INFECTIONS,

VESICULOBOLLOUS DISEASES,

AND ULCERATIONS IN THE

ORAL CAVITY

Dr. Ahmad Jumaa

INFECTIONS OF THE ORAL MUCOSA

Infections of the oral mucosa

1) Viral infections

2) Bacterial infections

3) Fungal Infections

VIRAL INFECTIONS

Herpetic stomatitis HSV-1,2

Chickenpox & shingles Varicella zoster

Herpangina Coxsackie A

Hand, foot, and mouth disease Coxsackie A

Infectious mononucleosis EBV

Hairy leukoplakia EBV

HERPETIC STOMATITIS• DNA virus

• The most frequent cause of viral infection of the oral cavity.

• Two types:

1) HSV-1: skin and oral mucous membrane infections

2) HSV-2: genitalia infections

• Two patterns of infections are seen:

1) Primary infection

2) Secondary recurrent infection

PRIMARY INFECTION

• Transmitted by droplet spread and contact with the lesion

• Occurs predominantly in young children

• Mostly subclinical or cause mild pharyngitis

• May present as primary herpetic gingivostomatitis

PRIMARY HERPETIC

GINGIVOSTOMATITIS

1. Incubation period is 5 days

2. Prodromal symptoms of malaise and fever

3. Development of numerous small vesicles

4. Then they ulcerate and become secondary infected

5. Regional lymphadenitis

6. Symptoms begin to subside about the sixth day

Self infection:

Chin (saliva drooling)

Fingers (sucking)

Eyes (rubbing)

SECONDARY INFECTION• 1/3 of those who had a primary infection develop recurrent HSV infection

• May result in asymptomatic shedding of HSV into the oral cavity

• Systemic symptoms are usually absent due to the immunity acquired during primary infection

• Most frequent presentation is herpes labialis

• Recurrent intraloral lesions occur almost always on the hard palate or gingiva

• Causes of recurrence:

• 1) febrile infection

• 2)UV

• 3) mechanical trauma

• 4)menstruation

• 5) stress

• 6)immunosuppression

HERPES LABIALIS1. Prodromal symptoms of itching and tingling

2. A few hours later: appearance of clusters of vesicles on the lip and adjacent skin

3. Rupture of vesicles then they become crusted

4. Heal within one week

HSV-1• Primary infection: transmitted by droplet spread/ young/ subclinical

• Secondary infection: no systemic symptoms

• Most common presentation of primary infection is primary herpetic stomatitis.

• Most common presentation of recurrent infection is herpes labialis.

HISTOPATHOLOGY• Infection of epithelial cells

• Ballooning degeneration: Infected cells have eosinophilic cytoplasm and large

nuclei

• Test: smear taken:

this shows multinucleated giant cells and balloon cell

• Degeneration and rupture of infected cells result in intraepithelial vesicles

• Rupture of cells release new viral particles

• Virus gain access to axons of sensor

CHICKENPOX AND SHINGLES

• Caused by varicella-zoster virus (part of herpesviruses)

• Zoster is the manifestation of recurrent chickenpox

• Chickenpox lesions may be found orally, on the skin

• Shingles (zoster/ herpes zoster):

1) Rare

2) Unilateral vesicular eruption

3) Preceded by prodromal symptoms of pain and paraesthesia for two weeks

4) When trigeminal is involved: ophthalmic is the most common

5) If the V2 V3 are infected: toothache and facial pain

CONT,• MOST distressing complication of zoster is: post herpetic neuralgia which is caused

by fibrosis in and around the sensory nerve and ganglia

• If happens in facial nerve it is called Ramsay-Hunt syndrome:

lower motor neuron-type facial paralysis

HERPANGIA

• Caused by coxsackievirus A (RNA virus)

• Most commonly in children

• Characterized clinically by sudden onset of a mild illness with fever, anorexia,

dysphagia, and sore throat

• Vesicles rapidly breakdown into ulcers 1-2 mm in diameter

• Seen in tonsils, soft palate, and uvula

• Symptoms persist for 2-3 days only

• Clinically hard to differentiate from acute primary herpes

• Acute primary herpes: Gingivostomatitis

• Herpangina: Oropharyngitis

HAND, FOOT, MOUTH DISEASE

• Caused by coxsackievirus A – 16

• Occurs predominantly in children

• Shallow, painful oral ulcers together with vesicles and ulcers on the hand and feet

• Usually lasts for 7-10 days

INFECTIOUS

MONONUCLEOSIS

• Caused by EBV (member of herpes group)

• Occurs predominantly in teenagers and young adults

• Characterized by lymph node enlargement, fever, inflammation of pharynx,

prolonged periods of malaise, petechial hemorrhages at the junction of the soft

and hard palate

• Oral changes are non-specific

MEASLES• Caused by measles virus (RNA virus)

• Prodromal symptoms may resemble common cold

• Koplik’s spot: 1) pin-point bluish-white spots against erythematous background,

opposite to buccal mucosa molar teeth

• 2) most of the times they are overlooked

• 3) they start to disappear as the characteristic skin rash develops 3-4

days later

CYTOMEGALOVIRUS• CMV herpes virus

• Important pathogen in immunocompromised hosts

• Subclinical infection is common, affecting 40-80% of adults

• Most common oral manifestations is non-specific oral ulcerations

• Infection of salivary glands is also common but usually asymptomatic

• CMV is strongly associated with the xerostomia seen in AIDS patients

BACTERIAL INFECTIONSNecrotizing ulcerative gingivitis

Noma (cancrum oris)

Actinomycosis

Syphilis

Tuberculosis

Leprosy

NECROTIZING ULCERATIVE GINGIVITIS• Endogenous, opportunistic polymicrobial infection

• Decreased host immune response disturbs host – parasite relationship

• Overgrowth of endogenous flora

• Fuso-spirochaetal complex

• Punched-out necrotic ulcers at the tips of the interdental papillae spreading to

involve gingival margins

• Ulcers are covered by greyish-green pseudomembrane

• Metallic taste, malaise, fever, and cervical lymohadenopathy

• Stress, decreased host resistance, poor oral hygiene, pre-existing gingivitis

NOMA• Severe, rapidly developing gangrene of orofacial tissues and jaws

• Preceded by NUG

• Spread of necrosis from gingival tissue into the cheek

• Development of demarcated gangrene of the orofacial tissues

• Almost all cases develop in malnourished children

ACTINOMYCOSIS• Chronic, suppurative, polymicrobial infection caused by endogenous anaerobic

bacteria

• Actinomyces israelii

• In cervicofacial: soft tissue of the submandibular area and neck are most commonly

involved

• Multiple foci of chronic suppuration

• Development of firm swelling which eventually soften

• Pus discharge through multiple sinuses

• Pus contains characteristic granules (sulfur granules)

• Due to the appearance not actually composed of sulfur

SYPHILIS• Caused by spirochaete Treponema pallidum

Primary lesion: chancre _ shallow painless ulcer

_ usually in genitalia

_ heals spontaneously within a 3-6 week period

Secondary lesion: mucous patches: - flat areas of ulceration

Tertiary: Gummas: - areas of necrosis associated with delayed HTN (IV) reaction to

syphilitic granules

- usually in the hard palate, which may perforate to nasal cavity

Atrophic glossitis: due to endarteritis obliterans

TUBERCULOSIS• Caused by mycobacterium tuberculosis

• Primary oral lesions may occur

• Secondary are more common; associated with the coughing-up of infected

sputum from pulmonary tuberculosis

• Classical description: chronic, painless undermined ulcer on the tongue

LEPROSY

• Caused by Myobacterium leprae

• Could be generalized (lyrpromatous type) or localized (tuberculoid type)

• Oral lesions only in lepromatous type

• Facial deformity of nasomaxillary complex

• Nodular masses on the palate /anterior maxialla

FUNGAL INFECTIONS

• Posterior dorsum of the tongue is the main reservoir

• Carriers rate about 40% of the population

• Opportunistic pathogens

• Predisposing factors disturb balance between host and organism

• PF: trauma, denture, extremes of age, drugs, xerostomia, AIDS, DM, anaemias

• Candida albicans is the most common pathogenic species

CLASSIFICATION OF ORAL

CANDIDOSIS• Acute pseudomembranous candidosis

• Chronic pseudomembranous candidosis

• Acute erythematous candidosis

• Chronic erythematous candidosis

• Chronic hyperplastic candidosis

• Candida-associated denture stomatitis

• Candida-associated angular chelitis

• Median rhomboid glossitis

PSEUDOMEMBRANOUS

CANDIDOSIS

• Called thrush

• S&S of acute and chronic are the same, duration is the distinguishing feature

• Presented clinically: thick white coating, can be wiped away, to leave red inflamed

base

• Pseudomembranous plaque consists of the superficial necrotic and desquamating

parakeratotic layers of the epithelium infiltrated by hyphae

ERYTHEMATOUS CANDIDOSIS

• Most commonly on the dorsum of the tongue

• Seen in patients with prolonged use of steroids

• Ab alters the normal bacterial flora, allowing candida to flourish

• Painful red area at the dorsum of the tongue

CHRONIC HYPERPLASTIC

CANDIDOSIS• Clinically: persistant white patch on the oral mucosa, indistinguishable from

leukoplakia

• Dense, opaque, irregular thickness

• Cannot be removed by scraping

• Buccal mucosa adjacent to the commissure of the lips

• Considered to be premalignant lesion

CANDIDA-ASSOCIATED DENTURE

STOMATITIS

• Characterized clinically by chronic erythema and edema of the mucosa directly

covered by the denture

• Ill fitting denture

• Poor oral hygiene

CANDIDA-ASSOCIATED

ANGULAR CHEILITIS

• Soreness, erythema, and fissuring at the corners of the mouth

• Local maceration of the keratinized layers of the skin as a result of continual wetting

by saliva

MEDIAN RHOMBOID

GLOSSITIS• Located un the midline of the dorsal surface of the tongue, just anterior to the

foramen caecum

• Rhomboidal in shape

• Devoid of papillae

• Surface appears reddish and may be smooth

• Asymptomatic

• Surface is covered by parakeratotic acanthotic squamous epithelium

ORAL MANIFESTATIONS OF

HIV INFECTIONS

• Vary in their strength according to their association with HIV

• Oral manifestations are numerous

• Oral signs may be the initial manifestations

• Opportunistic infections are a major feature

• Oral candidosis

• HIV-associated periodontal disease

• Viral infections

• Hairy leukoplakia

• Kaposi’s sarcoma

• Non-Hodgkin’s lymphoma

• Atypical ulcerations, xerostomia, and oral pigmentation

ORAL ULCERATIONS• Localized defect in the continuity of epithelial cover of the tissue

• Classified on an aetiological basis

• Infective

• Traumatic

• Idiopathic

• Associated with systemic disease

• Associated with dermatological disease

• Neoplastic

TRAUMATIC ULCERATION• Mechanical, chemical, thermal, friction, radiation

• Must fulfill three criteria:

• 1) cause must be determined

• 2) cause must fit the size, site, and shape of ulcer

• 3) by removal of cause, signs of healing must be shown within 10 days

• Examples:

• Mechanical: sharp cusp, ill-fitting appliance

• Chemical: aspirin misuse

• Thermal: hot food

• If lesion persists: take biopsy

RECURRENT APHTHOUS ULCER

• Group of idiopathic ulcers whose natural history is characterized by frequent

recurrence over a number of years

• Based on clinical features:

• 1) minor AU

• 2) major AU

• 3) Herpetiform AU

• Clinical picture:

• Prodromal symptoms of soreness, burning 1-2 days before the onset of ulceration

MINOR APHTHOUS ULCER

• 80% of RAS cases

• 1-5 in number

• Shallow, round or oval ulcers

• Affects the non-keratinized areas of oral mucosa

• Less than 10 mm in diameter

• Recur at 1-4 month intervals

• Heal within 10 days without scarring

MAJOR APHTHOUS ULCER• Larger than 10 mm in diameter

• Number 1-10

• May take 4-6 weeks to heal

• May heal with scarring

• May be associated with severe discomfort and with difficuly in eating and

speaking

• Differentiation of an isolated lesion from malignant ulcer may be difficult

HERPETIFORM ULCERATION

• Characterized by multiple, small, pin-head sized ulcer

• 1-2 mm

• May coalesce forming larger ulcers with irregular outline

AETIOLOGY OF RAS• Unknown

• There is increasing evidences that damaging immune responses are involved

• Number of local and general factors are also involved

• Hereditary predisposition: 45% of patients have family history

• Emotional stress

• Infective agents: Streptococcus sangius

• Allergic disorders: raised level of IgE

• Haematological disorders: 20% of patients show this (IRON, B12)

• Gastrointestinal diseases: coeliac disease, Crohn’s disease

BEHCET’S DISEASE

• rare immune-mediated small-vessel systemic vasculitis

• Vasculitis associated with the hyperactivity of polymorph neutrophils

• Characterized by:

• 1) RAS + at lease two of the following:

• 1) genital ulcers

• 2) eye lesions

• 3) skin lesions

• 4) rapid acute inflammation of skin in response to minor trauma (pathergy test)

VESICULOBULLOUS DISEASES

• Following rupture of the vesicle or bullae, presented as an ulcer

• Collection of clear fluid within or just below the epithelium

• Distinction between a vesicle and a bulla is simply one of size

• Divided into two major groups depending on the histological location of the lesion:

• 1) intraepithelial: lesions from within the epithelium

• 2) subepethelial: lesions between epithelium and lamina propria

• Intraepethelial can be subsubdivided into two groups depending on the mechanism of

formation:

• 1) acantholytic: lesions are formed by the breakdown of desmosomes between epithelial

cells (loss of cohesion between keratinocytes)

• 2) non-acantholytic: lesions produced by the death and rupture of groups of epithelial

cells

PEMPHIGUS VULGARIS

• Intraepethelial acantholytic lesion

• Autoimmune disease caused by AB directed against desmosome

• Middle age, F more than M

• Characterized by widespread bullous eruption involving the skin and mucous

membrane

• Oral mucosa is ultimately involved in nearly all patients

• 50% of the cases oral mucosa is the site of initial lesion

• Soft palate, buccal mucosa, and lips

• Bullae are fragile and readily rupture

DIAGNOSIS• Physical exam.: flat bullae and a positive Nikolsky’s sign

• NS: dislodgement of intact superficial epidermis by a shearing force, indicating a

plane of cleavage in the skin

• Gold standard for ddx is: punch biopsy from the area around the lesion that is

examined by direct immunofluoroescent staining, showing acantholytic cells

• Tzanck smear: look for multinucleated giant cells

• Circulating autoantibodies are important in establishing ddx, and monitoring the

progress of the disease (by monitoring their titre)

ERYTHEMA MULTIFORME• Immune complex vasculitis

• Disease of abrupt onset involving skin and mucous membrane

• Has wide range of clinical presentations, hence “multiform”

• Deposition of immune complex, mostly IgM, in the superficial microvasculature

• Antigen may be drug, sulfonamides, or viral, herpes

• Young adults, M more

• Disease tends to subside after 10-14 days

• Recurrence may occur

• Type III hypersensitivity

• Biopsy is non specific, but may be helpful in exclusion

• Characteristic target (iris) lesions: concentric rings of varying erythema, in the center of which may be intact or ruptured bulla

• Stevens-Johnson syndrome: widespread form of EM

• Ocular involvement can lead to conjunctival scarring and visual impairment

PEMPHIGOID• Subepithelial, non-acantholytic

• Autoimmune disease

• Similar in general appearance to pemphigus

• Production of AB against hemidesmosomes

• Can be divided into:

• Bullous pemphigoid: skin mostly

• Mucous membrane pemphigoid: mucous membrane mostly

MUCOUS MEMBRANE

PEMPHIGOID• Women in the 6th decade

• Full separation of the full thickness of the epithelium from the lamina propria

• Occasionally intact oral vesicles and bullae

• When they rupture they give rise to erosions which heal slowly, sometimes with

scarring

• Ocular involvement is the most serious complication; might lead to opacity of the

cornea, and blindness

DERMATITIS HERPETIFORMIS

• Chronic, intensly pruritic subepidermal AI blistering disease of skin

• Despite its name, its neither related to nor caused by herpes virus

• Oral manifestations are variable and range from small symptomless erythematous

areas to extensive erosions

• Granular deposits of IgA in the tips of the CT papilla together with complement

pathway

• 90% of patients have abnormalities of their jejunal mucosa associated with gluten

hypersensitivity

LINEAR IGA DISEASE

• Rare subepidermal blistering disease of skin

• Clinically overlaps with dermatitis herpetiformis and bullous pemphigoid

• Immunopathological studies show linear binding of IgA along the basement

membrane zone similar to the pattern seen in pemphigoid

MISCELLANEOUS DISORDERS• Fordyce’s granule

• Geographic tongue (benign migratory glossitis)

• Orofacial granulomatosis

• Crohn’s disease

• Sarcoidosis

• Wegner’s granulomatosis

• Scleroderma

• Amyloidosis

FORDYCE’S GRANULES• Sebaceous glands

• Small yellowish bodies

• Consist of a number of lobules of sebaceous cells grouped around glands

• Do not have any function in the oral cavity

• No significant pathological changes are associated with them

GEOGRAPHIC TONGUE• Condition of an unknown aetiology

• Seen clinically as irregular, Partially depapillated, red areas on the ant 2/3

• Affected area may begin as small lesion

• Gradually enlarging

• Heal then reappear on another location

• Symptomless, with some irritation associated with spicy food

• There is often a family history

OROFACIAL

GRANULOMATOSIS• Not a disease but a term used to describe the common clinicopathological

manifestations of a variety of disorders

• Recurrent or persistent diffuse enlragement of the lips and cheeks

• Time of onset varies from infancy to old age

• Should be regarded as a provisional ddx indicating the need for further investigations

• Possible causes:

• Crohn’s disease

• Sarcoidosis

• Allergy

• idiopathic

CROHN’S DISEASE• Chronic granulomatous disease involving any part of the GIT, but most commonly the terminal

ileum

• Aetiology is unknown

• Excessive cell-mediated immune response to bacteria

• Intestinal involvement usually causes recurrent episodes of abdominal pain, and nutritional deficiencies

• Orofacial manifestations:

• Diffuse swelling of the lip and cheeks

• Edematous and hyperplastic thickening of the buccolabial mucosa together with fissuring, producing “cobble-stone” appearance

• Edematous and hyperplastic enlargement of the bucco-labial mucosa, often involving the sulci, presenting as polypoid tag-like lesions or deep folds of mucosa that can mimic denture irritation hyperplasia

• Apthous ulcers involving any part of the mouth

• Glossitis secondary to iron, B12, folic acid deficiencies

SARCOIDOSIS• Systemic granulomatous disorder of unknown aetiology

• Affects young adults

• Presents with

• 1) bilateral hilar lymphadenopathy

• 2) pulmonary infiltration

• 3) skin or eye lesions

• Oral involvement is rare

• Submucosal, painless red nodules covered by normal mucosa

• Erythema, and hyperplasia of the gingiva

• Orofacial granulomatosis

• Salivary gland (parotid) involvement

• uveitis + parotitis + facial paralysis = Heerfordt syndrome

WEGNER’S

GRANULOMATOSIS• Systemic disease characterized by a necrotizing, destructive granulomatous

inflammation

• Involving respiratory tract, and a generalized necrotizing vasculitis

• Aetiology is obscure

• autoAB directed against cytoplasmic constituents of neutrophils

• Antineutrophil-cytoplasmic AB type-c (c-ANCA)

• Prevalence of oral lesions is about 15%

• Characterestic type of hyperplastic gingivitis (strawberry gingivitis) with heavily

inflamed granular exophytic lesions, and deep necrotic oral ulceration

SCLERODERMA• Chronic multisystem disease characterized by diffuse fibrosis (sclerosis) of the skin

with similar involvement of internal organs

• Face may be involved leading to restricted mouth opening, smoothing of facial

expressions’ lines, and expressionless (mask-like)

• Widening of PDL on posterior teeth

• Females between 20-50 yrs

• Associated with other CT disease, such as SLE, Sjogren syndrome

AMYLOIDOSIS• Disease characterized by extracellular deposition of fibrillary proteinaceous

material –amyloid- in a wide variety of tissues

• Amyloid’s chemical structure:

• Primary idiopathic: it arises as a result of derangement of IG synthesis, and thus it contains of fragments of IG light chain

• Secondary reactive: Rheumatoid arthritis. They do not contain light chain fragments. Fibrils composed of amyloid A protein (polypeptide related to an acute-phase protein found in serum)

• Oral manifestations:

• Macroglossia. Tongue indented, firm and immobile

• Petechiae, ecchymosis, haemorrhagic bullae which rupture leaving shallow ulcers

• Involvement of salivary glands leads to xerostomia

THANK

YOU