6. HERPES SIMPLEX STOMATITIS
• HSV-1: Primary herpetic Gingivostomatitis
Recurrent herpes labialis
• HSV-2:
• Primary herpetic Gingivostomatitis:
-most frequent cause of acute stomatitis in
children
-varies in severity, many infections -
subclinical
-misdiagnosed as “teething”
-malaise, anorexia, irritability, fever, anterior
cervical lymphadenopathy, diffuse, purple,
boggy gingivitis
-multiple vesicles scarred ulcers(1-3mm)
-occasionally in adults
7. Diagnosis:
-clinically
-scrapping or smears from the lesion
-immunofluorescent staining
-exfoliative cytology- typical multinucleated
giant cells
Treatment:
-symptomatic
-acyclovir (systemic)-severe cases
8. Recurrent Intraoral Herpes Simplex Infection:
-may affect healthy individual
-persistent lesions in immunocompromised
-chronic ulcer, raised, white border
-esp. at sites of trauma
-acyclovir
9. HERPES ZOSTER (SHINGLES)
• Reactivation of Varicella –Zoster virus
• Predisposing factor:
Immunocompromised status
• One dermatome affected (trigeminal
nerve)
• Unilateral
• Ulcers in the distribution of dermatome
• Mandibular nerve: ulceration of one
side of tongue, floor of the mouth, lower
labial & buccal mucosa
• Maxillary nerve: one side of palate, the
upper gingiva, buccal sulcus
• Lesions persists for 2-3 wks
Lesions on lips and chin
10. • Herpes Zoster Oticus (Ramsay Hunt
Syndrome)
• Ophthalmic Herpes Zoster
• Post Herpetic Neuralgia
• Diagnosis: clinically
• Treatment:
-Analgesics
-Antivirals(within 72 hrs of onset of
the lesions):acyclovir, famciclovir,
valacyclovir, & gabapentin
11. HERPANGINA
Common in children
Coxsackie virus group A,
Enteroviruses(30 & 71)
Self limiting vesicular eruptions in the
oropharynx eg. soft palate, uvula,
tonsillar pillars, posterior pharyngeal
wall
Similar to herpes simplex except the
lesions more commonly in oropharynx
rather than oral cavity
Diagnosis: Clinically
Treatment: Supportive
12. HAND, FOOT AND MOUTH
DISEASE
Enterovirus 71,Coxsackie viruses, some
untypeable enteroviruses
Young children
Vesicular eruption in the oral cavity &
oropharynx dysphagia, dehydration
Vesicles on the hands & feet
Pyrexia, malaise, vomiting
Short lived(5-8 days)
Diagnosis: clinically
Treatment: supportive
22. PRIMARY SYPHILIS
• Lips, tongue, buccal mucosa, & tonsils
• Site of inoculation- 3 weeks after the
infection, Papule, breaks down to form
an ulcer (chancre)
• Oral chancre: painless ulcer with a
smooth surface, raised borders, &
indurated margin
• Non tender cervical lymphadenopathy
• Spontaneous healing
24. Hyperemia and inflammation of pharynx
& soft palate
Snail Track ulcer :-
-Oral cavity & oropharnyx
-Ulcerated lesion covered with
grayish white membrane
which when scraped has pink base
with no bleeding
25. SYPHILITIC
PHARYNGITIS
• May be congenital or acquired by
sexual intercourse
• Secondary stage most likely
• HIV positive patients
26. TERTIARY SYPHILIS
• Tertiary syphilis - after a period of 4–7 years
• Typically painless
• No lymphadenopathy unless secondary infection
• Gumma:
-Characteristic lesion
-Hard palate, Nasal septum, Tonsil, PPW, or
Larynx
• VDRL may be negative
27. CONGENITAL SYPHILIS
Early:
first 3 months of life, manifest as
snuffles nasal discharge purulent
Late:
Manifest at puberty
Gummatous lesion
• Oral lesions: high-arched palate, short
mandible, Hutchinson’s teeth, and
Moon’s or mulberry molars
28. Diagnosis:
1.Immunoflurorescence or dark field microscopy
2. Biopsy
3.Serology
Non-treponemal antibody tests:
-VDRL, RPR
-For screening and treatment follow up
Treponema specific antibody tests:
-FTA-ABS test, TPHA
-For confirmation
-Usually remains positive for life
Treatment: Penicillin( DOC)
Ceftriaxone, Erythromycin, or Doxycycline
29. LEPROSY
Mycobacterium Leprae
Optimum temperature growth-less than body
temp preference for skin, mucosa & superficial
nerve
Transmission- nasal discharge
Both Humoral & cellular immune response
Clinically- Chronic granulomatous disease skin,
peripheral nerve & nasal mucosa
40. SJOGREN’S SYNDROME
• Autoimmune
• Female
• Primary Sjogren’s Syndrome:
• Secondary Sjogren’s Syndrome:
associated with RA, SLE, Scleroderma,
Polymyositis, Polyarteritis Nodusa
• Presents with xerostomia & parotid
enlargement
• Oral findings:
-Due to decreased salivadysphagia,
disturbances in taste & speech, burning
pain of mouth & tongue, increased dental
caries, increased predisposition to
infection (candidiasis)
41. Mucosal changes: dry, red & wrinkled mucosa
Fissured tongue, atrophy of tongue papillae and
redness of tongue, cracked & ulcerated lips
Diagnosis:
-Minor salivary gland biopsy (mucosa of lower lip)
-Periductal lymphocytic infiltrate
-Serum: Autoantibodies (ANA, antilacrimal &
antithyroid antibodies, RA factor)
Treatment :
-Steroid & immunossuppresive drugs
-Artificial saliva
-Constant dental evaluation
42. SYSTEMIC LUPUS
ERYTHEMATOSUS(SLE)
Approx. one quarter of SLEoral
lesions
Oral lesions: superficial ulcers with
surrounding erythema
Lips & all oral mucosal surfaces
Periodontal diseases, xerostomia
43. SCLERODERMA
• Deposition of collagen in the tissues
or around nerves & vessels
• Difficulty in opening mouth(due to
fibrosis of masticatory muscles),
immobility of tongue, dysphagia,
xerostomia
• Telangiectasia: lips, oral mucosa
• Association with Sjogren’s
Syndrome & CREST
Syndrome(Calcinosis, Raynaud’s
phenomena, Esophageal
hypomotility, & Sclerodactly)
44. KAWASAKI DISEASE
• Mucocutaneous lymph node syndrome
• Vasculitis- medium & large arteries
• Children <5 yrs of age
• High grade fever
• Cardiovascular complications
• Oral findings: swelling of papillae on the
surface of tongue(strawberry tongue),
erythema of the buccal mucosa & lips
Lips are cracked, cherry red, swollen &
hemorrhagic
45. Laboratory tests: polymorphonuclear leukocytosis, thrombocytosis, raised
ESR & CRP
Diagnosis: 4 out of 6 clinical features with evidence of coronary dilatation
1.Fever persisting>5 days
2.Bilateral conjunctival congestion
3.Erythema of lips, buccal mucosa & tongue
4.Acute non-purulent cervical lymphadenopathy
5.Polymorphous exanthema
6.Erythema of palms & soles (edemadesquamation)
Treatment: Aspirin, IVIg
Steroid avoided- risk of worsening coronary artery dilatation
46. DERMATOMYOSITIS-POLYMYOSITIS
• Immunologic disease muscle
• Tongue & the upper portion of the
esophagus
• Clinical features:
-Difficulty in phonation, chewing &
deglutition
-Stomatitis
• Difficulty in swallowingaspiration
pneumonia
• Xerostomia & salivary hypofunction
(2* sjogren’s syndrome)
47. WEGENER’S GRANULOMATOSIS
• Rare chronic granulomatous disease
• Immunological
• Clinical features: necrotizing
granulomatous lesions of the
respiratory tract, generalized focal
necrotizing vasculitis, and
necrotizing glomerulitis
• Oral lesions: solitary or multiple
irregular ulcers, surrounded by an
inflammatory zone
• Tongue, palate, buccal mucosa &
gingiva
• Laboratory tests: HPE, c-ANCA
• Treatment: Steroids, Azathioprine,
& Cyclophosphamide
49. HEERFORDT SYNDROME
Uveoparotid Fever
Rare form of Sarcoidosis
Clinical features: B/L painless, firm,
parotid swelling, ocular
involvement(uveitis, conjunctivitis,
keratitis), facial paralysis, low grade fever,
sublingual & submandibular gland may
also enlarge
50. BEHCET’S SYNDROME
• Chronic, multisystemic inflammatory
disorder
• Triad of symptoms: Aphthous ulcers,
Genital ulcers & Ocular lesions (uveitis,
conjunctivits, keratitis)
• Etiology – unclear
• Immunogenetic basis
• Clinical features - common in males
• Onset -20–30 years age
51. Diagnostic criteria :
1. Recurrent oral ulcers (aphthae)
2. Recurrent genital ulcers
3. Ocular lesions (conjunctivitis, iritis
with hypopyon, uveitis, retinal
vasculitis, reduced visual acuity
4. Skin lesions (papules, pustules,
folliculitis, erythema nodosum,
ulcers, & rarely necrotic lesions)
5. Positive Pathergy test:
The test is called positive, when
the needle puncture causes a
sterile red nodule or pustule that is
greater than 2mm in diameter at
24 to 48 hours
52. • Diagnosis:
• For accurate diagnosis, recurrent oral
ulcers plus two of the four criteria must
be present
• Treatment:
• Mild cases- Topical steroid
• Severe cases- Systemic steroid, & other
immunosuppressive drugs (Ciclosporin,
Thalidomide, Colchicine, Dapsone)
53. RHEUMATOID ARTHRITIS
• Progressive destruction of articular &
periarticular structure eg. TMJ
• TMJ pathology: clicking, locking, crepitus,
tenderness in the preauricular area, pain during
mandibular movement
• Oral cavity involvement-not common
• Association with secondary Sjogren’s
Syndrome
• Immunosuppressive drugsacute stomatitis,
candidiasis, recurrent HSV infection
54. REITER’S SYNDROME
• Triggered by infectious agent in
genetically susceptible
• Young male (20-30 yrs)
• Characterized by conjunctivitis,
asymmetric lower extremity arthritis,
non-gonococcal urethritis, circinate
balanitis, keratoderma blennorrhagia
• Mnemonic : “can’t see, can’t pee,
can’t climb a tree”
• Oral lesions: papules & ulcerations on
the buccal mucosa, gingiva, palate, &
lips
• Lesions on the tongue mimic
geographical tongue
• Diagnosis: HPE
• Treatment: Systemic steroid, NSAID
60. PLUMMER VINSON SYNDROME
(PATTERSON-BROWN-KELLY
SYNDROME)
• Oral manifestations: Dysphagia, iron def.
anaemia, atrophic glossitis, angular
stomatitis, & koilonychia
• Female, in fourth decade
• Barium swallow: web in post-cricoid
region
• Pre-malignant Post-cricoid carcinoma
• Treatment:
-Esophageal dilatation
(if symptoms from web)
-Follow up-developing carcinoma
61. IDIOPATHIC THROMBOCYTOPENIC
PURPURA (ITP)
• Oral lesions may be the first
manifestation of this condition
• Petechiae, ecchymoses,
& haematoma anywhere on the
oral mucosa
• Spontaneous bleeding from the
gingiva
• Treatment:
-Systemic steroids, Splenectomy
63. CROHN’S DISEASE
Diffuse nodular swelling in lips
(painless), angular cheilitis,
cobblestone appearance of buccal
mucosa or mucosal tag, Aphthous ulcer
May precede intestinal symptoms or
may be the only manifestations in
some cases
Systemic steroids
64. ULCERATIVE COLITIS
Destructive oral ulceration due to
immune mediated vasculitis
Polystomatitis Vegetans: microabscess
on lips, palate, ventral tongue
May manifests as aphthous ulcers
Exacerbation & remission
77. Vitamin A deficiency:
-Dyskeratotic changes of the skin & mucous
membranes
-Angular cheilitis
-Defects in the dentin & enamel of developing teeth
Vitamin B2 (Riboflavin) deficiency:
-Angular cheilitis
-Burning pain in the lips, mouth, & tongue
Vitamin B3 (Niacin) deficiency (Pellagra):
-Dermatitis, dementia,& diarrhoea
-Oral manifestations: glossitis (red, swollen) &
stomatitis, burning tongue
78. • Vitamin B6 deficiency:
-Peripheral neuropathy
-Oral lesions-similar to pellagra
(i.e. glossitis & stomatitis)
• Vitamin C deficiency (Scurvy):
-Cofactor for collagen synthesis
-Weakened vessels are responsible for
petechiae, ecchymoses, delayed wound
healing
• Deficiency of Vitamin B12 & Folic acid:
-Megaloblastic anemia
-Oral findings: angular cheilitis, recurrent
aphthous ulcers, & glossitis
79. • Vitamin D deficiency & Calcium deficiency:
-Calcium metabolism
-Mandibular osteopenia/osteoporosis, enamel
hypoplasia
• Vitamin k deficiency:
-Haemorrhagic diathesis
-Oral haemorrhagic bullae
• Zinc deficiency:
-Taste changes
-Acrodermatitis Enteropathica: angular cheilitis,
ulcers, glossitis, crusting, scaling of the lips as well
as ulcers, erosions & fissures
80. ORAL LESIONS ASSOCIATED
WITH HIV
• Early recognition, diagnosis, & treatment of
HIV associated oral lesions - reduce
morbidity
• Oral lesions-
-Early diagnostic indicator of HIV infection
-Stage of HIV infection
-Predictor of the progression of HIV disease
83. HAIRY LEUKOPLAKIA
Epstein Barr virus
Common, characteristic lesion-HIV infection
White, asymptomatic, raised, corrugated,
unremovable patch on lateral marigns of tongue
The surface is irregular and may have prominent
folds or projections, sometimes markedly
resembling hairs
Lateral margins may spread to dorsum of tongue
Diagnosis: Biopsy
Treatment:
-Usually asymptomatic-Rx not required
-Antiviral(Aciclovir/valaciclovir)
84. KAPOSI’S SARCOMA
Most common malignancy in HIV (+Ve)
Human Herpes Virus-8(KSHV)
Derived from capillary endothelial cells
Occur intraorally, either alone or in a/w skin &
disseminated lesions (lymph nodes, salivary
gland)
Intraorally- hard palate, buccal mucosa, & gingiva
-bluish, purple or red patches or
papulesnodular, ulcerate & bleed
Diagnosis: Biopsy
Treatment:
-Low dose radiation & chemotherapy
(eg.Vinblastine)
-Surgical excision (eg.CO2 laser)
-Immunotherapy (Interferon)
85. NON-HODGKIN’S LYMPHOMA
• Etiology: Unknown, genetic &
environmental factors (viruses,
radiation)
• Clinical features:
• Both sexes - any age
• Lymph nodes involved
• Oral lesions - part of a
disseminated disease, or the only
sign
• Oral Lymphoma: diffuse, painless
swelling, which may or may not be
ulcerated -soft palate, the posterior
part of the tongue, the gingiva, & the
tonsillar area
• HPE & Immunohistochemical examn
• Treatment: Radiotherapy &
chemotherapy
86. • Junction between skin & mucosa
• Pink/brown in colour
• Vermilion border
• Fordyce’s granules
• Pits
• No swellings or indurations
NORMAL LIP
87. What you need to DO:
• History:
o Time first noticed
o Any changes in size, consistency, colour,…
o Any associated symptoms
o Any discharge
• Examination
o Determine whether it is diffuse or localized
o Determine it’s consistency
o Determine it’s colour
• Further investigations
1- SWELLINGS
88. What you need to KNOW
• Differential diagnoses …
• More you know a longer list of differential
diagnosis and better diagnosis
1- SWELLINGS
89. INTRODUCTION
• What is Cleft Lip and Palate?
• Congenital abnormal space or gap in the upper lip, alveolus and palate
90. INCIDENCE
• More common in south far Asians:
• 1 in 500
• Less frequent in Africans:
• 1 in 2000
• Prevalence in Europeans and Americans:
• 1 in 750
• *Prevalence in Pakistan:
• 1 in 523
*Elahi MM, Jackson IT, Elahi O, Khan AH, Mubarak F, Tariq GB, Mitra A. Epidemiology of
cleft lip and cleft palate in Pakistan. Otolaryngol Clin North Am. 2007 Feb; 40(1):27-60
91. INCIDENCE
• Boys are more affected than girls by 3:2
• Cleft Lip and Palate occur twice as often in boys as in girls
• Isolated Clefts of Palate are more often in girls
• 75% of Clefts are Unilateral, rest are Bilateral
• Left side is more involved than right side
92. CLASSIFICATION
• We classify as the follows:
• its combined (cl+cp) or isolated cleft(cl or cp)?
• is it unilateral or bilateral?
• is it complete (if it cross the nasal philtrum) or incomplete ( if it
doesn’t cross the nasal philtrum.
93. PRENATAL DIAGNOSIS
• Cleft lip can be easily diagnosed
by performing ultrasonography
in the second trimester
• Diagnosing a cleft palate with
ultrasonography is very difficult
• Three-dimensional imaging has
been introduced to prenatal
ultrasonography diagnostics of
cleft anomalies
94. DIAGNOSIS
• Advantages of Prenatal Diagnosis:
1. Time for parental education
2. Time for parental psychological preparation
3. Opportunity to investigate other associated
anomalies
4. Gives parents the choice of continuing the
pregnancy
5. Opportunity for fetal surgery
95. ETIOLOGY
• “Actually no one knows exactly what causes clefts”
• Multiple factors may be involved, like:
• Genetics (inherited characteristic) from one or both
parents .
• Environmental factors
• Drugs: corticosteroids (anti-inflammatory), phenytoin
(anticonvulsant), retinoid.
• Infections: like rubella during pregnancy.
• Alcohol consumption, smoking, hypoxia during
pregnancy, some of dietary and vitamins deficiencies (like
folic acid and vitamin A deficiency)
• Maternal Age
96. PROBLEMS ASSOCIATED WITH CLEFT LIP AND
PALATE
• Feeding
• Dental problems
• Nasal Deformity and Esthetic Problems
• Ear Problems
• Speech Difficulties
• Associated Anomalies
97. FEEDING DIFFICULTIES
• Cleft lip= makes it more difficult for an infant to
suck on a nipple
• Cleft Palate= may cause formula or breast milk to
be accidently taken up into the nasal cavity
• Inability to create negative pressure inside oral
cavity
• Frequent regurgitations
• Upper respiratory tract infections
98. NASAL DEFORMITY AND ESTHETIC PROBLEMS
• Facial Disfigurements
• Poor nasal shape
• Scar marks of surgeries
• Poor lip function during speech
• Poor dental alignment and smile
101. SCHEDULE OF TREATMENT
Birth:
Initial Assessment
Pre-surgical assessment
3 Month:
Primary Lip repair
9-18 month:
Palate Repair
2 Year:
Speech assessment
3-5 Year:
Lip Revision Surgery
8-9 Year:
Initial interventional Orthodontics
Preparation for alveolar bone grafting
10 Year:
Alveolar Bone Grafts
12-14 Year:
Definite Orthodontics
16 Year:
Nasal Revision Surgery
17-20 Year:
Orthognathic Surgery
102. MULTIDISCIPLINARY CLEFT LIP AND PALATE
TEAM
• Genetic Scientist
• Pediatrician
• Pedodontist
• Orthodontist
• Oral and Maxillofacial Surgeon
• Prosthodontist
• ENT Surgeon
• Plastic Surgeon
• Psychiatrist
• Speech Therapist
• Social Worker
103. FEEDING
• Cleft lip= makes it more difficult for an infant to suck on a nipple
• use special nipples to allow the baby to latch properly
(either pump or use formula)
• Cleft Palate= may cause formula or breast milk to be accidentally
taken up into the nasal cavity
• don’t feed baby without palatal obturator (prosthetic
palate)
• feed in an upright position to keep milk from coming out
of the nose
104. Mead Johnson/Enfamil Cleft Feeder Special Needs Feeder /
Haberman Feeder
Pigeon Feeder Dr. Brown’s Natural
Flow to relieve gas
106. RULE OF TEN
Primary repair- repaired at approximately 10 weeks
• The surgeon usually uses the “Rule of Ten”
• The child weighs 10 pounds
• The child has a hemoglobin of at least 10 grams
• The child has a white count of no higher than 10,000
• The child is at least 10 weeks of age
108. CLEFT PALATE REPAIR
FURLOW PALATOPLASTY
• Lengthens the soft palate
• Reconstructs the muscle sling.
• Also commonly used to correct velopharyngeal insufficiency in
patients with submucous cleft palate
• Speech outcomes are improved compared with other palatoplasty
techniques.
119. Exfoliative chelitis
WHITE LESIONS OF THE LIP
• Excessive production of keratin
• More common in females
• Associated with stress &
anxiety
• Some improve by antidepressant/tranquilizers
• Spontaneous remission
121. Causes:
• Allergic reaction to topical ointments/creams or lipstick
• Tooth paste
• Food
• Medication
Management:
• Detailed history to identify allergen confirmed by patch testing eliminate
• Topical steroid (short course)
ALLERGIC CHEILITIS
122. • Is a clinical entity with many
etiological factors
• Most common in females
• Could be allergic / idiopathic
• Some cases respond to long term
tetracycline others to topical steroid
(1% hydrocortisone)
*DO NOT USE MORE POTENT STEROID ON
FACE
PERIORAL DERMATITIS
123. • Mainly children are affected
• Might not be aware of the habit
• Heals by stopping the
licking
Management:
• Appliance can be used to interfere with tongue
LESIONS OF THE LIP
LICK ECZEMA
124. • Less common than angular cheilitis
• Common in OFG and Down’s patients
• Usually persist due to secondary infection (s.aurius or
candida)
• Management:
o Remove pathogen by topical antibacterial
/ antifungal
o Steroid ointment
• Usually it recure
LESIONS OF THE LIP
LIP FISSURES
125. Cheilocandidosis
LESIONS OF THE LIP
Causes:
1.Candidal infection affecting
unstable epithelium (Solar
irritation) in healthy individual
1.Associated with IO candida
Treatment:
Early treatment by antifungal
might lead to resolution
127. • History:
o Generalized ill health
o Xerogenic medication
o Antibiotics / steroid therapy
o Ill fitting denture / night wearing
• Examination
o Signs of anemia
o Salivary gland swelling (xerostomia / diabetes)
o Intraoral candidosis
o Oral dryness
o Signs of OFG
o Lymphadinopathy
o Ill fitting denture / reduced vertical dimension
HOW TO DETERMINE CAUSING
FACTOR?
128. • Special investigations
o Swab & smear
o Blood test (CBC, B12, ferritin, folate)
o Blood glucose
• when blood testing should by performed?
o If suspecting an underlying systemic factor
o If local therapeutic measures fail
HOW TO DETERMINE CAUSING
FACTOR?
132. • Only will consider lesions specific to the
tongue NOT ones which are presentation
of systemic conditions
• Mobile organ
• Specialized epithelial lining
• Rich in sensory nerve endings
THE TONGUE
135. GLOSSITIS
• Glossitis is inflammation of the tongue. It
causes the tongue to swell and change color.
Finger-like projections on the surface of the
tongue (papillae) may be lost, causing the
tongue to appear smooth.
136. CAUSES
• Bacterial or viral infections (including oral herpes simplex).
• Poor hydration and low saliva in the mouth may allow bacteria to grow more readily.
• Mechanical irritation or injury from burns, rough edges of teeth or dental appliances, or other
trauma
• Tongue piercing. Glossitis can be caused by the constant irritation by the ornament and by
colonization of Candida albicans in site and on the ornament.
• Exposure to irritants such as tobacco, alcohol, hot foods, or spices.
• Allergic reaction to toothpaste, mouthwash, breath fresheners, dyes in confectionery, plastic
in dentures or retainers, or certain blood-pressure medications (ACE inhibitors).
• Administration of ganglion blockers (e.g. Tubocurarine, Mecamylamine).
• Disorders such as iron deficiency anemia, pernicious anemia and other B-
vitamin deficiencies, oral lichen planus, erythema multiforme, aphthous ulcer, pemphigus
vulgaris,syphilis, and others.
• Occasionally, glossitis can be inherited.
• Albuterol (bronchodilator medicine)
137. SYMPTOMS
• Tongue swelling.
• Smooth appearance to the tongue due to pernicious anemia (vitamin B12 deficiency).
• Tongue color changes (usually dark "beefy" red).
• Sore and tender tongue.
• Difficulty with chewing, swallowing, or speaking.
138. TREATMENT
• Treatment usually does not require hospitalization unless tongue swelling is severe.
Good oral hygiene is necessary, including thorough tooth brushing at least twice a day, and
flossing at least daily.
• Corticosteroids such as prednisone may be given to reduce the inflammation of glossitis.
• For mild cases, topical applications (such as a prednisone mouth rinse that is not swallowed)
may be recommended to avoid the side effects of swallowed or injected corticosteroids.
• Antibiotics, antifungal medications, or other antimicrobials may be prescribed if the cause of
glossitis is an infection.
• Anemia and nutritional deficiencies (such as deficiencies in niacin, riboflavin, iron, or vitamin
E) must be treated, often by dietary changes or other supplements.
• Avoid irritants (such as hot or spicy foods, alcohol, and tobacco) to minimize the discomfort.
139. LEUKOPLAKIA
• Leukoplakia are patches on the tongue, in
the mouth, or on the inside of the cheek
that occur in response to long-term
irritation. Leukoplakia patches may also
develop on the outer female genitals.
140. CAUSES
• Irritation in the mouth may be caused by:
• Rough teeth
• Rough places on dentures, fillings, and crowns
• Smoking or other tobacco use (smoker's keratosis), especially pipes
• Holding chewing tobacco or snuff in your mouth for a long period of time.
• HPV, Candida albicans and possibly alcohol
SYMPTOMS
• Usually white or gray
• Sometimes red (called erythroplakia, a condition that can lead to cancer)
• Thick and slightly raised with a hard surface that can't be easily scraped off
141. TREATMENT
• Treat dental causes such as rough teeth, irregular denture surface, or fillings as soon as
possible.
• Stop smoking or using other tobacco products.
• Do not drink alcohol.
142. CARCINOMA ORAL TONGUE
• Involving 2/3rd of tongue
• Age of 50-70 years.
• SITE
• Middle of the lateral border or ventral
aspect
• CAUSE
• Pre-existing leukoplakia
• Longstanding dental ulcer or syphilitic
glossitis
143. CLINICAL PRESENTATION
• An exophytic lesion like a papilloma
• Non healing ulcer with rolled edges, greyish white shaggy base and induration
• SYMPTOMATOLOGY
• Early lesion are painless and asymptomatic for a longer time
• Pain at the site of ulcer
• Pain in ipsilateral ear due to common nerve supply of tongue(lingual nerve)
and ear (auriculo temporal) from the mandibular division of trigeminal nerve.
• Lump in mouth.
• Enlarge lymph node mass in the neck
• Dysphagia, difficulty to protrude the tongue, slurred speech and bleeding
from the mouth are late features
144. TREATMENT
• Aim of treatment is to treat primary tumour in the tongue, control neck disease(nodal
metastasis) and preserve function of the tongue.
145.
146.
147. HYPOGLOSSIA
• It is a short, incompletely
developed tongue.
• CAUSES - malformation, other
deformities, such as Hypodactylia,
Peromelia, micrognathia.
• SYMPTOMS – underdeveloped tongue,
feeding problems, breathing problems,
speech problems, swallowing problems,
missing teeth, tooth enemel defects.
• TREATMENT – speech therapy ,
orthodontic treatment
148. FISSURED TONGUE
• Also known as "scrotal tongue," "lingua
plicata," "Plicated tongue” "furrowed
tongue.
• Is a benign condition characterized by
deep grooves (fissures) in the dorsum of
the tongue. The condition is painless and
individuals experience no physical
discomfort.
• Fissured tongue is seen in Melkersson-
Rosenthal syndrome, in most patients
with Down syndrome, in association
with geographic tongue, and in healthy,
normal individuals.
149. GLOSSODYNIA
• Glossodynia refers to a painful or burning feeling of the
tongue.
• CAUSES
• Long-term irritations in the mouth
• Nerve damage from tooth extractions
• Trauma (injury)
• Dry mouth (xerostomia)
• Vitamin or mineral deficiencies (such as vitamin
B, iron or zinc)
• Allergies
• Changes in hormones or the immune system
• Tobacco use
• Psychological conditions such as anxiety or
depression
• Infections of the mouth, caused by bacteria or
fungus (thrush)
• Anemia
150. TREATMENT
Treatment depends upon the cause. Treatments may include:
1. Removal of irritants (rough edges on fillings, crowns or dentures)
2. Construction of a soft plastic tray to correct or cover irregular areas of the teeth
3. Pain relievers applied to the area
4. Microsurgery to repair the lingual nerve, if nerve damage is a cause
5. Low doses of benzodiazepine, antidepressant or anticonvulsant drugs
6. Changes in current medicines, which may be causing the pain
7. Supplements or diet changes for nutritional deficiencies
8. Antifungal medicines
151. MACROGLOSSIA
• Macroglossia is the medical term for
unusual enlargement (hypertrophy) of
the tongue. Severe enlargement of the
tongue can cause cosmetic and functional
difficulties including in speaking, eating,
swallowing and sleeping.
152. • CAUSE
• Amyloid Disorders
• Amyloidosis is an accumulation of insoluble proteins in tissues that impedes normal
function
• Hypothyroid Macroglossia
• Macroglossia is also a clinical feature in Hypothyroid disorders which include
• Overgrowth Disorders
• Acromegaly
• Chromosomal disorders
• Downs Syndrome
153. TONGUE- TIE (ANKYLOGLOSSIA)
• Ankyloglossia, commonly known as
tongue tie, is a congenital oral
anomaly which may decrease mobility of
the tongue tip and is caused by an
unusually short, thick lingual frenulum.
• there may be a V shaped notch at the tip.
154. • CAUSE
• congenital oral anomaly
• SYMPTOMS/EFFECT
• can affect feeding,
• speech, and
• oral hygiene
• as well as have mechanical/social effects.
• TREATMENT
• Physician education
• Parental education and reassurance
• Monitor for appropriate weight gain if exclusively breastfeeding
• Complete fusion requires surgery
155. HYPERKERATOSIS OF THE TONGUE
• Hyperkeratosis is a thickening of the outer
layer of the skin. This outer layer contains
a tough, protective protein called keratin
156. • CAUSE
• Chronic (long-lasting) inflammation
• Infection (HPV)
• Radiation
• Irritating chemicals
• SYMPTOMS
• Painless
• TREATMENT
• The treatment of hyperkeratosis depends on the type and possible cause.
• corticosteroid ointment or cream
• cryosurgery to remove a single actinic keratosis. Multiple keratoses can be treated with
skin peels, laser therapy or dermabrasion.
157. FIBROMA OF TONGUE
• Fibromas are over growths of soft tissue.
They appear as raised, relatively small
areas.
• SITE- the lips, inside the cheeks and on
the tongue.
• Fibromas are usually pink. They also can
be whitish or light-colored. If injured,
fibromas may be reddish or bluish
158. • CAUSE
• A habit of biting these areas
• Tooth grinding (bruxism)
• Rubbing from poorly fitting dentures or sharp areas on a tooth
• SYMPTOMS
• They are usually no symptoms. Fibromas may get bigger over time
• TREATMENT
• Surgery
159. TONGUE WARTS (PAPILLOMA)
• A Squamous cell papilloma is a
generally benign papilloma that arises
from the stratified squamous epithelium of
the skin, lip, oral cavity,
tongue, pharynx, larynx, esophagus, cervi
x, vagina or anal canal.
160. • CAUSE
• Squamous cell papillomas are a result of infection with human papillomavirus (HPV)
• SYMPTOMS
• Oral papillomas are usually painless, and not treated unless they interfere with eating or
are causing pain. They do not generally mutate to cancerous growths, nor do they
normally grow or spread. Oral papillomas are most usually a result of the infection with
types HPV-6 and HPV-11
• TREATMENT
• cryotherapy,
• application of a topical salicylic acid compound,
• surgical excision and
• laser ablation
161. RANULA
• A ranula is a type of mucocele found on
the floor of the mouth.
• Ranulas present as
a swelling of connective tissue consisting
of collected mucin from a ruptured salivary
gland duct.
• A large mucocele in the floor of the oral
cavity. It usually results from obstruction of
the ducts of the sublingual salivary glands.
Less often, it results from obstruction of
the ducts of the submandibular salivary
glands.
162. • CAUSE
• local trauma.
• SYMPTOMS
• Asymptomatic
• can fluctuate rapidly in size, shrinking and swelling
• interfere with swallowing
• swelling is not fixed and is non-painful unless it becomes secondarily infected.
• TREATMENT
• excision of both the gland and lesion
• Marsupialization in which the cyst is opened to create a pocket. The pocket will lie flat
and be unable to fill with fluid again. However, sometimes the opening of the pocket
heals over, allowing the cyst to develop again. In this case, the growth must be removed
along with the attached blocked gland to prevent reformation of the ranula.
163. LINGUAL THYROID
• In the first trimester of embryonic
development, the thyroid gland originates
in the back of the tongue and migrates to
the front of the neck. If it fails to migrate
properly, it can remain high in the neck or
even in back of the tongue. In rare
instances, the thyroid gland can also
migrate too far into the mediastinum; it is
then called a substernal thyroid.
• When migration fails and the gland
remains in the base of the tongue, it is
called lingual thyroid or ectopic lingual
thyroid
164. PATHOLOGY
• A lingual thyroid results from failure of the normal caudal migration of the thyroid
from foramen caecum down to its normal location anterior to the larynx and upper trachea.
Thyroid tissue may be found anywhere along the course of the thyroglossal duct, however
complete arrest with thyroid tissue located at the base of tongue is most common, and
represents 90% of all cases of ectopic thyroid 1-2. Microscopic deposits of thyroid tissue along
its route of descent have been identified in up to 10% of the population, representing small
amounts of tissue being 'left behind' during normal development 2.
• The thyroid tissue is normal histologically and functionally.
• Carcinoma of a lingual thyroid has been reported but is very rare, presumably no higher than
normal thyroid.
165. • CAUSE
• SYMPTOMS
• interfere with swallowing and breathing
• INVESTIGATION
• MRI
• Ultrasound
• absent thyroid tissue in the normal location thyroid tissue both at the tongue base
and elsewhere in the neck
• CT
• hyperdense soft tissue mass due to accumulation of iodine within the gland.
• TREATMENT
• surgical excision
166. • Differential diagnosis
• The differential of a posterior midline mass includes 3:
• lingual tonsil
• thyroglossal duct cyst
• malignancy
• haemangioma
• dermoid
167. PRE-MALIGNANT LESIONS
• Leukoplakia - chronic, white, verrucous plaque with
histologic atypia
• Severity linked to the duration and quantity of tobacco and
alcohol use
• Occur anywhere in the oral cavity
• Lip, tongue, or floor of the mouth lesions are prone for
progression to SCC
• Erythroplakia - non-inflammatory erythematous
plaque
• Analagous to intra-oral erythroplasia of Queyrat or SCC in situ
• Biopsies - severe dysplasia and areas of frank invasion
170. PRE-MALIGNANT LESIONS…
• Submucous fibrosis
• generalized white discoloration of oral mucosa with
progressive fibrosis, painful mucosal atrophy and
restrictive fibrotic bands
• individuals who chew betel quid, a concoction of
tobacco, lime, areca nut and betel leaves
• Ultimately leads to trismus, dysphagia and severe
xerostomia
• 5 - 10 % progress to SCC
171. CANCEROUS LESION OF LIPS& ORAL
CAVITY
• Lips –SCC, Melanoma, BCC(rare)
• Oral cavity:
-- scc: 9/10 incidence
--verrucous ca: <5% low grade, slow growing rarely metastasizes with
tendency to invade deep tissue.
172. CANCEROUS LESION OF LIPS& ORAL
CAVITY
• Minor salivary gland tumor:
-in the glands lining the oral cavity
-adenoidcystic ca, mucoepidermoid ca,
adenocarcinoma.
-Sarcoma
173.
174. INCIDENCE
• Globally >300,000 people diagnosed/year
• Eighth most common malignancy
• India –upto 40% of all malignancies
• M>F
• Raising trend
• 6-7th decade
• Most of the people are dying because of ignorance
175. INCIDENCE
• Demographic and clinical profile of oral squamous cell carcinoma patients: a
retrospective study ( Shenoi R, Sharma BK, et.al, Indian J Cancer. 2012
Jan;49(1):21-6:
Most common site: mandibular alveolus
Major cause: tobacco chewing
Majority of patients presented in stage III
Majority presented within 6 months of onset
176. RISK FACTORS
Tobacco: About 90% of people with oral cavity and
oropharyngeal cancer use tobacco
Alcohol: Drinking alcohol strongly increases a smoker's
risk of developing oral cavity and oropharyngeal cancer.
Ultraviolet light: More than 30% of patients with cancers
of the lip have outdoor occupations associated with
prolonged exposure to sunlight.
Irritation: Long-term irritation to the lining of the mouth
caused by poorly fitting dentures
177. RISK FACTORS CONT…
• Poor nutrition: A diet low in fruits and vegetables is
associated with an increased risk
• Mouthwash: Some studies have suggested that
mouthwash with a high alcohol content
• Human papillomavirus (HPV) infection:
• Immune system suppression:
• Age: The likelihood of developing oral and
oropharyngeal cancer increases with age, especially
after age 35.
• Gender: Oral and oropharyngeal cancer is twice as
common in men as in women
178. HOW TOBACCO AFFECTS
• Tobacco smoke contains >4000 chemicals, at least 60 shown to be
carcinogens.
• Smoke less tobacco:
main form: chewing, snuff
at least 28 carcinogens found in smokeless
form
180. HOW ALCOHOL AFFECTS
• Chronic alcohol exposure results in increased
cancer incidence in animal model.
• Acetaldehyde , reactive oxygen species- main
mutagen
• Acetaldehyde: directly binds to DNA, alters methyl
transfer leading to hypomethylation leading to
alerted gene products
• Alcohol promotes cytochrome P450- which
increases activation of procarcinogens( tobacco,
alcohol).
• Alcohol can act as solvent facilitating entry of
carcinogens into cells
181. ROLE OF HPV IN ORAL SCC
• Role of human papilloma virus in the oral carcinogenesis:
an Indian perspective (Chocolatewala NM, et.al. J Cancer R
Ther. 2009 Apr-Jun;5(2):7-17).
• Association strongest for Oropharynx, specially cancer of
tonsils followed by base of tongue.
• High risk HPV-16 predominate type.
• Commonly affects younger age groups , male, non
smokers.
• Better outcomes, more responsive to RT, higher survival
rate.
186. SYMPTOMS
a sore in the mouth that does not heal (most common
symptom)
pain in the mouth that doesn't go away (also very
common)
a persistent lump or thickening in the cheek
a persistent white or red patch on the gums, tongue,
tonsil, or lining of the mouth
a sore throat or a feeling that something is caught in the
throat that doesn't go away
Increased salivation
187. MORE SYMPTOMS
difficulty chewing or swallowing
difficulty moving the jaw or tongue
swelling of the jaw that causes dentures to fit poorly or
become uncomfortable
loosening of the teeth or pain around the teeth or jaw
voice changes
a lump or mass in the neck
weight loss
persistent bad breath
190. PATIENT WORKUP
Investigations: for staging
- CT face + neck ± CT chest
- MRI
- USG of neck or primary ± USG guided
FNAC of suspicious lymphadenopathy
- PET
191. STAGING OF THE DISEASE
American joint committee on cancer:
T , N , M
Tx- primary tumour cannot be assessed
T0- No evidence of primary tumour
T1- ≤ 2cm in greatest dimension
T2- 4cm < 2cm> in greatest dimension
T3- > 4cm in greatest dimension
192. STAGING OF THE DISEASE
T4a- Oral cavity: tumour invades through cortical bone, into deep(extrinsic)
muscle of tongue, maxillary sinus or skin.
Lips: cortical bone, inferior alveolar nerve, floor of mouth, skin i.e. chin or
nose.
T4b- involves masticator space, pterygoid plates, skull base and/or encases
internal carotid artery
193. STAGING OF THE DISEASE
N stage:
Nx- regional lymph nodes can not be assessed.
N0- no regional lymph node metastasis.
N1- metastasis in a single ipsilateral lymph node ≤ 3cm in greatest
dimension.
N2a- metastasis in a single ipsilateral LN > 3cm but < 6cm in greatest
dimension.
194. STAGING OF THE DISEASE
N2b- metastasis in multiple ipsilateral LNs, none > 6cm in greatest dimension.
N2c- metastasis in B/L or C/L LNs, none > 6 cm.
N3- metastasis in a LN > 6 cm in greatest dimension
M stage: Mx- cannot be assessed, M0- no distant metastasis, M1- distant
metastasisi.
195. Stage Grouping
Stage 0 Tis N0 M0
Stage I T1 N0 M0
Stage II T2 N0 M0
Stage III T1, T2 N1 M0
T3 N0, N1 M0
Stage IV A T1, T2, T3 N2 M0
T4a N0, N1, N2 M0
Stage IV B Any T N3 M0
T4b Any N M0
Stage IV C Any T Any N M1
196. TREATMENT
• Treatment goals: to eradicate primary tumor and LN metastasis, to maintain
function, cosmetic reconstruction
• Factors affecting choice of treatment:
tumor factor
patient factor
resource factor
197. TREATMENT GOALS FOR
CANCER OF THE ORAL CAVITY
• • Cure of cancer
• • Preservation or restoration of form and function
• • Avoid or minimize sequelae of treatment
• • Prevent second primary cancers
198.
199. TUMOR FACTORS AFFECTING
TREATMENT
• • Site
• • Size (T stage)
• • Location
• • Multiplicity
• • Proximity to bone
• • Pathological features
• • Histology, grade, depth of invasion, tumor
• type
• • Status of cervical lymph nodes
• • Previous treatment
200. TREATMENT
• Patient factors:
age, general medical condition,
performance status, occupation,
lifestyle(smoking/drinking)
socioeconomic considerations
previous treatment
203. TREATMENT OF CHOICE
Stage I , II: single modality treatment is effective and preferable.
Stage III , IV: multimodal therapy is essential
204. TREATMENT
• SURGERY:
Early stage T1/2No tumor: Wide excision +/ - ND
High risk of locoregional recurrent (40%)
• Management of No Neck:
High incidence of occult metastasis in the clinically No
Neck (15-43%)
Controversy : Observation or Surgery/Radiation
Depend on primary site.
Should be have minimal morbidity
ELND if risk of occult meta >20%. (SND/SOHND).
• Locally advanced tumor: Combined modality treatment
205. CLASSIFICATION OF ND
1991 Classification:
• RND
• Modified RND
• Selective ND:
Supraomohyoid
Lateral
Posterolateral
Anterior
• Extended ND
2001 Classification:
• RND
• Modified RND
• Selective ND (SND):
SND (L.I-III/IV)
SND (L.II-IV)
SND (L.II-V)
SND (L.VI)
• Extended ND
Proposed by American HN Society and AAOHNS
207. Standard treatment options for management of
lymph node:
Radiation therapy alone or neck dissection:
N1 (0–2 cm).
N2b or N3; all nodes smaller than 2 cm. (A
combined surgical and radiation therapy
approach should also be considered.)
Radiation therapy and neck dissection:
N1 (2–3 cm), N2a, N3.
Surgery followed by radiation therapy, indications for
which are as follows:
Multiple positive nodes.
Contralateral subclinical metastases.
Invasion of tumor through the capsule of the
lymph node.
N2b or N3 (one or more nodes in each side of
the neck, as appropriate, >2 cm).
Radiation therapy prior to surgery:
Large fixed nodes.
209. SURGICAL APPROACH DEPENDS ON
• • Tumor size
• • Tumor site
• • Tumor location
• • Proximity to mandible or maxilla
• • Need for neck dissection
• • Need for reconstructive surgery
210. SURGICAL MARGINS
UK Royal college of pathologist guidelines:
Clear margin: histological clearance >5mm
Close margins: 1-5mm
Positive margin: <1mm
Incidence higher in oral cavity cancer than other HN sites.
Potentially due to complex anatomy and 3D shape.
212. RADIOTHERAPY
• Applications:
- Radical : early tongue, fom cancer
- palliative : advanced total control not possible: 20Gy x5 daily fractions x 1
week.
-combined therapy.
-preoperative.
-postoperative.
213. RADIOTHERAPY
• Small (T1/T2), superficial (<5mm thickness) lesions of tongue & FOM:
interstitial brachytherapy.
• Dose: 60 Gy/6days with iridium-192
214. POST-OP RT
Indications:
-presence of nodal disease with exptracapsular spread.
-presence of involved surgical margin
-excision margin less than 5mm.
-stage III/IV.
-perineural or vascular invasion.
-poor differentiation.
-oral cavity primary.
-multicentric primary.
->4 nodes positive.
-soft tissue invasion.
-dysplasia or carcinoma insitu at resection margin.
215. IMMUNOTHERAPY
Based on two principles:
-immune system should recognise and destroy abnormal
cells.
- tumor cells are poorly immunogenic and strongly
immunosuppressive.
. Tumors downregulate antigen presenting molecule
. PGE2 produced by tumors inhibit lymphocyte
proliferation.
. Cytokines produced by tumors inhibit lymphocytes
function.
216. IMMUNOTHERAPY
IL-2 : stimulate growth, diffrentiation and survival of
cytotoxic T cells.
-systemic injection associated with sever
reaction.
- Local injection in tumour: short half life requiring frequent
injections.
-IRX2 human cytokine mixture injected perilymphatically
near tumour: in clinical trial
217. IMMUNOTHERAPY
• A trial of IRX-2 in patients with squamous cell
carcinomas of the head and neck(Hadden J, et. al.
Int Immunopharmacology. 2003 Aug;3(8):1073-
81:
using immunotherapy with 10-20 days of
perilymphatic injections of a natural cytokines
mixture (NCM:IRX2;200 units IL2 equivalence)
Found - significant reduction in tumour mass.
-increased area of leukocyte infiltration
218. IMMUNOTHERAPY
Non-Specific Active Immunomodulation
BCG vaccine
Used to induce active, non specific stimulation of the immune system
Reports of increased tumor free survival which could not be substantiated
Trials with other vaccines (strep pyogenes, trypanosoma cruzi, levamisole) show no
benefits in long term survival
219. IMMUNOTHERAPY
HPV Vaccines
Estimated that 25% of HNSCC are HPV associated
Tend to arise in younger patients
Lingual and palatine tonsils
Occur predominantly in non smoker/drinker
Associated with a more favorable prognosis
HPV viral oncogenes E6 and E7 are consistently expressed in HPV
associated cancers
Thought to integrate into the host DNA, and when expressed, bypass the
regulation of cell proliferation
Both protein and DNA vaccines targeting HPV DNA are currently in phase I
and phase II trials
220. TARGETED THERAPY
Targeted therapy in head and neck cancer: state of the art
2007 and review of clinical applications( Langer CJ.
Cancer 2008 Jun 15;112(12):2635-45:
-anti-EGFR monoclonal antibody(MoAb) cetuximab first
targeted therapy to be developed
-single agent cetuximab confer clinical benefits in patient
with cisplatin refractory metastatic disease.
221. WHAT HAPPENS AFTER TREATMENT?
• Speech and Swallowing Therapy
• Follow-up tests
• Chemoprevention
• Watch for new symptoms
• General health considerations
222. SUMMARY
The main problem of oral cancer is early detection
Surgery is still the most important modality in
management of oral cancer.
Better understanding of molecular biology of HNSCC.
Bio-molecular markers can be used in the management of
SCC oral cancer.
High risk of second primary cancer, Chemoprevention?
