb, calendula (Calendula officinalis), in tincture form (an alcoholbased herbal extract) and diluted for a mouth rinse, can be quite effective in treating aphthous stomatitis and other manifestations of stomatitis.

 More

recently, a group of researchers in Brazil have reported that an extract made from the leaves of Trichilia glabra, a plant found in South America, is effective in killing several viruses that cause stomatitis.

Colder

Dry Imb:.

Internal Use:. Afternoon (D)

:Gargles:.

Mazo(3g), Anar(3g), Simaq(3g), Dharia(3g), 120 ml water .

Hot

& Dry Imbalance:.

Powder for external Use: Katta safaid, dana ela (3gm), ichi Khurd(3g), Kabab chini(3gm), Tabashir (3gm).

For Internal Use:.

Arqe. Gaozaban, luabe behidea, Shira-eUnnab, Sharbat-e-Nelofer, if constipation occurs add Gulqand in add of Sh. Nelofer.

 The

prognosis for the resolution of stomatitis is based on the cause of the problem. Many local factors can be modified, treated, or avoided. Infectious causes of stomatitis can usually be managed with medication, or, if the problem is being caused by a certain drug, by changing the offending agent.

 Stomatitis

caused by local irritants can be prevented by good oral hygiene, regular dental checkups, and good dietary habits. Problems with stomatitis caused by systemic disease can be minimized by good oral hygiene and closely following the medical therapy prescribed by the patient's health care provider.

 33

yo male admitted for throat pain, fever. Patient developed a vesiculopapular rash, fever as high as 103F, and thick coating on tongue, and penile ulcers following one week history of fevers and sore throat. Physical exam- Crusted lesions over face and neck,3 mm tender lesion on upper lip, tongue-tender, thick white coating with 2 erythematous areas on tip, numerous white lesions across uvula, hard and soft palate, Neck- No lymphadenopathy ESR- 44

 Diffuse,

filmy grayish surface with white streaks, wrinkles, or milky alteration Symmetric, usually involving the buccal mucosa, lesser extent labial mucosa Normal variation; present in the majority of black adults, and half of black children At rest, opaque appearance. When stretched dissipates

 Clinically

defined white patch or plaque that has been excluded from other disease entities Presence of dysplasia, carcinoma in situ, and invasive carcinoma from all sites 17-25% (Bouqot and Gorlin 1986) Etiology- associated with tobacco (smoking, smokeless tobacco), areca nut/betel preparations

 May

be macular, slightly elevated, ulcerative, erosive, speckled, nodular, or verrucous Clinical shift in appearance from homogenous to heterogenous, speckled, or nodular, a rebiopsy is mandatory Correlation between increasing levels of dysplasia and increases in regional heterogeneity or speckled quality

 Uncommon

variant of leukoplakia Multifocal, occurring more in women, and in those without the usual risk factors Evolution from a thin, flat white patch to leathery, then papillary to verrucous Development of squamous cell CA in over 70% of cases

 Risk

of dysplasia/carcinoma higher with floor of mouth, ventrolateral tongue, retromolar trigone, soft palate than with other oral sites

Trial of cessation of offending agent, follow-up Guided by microscopic characterization Benign, minimally dysplastic- periodic observation or elective excision Complete excision can be performed with scalpel excision, laser ablation, electrocautery, or cryoablation Chemoprevention

Asymptomatic, seen with systemic immunosuppression EBV Lateral tongue bilaterally; subtle white keratotic vertical streaks to thick corrugated ridges Diagnosis by microscopy and in situ hybridization Management includes establishing diagnosis and treating immunosuppression

 0.2%-

2% population affected Usually asymptomatic, reticular from, white striaform symmetric lesions in the buccal mucosa T-cell lymphocytic reaction to antigenic components in the surface epithelial layer Other variants: plaque, atrophic/erythematous, erosive

 Small

risk of squamous cell carcinoma, more likely seen in the atrophic or erosive types Studies show that dysplasia with lichenoid features have significant degree of alleic loss. Recommendation is to remove these lesions/follow patient closely

 Opportunistic

infection, Candida albicans Pseudomembranous (thrush), erythematous, atrophic, hyperplastic Risk factors: Local- topical steroids, xerostomia, heavy smoking, denture appliances. Systemic- Poorly controlled diabetes mellitus, immunosuppression

 Symptoms:

burning, dysgeusia, sensitivity, generalized discomfort Angular cheilitis, coinfection with staph may be present Acutely- atrophic red patches or white curdlike surface colonies Chronic- denture related form confined to area of appliance

 Confirmation

with KOH smear, tissue PAS or

silver stains Treatment- topical or systemic, polyene,azoles

Acute Chronic Recurrent

Bacterial Acute necrotizing ulcerative gingivostomatitis Poor oral hygiene, Punched-out ulcer at interdental papillae, seen in young adults with poor nutrition, heavy smoking Streptococcal gingivostomatitis B hemolytic strep, bright red gingivae Oral tuberculosis Gonococcal stomatitis

Syphilis Congenital syphilis- Hutchinsons incisors, moons molars Primary-painless, indurated, ulcerated, usually involving the lips, tongue Secondary- mucous patches, split papules Tertiary- Gummas, can involve palate, tongue Fungal Oral Candidiasis Histoplasmosis- disseminated form, oropharyngeal lesions may present as ulcerative, nodular, or vegetative. Biopsy will provide the diagnosis

Viral Infections Herpes simplex- 600,000 new cases annually, prodrome followed by small vesicles that ulcerate, primary infection involves the gingiva, and can involve the entire oral cavity Recurrent herpes simplex- prodrome present, herpes labialis, limited to keratinized epithelium and can involve the gingiva and hard palate Varicella zoster virus- distribution of trigeminal nerve Coxsackie- prodrome, vesicular, pharynx,tonsils, soft palate

 Erythema

multiforme Mucocutaneous hypersensitivity reaction Etiology- infectious (strong association with HHV-1, viral, mycoplasma), drugs (antiseizure medications, sulfonamides) Clinically- target lesions develop over the skin with erythematous periphery and central area that can develop bullae, vesicles.

Clinically- Oral mucosa and lips demonstrate aphthous like ulcers and occasionally vesicles or bullae may be present. Gingiva rarely involved; common sites include labial mucosa, palate, tongue, and buccal mucosa Mucosal ulcers are irregular in size and shape, tender and covered with fibrinous exudate Sialorrhea, pain, odynophagia, dysathria Severe EM are associated with involvement of other mucosal sites- eyes, genitalia, and less common esophagus and lungs

 Histopathology-

Intense lymphocytic infiltration in a perivascular distribution and edema from submucosa into the lamina propria, epithelium lack antibodies, blood vessels contain fibrin, C3, IgM Treatment- with oral involvement only can treat symptomatically/short course of corticosteroids

Lupus erythematosus- chronic discoid and systemic lupus erythematosus (SLE) forms Discoid type- lip, intraoral lesions, most common site is buccal mucosa; central depressed, red atrophic area surrounded by slightly, raised keratotic border SLE form- common site posterior hard palate, superficial ulcerations that vary in size without keratinization of the oral mucosa Immunofluorescence shows staining of the basement membrane with immunoglobulin, and complement

 Reiters

Syndrome- mainly young men 20 to 30. Classis triad of conjunctivitis, arthritis, and urethritis. Oral lesions range from erythema to papules to ulcerations involving the buccal mucosa, gingiva, and lips. Lesions on the tongue resemble geographic tongue Behcets Syndrome- recurrent oral and genital ulcers, athritis, and inflammatory disease of eyes and GI tract.

 Drug

reactions Barbiturates, salicylates, phenolphthalein, quinine, digitalis, griseofulvin, and dilantin

 Pemphigus

vulgaris- 0.1 to 0.5 patients/100,000; 70% present with upper aerodigestive lesions Desmoglein 3 is the pemphigus antigen IgG, IgA Deposition of antibodies in the intracellular spaces produces direct damage to the desmosomes

Clinical presentation- ulceration and pain with collapse of vesicles Lesions extend from gingival margin to alveolar margin Oropharyngeal lesions favor lateral aspects of soft palate to lateral pharyngeal wall Lesions heal quickly without scarring Treatment- immunosuppression with steroids supplemented with azathioprine 5% mortality with immunosuppression

 Mucous

Membrane (Cicatricial) Pemphigoid Autoantibodies directed at molecular components of the basement membrane Most common Head and Neck sitesoral, followed by ocular, nasal, and nasopharynx sites Ocular scarring- symblepharon, corneal opacification, entropion

 Diagnosis

is with immunofluorescence showing linear immune deposits along the basement membrane Site directed therapy. Oral cavity- topical vs. systemic steroids.

Traumatic (Eosinophilic) Granulomaself-limiting, relatively long duration, deep mucosal injury, origin unknown Clinical presentation- 5th to 7th decade, painful rapid onset, 1 to 2 cm in diameter with crater center and firm periphery that is white in appearance Pathology- deep ulceration extending into skeletal muscle, intense, diffuse inflammatory infiltrate of histiocytes, endothelial cells, and eosinophils Treatment- observation, topical or intralesional corticosteroids, excision if clinical presentation in question

 Recurrent

aphthous stomatitis (RAS) Frequency range of 20-40% of population, most common non-traumatic form of oral ulceration Data indicates a greater prevalence among those in professional groups, higher socioeconomic status, and non-smokers

Seen in a variety of conditions Crohns disease, Behcets syndrome, gluten-sensitive enteropathy, food hypersensitivity (nuts, spices, chocolate) Certain medications- NSAIDS, B-blockers, K+channel blockers Sweets syndrome- acute febrile neutrophilic dermatosis PFAPA- Periodic fever, aphthous ulcers, pharyngitis, and adenitis Familial variety

 Pathogenesis-

No sign of vesicle or blistering

formation Lesions over non-keratinizing mucosal surfaces (labial, buccal, ventral, and lateral tongue, floor of mouth, soft palate, tonsillar pillars)

ClassificationMinor <1.0cm, comprise 85% of all ulcers usually anterior portion of oral cavity, ulcerative episode 7 to 10 days, no scarring Major > 1.0 cm deeper, more painful, posterior aspect of oral cavity, 6 weeks or longer in immunocompromised Herpetiform- multiple pinhead-sized, pain greater than size of lesion Treatment- symptomatic, topical steroids, for larger lesions intralesional steroids. Severe- short term systemic steroids.

 Prodrome
Rash

present, major aphthous ulcers, genital findings No eye findings No prior history

 Must

rule out dysplasia, squamous cell carcinoma with leukoplakia Duration of lesion, as well as location help to narrow your differential diagnosis Biopsy of persistent lesions can help guide management

 Cohen,

Lawrence. Ulcerative Lesions of the Oral Cavity. International Journal of Dermatology Sept 1980, 362-373. Sciubba, James. Oral Mucosal Lesions. Cummings Otolaryngology Head and Neck Surgery. Philadelphia, 2005, 144891.