Common Benign Oral cavity disorders by. Dr.vijay kumar

Oral cavity

◦ Lips◦ Tongue◦ Floor of Mouth◦ Buccal mucosa◦ Palate◦ Retromolar

trigone

Lesion is a broad term for abnormal tissues in the oral cavity that includes wounds, sores, and any other tissue damage caused by injury or disease.

Determining the type of lesion in a disease is one of the earliest steps in formulating a differential diagnosis.

Types of lesions of the oral mucosa are classified as to whether they:• Extend below or above the surface. • Are flat or raised on the surface.

Ulcer: A defect or break in continuity of the mucosa (epithelium) that creates a punched-out area similar to a crater.

Erosion: A shallow defect in the mucosa caused by mechanical trauma.

Abscess: A localized collection of pus in a circumscribed area.

Cyst: A closed sac or pouch that is lined with epithelium and contains fluid or semisolid material.

Blisters: Also known as vesicles, lesions filled with a watery fluid.

Pustule: Similar in appearance to a blister, but contains pus.

Hematoma: Also similar to a blister, but it contains blood.

Plaque: Any patch or flat area that is slightly raised from the surface.

Congenital Conditions Inflammatory lesions/Traumatic condition Autoimmune diseases Precancerous lesions(Leukoplakia &

erythroplakia) Benign Tumors of Oral Cavity

• Solid Tumours • Cystic Lesions

Miscellaneous lesions of tongue and oral cavity

Torus : Torus palatinus and torus mandibularis represent developmental anomalies ,present in the second decade of life and continue to grow slowly throughout life

Mucosally covered bony outgrowths of the palate and mandible

Occur in 3% to 56% of adults and are more common in women

Tori of the palate are found only in the midline of the hard palate.

Mandibular tori are found to involve only the lingual surface of the anterior mandible, primarily in the premolar region.

Tori are typically pedunculated or multilobulated, broadly based, smooth , bony masses , consist of dense lamellar bone with relatively small marrow spaces.

Usually asymptomatic , In symptomatic patients, the tori can be treated by removing them from the underlying cortex with osteotomes or cutting burs.

Recurrence is occasionally seen; malignant transformation has not been reported.

Lingual Thyroid: Due to lack of descent of thyroid tissue during development.

Approximately 90% of all ectopic thyroid tissue is associated with the dorsum of the tongue.

found in the midline in the area of foramen cecum. approximately 1/18,000 to 1/100,000 live births were

associated with ectopic thyroid tissue involving the tongue. usually asymptomatic, the presence of lingual thyroid can

be associated with hypothyroidism. Other symptoms are due to mass effect of lingual thyroid

and cause airway obstruction and/or difficulties with swallowing ,or the sensation of a lump in throat , dysphonia or bleeding.

Symptoms occur at times of increased metabolic demands such as growth spurts during adolescence or during pregnancy.

Malignant transformation is rare.

Treatment : hypothyroid patients –thyroid hormone replacement therapy, which may also reduce the size of the lingual thyroid .

for symptomatic euthyroid patients- surgical excision. different approaches for surgical excision of lingual thyroid include transcervical routes by means of lateral pharyngotomy or transhyoid pharyngotomy, as well as transoral excision with use of the CO2 laser.

postoperative exogenous thyroid hormone replacement therapy because approximately 70% of patients have lingual thyroid as the only functioning thyroid tissue.





Fibroma (fibroepithelial polyp):

Most common Found in1.2% of adults and has a 66% female

predilection. Can occur throughout the oral cavity Most common along the "bite line." usually solitary and seldom are larger than 1.5

cm. Asymptomatic, sessile or pedunculated, firm mass Microscopically: dense and minimally cellular

fascicles of collagen fibers and have a relatively avascular appearance.

Treatment -conservative excision,recurrence unlikely, unless the precipitating trauma is continued or repeated.

Pyogenic granulomas 12 % Due to acute or chronic

trauma or infection Highly vascular lesions

similar to granulation tissue. raised or pedunculated

lesions that remain less than 2.5 cm in size.

Histologically , Aggregation of multinucleated foreign body-like giant cells Separated by fibroangiomatous stroma.

Treatment- excision and removal of potential traumatic or infective factors

1. Viral infection2. Fungal infection3. Bacterial infection

Vincent’s angina

Inflammation of the mouth (Stomatitis)(Stomatitis) Inflammation of the Lips (Cheilitis)(Cheilitis) Inflammation of the soft tissues around teeth

typically resulting from inadequate oral hygiene (Gingivitis)(Gingivitis)

Inflammmation of the tongue (Glossitis).(Glossitis). GlossitisGlossitis more commonly applied to the "beefy-"beefy-

red" tonguesred" tongues of certain deficiency states (e.g.; (e.g.; vitamin B12, and iron, deficiencies).vitamin B12, and iron, deficiencies).

Herpetic Gingivostomatitis Primary infection Presentation

Multiple small vesicles involving many oral cavity sites

Vesicles rupture in 24 hours leaving ulcerations

Ulcerations typically heal over a 7-14 day course

Fever, arthralgia, malaise, headache, cervical lymphadenopathy

Greatest infectivity rate when vesicles rupture

Reactivation Phase Occurs in roughly 16-45% of patients with HSV Triggers: UV light, stress, infection, immunosuppresion Presentation

Vesicles typically erupt on mucocutaneous junction of lips, hard palate, and other attached gingiva Prodrome of tingling, itching, burning at site of lesion just prior to vesicular eruption Vesicles -> ulcers -> crusting in 7-14 days

Diagnosis Clinical picture Obtain fluid from unruptured vesicle as it is

most likely to contain virus PCR – much better than cultures Culture Smear – multinucleated giant cells

Serology ELISA testing for antibodies to HSV Western Blot – very accurate, but very

time consuming

Vesicles and Ulcerations

Gingivostomatitis Gingivostomatitis

Treatment Antipyretics, analgesics, hydration Valacyclovir and famciclovir inhibit

viral DNA polymerase – help to suppress and control symptoms, but does not cure (given for 1 week)

If catch in the prodrome - 5% acyclovir cream for 1 week has shown to shorten course or completely abort reactivation altogether

○ InformationPrimary infection is chicken pox; secondary

infection is shinglesSpread by respiratory droplets and less commonly

by direct contact Incubation time is 2 weeks

○ Primary infectionFever, headaches, malaise, and a rashRash- Vesicles -> Pustules -> Rupture (ulcers) -> Crust- Oral cavity involvement typically involves buccal

mucosa and hard palate – resembles aphthous ulcers in oral cavity

- Lasts 7-10 days

Secondary infection (Shingles) Rare in the immunocompetent Presentation

Prodrome of burning or pain over dermatome

Maculopapular rash develops -> vesicles form -> pustules -> ulcerations -> crust

Oral lesions typically occur after skin involvement

Treatment Supportive Severe forms can be treated with Valacyclovir or acyclovir

○ BasicsCandida species part of normal oral flora – 40-

65% of patientsInfections typically the result of

immunocomprimised state, oral trauma, or recent antibiotic use; rare in healthy individuals

90% of HIV patients typical affected○ Forms

Pseudomembranous candidiasis (Thrush)- Most common form- Whitish plaque that can be scrapped off to reveal a “beefy” red base or ulceration that is tender to palpation

Thrush Angular Chelitis

Atrophic Candidiasis

○ TreatmentMild, acute forms – topical NystatinMild, chronic – topical Nystatin +

Clotrimazole trochesRefractory or immunocomprimised

WITHOUT systemic involvement – add oral Fluconazole

Severe forms – IV Amphotericin B with or without Fluconazole

○ KEY TO DIAGNOSIS: Clinical + KOH Prep; culture and serum (1,3)β-D-glucan detection assay if unclear

Erythematous Candidiasis

Caused by Borellia vincenti and fusiform bacilli

Both are normal inhabitants of oral cavity

Decreased resistance (inadequate nutrition, immunofeciency) is a predisposing factor to infection

Punched out erosions → ulceration → spreads → invovles all gingival margin, which become covered by a necrotic pseudomembrane





Lupus Erythematosus 40-50 cases per 100,000 people Two main types

Discoid –skin + oral cavity WITHOUT visceral involvement

Systemic – skin, oral, and visceral involvement

Both can present with oral lesions DLE – 25% of cases SLE – 40% of cases

Oral manifestations Erythematous plaques or erosions that can

evolve into ulcerations White keratotic striae radiating from lesion

margins Areas of involvement: buccal mucosa,

gingiva, labial mucosa, and vermillion border

Diagnosis: clinic appearance, immunofluorescence test of antibody-antigen complex, ANA, SS-A/SS-B antibodies, anti-dsDNA antibody

Treatment Oral lesions typically do not need to be

treated. However, topical corticosteroids can improve lesions

corticosteroids with or without cytotoxic agents (cyclophosphamide and azathioprine)

Methotrexate

• Rare – reported as affecting less than 200,000 people in the United States

Bullous pemphigoid Antibodies directed at the epithelial basement

membrane illicit an inflammatory response Lesions appear as vesicles that can then rupture to form

open ulcerations Oral involvement- 40%, self limiting Skin involvement first and then oral involvement Diagnosis: biopsy and immunofluorescence showing IgG

and C3 in a linear fashion along basement membrane Treatment

Systemic steroids with or without cytotoxic agents Topical steroids improve lesions IV immunoglobulin when patients are resistant to

steroid and cytotoxic treatment

Cicatricial pemphigoid - Oral involvement occurs in 85% of cases, and can be the only presentation

Pemphigus vulgaris Most common presentation of pemphigoid in

the United States Antibodies directed at intercellular bridges –

leads to separation of cells in the epithelial layer with formation of very thin walled bullae

Lesions occur in oral cavity first and then skin becomes involved

Lesions appear as ulcerations with a grey membranous covering

Nikolsky sign – scrapping the mucosa around the lesion results in slothing of the mucosa

Diagnosis Biopsy shows “tombstone” appearance

with Tzanck cells (free squamous cells forming a spherical shape)

Direct immunofluorescence shows IgG against cell-cell adhesion junctions

Treatment Typically requires high doses of systemic

steroids + cytotoxic agents Plasmapheresis has been utilized with

good results

◦Theory:: Vasculitis secondary to a hypersensitivity reaction to HSV and/or

streptococcal antigen◦ Incidence in Asian/Middle Eastern countries -

1/10,000◦ M: F 20:1◦ Aphthous ulcerations are the most common oral

presentation◦ Other symptoms: recurrent genital lesions, eye

lesions (uveitis, retinal vasculitis), skin lesions (erythema nodosum), polyarthritis, meningioencephalitis

◦Treatment Tetracycline solution Topical steroids for both oral and genital lesions Systemic steroids have been shown to improve

acute symptoms, but do not slow progression or prevent recurrence

T cells destroy basal cell layer of epidermis Hepatitis C 5 P’s of cutaneous lesions

Purple, Pruritic, Planer, Polygonal, Papules Oral involvement in 70% of cases Oral lesion appearance

Reticular – white striae on buccal mucosa that does not scrape off

Plaque – resemble leukoplakia, and typically located on dorsum of tongue or buccal mucosa

Bullous – rare form, appear as bullae that rupture leaving areas of ulceration

Erosive – very painful, erythematous erosions with fibrous covering

Malignancy arising from lesions in 1-5% of cases Cutaneous lesions typically resolve in 6 months,

but oral lesions tend to last longer, up to 5 years Diagnosis: Clinical, biopsy of lesions with HPE and

DIF examtn

Treatment Oral treatment

Topical steroids Cyclosporine mouth wash for 4-8 weeks

improves oral disease Severe disease – systemic steroids

Lichen planus

White plaques

whitish linear lesions in lacy patternwhitish linear lesions in lacy pattern

Most common cause of non-traumatic ulcerations of the oral cavity Etiology unknown 10-20% of general population Classifications

Minor aphthous ulcer< 1cm in diameterLocated on freely mobile oral mucosaAppears as a well-delineated white lesion with an erythematous haloProdrome of burning or tingling in area prior to ulcer’s appearanceResolve in 7-10 days, never scar.

Sutton disease or periadenitis mucosa necrotica recurren.

> 1cm in diameter Involves freely mobile mucosa, tongue, and palate

Last much longer – 6 weeks or more

Typically scar upon healing

Aphtha = Whitish spot

Treatment : topical application of steroids Cauterisation with 10% silver nitrate Severe cases: 250 mg of tetracycline

dissolved in 50 ml of water is given as mouth rinse and then to be swallowed, four times a day.

Local pain can be relieved with lignocaine viscous.





◦ Any ulceration that fails to heal in 1-2 weeks should be biopsied

Leukoplakia Whitish plaque that cannot be

scrapped off 5-20% malignant potential Microscopic examination reveals

hyperkeratosis and atypia

Aetiologic factors include smoking, tobacco chewing, alcohol abuse particularly, if combined with smoking

chronic trauma: due to ill-fitting dentures or cheek bites

Sites : Buccal mucosa and oral commissures are the most common sites, also involves floor of mouth, tongue, gingivobuccal sulcus and the mucosal surface of lip.

Buccal mucosa is the most common site in india. Lesions on lateral tongue, lower lip, and floor of

mouth more likely to progress to malignancy

Leukoplakia usually shows hyperkeratosis with or without dysplasia (20% show dysplasia)

white colour change is the sign of hyperkeratosis

Clinical Types:

Homogeneous: non-palpable, faintly translucent white discoloration

non-homogeneous: ◦ verrucous or nodular◦ speckled: hyperkeratotic white areas and

red areas◦ errosive: fissuring and ulcer formation

Management: Many of the lesions will disappear

spontaneously if causative agent is removed.

In lesions with higher potential for malignant change, a biopsy is taken to rule out malignancy.

In suspicious small lesions, surgical excision or ablation with laser or cryotherapy can be done.

Erythroplakia Red patch or macule with soft, velvety

texture Much higher chance of malignancy =

60-90% Biopsy is mandatory Treatment is surgical excision or laser

ablation

Erythroplakia

◦ Inflammation of mucus membranes caused by chemotherapy and/or radiation therapy

◦ Incidence – 30-40% of patients receiving chemotherapy or radation

◦ Drug induced - 5-10 days of starting therapy◦ Radiation induced - 2nd week of therapy◦ Intense pain, trismus, oral bleeding

◦ Disease course lasts 2-3 weeks◦ Treatment

Good oral hygiene Rinses with dilute hydrogen peroxide.

Prevent/Eradicate infection Fluoride rinses for bacterial infection Nystatin rinses or Oral Fluconazole for

candidal infection Maintain moisture – petroleum jelly, mineral oil Pain control

Topical lidocaine Sulcralfate – coats, protects, and decreases

pain Systemic pain medications





Squamous cell papilloma

Associated with HPV-6 and HPV-11 virus subtypes.

Single, asymptomatic, soft, pedunculated mass with numerous finger-like projections at the surface. Histologically, the projections have fibrovascular cores and demonstrate a relatively narrow base.

Treatment -surgical excision or ablation with use of a CO2 laser.

Granular cell tumors

Neural in origin. Usually diagnosed in third decade of life. Found throughout the body, more than half of all cases

occur in the oral cavity. Site - dorsum of the tongue , soft palate, uvula, and

labial mucosa Typically present as firm, painless, relatively immobile,

sessile, nodular-appearing lesions less than 1.5 cm in greatest dimension.

Histologically -large polygonal, oval, or bipolar cells with abundant granular eosinophilic cytoplasm. Cells often appear in a ribbon pattern and extend to the surface epithelium and demonstrate pseudoepitheliomatous hyperplasia.

Treatment -Surgical excision. Recurrence is less than 10%, even with a microscopically positive margin

Hemangioma Hemangioma of the oral cavity represents 14% of all

hemangiomas. Present at birth with a rapid proliferative phase. May be associated with a number of conditions including Sturge-

Weber-Dimitri syndrome and von Hippel-Lindau syndrome. Lip is the most frequent site of hemangioma involving the oral

cavity. Present as a soft, painless mass that is red or blue , typically less

than 2 cm in greatest dimension Can become quite extensive to involve significant portions of the

oral cavity and oropharynx to include the tongue. Hemangiomas tend to spontaneously regress over the years.

Those limit the form and function of the oral cavity and oropharynx are usually treated with conservative surgical excision.

Intralesional sclerosing agents, interferons, laser treatment, local and systemic steroids, and radiation have been reported as primary or adjunctive treatment with varying success.

Cavernous hemangioma

Ameloblastoma Odontogenic origin can present as tumors or tumor-like

conditions of the oral cavity Most common neoplasm of odontogenic origin. Thought to arise from rests of primitive dental lamina related to

the enamel organ in alveolar bone. Typically seen in the third decade of life with a painless mass

involving the mandible (molar/ramus area) or maxilla. Histologically - solid infiltrating tumors with a follicular or

plexiform pattern, which exhibit an element of cystic change. Treatment - En bloc resection with at least 1cm margins of normal-appearing tissue.

Overall recurrence rate is 22% Malignant transformation can occur but is rare

Pleomorphic Adenoma Minor salivary glands are

unencapsulated seromucinous glands located immediately beneath the mucosa throughout the oral cavity and oropharynx.

Less than 10% of salivary gland tumors arise from minor salivary glands.

Approximately 40% of tumors arising from minor salivary glands are benign.

Pleomorphic adenoma is the most frequently encountered benign tumor of minor salivary glands.

Other benign minor salivary gland tumors include canalicular adenoma, papillary cystadenoma, oncocytoma, and myoepithelioma

Treatment - complete surgical excision.





Mucocele Most common site -

lower lip. It is a retention cyst

of minor salivary glands of the lip.

The lesion appears as a soft and cystic mass of bluish colour.

Treatment is surgical excision.

Ranula Cystic translucent lesion seen in the floor of

mouth on one side of the frenulum and pushing the tongue up.

Arises from the sublingual salivary gland due to obstruction of its ducts.

Some ranulae extend into the neck (plunging type).

Treatment - complete surgical excision if small, or marsupialisation, if large.

Often it is not possible to excise the ranula completely because of its thin wall or ramifications in various tissue planes.

Median rhomboid glossitis It is red rhomboid area, devoid of papillae, seen

on the dorsum of tongue in front of foramen caecum.

It is developmental anomaly that occurs due to persistence of tuberculum impar, which fails to invaginate.

Recent studies reveal this condition to be due to chronic candida infection. The condition is asymptomatic and no treatment is necessary.

Geographical tongue Characterised by

erythematous areas, devoid of papillae, surrounded by an irregular keratotic white outline.

The lesions keep changing their shape and hence the condition is also called "migratory glossitis".

The condition is asymptomatic and may not require any treatment.

Hairy tongue

Due to excessive formation of keratin, the filiform papillae on the dorsum of the tongue become elongated.

They get coloured, brown or black, due to chromogenic bacteria and look like hair. Smoking seems to be one of the factors.

Treatment consists of scraping the lesions with a tongue cleaner, application of half-strength hydrogen peroxide and improving the general nutritional status of the patient by vitamins.

Ankyloglossia (Tongue tie)

True tongue tie which produces symptoms is uncommon.

If tongue can be protruded beyond the lower incisors, it is unlikely to cause speech defects.

Treatment -Transverse release and vertical closure. Thin mucosal folds can be simply incised.

Oral submucous fibrosis (OSF) is a chronic insidious process characterised by juxta-epithelial deposition of fibrous tissue in the oral cavity and pharynx.

The condition was first described in India by Joshi in 1953. Aetiology 1. Socio-economic status. In India poor socio-economic status

has been associated with higher risk of precancerous lesions like leukoplakia, erythroplakia and submucous fibrosis. This is related to education, diet, life-style and access to medical care.

2. Tobacco chewing. It is a major risk factor in submucous fibrosis.

3. Areca nuts. Areca nuts are chewed alone, with tobacco or in the form of pan (containing lime, catechu and other ingredients on a betel leaf).

4. Alcohol. It is observed that drinking increases the risk of OSF by 2-fold.

5. Nutritional. Deficiency of vitamins and micronutrients has been suggested.

6. Immune process. OSF is considered a cell-mediated immune reaction to arecoline in areca nuts. It may also reflect a localized collagen disorder or an autoimmune process in the oral cavity.

7. Multifactorial. Several factors may operate together in the causation of OSF. Habit of betel-nut chewing, drinking or smoking tobacco coupled with dietary deficiencies may have synergistic effect.

Pathology-The basic change is fibroelastotic transformation of connective tissues in lamina propria associated with epithelial atrophy.

It is a premalignant condition and malignant transformation has been seen in 3-7.6% of cases.

Symptoms : 1. Intolerance to chillies and spicy food. 2. Soreness of mouth with constant burning sensation; worsened during meals particularly of pungent spicy

type. 3. Repeated vesicular eruption on the palate and pillars. 4. Difficulty to open the mouth fully. 5. Difficulty to protrude the tongue.

Treatment Medical. 1. Steroids: Topical injection of steroids into the affected

area is more effective than their systemic use with fewer side effects. Dexamethasone 4 mg (1 ml) combined with hyalrunidase, 1500 I.U. in one ml is injected into the affected area biweekly for 8-10 weeks.

2. Avoid irritant factors, e.g. areca nuts, pan, tobacco, pungent foods, etc.

3. Treat existent anaemia or vitamin deficiencies. 4. Encourage jaw opening exercises.

Surgical It is indicated in advanced cases to relieve trismus. 1. Simple release of fibrosis and skin grafting. There is high

recurrence rate due to graft contracture. 2. Bilateral tongue flaps. Requires flap division at a second

stage.

3. Nasolabial flaps. They are small to cover the defect completely, cause facial scar and require division of flaps at second stage.

4. Island palatal mucoperiosteal flap. It is based on greater palatine artery. Possible only in selected cases. Requires extraction of 2nd molar for the flap to sit without tension. Not suitable for bilateral cases.

5. Bilateral radial forearm free flap. It is bulky and hair-bearing. May require debulking procedure, 3rd molar may require extraction.

6. Surgical excision and buccal fat pad graft. 7. Superficial temporal fascia flap and split skin graft. 8. Coronoidectomy and temporal muscle myotomy.

THANK YOU

Health & Medicine

Common Benign Oral cavity disorders by. Dr.vijay kumar