OESOPHAGUS

i) Anatomy and Physiology of Oesophagus

Anatomy:
• It is a fibromuscular tube, about 25 cm long in an adult.
• It extends from the lower end of pharynx (C6) to the cardiac end of stomach
(T11)
• It shows 4 normal constrictions. They are:

1. At pharyngo-oesophageal junction or cricopharyngeal junction (C6)—15

cm from the upper incisors.
2. At crossing of arch of aorta (T4) —22.5 cm from upper incisors
3. At crossing of left main bronchus (T5)—27 cm from upper incisors.
4. Where it pierces the diaphragm (T10)—40 cm from upper incisors.
• The wall of oesophagus consists of four layers.
• From within outwards, they are:
(a) Mucosa: which is lined by stratified squamous epithelium
(b) Submucosa: which connects mucosa to muscular layer.
(c) Muscular layer: which has inner circular and outer longitudinal fibres.
• Circular fibres at the lower end are thickened to form a cardiac sphincter.
• The upper third of oesophagus has striated, lower third has smooth, and
middle third has both striated and smooth muscle fibres
d) Fibrous layer: which forms loose covering of oesophagus.

Nerve supply:
• Vagus:- parasympathetic supply
• Intrinsic innervation by intramular myenteric and submucosal plexus:
i) Auerbach’s plexus (myenteric plexus):
• Lies between longitudinal and circular layers of muscular layer.
• Regulates contraction of outer muscle layers
ii) Meissner’s plexus (submucosal plexus):
Lymphatic drainage:
• The cervical, thoracic and abdominal parts drain respectively into deep cervical,
posterior mediastinal and gastric nodes.

Blood supply:
• Cervical oesophagus: by inferior thyroid artery of thyrocervical trunk
• Thoracic oesophagus: Segmentally from branches of descending aorta or by branches
of bronchial and oesophageal arteries
• Abdominal oesophagus: Left gastric and left inferior phrenic arteries.

Venous drainage:
• Cervical oesophagus: Inferior thyroid vein via brachiocephalic veins
• Thoracic oesophagus: azygos vein, hemiazygos and intercostal vein
• Abdominal oesophagus: left gastric vein

Physiology:
• The upper oesophageal sphincter starts at the upper border of oesophagus and is
about 3–5 cm in length and functions during the act of swallowing.
• The lower oesophageal sphincter is situated at lower portion of oesophagus. It is also
Physiology of swallowing:
act of swallowing is divided into three phases:
i) Oral or buccal phase: food which is placed in the mouth is chewed, lubricated with
saliva, converted into a bolus and then propelled into pharynx by elevation of the
tongue against the palate
ii) Pharyngeal phase: It is initiated when bolus of food comes into contact with
pharyngeal mucosa.
The communications into nasopharynx, oral cavity and larynx are cut off.
a) Closure of nasopharynx:
• Soft palate contracts against the Passavant’s ridge on the posterior pharyngeal wall
and completely cuts off the nasopharynx from the oropharynx.
b) Closure of oropharyngeal isthmus:
• The entry of food back into oral cavity is prevented by contraction of tongue against
the palate and sphincteric action of palatoglossal muscles.
c) Closure of larynx:
• Aspiration into the larynx is prevented by temporary cessation of respiration, closure
of laryngeal inlet by contraction of aryepiglottic folds, closure of false and true cords,
and rising of larynx under the base of tongue.
d) Contraction of pharyngeal muscles and relaxation of cricopharyngeus:
• Relaxation of cricopharyngeus muscles is so timed and synchronous that food passes
from pharynx into the oesophagus during contraction of pharyngeal muscles
iii) Oesophageal phase:
• After food enters oesophagus, cricopharyngeal sphincter closes
and peristaltic movements of oesophagus take the bolus down the
stomach.
• Gastro-oesophageal sphincter at the lower end of oesophagus
relaxes well before peristaltic wave reaches and permits fluids to
pass.
• Bolus of food is passed by contraction of peristaltic waves and then
the sphincter closes.

Regurgitation of food back from stomach into oesophagus is

prevented by:
(i) tone of gastro-oesophageal sphincter,
(ii) negative intrathoracic pressure,
(iii) pinch-cock effect of diaphragm,
(iv) mucosal folds,
ii) Disorders of Oesophagus

a) Perforation of oesophagus:
Perforation or rupture of oesophagus results from:
1. Instrumental trauma: i.e. oesophagoscopy or dilatation of strictures with bougies.
• The common site or rupture in these cases is just above the upper sphincter; sometimes it is
the lower oesophagus near the hiatus.

2. Spontaneous rupture: This usually follows vomiting and involves mostly lower third of
oesophagus. Post emetic rupture of all layers of oesophagus is called Boerhaave syndrome

NOTE:
Mallory Weiss tear: violent coughing or vomiting can tear the tissue of your lower esophagus and it can
start to bleed. Most often caused from violent coughing or vomiting. There will tear in the mucosal layer of
oesophaus. Common in alcoholic patient

Diagnosis:
i) features of cervical oesophageal rupture:
• pain, fever, difficulty to swallow and
• local tenderness, along with
• signs of surgical emphysema in the neck (swelling, crackling sound when pressing the swelling,
ii) features of thoracic oesophageal rupture:
• pain, referred to the interscapular region,
• fever 102–104 °F (39– 40 °C),
• signs of shock, surgical emphysema in the neck,
• crunching sound over the heart (Hamman’s sign, because of air in the
mediastinum) and
• pneumothorax.

X-rays of chest and neck:

• widening of mediastinum and retrovisceral space, surgical emphysema,
pneumothorax, pleural effusion or gas under the diaphragm.

Treatment:
• All oral feeds are stopped immediately.
• Nutrition is maintained through i.v. route.
• i.v. antibiotics
• Small perforation: conservative management
b) Corrosive burns of oesophagus:
Aetiology:
• Acids, alkalies or other chemicals may be swallowed accidentally in children or taken with
the purpose of suicide in adults.

Pathology:
Oesophageal burns run through three stages:
1. Stages of acute necrosis.
2. Stage of granulations: Slough separates leaving granulating ulcer.
3. Stage of stricture: Stricture formation begins at 2 weeks and continues for 2 months or
longer.

Management:
• Hospitalize the patient.
• Treat shock and acid-base imbalance by i.v. fluids and electrolytes. Monitor urine output
for renal failure.
• Relieve pain.
• Relieve airway obstruction: Tracheostomy may be required.
• Parenteral antibiotics
• Pass a nasogastric tube: It is useful to feed the patient and to maintain oesophageal
• Steroids should be started within 48–96 h and continued for 4–6 weeks to prevent
• Follow the patient with oesophagoscopy every 2 weeks, till healing is complete to look for
the development of any stricture.

• If stricture develops it can be treated by:

 Oesophagoscopy and prograde dilatations, if permeable.
 Gastrostomy and retrograde dilatation, if impermeable.
 Oesophageal reconstruction or by-pass, if dilatations are impossible.

c) Hiatus hernia:
• It is displacement of stomach into the chest through oesophageal opening of the
diaphragm.
• Most patients are elderly, past 40 years.

This disorder is of two types:

i) Sliding:
• Stomach is pushed into the thorax, in line with the oesophagus.
• Reflux oesophagitis is common and may give rise to ulceration and stenosis.
• Haematemesis may occur.
ii) Paraoesophageal:
• A part of stomach along with its peritoneal covering passes up into the
thorax by the side of oesophagus.
• The gastro-oesophageal junction still remains below the diaphragm and
the angle between oesophagus and stomach is maintained.
• There is no reflux oesophagitis in this type of hernia.
• The main symptom is dyspnoea on exertion due to position of stomach in
the thorax and sometimes bleeding.

Diagnosis:
Treatment:
• Mainly it is surgical; hernia is reduced and diaphragmatic opening
repaired.
• Early cases and those unfit for surgery may be treated conservatively to
reduce reflux oesophagitis by measures such as
(i) sleeping with head and chest raised,
(ii) avoidance of smoking,
(iii) use of drugs that reduce acidity (antacids and proton pump inhibitors),
(iv) reduction of obesity and
(v) attention to the causes which raises intra-abdominal pressure. Eg:
straining, forceful coughing

d) Plummer vinson (Patterson brown Kelly) syndrome:

• Classical features: dysphagia, iron-deficiency anaemia, glossitis, angular
stomatitis, koilonychia (spooning of nails) and achlorhydria.
• There is atrophy of mucous membrane of alimentary tract.
• Predominantly, it affects females past 40 years.
• About 10% of cases with this syndrome will develop postcricoid
carcinoma.
• It also predisposes to development of carcinoma in the tongue, buccal
mucosa, pharynx, oesophagus and stomach

Treatment:
• To correct anaemia by oral/parenteral iron.
• Associated B12 and B6 deficiency should also be corrected.
• Dilatation of webbed area by oesophageal bougies

e) Globus (Hystericus) pharyngeus

• Functional disorder where patient complains of “lump” in the throat.
• There is no true dysphagia.
• Such a patient may have fear of cancer in the throat.
• Clinical examination of pharynx, larynx and base of tongue is normal.
f) Motility disorders of oesophagus
They can be divided into:
1. Hypermotility disorder: e.g. cricopharyngeal spasm, diffuse
oesophageal spasm, nut cracker oesophagus.
2. Hypomotility disorders: e.g. cardiac achalasia, gastro-oesophageal
reflux, scleroderma, amyotrophic lateral sclerosis.

They may involve upper sphincter, lower sphincter or body of

oesophagus.

i) Cricopharyngeal spasm
• Is caused by failure of upper oesophageal sphincter to relax properly.
• There is incoordination between relaxation of upper oesophageal
sphincter and simultaneous contraction of pharynx.
• The common causes are cerebrovascular accidents, Parkinson’s
disease, bulbar polio, multiple sclerosis and muscular dystrophies.
ii) Diffuse oesophageal spasm
• It is characterized by strong non peristaltic contractions of body of
oesophagus while sphincteric relaxation is normal.
• Symptoms: dysphagia or odynophagia with substernal chest pain,
simulating angina pectoris.
• Barium swallow may show segmented oesophageal spasms giving a
rosary bead or a cork-screw type of oesophagus.
• Manometry shows normal relaxation of sphincter on swallowing.
Treatment:
• dilatation of lower oesophagus.
• Severe cases may require myotomy of oesophagus from arch of aorta
to lower sphincter

iii) Nut cracker oesophagus

• These are strong, high amplitude oesophageal contractions but
contractions remain peristaltic (compare diffuse oesophageal spasm
where contractions are nonperistaltic).
iv) Achalasia cardia
• It is characterized by absence of peristalsis in the body of
oesophagus and high resting pressure in lower
oesophageal sphincter which does not relax
during swallowing.

Symptoms:
• dysphagia, which is more to liquids than solids (reverse of that
seen in malignancy or strictures) and
regurgitation of swallowed food particularly at night.

Diagnosis by:
(i) radiography (barium swallow shows dilated oesophagus with narrowed rat tail lower
end), sometimes also called bird-beak appearance;
(ii) manometric studies (low pressure in the body of oesophagus and high pressure at lower
sphincter and failure of sphincter to relax);
(iii) endoscopy (to exclude benign stricture or any development of carcinoma which is a
common complication of this disorder.

Treatment of choice:
• modified Heller’s operation (myotomy of the narrowed lower portion of the oesophagus).
v) Gastro-oesophageal reflux
• It is due to decreased function of lower oesophageal sphincter thus permitting
regurgitation of gastric contents into oesophagus.
• Other causes of gastro-oesophageal reflux are:
pregnancy, hiatus hernia, scleroderma, excessive use of tobacco and alcohol, and
drugs that relax the smooth muscle (anticholinergic, beta-adrenergic drugs and
calcium-channel blockers).
Symptoms:
• substernal pain, heartburn and regurgitation

Treatment:
1. Elevation of head of bed at night.
2. Avoiding food at least 3 hr before bedtime.
3. Using Antacids.
4. Drugs that increase tone of lower oesophageal sphincter, e.g.
metoclopramide.
5. H2 receptor antagonists, e.g. cimetidine and ranitidine.
6. Avoiding smoking, alcohol, caffeine, chocolates, mints and carbonated drinks.
Complications of Gastro-oesophageal Reflux:
1. Oesophagus
• Oesophagitis, oesophageal mucosal erosion and haemorrhage.
• Benign oesophageal stricture.
• Barrett’s oesophagus (normal squamous epithelium of oesophagus is replaced by
columnar epithelium as a result of continuous inflammation). It is a precancerous
condition.

2. Lung
• Aspiration pneumonia. • Chronic cough.
• Asthma.
• Bronchiectasis.
3. Larynx
• Posterior laryngitis causing vague pain in throat, hoarseness and repeated throat
clearing.
• Pachydermia laryngis. • Contact ulcers and granulomas.
• Posterior glottic stenosis. • Paroxysmal laryngospasm.
• Carcinoma larynx.

4. Ear: • Otitis media with effusion.

vi) Scleroderma
• It is a systemic collagen disorder primarily neural, but secondarily
weakening smooth muscles of lower two thirds of oesophagus and lower
oesophageal sphincter.
• Dysphagia may precede cutaneous lesions.
• Barium swallow shows absence of peristalsis in distal two-thirds of
oesophagus.
• Many of these patients have hiatus hernia, or reflux oesophagitis and may
develop stricture in distal part of the oesophagus due to recurrent
inflammation.

vii) Schatzki’s ring:

• It occurs at the junction of squamous and columnar epithelium at lower
end of oesophagus and also called lower oesophageal ring.
• Usually seen in patients above 50 years of age.
• Cause is unknown.
• Symptoms: intermittent dysphagia, bolus obstruction. It may be associated
with hiatus hernia.
NEOPLASMS OF OESOPHAGUS
i) Benign neoplasms:
• Leiomyoma is the most common of all benign neoplasms. It arises from the
smooth muscle and grows in the wall of oesophagus.
• Mucosal polyps, lipomas, fibromas and haemangiomas are other benign tumour

ii) Carcinoma oesophagus

• Smoking and alcohol consumption are high-risk factors
• Squamous cell carcinoma is the most common (93%). Adenocarcinoma (3%)
and other are rare

DYSPHAGIA
• Dysphagia is difficulty in swallowing
• odynophagia is painful swallowing

Aetiology:
a) Oral phase: Trismus, fractures of mandible, tumours of upper or lower jaw and
disorders of temporomandibular joint, Paralysis of tongue, painful ulcers, tumours
b) Pharyngeal phase:
• Tumours of tonsil, soft palate, pharynx, base of tongue, supraglottic larynx, acute
tonsillitis, peritonsillar abscess, retro or parapharyngeal abscess, acute epiglottitis,
oedema larynx, tetanus, rabies.

c) Oesophageal phase:
• Obstruction to lumen: atresia, foreign body, strictures, benign or malignant
tumours
• Hypomotility disorders, e.g. achalasia, scleroderma
• Hypermotility disorders, e.g. cricopharyngeal spasm, diffuse oesophageal spasm

Investigations:
1) History:
a) Sudden onset: Foreign body or impaction of food on a pre-existing stricture or
malignancy, neurological disorders.
b) Progressive: Malignancy.
c) Intermittent: Spasms or spasmodic episodes over an organic lesion.
d) More to liquids: Paralytic lesions.
(e) More to solids and progressing even to liquids: Malignancy or stricture.
Note any associated symptoms, e.g.
• regurgitation and heart burn (hiatus hernia);
• regurgitation of undigested food while lying down, with cough at night
(hypopharyngeal diverticulum);
• aspiration into lungs (laryngeal paralysis);
• aspiration into the nose (palatal paralysis)

2. Clinical examinations:
• Examination of oral cavity, oropharynx, and larynx and hypopharynx can exclude most
of the pre-oesophageal causes of dysphagia.
• Examination of the neck, chest and nervous system, including cranial nerves should
also be undertaken

3. Blood examination:
• Haemogram is important in the diagnosis and treatment of Plummer–Vinson
syndrome and to know the nutritional status of the patient.

4. Radiography
(a) X-ray chest. To exclude cardiovascular, pulmonary and mediastinal diseases.
(b) Lateral view neck. To exclude cervical osteophytes and any soft tissue lesions of
c) Barium swallow: It is useful in the diagnosis of malignancy, cardiac
achalasia, strictures, diverticula, hiatus hernia or oesophageal spasms.

5. Manometric and PH studies:

• These studies help in motility disorders, gastro-oesophageal reflux
and to find whether oesophageal spasms are spontaneous or acid
induced.

6. Oesophagoscopy:
• It gives direct examination of oesophageal mucosa and permits
biopsy specimes. Flexible fibreoptic or rigid scopes can be used.

7. Other investigations:
• Bronchoscopy (for bronchial carcinoma),
• cardiac catheterization (for vascular anomalies),
• thyroid scan (for malignant thyroid) may be required, depending on
Foreign Bodies of Food Passage:
An ingested foreign body (FB) may lodge in:
1. tonsil: Sharp fish bone, needle in tonsillar crypts
2. base of tongue/vallecula: fish bone, needle
3. Posterior pharyngeal wall: A wire, a needle or a staple
4. Pyriform fossa: Fish bone, chicken or a mutton bone, needle or
a denture
5. Oesophagus: coin, piece of meat, chicken bone, denture, safety
pin or a marble

• Most of oesophageal foreign bodies lodge just below the

cricopharyngeal sphincter
• If they lodge lower down, an underlying condition such as
congenital or acquired stricture or a malignancy (in adults)
should be suspected and/or a follow-up barium swallow should
Aetiology:
1. Age: Children are most often affected. They have a tendency to put
anything in the mouth. Playing while eating is another factor. Education
of parents is important to prevent such accidents in toddlers and young
children.
2. Loss of protective mechanism: Loss of consciousness, epileptic seizures,
deep sleep or alcoholic intoxication.
3. Carelessness: Poorly prepared food, improper mastication, hasty eating
and drinking.
4. Narrowed oesophageal lumen: Pieces of food may be held up in cases of
oesophageal stricture or carcinoma.
5. Psychotics: Foreign body may be swallowed with an attempt to commit
suicide.

Site of lodgement of foreign body:

• commonest site is at or just below the cricopharyngeal sphincter.
• Foreign bodies which pass the sphincter can be held up at the next
narrowing at bronchoaortic constriction or at the cardiac end.
Clinical features:
Symptoms:
i) History: of initial choking or gagging
ii) Discomfort or pain in throat
iii) Dysphagia
iv) Drooling of saliva
v) Respiratory distress
vi) Substernal or epigastric pain

Signs:
vii) Tenderness in the lower part of neck on the right or left of trachea.
viii) Pooling of secretions in the pyriform fossa on indirect laryngoscopy. They
do not disappear on swallowing

Investigations:
• Posteroanterior and lateral views of neck and similar views of the chest
including abdomen are taken.
Management:
i) Endoscopic removal: using rigid and flexible scopes
ii) Cervical oesophagotomy: Impacted foreign bodies or those with sharp
hooks such as partial dentures located above thoracic inlet may require
removal through an incision in the neck and opening of cervical
oesophagus
iii) Transthoracic oesophagotomy: For impacted foreign bodies of thoracic
oesophagus, chest is opened at the appropriate level

Complications of oesophageal foreign body:

i) Respiratory obstruction: due to tracheal compression by foreign body in the
oesophagus, or laryngeal oedema especially in infants and children.
ii) Perioesophageal cellulitis and abscess: It occurs in the neck.
iii) Perforation: Sharp objects may perforate the oesophageal wall leading to
mediastinitis, pericarditis or empyema. They may perforate the aorta and
prove fatal.
iv) Tracheo-oesophageal fistula: Rare.
v) Ulceration and stricture: Overlooked foreign bodies may cause slow
ulceration and stricture formation.
DISC BATTERIES
• Ingestion of disc batteries is common because of their
widespread use in hearing aids, toys, calculators and other
electronic devices.
• They contain sodium hydroxide, potassium hydroxide and
mercury which leaks through them to cause oesophageal
injury.
• Prolonged disc battery at one place causes complications
like stricture, perforation, tracheo-oesophageal fistula,
mediastinitis and death.
• If lodged in stomach, a radiographic follow up is conducted
every 4–7 days and parents instructed to observe stools
daily for spontaneous passage.
ORAL CAVITY:
Anatomy:

• The oral cavity extends from lips to the oropharyngeal isthmus,

i.e. up to the level of anterior pillar of tonsils. It is divided into
the following sites:
1. Lips
2. Buccal or cheek mucosa
4. Retromolar trigone
5. Hard palate

6. Oral tongue: Only anterior two-thirds of tongue are included in the oral cavity.
• Posterior one-third or base of tongue is situated behind the circumvallate
papillae and forms part of the oropharynx.
• Oral tongue is divided into tip, lateral borders, dorsum and undersurface.

7. Floor of mouth:

Lymphatic drainage of oral cavity:

1. Lips:
• Lower: Medial portion of lower lip drains into submental and lateral portion to
submandibular nodes.
• Upper: Drain into preauricular, infraparotid and submandibular nodes.
2. Buccal mucosa: Submental and submandibular nodes
3. Upper and lower alveolar ridges: drains into submental and submandibular
nodes.
4. Hard palate: Upper deep cervical and lateral retropharyngeal nodes. Anterior
part of palate drains into submandibular nodes.

5. Floor of mouth: Anterior portion of floor of mouth drains into submandibular

nodes. Lymphatics from this area also cross the midline. Posterior portion drains
into upper deep cervical nodes.

6. Tongue: Tip of tongue drains into submental and jugulo-omohyoid nodes,

lateral portion drains into ipsilateral, submandibular and deep cervical nodes.
• Central portion and base drain into deep cervical nodes of both sides.

NOTE:
There are four types of papillae in
the tongue:
• Circumvallate (or vallate)
• Fungiform
• Filiform:- most common type,
does not contain taste bud
Common Disorders of Oral Cavity:
1) Ulcers of oral cavity:
a) Infection:
Viral
i) Herpangina:
• Coxsackie viral infection mostly affecting children.
• begins with multiple small vesicles appear on the faucial pillars, tonsils, soft palate and
uvula.
• They rupture to form ulcers which are usually 2-4 mm in size, have a yellow base and red
areola around them.

ii) Herpetic gingivostomatitis: Also known as orolabial herpes.

It is caused by herpes simplex virus and is of two types: primary and secondary
(a) The primary infection affects children and is characterized by clusters of multiple
vesicles which soon rupture to form ulcers.

(b) Secondary or recurrent herpes chiefly affects adults.

• It is milder in form as adults have some immunity to this virus.
• Most commonly, it involves vermilion border of lip (herpes labialis) but less often lesions
appear intraorally on the hard palate and gingiva.
• In recurrent herpes virus lies dormant in trigeminal ganglion and, when reactivated,
Treatment:
• is mostly symptomatic.
• Acyclovir, 200 mg, five times a day for 5 days helps to cut down the course of
recurrent herpes labialis.

Bacterial:
a) Vincent infection (acute necrotizing ulcerative gingivitis)
• It is similar to Vincent’s angina.
• Causative organisms are the same (a fusiform bacillus and a spirochaete
Borrelia vincentii).
• Clinical features: ulcers in oral cavity and necrotic slough.
• Similar ulcer and necrotic membrane may also form over the tonsil (Vincent’s
angina).
• Diagnosis is made by smear from the affected area.

Treatment:
• systemic antibiotics (penicillin or erythromycin and metronidazole),
• frequent mouth washes (with sodium bicarbonate solution) and
Fungal:
Moniliasis (candidiasis): caused by Candida albicans and occurs in
two forms:
i) Thrush:
• It appears as white grey patches on oral mucosa and tongue.
• When wiped off, they leave an erythematous mucosa.
• Can be treated by topical application of nystatin or clotrimazole

ii) Chronic hypertrophic candidiasis: Also called candidal leukoplakia.

• The lesion appears as white patch which cannot be wiped off and
usually requires excisional surgery

b) Immune disorders:
i) Behcet syndrome (oculo-oro-genital syndrome): has a triad of
aphthous-like ulcers in the oral cavity, genital ulcerations and uveitis
ii) Aphthus ulcer:
• recurrent and superficial, usually involving movable mucosa, i.e. inner surfaces
of lips, buccal mucosa, tongue, floor of mouth and soft palate, while sparing
mucosa of the hard palate and gingivae.
• In the minor form, which is more common, ulcers are 2-10 mm in size and
multiple with a central necrotic area and a red halo. They heal in about 2
weeks without leaving a scar.
• In the major form, ulcer is very big, 2-4 cm in size and heals with a scar but is
soon followed by another ulcer
• Aetiology of aphthous ulcers is unknown.
• It may be an autoimmune process, nutritional deficiency (vitamin B12, folic
acid and iron), viral or bacterial infection, food allergies or due to hormonal
changes or stress.

Treatment:
• topical application of steroids and
cauterization with 10% silver nitrate.
• In 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.
MISCELLANEOUS LESIONS OF TONGUE AND ORAL CAVITY
i) Ankyloglossia (tongue tie): Unable to protrude tongue completely.
ii) Fordyce spots: They are aberrant sebaceous glands present under the buccal or labial
mucosa and appears as yellowish or yellow-brown spots.

SUBMUCOUS FIBROSIS
• characterized by fibrosis in submucosal layers of oral cavity
Etiology
• Prolonged local irritation: Due to mechanical and chemical irritation caused by chewing betel
nut, areca nut, tobacco, etc
• Dietary deficiency: Vitamin A, Zinc and antioxidants.

Clinical Features:
• Most common in ages between 20 and 40 years.
• Intolerance to spicy food.
• Soreness of mouth with constant burning sensation.
• Redness and repeated vesicular eruptions on palate and pillars.
• Difficulty in opening mouth fully and protruding the tongue .

Blanching of mucosa over soft palate, facial pillars and buccal mucosa (three most common sites
Treatment
Medical
• Avoid irritant factors.
• Treat anemia and vitamin deficiencies.
• Topical injection of steroids combined with hyalase.

Surgical
• Indicated in advanced cases to relieve trismus.
• Includes release of fibrosis followed by skin grafting or use of flaps.

TUMORS OF ORAL CAVITY:

• Most common cancer of oral cavity in World: Ca tongue
• Most common type of oral cancer: Squamous cell carcinoma

Premalignant conditions: Conditions increasing risk:

• Leukoplakia (most common) Oral submucosa fibrosis
• Erythroplakia (maximum risk of Ca) Syphilitic glossitis
 Diseases Most common site
Most common site for:
Lip carcinoma Vermilion of lower lip
Tongue carcinoma Lateral border
Cheek carcinoma Angle of mouth
Larynx carcinoma Glottis
Nasopharynx carcinoma Fossa of rosenmuller
Ranula Floor of mouth beneath
the tongue
Epulis Root of teeth

DENTIGEROUS (FOLLICULA R CYST )

• cyst which envelops the whole or part of the crown of the uninterrupted
permanent tooth
• Most common site: mandibular 3rd molar tooth
• Most common type: Central type, i.e. cyst surrounds the crown of tooth
• Cyst lining: Non-keratinzing stratified squamous epithelium. The fluid
inside is cholesterol rich
SALIVARY GLAND:
Embryology:
• Major salivary glands develop from 6th to 8th weeks of gestation as outpouchings
of oral ectoderm into the surrounding mesenchyme.
• The parotid develops first, growing in a posterior direction as the facial nerve
advances anteriorly so that eventually, the parotid gland surrounds the facial nerve.
• After the parotid glands are formed, submandibular glands develop at 6 weeks and
sublingual glands at 8 weeks.
• The minor salivary glands arise from oral ectoderm and nasopharyngeal endoderm
• While the parotid is the first to develop, it is the last to become encapsulated,
after the lymphatics develop.
• This results in entrapment of lymphatics
deep to the capsule in the parenchyma
of gland. Salivary epithelial cells can be
included within these lymph nodes and
this may be important in the development
of Warthin’s tumours and lymphoepithelial
cysts within the parotid gland.
a) Parotid gland:
• Facial nerve divides gland into superficial and deep lobes comprising approximately
80% and 20% of the gland respectively.
• The nerve lies superficial to the retromandibular vein, which is in turn superficial to
the external carotid artery. The vein can be a useful radiological landmark for the
nerve.
• Parotid duct: Stensen duct

• Nerve suppy of parotid:

 Auriculotemporal nerve: secretomotor parasympathetic nerves are secretomotor,
sensory supply
 Vasomotor: Sympathetic nerve from plexus around middle meningeal artery

b) Submandibular gland:
• Submandibular duct: Wharton’s duct
• Submandibular duct lies between hypoglossal and lingual nerves.

c) Sublingual glands:
• most of the small excretory ducts (ducts of Rivinus) open directly on the summit of
the sublingual fold, but some may open into the submandibular duct itself
Physiology of salivary glands:
• Major salivary glands: Parotid, submandibular and submental
salivary gland
• there are 600–1000 minor salivary glands present in the
mucosal lining of the oral cavity and oropharynx.
• In general, saliva comprises 99.5% water, in addition to proteins,
glycoproteins and electrolytes.
• The saliva is high in potassium (7x that of plasma), low in
sodium (1 / 10 x that of plasma), calcium, phosphorous,
chloride, thiocyanate, and urea resulting in a pH of 5.6–7

Salivary flow:
• The average volume of saliva secreted from the major salivary
gland in a 24-hour period is 1–1.5 litres
• The basal salivary flow rate is 0.001–0.2 ml / minute / gland,
while the stimulated salivary flow rate increases to 0.18–1.7ml /
In an unstimulated state the contribution of measured
salivary gland is:
• submandibular gland: 69%
• parotid gland: 26%
• sublingual gland: 5%

In stimulated phase relative

contributions of major
salivary glands are:
• parotid gland: 69%
• submandibular gland: 26%
• sublingual gland: 5%.
Non-neoplastic Disorders of Salivary Glands
i) Mumps (viral parotitis):
• It is a viral infection caused by paramyxovirus.
• Disease is contracted by droplet infection and fomites.

Complications:
• Orchitis
• Ophritis
• Pancreatitis
• Aseptic meningitis or meningoencephalitis
• Unilateral sensorineural hearing loss
• Other complications include thyroiditis, myocarditis, nephritis and
arthritis.

Prevention:
• An infant has maternal immunity for 1 year.
• After that immunization can be given by MMR (Mumps, Measles, Rubella)
ii) Acute suppurative parotitis
• Staphylococcus aureus is the usual causative organism though
other Gram-positive and anaerobic organisms have also been
observed.

iii) Sialolithiasis (salivary gland stone)

• 80-90 % of calculi develop in whartons duct of submandibular
gland . Stensons duct of parotid constitutes 10-20 % and
sublingual only 1% .
• 80 % submandibular stones are radiopaque while parotid stones
are radiolucent.

iv) Mikulicz syndrome: there is generalized enlargement of all

major salivary glands including lacrimal glands.

v) Sjogren’s syndrome (Sicca syndrome): in which mikulicz

SALIVARY GLAND TUMORS
i) Pheomorphic adenoma (mixed tumor):
• Most common benign salivary gland tumor
• Most common tumor of major salivary gland
• Mixed tumour : because both epithelial and mesenchymal elements are seen
• Most common site: superficial lobe of parotid gland
• Encapsulated but sends pseudopods into surrounding glands (so enucleation is
not done as treatment)
• Malignant transformation occurs in 3-5% of cases
• Facial nerve infiltration indicates carcinomatous change

• Treatment: Superficial parotidectomy (Patey's operation)

Incision for parotid surgery: Blair’s incision, modified blair’s incision, lazy S incision

ii) Warthin tumour/ Adenolymphoma/Papillary cystadenoma lymphomatosum:

• occurs in Parotid gland exclusively
• Most common site: tail of parotid and and bilateral in 10%
• Common in males (5:1).
• Smoking is its risk factor
iii) Adenoid cystic carcinoma (Cylindroma
• Most common cancer of minor salivary gland followed by
adenocarcinoma and mucoepidermoid carcinoma
• Invades perineural space and lymphatics
• Most common head and neck cancer associated with perineural
invasion so it is painful tumour
• Unlike other salivary gland tumors it is more radiosenstive
Management: Radical parotidectomy followed by postoperative
radiotherapy if margins are positive

iv) Mucoepidermoid carcinoma

• Most common site: Parotid gland
• Most common malignant salivary gland tumor in children
• Most common malignant tumour of parotid
• Most common radiation induced neoplasm of salivary gland
v) Acinic cell adenocarcinoma:
• Most common site: Exclusively parotid gland affecting women mostly

Frey’s syndrome (Gustatory sweating):

• Frey’s syndrome arises as a complication of parotid surgery usually manifesting
several months after the operation.
• It is characterized by sweating and flushing of preauricular skin during
mastication causing social embarrassment.
• It is the result of aberrant innervation of sweat glands by parasympathetic
secretomotor fibres which used to suppy parotid.(cross innervation)
• Now instead of causing salivary secretion from the parotid, they cause
secretion from the sweat glands.

Treatment:
• reassurance
• tympanic neurectomy
• place a sheet of fascia lata between skin and underlying fat to prevent
secretomotor fibres reaching the sweat glands.
NOTE:
• Major salivary gland tumor are mostly benign:- pheomorphic adenoma
• Minor salivary gland tumor are mostly malignant.
• Most common malignant tumor of major salivary glands - Mucoepidermoid
carcinoma.
• Most common malignant tumor of minor salivary galnds - Adenoid cystic
carcinoma.
• Most common site of minor salivary glands tumor-Hard palate
• Malignancy varies inversely with the size of gland (90% o f minor salivary
gland tumor s are malignant).
• All salivary gland tumors are mostly present in parotid gland except adenoid
cystic carcinoma which is seen most commonly in minor salivary glands and
squamous cell carcinoma which is seen most commonly submandibular
gland.
• Most common Benign tumor/overall tumor of salivary glands in children is
hemangioma
• Most common malignant salivary gland tumor in children -
Mucoepidermoid
• Most common etiological agent for salivary gland tumor is
exposure to radiation
• Open surgical biopsy is contraindicated in salivary gland
tumors as it seeds the tumor to the surrounding tissue.
• Investigation of choice for salivary gland swellings - FNAC. as
MRI cannot distinguish between benign and malignant
lesions.
• Treatment is exicision not enucleation as tumor has
microscopic extensions outside the capsule.
• Majority of salivary gland tumors are radioresistant.
THANK YOU…..