ORAL CAVITY

GENETIC DISORDERS AFFECTING THE ORAL MUCOSA AND

LIPS:
1. WHITE LESIONS:

conditions Features
FORDYCE SPOT They are sebaceous glands containing neutral lipids and are seen after
puberty. They are extremely common and 80% of the populations have them.
They are usually seen in buccal mucosa inside the commisures and
sometimes in the retromolar regions and upper lip. They appear as
YELLOWISH SMALL GRAINS seen beneath the buccal and labial mucosa and
are totally benign. No treatment is required.
Bohn’s and Discrete, pearly white or yellow, freely movable elevations, 2-3 mm in
Epstein’s pearls diameter at the gingival margins or midline of the hard palate are seen in
(gingival cyst of upto 85% of newborn infants. They are superficial white lesions containing
the newborn) cysts and are shed in a few weeks.

White sponge It is a rare familial disorder(FAMILY HISTORY IS POSITIVE) seen in CHILDHOOD

nevus and is a AD disorder. They appear as defects in keratin 4 and 13 with
abnormal tonofilament aggregation. There is hyperplastic acanthotic
epithelium in which gross edema causes a basket weave appearance. The
oral mucosa is almost invariably affected ( affects the buccal mucosa
bilaterally). It may also affect the upper respiratory tract, anus and genitalia.
IT IS IN THE FORM OF PAINLESS SHAGGY OR FOLDED WHITE LESIONS. It is a
benign condition and reassurance is all that is required.
Dyskeratosis See notes.
congenita

Pachyonychia It is a benign disorder characterized by mutations in keratin. 60% of patients

congenita have oral keratoses, 16% have natal or neonatal teeth and 10% have angular
stomatitis.

Tylosis and Associated with oral white lesions

focal PPK
Hereditary It is a autosomal dominant condition .There is oral milky white smooth and
benign transluscent plaques appear by childhood and become more obvious by
intraepithelial adolescence. They appear in the buccal mucosa, lips and ventrum of the
dyskeratosis tongue.
Darier’s Seen in 50% cases of Darier’s disease. They are most marked in the patients
disease with the most severe skin changes and typically flattish, coalescing red
plaques that eventually turn white and affect the keratinized epithelia of the
dorsum of the tongue, palate and gingival. They resemble nicotinic stomatitis
clinically.salivary duct abnormalities including dilations and periodic
stricturea and indentations may affect the main ducts.
Warty It typically presents as a nodule or papule on the gingival, palate or alveolar
dyskeratoma ridge. There is suprabasal epithelial clefts and corps ronds.
Chronic Persistant adherent white lesions are seen in the mouth often with angular
mucocutaneous stomatitis.
candidiasis
KID syndrome There is dental dysplasia, chronic mucocutaneous candidiasis
 2. PIGMENTED LESIONS:

condition feature
Melanotic macule It is an acquired small (< 2 cm) flat brown to brown black asymptomatic
macule usually solitary, benign lesion unchanging in character. It is similar to
ephelides and lentigo. They are seen on the vermillon border of the lips,
gingival, buccal mucosa and palate. On the lips they are most on the midline
of lower lip in the vermillon border. There are no nevus cells and there is only
increased pigmentation at the tip of rete ridges.

Peutz- Jeghers notes

syndrome
Psuedoxanthoma
elasticum
Lentiginosis They include Peutz- Jeghers syndrome and the LEOPARD syndrome.

Centrofacial There is centrofacial lentigens with bone abnormalities, malformations due to

lentiginosis dysraphia, endocrine dysfunctions and neurological diseases
syndrome
Carney complex It is a autosomal dominant condition. It is a complex of myxomas, spotty
pigmentation and endocrine overreactivity. There is cardiac and cutaneous
myxomas, mammary myxoid fibroadenomas, spotty cutaneous pigmentation,
primary pigmented nodular Adrenocortical disease, testicular Sertoli cell
tumours and growth hormone secreting pituitary adenomas. The
hyperpigmentation in Carney complex is FACIAL and occurs in the vermillon
borders of the lips in 35%, oral mucosa in 8%. 2% have oral myxomas on the
tongue and palate. It differs from the Peutz-Jegher’s syndrome in that
hyperpigmentation is less intraorally but more common on the conjunctiva
and other manifestations are also present. Cases previously desribed as
NAME(nevi, atrial myxomas, myxoid nerofibroma, ephelides) syndrome and
LAMB(lentigens, atrial myxomas, mucocutaneous myxomas, blue nevi)
syndrome may represent this complex.

Naevi They are much less common than the skin. Majority(60%) are Intradermal
and 25% are blue nevi. The other types are also seen. They are seen
particularly on the vermillon border of the lips and on the palate or buccal
mucosa. They are generally brown macular. There is no evidence that most
nevi except junctional nevi progress to melanomas. But excisional biopsy
should be done for ruling out melanoma in every case more so if the lesions
are raised.

CAUSES OF MUCOSAL PIGMENTATION:

localised generalised
Amalgam tattoo Racial
Ephelides Smoking
Nevus Drugs --- phenothiazines, antimalarial,
Melanotic macule minocycline, contraceptive, mephenytoin
Carney complex Addisons disease
PJ syndrome Nelson’s syndrome
Malignant melanoma Heavy metal
Kaposi sarcoma Albright syndrome
 Malignant acanthosis nigricans
Hemochomatosis
Generalised neurofibromatosis
Incontitentia pigmenti
Ectopic adrenocorticotropic hormone e.g.
bronchogenic carcinoma.

3. RED LESIONS:

condition feature
Hereditary There are multiple telangiectasia of the lips, oral and nasal mucosa and
hemorrhagic perioral areas as well as GIT. Occasionally there are colomic or hepatic
telangiectasia(o complications.
sler rendu weber
syndrome)

hemangiomas Most are solitary but a few may be multiple and or part of a wider
syndrome such as Maffucci syndrome. Also oral hemangiomas are seen in
Sturge weber syndrome, Klippel Trenauney weber syndrome, blue rubber
bleb syndrome or Dandy walker syndrome or other posterior cranial fossa
malformation.

Hereditary It is an autosomal dominant dyskeratotic epithelial syndrome affecting

mucoepithelial oral, conjunctival, nasal, vaginal, urethral, anal and bladder mucosa with
dysplasia cataract, follicular keartosis, nonscarring alopecia anf terminal lung
disease. It is probably a pan epithelial cell defect of desmosomal and gap
junction structure with a lack of keratinisation and cornification.
Histologically the mucosal epithelium shows dyshesion, thinning of the
epithelial layer and dyskeratosis. There is red periorificial mucosal lesions
are typically noted during infancy and persist throughout life. The oral
lesions are painless red macules or maculopapules and are seen
predominantly on the palate and gingiva. Severe photohobia, tearing and
nystagmus herald the development of keratitis, corneal vascularisation
and lens cataract. In addition there are various cardiorespiratory
complications especially potentially lethal bullous lung disease ----
spontaneous pneumothorax, bullous emphysema terminating in cor
pulmonale.

4. VESICULOEROSIVE LESIONS:
condition feature
Epidermolys Oral lesions are common in the dystrophic and lethal forms of EB. Overall oral
is bullosa lesions are found in the 30% cases of EB. There is also a predisposition for SCC
mainly in the Hallopeau-Siemens type. Dental hypoplasia, pitting,
hypomineralisation and delayed eruption of teeth esp. in junctional variety.
There is difficulty in maintaining oral hygiene leading to caries formation.
Patients with recessive dystrophic EB suffer from severe growth retardation
due to severe orophartngeal and esophageal blistering and scarring.
Acrodermati It is a inborn error of metabolism resulting in zinc malabsorption and severe
tis zinc deficiency. See notes.
enteropathi
ca
Felty’s
syndrome
Immune Mouth ulcers (and early onset periodonditis) feature in congenital immune
defects defects including Chediak-Higashi Syndrome, Papillon Lefevre syndrome,
familial neutropenia, cyclic neutropenia, Job’s syndrome. Chronic
granulomatous disease and glycogen storage disease type 1b.

5. LUMPS AND SWELLINg

conditions feature
Hereditary Occurs due to deficiency or dysfunctional C1 esterase levels. It produces a
angioedema more severe reaction with edema affecting the lips, mouth, face and neck
region, the extremities and gastrointestinal tract. Blunt injury is the most
consistent precipitating event. The trauma of dental treatment is a potent
trigger and some attacks even follow emotional stress. The edema may
persist for many hours and even upto 4 days. Airway involvement is a
constant threat. There is low C4 levels but C3 levels are normal.
Acanthosis Oral papilliferous lesions may be a feature of both familial and malignant
nigricans acanthosis. Between 30-50% of patients with acanthosis nigricans
secondary to neoplasia( malignant acanthosis nigricans ) have oral lesions
which involve the tongue and lips predominantly.
lymphangioma Frog spawn appearance , usually in the tongue and solitary.
Dermoid cyst It is a hamartoma arising in the midline of the neck above the mylohyoid
muscle, occasionally elsewhere, even in tongue and antrum. It usually
becomes evident in the second decade. It causes elevation of the tongue.
Lingual tonsil It is a mass of lymphoid tissue in the posterior surface of the tongue
between the epiglottis posteriorly and the circumvallate papilla anteriorly.
If it enlarges , it can cause globus sensation, alteration of voice,
obstructive sleep apnoea or airways obstruction. It tends to involute with
increasing age. There may be tonsillitis.
Lingual thyroid It is a smooth surfaced lump in the midline of the base of the tongue at
the site of foramen caecum. Occasionally it may produce dysphagia,
cough, pain or rarely airways obstruction. The thyroid tissue may be
functional or non functional. Malignant change is rare.
Multiple mucosal The syndrome of multiple endocrine neoplasia (MEN) type 2b is inherited
neuroma as an autosomal dominant trait , some sporadic. It is characterized by
syndrome medullary carcinoma of the thyroid and pheochromocytoma in association
with multiple mucosal neuroma and an abnormal phenotype ---- a striking
facial appearance with thick everted lips that usually have a bumpy
surface due to multiple neuromas. These are actually mucosal and
submucosal hamartomatous proliferations of nerve axons, Schwann cells
and ganglon cells. Lesions may also involve the tongue and commisures
but are less frequent on the buccal mucosa, gingiva, palate, pharynx or
larynx. Ganglioneuromatosis may also occur throughout the GIT . ocular
changes include yellowish masses on the conjunctiva, thickened corneal
nerves and keratitis due to decreased tear production. Most patients have
asthetic marfanoid habitus, high arched palate, pectus excavatum.
Ararchnodactyly and kyphoscoliosis.

6. OROCUTANEOUS DISORDERS

conditions Features
Cleft Are the most common congenital craniofacial abnormalities. They are often
lip/palate accompanied by impaired facial growth, dental anomalies, speech disorder,
poor healing and psychosocial problems. A cleft may involve only the upper lip
or may extend to involve the nostril and the hard and soft palate. Isolated cleft
lip may be unilateral ( mostly on the left) or bilateral. In combination with the
cleft palate, they are mostly bilateral.
Cowden’s Oral lesions are typically smooth, pink or whitish benign fibromas found
syndrome especially on the palatal, gingival and labial mucosa. Other manifestations are
(multiple ------
hamartoma
syndrome)
Gorlin’s Odontogenic keratocysts of the jaw’
syndrome
(naevoid
BCC)
Xeroderma SCC of the lips
pigmentosa
NF-1 Intraoral neurofibromas of oral mucosa
Garder’s Multiple jaw osteomas are a feature of garder’s syndrome of familial polyposis
syndrome coli. Some also have dental anomalies such as supernumery or impacted teeth
or odontomas.
Erythropoeti Psuedoraghades are found.
c
protoporphy
ria
Down’s Angular cheilitis, lip fissures.
syndrome
Tuberous Pit shaped enamel defects and both dental and gingival fibromatosis
sclerosis

ACQUIRED DISORDERS OF THE ORAL MUCOSA AND LIPS

MOUTH ULCERS:

The causes of mouth ulcer are -----

1. Local Factors
 Accidental cheek bite or facial trauma ----- history, single ulcer of short duration (5-10
days)
 Orthodontic appliance ---- chronic trauma may cause a well defined ulcer with keratotic
halo.
 Child abuse
 Self mutilation
 Cunnilingus or fellatio
 Thermal burns
 Chemical burns
 Irradiation mucositis
2. Recurrent apthous stomatitis
 It is characterized by recurring episodes of ulcers, typically from childhood or
adolescence each lasting from 1-4 weeks before healing.
 Aphthae typically are multiple, round or ovoid ulcers with circumscribed
margins, erythematous halo and a yellow or grey floor.
 The etiology is unclear. A positive family history is found with about one third and
there is increased frequency of HLA-A2,A11, B12, DR2. There are identifiable
predisposing factors in some patients ----- low serum iron or ferritin, folate and
vit B12 deficiency, celiac disease, stress, trauma, cessation of tobacco
smoking.
 Ulcers like aphthae are also seen in Behcet’s syndrome, Sweet’s syndrome, HIV
infection, cyclic neutropenia and other immunodeficiencies.
 There is no evidence that RAS is an autoimmune disease. There is no association
with systemic autoimmune disorders, none of the common autoantigens are found and
RAS tends to resolve spontaneously with age. The serum immunoglobulins are normal.
 Attempts to implicate a variety of viruses or bacteria in the etiology of RAS has largely
been unsuccessful but there are cross reacting antigens between the oral mucosa and
microorganisms such as Strep. sanguis or its L form, or HSP.
 CMI mechanisms appear to be involved in the pathogenesis of RAS. IN THE
LESIONS HELPER T CELLS PREDOMINATE EARLY ON WITH SOME NK CELLS. CYTOTOXIC
CELLS THEN APPEAR AND THERE IS EVIDENCE FOR AN ADCC.
 Clinical features: it is of 3 types ------ the most common are minor apthous
ulcers(80%), major aphthous ulcers (10%) herpetiform type of ulceration
(10%).
 Minor aphthous ulcers or Miculitz ulcers occur mainly in the age group of 10-40
years. They cause minimal symptoms. They are usually 2-4 mm in diameter and
are found mainly on the nonkeratinized mobile mucosa. They are uncommon on
 the GINGIVA, DORSUM OF THE TONGUE AND PALATE. Only a few (1-6) appear at a
time, they heal in 7-10 days and recur at variable intervals. Heal without scar.
They are usually round to ovoid.
 Major aphthous ulcers or Sutton’s ulcers are larger(even more than 1 cm), recur
more frequently, last longer(10-40 days) and are more painful. They can occur
anywhere in the oral mucosa including the dorsum of the tongue and palate. They
heal with scarring.
 Herpetiform ulcers: it is found in older age group and commoner in female. It is
extremely painful an drecur so frequently that they seem almost continous. It
begins with vesiculation which proceeds to multiple minute ulcers at any oral site. They
then coalesce into large ragged ulcers that heal in 10 days or longer.
 Treatment: predisposing factors should be corrected.oral hygiene. Steroids,
pentoxyphylline, colchicines, dapsone, thalidomide, sucralfate, topical tacrolimus,
levamisole.

3. Neoplasms
4. Systemic conditions
(a) Hematologic

conditions Features
Deficiency Low iron, folate or vitamin B12 levels may predispose to aphthae. There may
states also be other oral features like glossitis, angular stomatitis.
Leucopenia Oral ulceration---- painful, deep, irregular ulcers often with only a minimal
and inflammatory halo involve the mouth and/or pharynx and tend to extend and
agranulocytosi penetrate slowly. Severe periodontitis is often also a feature.
s
leukemias Oral ulceration is a prominent feature especially in acute leukemia. Other
manifestations include mucosal pallor, gingival hemorrhage, gingival swelling,
petechiae and ecchymoses. Oral infections with Candida and gram negative
organisms are common.
Myelodysplasti Ulceration, paresthesia, petechia, burning mouth, gingival swelling, xerostomia
c syndrome and herpes labialis
lymphoma Usually on the palate and pharynx. Can occur elsewhere. They may appear as
oral swelling with or without ulceration. Herpes virus infection is common.
There is increased incidence of oral lymphomas in HIV.
Mycosis Red or white lesions on the tongue.
fungoides
psuedolympho Tumor like infiltrates are seen in the oral cavity mostly in the palate.
ma
histiocytosis Produce lytic bone lesions, gingival swelling, periodontal destruction with
loosening of the teeth, mouth ulcers. 111In- pentetreotide imaging may be
useful in the diagnosis of Langerhans’ cell histiocytosis.

(b) Gastrointestinal

condition Feature
Pyostomatitis They are mostly seen in inflammatory bowel disease and the course of the
vegetans disease follows the associated bowel disease. The oral lesions are deep
fissures, pustules and papillary projections.
Orofacial Ulcers classically involve the buccal sulcus where they appear as linear
granulomatosis(O ulcers often with granulomatous masses flanking them. There is also
FG) thickening and folding of the mucosa to produce cobblestone type
appearance and mucosal tags. Purple granulomatous enlargements may
appear on the gingival. The lips and face may swell. There may be splitting
of the lips and angular stomatitis. In HPE: non caseating granulomas and
lymphomas may be seen located very deep, close to muscle. They occur in
 Crohn’s, as an ADR to various food additives such as cinnamaldehyde or
benzoates or to menthol or cobalt. Clofazimine 100mg BD for 10 days then
twice weekly for 4 months appears to help a majority of cases. It is the
most effective drug during the early stages and works by clearing the
granulomas. Others include diet excluding additives, IL steroids.
Crohn’s disease Lesions are indistinguishable from OFG.

(c) Dermatological

condition Feature
Lichen It is a T cell mediated autoimmune disease in which autocytotoxic CD8+ T cells
planus trigger apoptosis of the epithelial cells. OLP occurs in 50% cases of LP and is
probably 8 times more common than cutaneous LP. It mainly affects adults > 40
years. It may be involved alone or in association with diseases in the skin and
other mucosa. The oral lesions may precede, follow or accompany lesions
elsewhere. The association of oral LP with gingival and vulvovaginal lesions is
called vulvovaginal- gingival syndrome. Most cases are idiopathic . some
lichenoid lesions are related to dental materials --- chromate. Gold and
thimerosal. Other lichenoid eruptions may be related to GVHD, drug intake
(NSAIDS, sulfones, antimalarials, beta blockers and ACE inhibitor),
diabetes or liver disease. Chronic liver disease esp, chronic active hepatitis
and hep.C are associated with erosive LP. Pathology is similar to that of skin. They
may present as -----
 Reticular pattern : an interlacing reticulated pattern of white streaks is
the most frequent form. Occurs B/L in the buccal and lingual mucosa.
 Papular pattern : it is sually seen with lesions of the reticular pattern
 Plaque form: it resembles leucoplakia though reticular pattern can be
ssen in the periphery.
 Atrophic pattern: red atrophic areas with a peripheral reticular pattern.
 Ulcerative or erosive pattern: may develop from an atrophic area or
bullous area. Usually affect the dorsum of the tongue or buccal mucosa.
The erosions are often large, irregular and surrounded by an area of
erythema and glazed surface (due to loss of papilla). Reticular lesions can
be seen in the periphery.
 Bullous pattern: it is rare. The most common area of involvement is the
buccal mucosa. Some patients present with desquamative gingivitis. The
atrophic and ulcerative types may be associated with pain and burning
sensation.
Malignant transformation occurs in less than 1% or so over 5 years
particularly with the chronic erosive or atrophic forms. SCC may develop.
Therefore follow up all patients at 6-12 monthly intervals. Tobacco and alcohol
should be minimized.
Treatment includes removal of the triggers, oral hygiene.
1. Mild OLP: Topical steroids(aerosols/pastes) or tacrolimus. Antifungals for
candidial superinfection.
2. moderate OLP: Topical ciclosporin or tacrolimus with super potent steroids
3. severe LP: systemic steroids, azoran, endoxan, HCQS, acitretin, thalidomide
or ciclosporin.
4. Other therapies ----- include retinoids, dapsone, LMW heparin.

There are 2 overlap syndromes ----

 LP pemphigoides
 LP/Lichen sclerosus overlap.
pemphigus Oral lesions are a rule in PV but are rare in the superficial forms of pemphigus.
The PV cases which have only oral lesions have antibodies to desmoglein 3.
usually the patients present with large painful irregular persistent red
lesions in any part of the oral mucosa. Intact blisters are rare. Rarely in PV there
may be acquired macroglossia or desquamative gingivitis. Treatment is largely
based on systemic immunesuppression . oral lesions are recalcitrant. Try topical
 steroids/prostaglandin E2/ topical tacrolimus.
Apart from PV, the other important pemphigus variant affecting the mouth is
paraneoplastic pemphigus with painful extensive stomatitis, painful
paronychia and lichenoid papules. Histology and DIF are characteristic.Treatment
is immunosuppression. Recent therapeutic advances include the use of anti-CD20
monoclonal antibody( rituximab) and mycophenolate.
Oral lesions may be seen in less common pemphigus variants especially in
most cases of IgA pemphigus and in some cases pf pemphigus associated
with IBD.
Subepithelia 1. mucous membrane pemphigoid: Here, autoantibodies are present against
l immune different molecules of BMZ. Sera of oral pemphigoid patients selectively
bullous and specifically bind to human α6 integrin. Mucous membrane
disease pemphigoid involves the oral mucosa in more than one third of the cases
commonly causing gingival lesions. The usual lesion, desquamative
gingivitis, is characterized by erythematous, glazed, sore gingival. Bulla
are less common and are seen particularly in the soft palate. They rupture
to form erosions. The bulla persist longer and may scar. They are typically
filled with serous fluid. Treatment: topical steroids, azathioprine, systemic
corticosteroids, tetracycline with or without nicotimanide. DAPSONE may be
useful especially in the treatment of desquamative gingivitis.
2. Epidermolysis bullosa acquisita, DH, Linear IgA disease and CBDC
are other conditions associated with oral erosions.
3. erythema multiforme ----notes
4. TEN --- notes
Lichen Oral LSEA is uncommon but since it presents with whitish plaques, papules
sclerosus or a reticular pattern or erosions, all features of LP, it may be
underdiagnosed. Histologically there is epithelial atrophy with hyperkeratosis,
oedema of the papillary dermis and the lymphocytic infiltrate is less close to the
epithelium than in LP. It has been suggested that mucosal lichen sclerosus is more
common than formerly thought and may even case dysplasia.
Lupus Almost 50% of LE patients have oral lesions. Which begin as red patches that
erythematos break down into irregular slit like ulcers and often heal with scarring. Palate is
us mostly affected. Sjogren’s syndrome may occur with SLE. Oral petechia and
herpetic infectios are also common.
Similar erosions with a white border are seen in DLE. It may predispose to
oral carcinoma. Oral ulcers are also described in drug induced lupus
Dermatomyositis and MCTD may be associated with non specific mucosal
erosions.
Oral lesions in Reiter’s syndrome may include red patches or superficial
painless mucosal erosions which may resemble erythema
migrans(geographical tongue) both clinically and histologically.

(d) Infective

viral bacterial fungal

Herpes simplex Acute necrotizing Candidiasis
Varicella (ulcerative) gingivitis Actinomycosis
Herpes zoster and noma (syn. Aspergillosis
HERPENGINA Vincent’s angina) Cryptococcosis(indolent oral
Hand, foot and mouth Syphilis ulcers)
disease Tuberculosis Mucormycosis(black necrotic
HIV ulcer in palate)
Leishmaniasis
Histoplasmosis(ulcerogranulom
atous disease)
Blastomycosis(do)
Coccidiodomycosis(do)
 (e) Vasculitis -----polyarteritis nodosa(oral nodules may occur singly or in crops
along the path of vessels and esp in the tongue. Other lesions --- erythema, papule,
hemorrhage, ulceration and necrosis) and giant cell arteritis (ischemic pain
during mastication, intermittent claudication, ulceration and necrosis of tongue or
occasionally lips).
(f) GVHD ---- oral manifestation of GVHD consist of painful mucosal desquamation
and ulceration and /or cheilitis, and the presence of lichenoid papules or
striae.

5. Drugs ---- caustics, cytotoxic drugs, drugs causing erythema multiforme/SJS/TEN.

6. Irradiation of the oral mucosa

ORAL SORENESS

Causes:
1. Burning mouth syndrome(syn: glossodynia, oral dysaesthesia)
It mainly affects the middle aged and elderly females. BMS with a tongue of normal
clinical appearance may be seen in deficiency states and with psychogenic causes (a
monosymptomatic hypochondriasis or an underlying anxiety about cancer or venereal
disease appear to be the basis of the disease in most cases), drugs (e.g. ACEI, cytotoxic
agents, protease inhibitors) and diabetes mellitus.
Although the tongue is mostly affected, patient may also complain of occasional
burning in the lips, gums and palate. THE BURNING SENSATION IS OFTEN BILATERAL AND IS
RELIEVED BY EATING OR DRINKING.
Diagnosis:

Causes of burning mouth ---------

LOCAL -----
 Candidiasis
 Other infections
 Geographical tongue
 LP
 Oral submucosal fibrosis
 Dentures

SYSTEMIC -----
 Psychogenic
--- cancerophobia
--- depression
--- anxiety states
---hypochondriasis
 Deficiency states
---- Pernicious anemia
---- vitamin B deficiency
---- folate deficiency
---- iron deficiency.
 Diabetes
 Drugs(captopril)

Management of BMS includes reassurance, treatment of underlying abnormality, psychological

treatment like antidepressants for 2-3 weeks. 50% resolve spontaneously over 6-7 years. Others
include topical benzydamine 0.01% rinse or spray, topical capsaicin cream 0.025%, clonazepam.

WHITE LESIONS
condition feature
Cheek Whitish shredded appearance usually of the buccal or lower labial mucosa at the
bite occlusional line. Seen in tense and anxious individuals.
burns Due to holding mouth washes, drugs against the buccal mucosa. They cause
white sloughing lesions in the mucosa. They typically heal in 1-3 weeks.
LP
Candidias notes
is
leukoplak It is defined as a white patch or plaque on the mucosa that cannot be rubbed off
ia and that is not recognized as a specific disease entity. The term is also used
irrespective of the presence or absence of epithelial dysplasia. It is common in
adults, around 1% is affected. Most cases are seen between 50-70 years age
group. It can be totally benign or sometimes can be precancerous or a marker of
cancer elsewhere in the upper aero digestive tract.
Oral See notes below.
keratoses
Hairy It is seen in severe immune defects especially HIV infection. Occasionally in
leukoplak immunocompetant. It is caused by EBV. HL is a white patch usually seen in the
ia parakeratinized mucosa of the tongue frequently bilaterally. The lesions are
hyperplastic whitish plaques with a corrugated hairy appearance. They are mostly
symptomless. Have no premalignant potential. Histologically there is
hyperparakeratosis. HL needs no treatment and in HIV resolves with antiretroviral
medications.
psoriasis Oral white lesions, lesions like geographical tongue can occur in the buccal
mucosa ( annulus migrans) particularly in pustular psoriasis
Kopliks White specks may be seen in the buccal mucosa opp the first upper molar tooth
spots in measles.

PIGMENTED LESIONS
condition Features
Black hairy The coating in most cases appears to be of epithelial food and microbial
tongue debris; indeed, the tongue is the main oral reservoir of some
microorganisms such as Candida albicans and viridans streptococci. The
filiform papilla are excessively long and stained by accumulation of
squames and chromogenic microorganisms. This mostly occurs in the
adults who are edentulous, on soft non abrasive diet, have poor
oral hygiene or are fasting. The coating appears more obvious in
xerostomia. Habits such as tobacco and betel use and various
medicaments such as chlorhexidine or iron can cause black or brown
superficial staining of the tongue. Occasionally a brown hairy
tongue may be caused by drugs that induce xerostomia,
lansoprazole or antimicrobial therapy. IT MAINLY AFFECTS THE
POSTERIOR PART OF THE DORSUM OF THE TONGUE, ESPECIALLY
CENTRALLY. Treatment: oral hygiene, avoid drugs, brush tongue with hard
tooth brush. Topical tretinoin may be effective.
Pigmentary In LP.
incontinence
Tattoos Amalgam tattoos are common causes of blue black pigmentation of
the gingival.
Food habits Causes include ----
 Foods and beverages ( beetroot, red wine, coffee and tea) cause
superficial staining
 Confectionary such as liquorice causes superficial staining
 Smoking tobacco is now a fairly common cause and cause
extrinsic discoloration as well as intrinsic pigmentary
incontinence. This is more in the case of reverse smoking.
 Chewing betel may cause superficial brownish red discoloration
mainly in the buccal mucosa with an irregular epithelial surface that
has tendency to desquamate. The epithelium in betel chewer’s
 mucosa is often hyperplastic and brownish amorphous material
from the betel quid may be ssen intracellularly and intercellularly
with ballooning of epithelial cells. Betel also predisposes to
submucous fibrosis and cancer.
 Drugs such as chlorhexidine, iron salts, griseofulvin, crack
cocaine, minocycline, lansoprazole and HRT. The first two
cause superficial staining. Drugs that cause intrinsic staining are
--------
 Antimalarials --- produce a variety of colors ranging
from yellow(mepacrine) to blue black(amodaquine).
 Minocycline ----- black discoloration of teeth, gingival and
bone, skin, sclera and even breast milk. In a minority it
produces a blue grey gingival pigmentation caused by
staining of the underlying bone an dsome intrinsic faint bluish
grey staining of the anterior teeth.
 Busulphan, OCP, phenothiazines, anticonvulsants may
occasionally produce brown pigmentation.
 ACTH, zidovudine and clofazimine may also produce
brown pigmentation.
 Gold produces purplish gingival discoloration .

ACTH induced The brown or black pigmentation is variable in distribution but is seen
hyperpigmentat typically on the soft palate, buccal mucosa and at sites of trauma.
ion
HIV infection Oral pigmentation is seen due to drug or adrenal hypofunction
Oral mucosal It occurs suddenly as a reactive lesions following trauma mostly in black
melanotic people. It appears in a course of days to weeks and resolves spontaneously
macule within 6 months. Melanin content is increased but not the number of
melanocytes.

Malignant Rare and occurs most in the palate and maxillary alveolus.
melanoma
Kaposi’s Occur mostly in HIV infected patients over the palate initially as red-
sarcoma purple macule that progresses to nodule that may be extensive and
ulcerative. Multiple lesions are common. They are often asymptomatic
but some are painful and bleed. Treatment is local radiotherapy/ laser
removal/ systemic vinca alkaloids/ IL vinblastin. Occasionally it may regress
spontaneously or with HAART, zidovudine or systemic vinca alkaloids.

RED LESIONS

Condition Feature
Goegraphic It is characterized by map like areas of erythema . the pattern changes from
al tongue day to day and even within a few hours. They may be asymptomatic or cause
( benign sore tongue. There is increased thickness of the intervening filiform papilla.
migratory There may be family history. There is association with HLA B15 AND DR7.
glossitis) some have atopy and some relate it to specific food items. Similar
lesions also seen in Reiter’s syndrome, generalized pustular psoriasis
and acrodermatitis continua of Hallopeau. Rarely other sites like the
labial and palatal mucosa may be affected. Pathologically there is
epithelial thinning at the centre of the lesion with an inflammatory
infiltrate mainly of PMNL.
Larva Irregular linear lesions with inflammatory border.
migrans
Strawberry Prominence of the lingual papilla may be seen in scarlet fever, Kawasaki
tongue disease and Riley Day syndrome.
Telangiectas In Osler rendu syndrome, CREST, chronic liver disease, pregnancy and after
ia irradiation.
Venous lake, pyogenic granuloma, hemangioma, angiosarcoma.
candidiasis
erythroplasi It is a red velvety lesion in level with or depressed below the surrounding
a mucosa. Uncommon. It occurs in 6-7th decade. 75-90% of cases of erythroplasia
prove to be carcinoma or carcinoma in situ or show severe dysplasia. The
incidence of malignant change in erythroplakia is 17 times higher than
leukoplakia. Therefore these areas should be excised and sent for HPE.
Glossitis,
desquamati
ve gingivitis

LOSS OF ELASTICITY OF ORAL LESIONS

Condition Feature
Oral It is a chronic disease of the oral mucosa that appears to be caused by the
submucos constituents of areca nut. There is a subepithelial chronic inflammatory
al fibrosis reaction with fibrosis extending to the submucosa and muscle.
Epithelial changes range from atrophy to keratosis and dysplasia. It
develops insidiously often presenting with dysaesthesia or vesicular stomatitis.
Later there may be symmetric fibrosis of the cheeks, lips and palate and noted as
bands. It can become very severe that the affected site becomes white and
firm with restricted mouth opening. It can predispose to oral carcinoma.
Diagnosis by biopsy.
Systemic Changes are --- restricted mouth opening with radiating fissures, telangiectasia,
sclerosis xerostomia, mandibular erosions, increased width of the periodontal ligament
space of all teeth on radiography. Caries and periodontal disease.

LUMPS AND SWELLING

Conditions Features
mucocele It is usually seen in lower labial mucosa usually resulting from the
escape of mucous into the lamina propria from damaged minor salivary
gland duct. They appear as painless, transluscent dome shaped
whitish blue papules or nodules
Oral papilloma These are caused by HPV. They are most common at the junction of
the hard an soft palate. It is a white or pink cauliflower like lesion that
may resemble a wart. They remain benign. Excision must be total deep
and wide enough to include any abnormal cells beyond the zone of the
pedicle.
warts Common wart and Condyloma acuminata are rare in the mouth but are
mosr common in HIV.
Focal epithelial It is a rare benign familial disorder characterized by multiple soft
hyperplasia circumscribed sessile nodular elevations of the oral mucosa. It is
(Heck’s disease) mostly caused by HPV-13 and HPV-32. it usually affects the lower lip
and tongue.
Denture This growth appears on the labioalveolar fold as a localized firm,
granuloma whitish, fissured. Fibrous granuloma.
epulis Any benign gingival tumor is called epulis. The most common is the
fibrous epulis which appears as a hard, broad based nodule. It is a
fibroma
Giant cell epulis It is a bluish red gingival tumor dur to reactional hyperplasia of
the mucoperiosteum and excess production of granulation tissue
due to chronic irritation. Pregnancy epulis is painless though unsightly
and may ulcerate and bleed.
Parotid duct cyst Develops opp upper second molar tooth on the buccal mucosa in
musicians who play wind instruments.
Fibroma Pedunculated or sessile nodule that may occasionally get ulcerated in an
area of the oral cavity but seems to have predilection for sites of
 trauma.
lipoma Soft, compressible yellowish nodules mostly on the buccal mucosa
or floor of the mouth.
Leiomyoma It is situated on the palate or tongue as bluish or red circumscribed
firm tumors
neurofibromas Oral lesions are not unusual and involvement of the tongue leads to
macroglossia.
Rhabdomyoma Most extracardiac rhabdomyomas present in the mouth typically as
lumps in the floor of the mouth, tongue or soft palate. Most are
seen in the 6th decade.
Rhabdomyosarco The most common oral presentation is a progressively enlarging
ma mass; some 20% have enlarged regional lymph nodes. In advanced
disease, there may be pain, paraesthesia, trismus or loosening of the
teeth.
Neurilemmoma The sites commonly involved in this tumor are the tongue and floor of
(schwannoma) the mouth. The lesions appear as sessile nodules softer than a
fibroma. Excision is the treatment of choice.
Salivary gland They appear mainly on the palate but may occur as slow growing tumors
adenoma anywhere in the mouth
Torus palatinus These are bone excesses found in the midline of the hard palate.

SCROTAL TONGUE

SYN: Fissured tongue, lingua plicata, lingua fissurata

Congenital fissuring of the tongue is a developmental disorder.
 The tongue is larger than normal. Its dorsal aspect exhibits numerous plicate and
superficial or deep grooves or fissures usually arranged in an arborized pattern
connected to longitudinal furrow along the median raphe.
 The malformation, which has a familial tendency, may affect 3-5 % of the population.
 It is frequently associated with Down’s syndrome and is a component of
Melkersson Rosenthal syndrome.
 It has a frequent association with geographic tongue
 It is usually asymptomatic
 Food deposits may get embedded in the tongue and cause chronic inflammation. Does
not usually require any treatment except for mouth washes.

MACROGLOSSIA
Causes:
1. Congenital -------------- lymphangioma, Hemangioma.
2. Metabolic disorders ---------- primary amyloidosis, mucopolysaccharidosis, and glycogen
storage diseases.
3. Endocrine disorders ------------ acromegaly, hypothyroidism
4. neoplastic (benign) --------- neurofibroma, granular cell myoblastoma, rhabdomyoma,
glomus tumors
5. malignant ------------- metastatic carcinoma, SCC, adenocarcinoma, sarcoma, multiple
myeloma.
6. miscellaneous ------ angioneurotic edema, nutritional disorder (iron deficiency, pellagra,
pernicious anemia), trauma, infections (TB, syphilis and actinomycosis).

INFECTIONS OF THE ORAL CAVITY

1. Acute necrotizing(ulcerating) gingivitis (ANUG) ----- Syn. Vincent’s infection

 It is a mixed, mainly anaerobic flora consisting mainly of fusobacterium
nucleatum and Borrelia vincentii is associated with this infection.
 Immune depression may be a predisposing cause
 It may occur in an epidemic form in institutions or in military camps.
  The mouth ulcer is restricted to the interdental papilla of the gingival which
appear blunted. Acute onset of gingival soreness and bleeding and halitosis is
characteristic. ANUG occurs in the anterior part of the mouth. Fever, cervical
lymphadenopathy are present. Failure to adequately treat ANUG may lead to
noma (cancrum oris).
 In noma, the infection extends onto the skin and bones to result in destructive
lesions with a fatal outcome. The condition occurs in malnourished and debilitated
children.
 Similar lesions of gangrenous stomatitis are increasingly reported in HIV
disease.
 Treatment consists of cleaning with hydrogen peroxide, soft tooth brush, oral
metronidazole 200 mg TDS for 3-7 days.

2. Tuberculosis:
Tuberculosis of the oral mucosa can be classified as -----
(a) Primary
------ inoculation ( tuberculous chancre)
------ hematogenous ( miliary tuberculosis)
(b) Secondary
----- ulceration or granuloma
----- tuberculosis cutis orificialis
----- mucosal extension of tuberculosis from osteomyelitis
(c) Mycobacterial oral ulcers by MAI in AIDS.
(d) M. chelonei may occasionally cause cervicofacial infection in the form of lymph node
abscess or occasionally intraoral swellings.

3. gonorrhoea:
Although rare, gonococcal stomatitis has been reported in oral sex with an infected
partner. The oral mucosa appears intensely inflamed with multiple superficial erosions and
ulcers which are covered by a yellowish psuedomembrane.
4. syphilis: notes
5. herpes simplex infection: notes
6. varicella
7. herpes zoster:
 the pain in trigeminal zoster may simulate toothache
 In mandibular zoster, there is ulceration of one side of the tongue, floor of
the mouth and lower labial and buccal mucosa.
 In maxillary zoster, one side of the palate, the upper gingival and buccal
sulcus.
 Rarely mandibular or maxillary zoster may disturb the formation of developing
teeth or cause jaw necrosis.
 If geniculate ganglion of the facial nerve is affected, there may be unilateral facial
palsy with vesicles in the ipsilateral ear and ulcers in the soft palate.
8. herpengina
 it is caused by Coxsakie virus in children.
 The incubation period is 3-7 days
 It begins with fever followed by the appearance of minute vescicles and erosions
scattered over the pharynx, soft palate(mainly) and tonsils. There is
enlarged and tender anterior cervical lymphadenopathy. There is sore throat.
 The condition is self limiting.
9. hand foot and mouth disease
 it is mainly caused by Coxsakie A virus but sometimes by Coxsakie B virus or
enterovirus.
 The I.P. is 3-10 days
 Young children are particularly affected.
 Many infections are subclinical but features of the clinical syndrome include the
following -----------
  General features like malaise, anorexia, irritability and fever.
 Anterior cervical lymphadenopathy ------- enlarged and tender
 Mouth ulcers are round or ovoid, usually sparse and may affect any site
 Rash ----- painful sometimes deep seated vesicles may appear usually on
the hand and/ or feet particularly on the digits or at he base of the
phalanges.
 It is self limiting. Occasional encephalitis.
 It is severe in adults.

ORAL KERATOSIS

Etiology:
1. Idiopathic
2. tobacco chewing ----- M
3. reverse smoking ------M
4. cigarette induced keratoses -------- U
5. pipe smoking ------ U
6. cigar smoking ------ U
7. Sniff dipper’s keratoses and other smokeless tobacco lesions -------- R
8. HPV induced proliferative verrucous leukoplakia --------- U
9. Candidial leukoplakia ------- U
10.Syphilitic leukoplakia -------U
11.Hairy leukoplakia -------- not recorded.

CLINICAL FEATURES:
 Leukoplakias vary in size, some are small and focal and others more widespread
 They may be homogenous white plaques that can be faintly white or very thick and
opaque. Or they can be nodular white lesions or lesions admixed with red lesions.
 The malignant potential depends on the following ----------
(a) Appearance
 Homogenous leukoplakia has little malignant potential
 Nonhomogenous or heterogenous leukoplakia are nodular, speckled with red
patches, ulceration ------- they have high risk of malignancy.
(b) Site
 soft palate complex, ventrolateral tongue and floor of the mouth ------ high
malignancy risk.

(c) Etiological factors ---- see chart.

Biopsy is mandatory in those leukoplakia which exhibit the following -----------

 Found in patients with previous or concurrent head and neck cancer.

 Are non homogenous ----- have red areas, ulcerated, verrucous, idurated.
 In high risk areas like the floor of the mouth and tongue
 Focal
 With symptoms
 Without obvious etiological factors.

Pathology:
 They show, to a varying degree, increased keratin production, change in
epithelial thickness and disordered epithelial maturation.
 Mild dysplasia is not usually regarded as of serious significance
 Severe epithelial dysplasia is thought to indicate a risk of malignancy.
 Pagetoid dyskeratosis is considered a selective keratinocyte response in which part of
the normal population of keratinocytes is induced to proliferate in response to friction.
 Pagetoid cells are more common in suprabasal location and in the labial mucosa.
  These cells show positivity for high molecular weight cytokeratin and negative reaction
for low molecular weight cytokeratin, epithelial membrane antigen, CEA and HPV.
 The Immunohistochemical profile and morphology is also different from surrounding
keratinocytes.

D/D:
 White sponge nevus.
 Leukodema.
 Oral koilocytosis.
 Hairy leukoplakia.
 Pagetoid SCC.
 Extramammary Paget’s disease of the oral mucosa.

Prognosis:

1. Leukoplakia: 2-5% of leukoplakias become malignant in 10 years and 5-20% of

leukoplakia is dysplastic.
2. 15-30% regress spontaneously.
3. At present, it is not possible to predict which dysplastic lesions will progress to
carcinoma and which will regress.

Management:
1. removal of risk factors (tobacco, alcohol and trauma).
2. surgery is an obvious option for the management of leukoplakia with high
predisposition for malignant predisposition to malignant transformation such as
leukoplakia that are -----
 speckled
 verrucous
 from high risk sites (e.g. floor of the mouth/ventrum of the tongue or soft
palate/ fauces)
 in a patient with previous cancer of the upper aerodigestive tract
 dysplastic
 polysomic (aneuploidy or tetraploidy)
 positive for genetic markers such as mutated tumor suppressor factor p53
or for loss of heterozygosity on chromosomes 3p and 9p.

3. Chemotherapy and chemoprevention:

 Topical 0.5% bleomycin
 Topical or systemic vitamin A derivatives
 Calcipotriol.

GINGIVAL SWELLING

Causes are -------

1. LOCAL
 Chronic gingivitis
 Chronic periodontitis
 Acute necrotizing gingivitis
2. SYSTEMIC
 Any condition causing exacerbation of gingivitis (e.g. pregnancy)
 Leukemia
 HIV infection
 Other causes of purpura
 Clotting defects
 Drugs ------- e.g.anticoagulants
 Scurvy.
Causes of gingival bleeding -------

 GENERALIZED SWELLING
 Chronic gingivitis
 Hyperplastic gingivitis due to mouth breathing
 Hereditary gingival fibromatosis
 Drugs
 Pregnancy
 Sarcoidosis
 Crohn’s disease
 Leukemia
 Wegener’s granulomatosis
 Scurvy
 Amyloidosis
 Mucopolysaccharidosis
 Mucolipidosis
 Lipoid proteinosis
 Juvenile hyaline fibromatosis
 LOCALIZED SWELLING
 Abscess > pregnancy
 Cysts > sarcoidosis
 Pyogenic granuloma > orofacial granulomatosis
 Neoplasm > Crohn’s disease, WG
 Wart > amyloidosis