 Extends from the lips to the

oropharyngeal isthmus

 The oropharyngeal isthmus:

 Is the junction of mouth
and pharynx.
 Is bounded:
 Above by the soft palate
and the palatoglossal folds
 Below by the dorsum of the
tongue
 Subdivided into Vestibule &
Oral cavity proper
 Slitlike space between the cheeks
and the gums

 Communicates with the exterior

through the oral fissure

 When the jaws are closed,

communicates with the oral cavity
proper behind the 3rd molar tooth on
each side

 Superiorly and inferiorly limited by

the reflection of mucous membrane
from lips and cheek onto the gums
 The lateral wall of the
vestibule is formed by the
cheek

 The cheek is composed of

Buccinator muscle, covered
laterally by the skin &
medially by the mucous
membrane

 A small papilla on the mucosa

opposite the upper 2nd molar
tooth marks the opening of the
duct of the parotid gland
 It is the cavity within the
alveolar margins of the maxillae
and the mandible

 Its Roof is formed by the hard

palate anteriorly and the soft
palate posteriorly
hard
 Its Floor is formed by the
mylohyoid muscle. The anterior soft palate
2/3rd of the tongue lies on the
floor.

mylohyoid
 Covered with mucous membrane

 In the midline, a mucosal fold,

the frenulum, connects the
tongue to the floor of the mouth

 On each side of frenulum a small

papilla has the opening of the
duct of the submandibular gland

 A rounded ridge extending

backward & laterally from the
papilla is produced by the
sublingual gland
o Sensory
 Roof: by greater palatine and nasopalatine nerves
(branches of maxillary nerve)
 Floor: by lingual nerve (branch of mandibular nerve)
 Cheek: by buccal nerve (branch of mandibular nerve)

o Motor
 Muscle in the cheek (buccinator) and the lip
(orbicularis oris) are supplied by the branches of the
facial nerve
 Leukoplakia
 Erythroplakia
 Oral submucous fibrosis
 Oral candidiasis
 Sideropenic dysphagia (Paterson-Kelly Syndrome)
 Oral lichen planus
 Oral leukoplakia is defined by the WHO as “a white patch
or plaque that cannot be characterized clinically or
pathologically as any other disease”.

 Thus a diagnosis by exclusion.

 The term is strictly a CLINICAL one and does not imply a

specific histopathologic tissue alteration.

 The clinical color (white) results from a thickened surface

keratin layer (which appears white when wet) or a
thickened spinous layer, which masks the normal
vascularity (redness) of the underlying connective tissue.
 Leukoplakia occurs most often in middle-aged and older
men and arises most frequently on the buccal mucosa,
alveolar mucosa, and lower lip.

 Overall, the malignant transformation potential of

leukoplakia is 4 % (estimated lifetime risk).

 However, specific clinical subtypes are associated with

much high potential malignant transformation rates (as
high as 47 %).
1. Tobacco chewing or smoking
2. Alcohol
3. Local irritations
4. Vitamin deficiency : Vit A and Vit B
5. Endocrine disturbances
6. Candidiasis
7. Syphilis
 More common in men than women
 Common above 4o years of age
Common Site: It can be found anywhere in oral cavity
1. Buccal mucosa and Alveolar mucosa
2. Tongue
3. Lower lip
4. Hard and soft palate
5. Floor of the mouth
6. Gingiva
 Proper history
 Prevention of the cause
 Surgical excision of the small lesion
 In females: supplementation of Oestrogen
 Topical chemotherapy and radiation
 These are red patches found in the oral cavity
 Erythroplakia not very common than Leukoplakia
 There is no sex difference
 Occurs in 6th and 7th decades of life

Etiology:
1. Smoking: Pipe smokers
2. Trauma
3. Dental irritation

Common Site:
 Buccal muosa,soft palate,Floor of the mouth,Retromolar
area,Tongue,Mandibular mucosa and sulcus
1.Homogenous form:
 Which appears as a bright red, soft, velvety lesions and
quite extensive in size
 Site: Commonly found in buccal mucosa and soft palate

2. Speckled erythroplakia:
 These are soft, red lesions, slightly elevated with an
irregular outline
 Surface being granular—These are often referred to as
speckled leukoplakia/erythroplakia
Common Site: Anywhere in the oral cavity
3.Erythroplakia interspersed with patches of
Leukoplakia:

 Inthis erythematous patches are not as

bright as the homogenous form
Common Site: Tongue and floor of the mouth
 This is due to fibroelastic change of oral mucosa with
epithelial atrophy leading to stiffness of oral mucosa and
causing trismus and inability to eat.

Etiology :
 Chewing bettel nut, Panmasala
 Vitamin B deficiency
 Protein deficiency
 Most common between 20-40 years of age, but can occur in any
decades of life

 The disease is characterized by burning sensation of mouth particularly

when eating spicy foods.

 This is accompanied by the formation of the vesicles, ulceration or

recurrent stomatitis with excessive salivation or xerostomia

 Ultimately the patient develops stiffing of certain area of the oral

mucosa with difficult in opening the mouth and swallowing.

 The fibroelastic band eventually appear on mucosa usually involving

the buccal mucosa,soft palate,lips and tongue

 Treated with Local Hydrocortisone injection and Systemic

corticosteroids
 Investigations for all premalignant
lesions:Biopsy

 Treatment:Radiation therapy
1.Acute candidiasis:
 Acute pseudo membranous oral candidiasis
 Acute atrophic oral candidiasis

2.Chronic candidiasis
 Chronic hyperplastic oral candidiasis—Resembles
leukoplakia
 Chronic atrophic oral candidiasis—found in dentures sore
mouth
 Chronic mucocutaneous oral candidiasis
 Involment of skin,scalp,nail and mucous
membrane
Types:
1.Chronic familial muco-cutaneous candidiasis
 It is an inheritant disorders occurs before the
age of 5 years
 There is equal sex distribution
 Oral lesions occurs in children
2.Chronic localised mucocutaneous candidiasis:
 This also occurs earlier in life but no genetic
transmission
 There is widespread involvement of face and
scalp,mouth is the primary site
3.Candidiasis endocrinopathy syndrome:
 It is genetically transmitted candidiasis and
infection of the skin scalp, nails and mucous
membrane classically in the oral cavity
 Seen in
Hypothyroidism,Hypoparathyroidism,Diabetes
mellitus
4. chronic diffuse mucocutaneous candidiasis:
 It has late onset over 55 years of age
 It is the least common form
 There is no family history and usually no
abnormality
Treatment:
 Fluconazole tablets
 Amphotericin B
 Nystatin Suspension
 This is an uncommon condition characterized by an iron-
deficiency anemia with an associated glossitis and
dysphagia.

 It is of significance because of its association with a high

frequency of oral and esophageal squamous cell
carcinoma.

 Sideropenic dysphagia
 This syndrome is most common in females between the
ages of 30 and 50 years.

 It is more common in patients of Scandinavian and

northern European background.

 Patients complain of a burning tongue/mouth.

 Smooth red tongue are often presenting features.

 koilonychia and brittle nail.

 The symptoms of anemia such as fatigue, shortness of

breath and weakness often lead the patient to seek
medical care.
 Hematologic studies show a hypochromic, microcytic
anemia consistent with iron-deficiency anemia.

 Biopsy of the oral mucosa reveals epithelial atrophy with

submucosal inflammation.

 In advanced case one may see epithelial atypia, dysplasia,

carcinoma in situ or frank squamous cell carcinoma.
 Treatment centers on correcting the iron-deficiency
anemia and if this is successful, the glossodynia and
esophageal symptoms improve.

 Patients should be evaluated periodically for oral,

pharyngeal and esophageal cancer.

 The frequency of malignancy in these patients has ranged

from 5 to 50 %.
 A chronic inflammatory disease that causes
bilateral papules, striations or plaques

 May cause erythema, erosions and blisters

 Found on buccal mucosa, tongue and gingiva

 Female:Male ratio: 1.4:1

 Predominantly seen in adults over 40 years.

 Oral Lichen planus is a purely T cell mediated
inflammatory response.

 keratinocyte apoptosis in OLP – cause unknown

 No microorganism
 Three common types
 Reticular
 Erosive

 Plaque

Variants of Plaque and Erosive types

Atrophic
Bullous

 Histopathology
Picture 1: Plaque-like OLP Picture 2: Reticular OLP

Picture 3: Erosive OLP Picture 4: Reticular OLP

 No treatment for OLP is curative
 Goal:
 Reduce painful symptoms
 Resolution of oral mucosal lesions
 Reduce risk of oral squamous cell carcinoma
 Improve oral hygiene
 Eliminate exacerbating factors
 Repair defective restorations or prosthesis
 Remove offending material causing allergy
 Diet
 Eliminate smoking and alcohol consumption
 Eat fresh fruit and vegetables (but avoid tomatoes and nuts)
 Reduce Stress
 Medication

 Topical corticosteroids

 Systemic Steroid Therapy

 Inflammation of lining of mouth

 Caused : by injury,
mechanically
chemically
thermal
radiotherapy
idiopathic
malnutrition
 Caused by: hard tooth brush,
ill-fitting denatures
jagged teeth
simple cuts & bruns

 Pain
 Movement restricted
 Increase salivation

 Remove causative factor

 mouth wash with NS
 Generalized debilitating disease

 Solitary or multiple aphthous ulcer

 Vesicle with hyperaemic base

Break to form small white circular ulcer
Painfull

 T/t oral hygiene rinse with Listerin or NS solution

 Send C/S -antibiotic if culture positive

 Infant first few week of life

 People debilitating disease

 Prolong antibiotic therapy

 Diabetics

 Fungus candida albicans

 Spots small red patches turn white (desquamated epithelium)

 Painful excessive salivation

 T/t oral hygiene glycerine nystatin

 Cracks or superficial ulcer at corner of mouth

 Children rub & lick corner of mouth

 Over closure of mouth

 Dribbling saliva corner of mouth

 Inflammed red brown fissures at corner of mouth

 Vitamin B,C & iron supplement