LESIONS OF ORAL CAVITY

DR JOEL G. MATHEW

ULCERS OF ORAL CAVITY

INFECTIONS VIRAL-HERPANGINA, HERPES SIMPLEX

BACTERIAL-Vincent’s infection, TB, syphilis

Fungal: Candidiasis

Immune disorders: Aphthous ulcer, Behcet’s syndrome

Trauma ill-fitting denture, phenol, aspirin burns, Hot food

Neoplasms

Skin disorders: Erythema multiforme, lichen planus, BMMP, bullous pemphigoid, lupus erythematosus

Blood disorders: Leukaemia, agranulocytosis, pancytopenia

Drug allergy: Mouth washes, tooth paste, etc.Reactions to systemic drugs

Vitamin deficiencies

Miscellaneous: Radiation mucositis, cancer chemotherapy, diabetes mellitus, uraemia

INFECTIONS

HERPANGINA

SYN: Vesicular stomatitis , Acute lymphonodular pharyngitis

Cause: Enteroviruses-Coxsackie A, EV 71

Characteristic vesicular rash on tonsillar pillars, soft palate, uvula, tonsils, posterior pharyngeal wall

Discrete 1- to 2-mm vesicles and ulcers

Enlarge over 2-3 days to 3-4 mm and are surrounded by erythematous rings up to 10 mm

1-15 lesions are present, usually around 5

Usually resolve without complications

Rarely, meningitis

Herpetic gingivostomatitis Syn: orolabial herpes

Cause: HSV

Primary Children

Clusters of multiple vesicles -> ulcers

Fever, malaise and headache , sore throat and lymphadenopathy.

Secondary Adults, mild

Vermilion border of the lip > hard palate and gingiva

Reactivation of dormant virus in trigeminal ganglion

Acyclovir, 200 mg, five times a day for 5 days to reduce viral load

Hand, foot and mouth disease Cause: Coxsackievirus A16 and enterovirus 71

(EV71)

spread via the fecal-oral and perhaps respiratory routes

primarily in children

vesicular palmoplantar eruption and erosive stomatitis.

Cloudy vesicles with a red halo are highly characteristic of this disease.  

Vincent’s infection Syn: acute necrotising ulcerative gingivitis, trench

mouth

Causative organisms include a fusiform bacillus and a spirochaete –borrelia vincentii

Affects young adults and middle-aged persons

Starts at the interdental papillae -> free margins of the gingivae

Lesions covered with necrotic slough.

Gingivae become red and oedematous.

Similar ulcer and necrotic membrane may also form over the tonsil (vincent’s angina). 

Diagnosis: smear from the affected area.

Treatment is Systemic antibiotics (penicillin or erythromycin and

metronidazole),

Frequent mouth washes (with sodium bicarbonate solution) and attention to dental hygiene.

Moniliasis (candidiasis) caused by Candida albicans

Thrush white grey patches on the oral mucosa and

tongue.

 infants and children

systemic malignancy and diabetes or taking broad spectrum antibiotics, cytotoxic drugs, steroids or radiation.

Thrush can be treated by topical application of nystatin or clotrimazole.

Chronic hypertrophic candidiasis. Also called candidal leukoplakia. White patch which cannot be wiped off.

Mostly affects anterior buccal mucosa just behind the angle of mouth.

Hypertrophic form usually requires excisional surgery.

IMMUNE DISORDERS

Aphthous ulcers Recurrent and superficial

Aetiology: Unknown. Autoimmune, Nutritional (Folate, B12, Iron), Viral, Bacterial, Food allergies, Hormonal, Stress

usually involving movable mucosa, i.e. inner surfaces of lips, buccal mucosa, tongue, floor of mouth and soft palate, sparing mucosa of the hard palate and gingivae.

Minor form more common,

ulcers are 2–10 mm in size and multiple with a central necrotic area and a red

They heal in about 2 weeks without leaving a scar.

Major form, ulcer is very big, 2–4 cm in size, and heals with a scar but is soon followed by another ulcer.

Topical application of steroids

Cauterisation 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.

Local pain can be relieved with lignocaine viscous.

Behcet’s syndrome (Oculo-oro-genital syndrome)

Behçet's disease is a complex multisystem disease characterized by oral and genital ulcers and other systemic features.

Diagnosis is based on the International Criteria for Behçet's Disease including: oral aphthae,

genital aphthae,

ocular lesions,

cutaneous lesions,

and a positive pathergy test.

Cutaneous lesions should display a neutrophilic vascular reaction on histopathologic examination.

Seen worldwide, with the highest prevalence reported in Turkey and Japan

prevalence and often the severity is increased in the Middle East and the Mediterranean

predominantly affect males

Cause and Pathogenesis Heredity, immunologic factors, infectious agents, inflammatory

mediators, and clotting factors likely contribute.

Oral aphthae, or Canker sores are often the initial feature of Behçet's disease and constitute a requisite diagnostic feature

usually occur in crops of more than 3 to 10s

painful and shallow, and they heal without scarring over 1 to 3 weeks

Genital ulcers typically occur on the scrotum and penis in males and on the vulva or vaginal mucosa in females.

These aphthae are similar in appearance to oral lesions, but they have a greater tendency to scar and may recur less frequently.[

Cutaneous- erythema nodosum–like lesions,

pyoderma gangrenosum–like lesions,

Sweet's syndrome–like lesions,

cutaneous small vessel vasculitis, and pustular vasculitic lesions including lesions induced by trauma—the so-called pathergy lesion.

Pathergy signifies the development of erythematous pustules or papules 24 to 48 hours following puncture of the skin with a 20- to 21-gauge sterile needle.

Specimens from all these lesions demonstrate a neutrophilic vascular reaction on histopathologic analysis.

Ophthalmic (83% to 95% of men and 67% to 73% of women)  anterior and posterior uveitis,

retinal vasculitis, and hypopyon, with secondary glaucoma,

cataract formation, decreased visual acuity, and synechiae formation

Arthritis of Behçet's disease is typically a nonerosive, inflammatory, symmetric, or asymmetric oligoarthritis

Central nervous system (CNS) involvement is most commonly characterized by brain stem or corticospinal tract syndromes (neuro-Behçet's syndrome),

venous sinus thrombosis,

increased intracranial pressure

isolated headache.

Cardiac complications include myocardial infarction,

pericarditis,

arterial and venous thromboses, and

aneurysm formation. 

Miscellaneous lesions of oral cavity and tongue

Median rhomboid glossitis red rhomboid area, devoid of papillae, seen

on the dorsum of tongue in front of foramen caecum.

Due to chronic oral candidiasis

TRAUMATIC ULCER lateral border of tongue -jagged tooth or ill-

fitting denture;

buccal mucosa -cheek bite;

palate - injury with a foreign object such as pencil or tooth brush

acute ulcerative lesions of oral and oropharyngeal mucosa - ingestion of acids or alkalies or hot fluids.

Aspirin burn - buccal sulcus

SKIN DISORDERS

Erythema multiforme Acute, self-limited, polymorphous eruption

Symmetrically distributed macules, papules, and bullae, with an edematous, petechial, vesicular, or bullous dusky violet center.

It is probably due to cell-mediated hypersensitivity reaction to certain drugs or infections, particularly in genetically predisposed individuals, those immunocompromised or with autoimmune disease.

Mucosal lesions are ocular (conjunctivitis, keratitis), oral (stomatitis, cheilitis), nasal, pharyngeal, tracheal, and genital (balanitis and valvulitis).

Dull red, flat or slightly raised maculopapules, which may remain small or may increase in size to reach a diameter of 1-3 cm in 48 h. Typical cases show at least some target (or iris) lesions.

The disease is self-limiting and management is mainly supportive. Steroids are used to treat the severe form.

Pemphigus vulgaris autoimmune disorder affecting older age group (50–70) [AMBD]

Oral ulcerations are superficial and involve palate, buccal mucosa and tongue.

Jagged intraoral erosions->Blisters

Treatment consists of systemic steroids and cytotoxic drugs.

Benign mucous membrane pemphigoid (BMMP)

Most common AMBD

autoimmune disorder.

Mucosal lesions involve cheek, gingivae and palate > Conjunctiva

Bulla filled with clear or haemorrhagic fluid -> ruptures to form superficial ulceration covered with shaggy collapsed mucosa.

Skin lesions may be absent.

Treatment consists of steroids.

Lichen planus Oral lichen planus (OLP) can occur without

cutaneous disease.

Onset before middle age is rare; the mean age of onset is in the sixth decade.

Women outnumber men by more than 2:1.

Mucous membrane involvement is observed in more than 50% of patients with cutaneous lichen planus

The most common location of OLP is the buccal mucosa (80% to 90%) followed by the tongue (30% to 50%)

Lavy white lesions on buccal mucosa

Geographic tongue Also called benign migratory glossitis,

Well-defined areas of atrophied filiform papillae bordered by arcs of normal or hyperplastic filiform papillae and by gradual changes in the location of these lesions over time 

Submucous Fibrosis Definition:

Submucous fibrosis represents a multifactorial disorder;

with the considered chief etiologic factor being the consistent and habitual use of areca (betel) nut, either in the form of chewing or simply placing a quid of material (paan masala) in the buccal or labial sulcus several time per day, or in a packaged powdered form with other components (guthka), over many years.

premalignant condition with transformation rates as high as 7.6%

Etiology and pathogenesis:   failure of collagen remodeling

altered epithelial-mesenchymal interactions ->formation of collagenous bands and aggregates within the submucosa and lamina propria.

diminished level of functional collagenase levels 

Clinical Features Changes of submucous fibrosis are most marked

over soft palate, faucial pillars and buccal mucosa

Initial mucosal alterations: erythema with or without vesiculation.

Later: slow diminishment of erythema and a progressive decrease in the degree of oral opening and tongue mobility

Pallor of the normally pink mucosa becomes evident as the underlying chronic inflammation recedes and fibrosis and hyalinization progress. 

Scar bands may become evident deep within the buccal soft tissues, further limiting jaw opening and function.

Development of squamous cell carcinoma is characterized by a gradual thickening of the epithelial surface with hyperplastic to verrucous surface qualities becoming evident.

Histology:

 juxtaposition of atrophic epithelium surfacing a subjacent fibrosis.

Early connective tissue alterations are characterized by delicate and loosely arranged collagen fibers with progressive degrees of hyalinization

In the late stages:

complete hyalinization of the supportive connective tissue.

Variable degrees of chronic inflammation occur in the form of lymphocytes and plasma cells.

Variable levels of dysplasia have been noted.

Management of oral submucous fibrosis is problematic, particularly in advanced cases and when the use of areca-containing products remains in place.

Medical:

Avoid irritant factors

Topical injection of steroids-Dexamethasone

Treat existent anaemia or vitamin deficiencies

Encourage jaw opening exercises.

Surgical

Surgical release procedures of scar bands have been only modestly successful.

More recently collagenase and pentoxifylline administration in separate studies has been proposed