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

 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.

 Congenital Conditions
 Inflammatory lesions/Traumatic condition
 Autoimmune diseases
 Precancerous lesions(Leukoplakia &
erythroplakia)
 Benign Tumors of Oral Cavity
• Solid Tumours
• Cystic Lesions


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 infection
2. Fungal infection
3. 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-red""beefy-red"
tonguestongues of certain deficiency states (e.g.; vitamin(e.g.; vitamin
B12, and iron, deficiencies).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

○ Information
 Primary infection is chicken pox; secondary infection is
shingles
 Spread by respiratory droplets and less commonly by
direct contact
 Incubation time is 2 weeks
○ Primary infection
 Fever, headaches, malaise, and a rash
 Rash
- 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

○ Basics
Candida species part of normal oral flora – 40-65% of
patients
Infections 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

○ Treatment
Mild, acute forms – topical Nystatin
Mild, chronic – topical Nystatin + Clotrimazole
troches
Refractory 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

 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 diameter
Located on freely mobile oral mucosa
Appears as a well-delineated white lesion
with an erythematous halo
Prodrome of burning or tingling in area
prior to ulcer’s appearance
Resolve 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

 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

◦ 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.

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.

Common Benign Oral cavity disorders by. Dr.vijay kumar

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Common Benign Oral cavity disorders by. Dr.vijay kumar

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