Oral manifestation of systemic disease - PowerPoint Presentation

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Oral manifestation of systemic disease

Bacterial infection Part II

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STREPTOCOCCAL TONSILITUS AND PHARYNGITIS

Most commonly caused by

Beta hemolytic streptococci.

Adenoviruses

Enteroviruses

Influenza and Para influenza viruses

Clinical Presentation (Symptoms)

Sore throat

Fever (either low- or high-grade)

Headache

Loss in appetite

Nausea & Vomiting

Painful

swallowing

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Signs

Redness of

orophyranx

and tonsil

Pus discharge from the tonsil

Palatal

petechiae

Cervical lymphadenopathy

Diagnosis

Clinical diagnosis that is presence of tonsillitis and cervical lymphadenopathy .

Treatment

Antibiotics-

Penicillin and Cephalosporin

Analgesic –

To control pain and inflammation

Warm saline gargle

Slide4

Leprosy

A chronic infectious disease with predilection to skin, nerve and mucous membrane

Caused by

Lepra

Bacillus Mycobacterium

Leprae

.

It was observed by Hansen in 1868.

The bacteria can not grow in culture media

M.

leprae

 has an affinity for the cooler regions of the body.

So the

preferential sites involved in

leprosy

, i.e. the peripheral nerves and the nasal

mucosa

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Oral Manifestation of Leprosy

The

hard palate

is the

most frequent site of oral involvement in leprosy, followed by the soft palate, labial maxillary gingival, tongue, lips,

buccal

maxillary gingival, labial mandibular gingival and the

buccal

mucosa.

The

anterior palate, which may be involved in up to 75% in cases with oral lesions, shows a mean surface temperature of 27.4°C.

Mouth breathing

is commonly seen in patients with

lepromatous

leprosy due to nasal obstruction and stuffiness. This lowers the mean surface temperatures, especially over the dorsum of the tongue and the hard and the soft palate

.

In the sequence of morphological changes seen in oral mucosa, Initially

, there is congestion of the mucosa followed by infiltration and formation of nodules, which may ulcerate.

In

advanced disease, complications arise due to fibrosis, leading to deformities, gross disfiguration and functional abnormalities.

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The oral lesions in leprosy are slow to progress and are usually asymptomatic.

The

spectrum of lesions may vary from relatively non-specific ones like

enanthem

of palate or uvula, which, on histopathology, may show no changes or non-specific infiltrate to more specific lesions like papules,

nodules

and ulcers, which may show bacillary

positivity.

Leprous involvement of the lips may present as

macrocheilia

,

Presence

of flat-topped nodules and

Microstomia

.

The swollen and rigid appearance of the lips may be marked and hence cosmetically quite troublesome

.

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Commonly observed lesions on tongue include

multiple superficial ulcers,

mild

glossitis

,

loss of papillae,

chronic atrophic candidiasis and fissured tongue

Nodular lesions may be present over the anterior part of the tongue, giving a pavement-stone appearance and ultimately lead to scarring.

The muscles of the tongue are usually spared unlike the extensive involvement seen in other subcutaneous muscles.

The

buccal

mucosa may appear paler than normal. In advanced cases, there may be diffuse infiltration, swellings,

papulonodules

and ulceration.

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Hard Palate

It is the

most common site of involvement and shows the most varied type of lesions.

The

disease may present as erythematous or reddish papules that gradually increase in size and number and coalesce to form a generalized nodular sub-mucosal infiltrate

As

the disease progresses, the mucosa loses its shininess and gives a matt-like appearance

.

Ultimately, there may be palatal ulceration and perforation leading to communication between the oral and nasal cavity

.

At this time, patients may develop functional abnormalities like difficulty in swallowing, eating and

drinking.

Noduloulcerative

lesions over the palate may at times mimic squamous

cell

carcinoma

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Further

in the course of disease, the mucosa of the soft palate, uvula and

fauces

of tonsils become infiltrated with the appearance of

miliary

papules or nodules.

These

may break down forming superficial ulcers, especially during leprosy

reactions.

The

uvula may initially appear swollen and later completely effaced or may become adherent to the soft palate

.

Scarring in the region of

fauces

may lead to a triangular deformity instead of the normal

faucial

arch.

Involvement of gums may be in the form of

gingivitis or periodontitis.

Gums

appear swollen with shiny and purplish mucosa and bleed easily with decreased sensitivity to pain.

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Images of oral involvement

Nodule on the right

fauci

(encircled) in case of

lepromatous

leprosy

Superficial erosion on the hard palate

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Tuberculosis

Tuberculosis is a chronic granulomatous disease caused by various strains of mycobacteria, usually 

Mycobacterium Tuberculosis

 in humans

.

Robert

Koch, a German physician, discovered the Tuberculosis bacillus in 1882

.

Although the disease’s prevalence reduced decades ago, it still has extremely high prevalence in Asian countries. India accounts for nearly one third of global burden of tuberculosis.

It

may take any form clinically, but with decline in number, these tuberculosis lesions of oral cavity have become so rare that they are frequently overlooked in the differential diagnosis of oral lesions

 

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Oral Manifestations of Tuberculosis

Oral TB lesions may be either primary or secondary in occurrence. Primary lesions are uncommon, seen in younger patients, and present as single painless ulcer with regional lymph node enlargement.

The

secondary lesions are common, often associated with pulmonary disease, usually present as single, indurated, irregular, painful ulcer covered by inflammatory exudates in patients of any age group but relatively more common in middle-aged and elderly

patients

.

Oral TB may occur at any location on the oral mucosa, but the

tongue

is most commonly affected. 

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Other sites include

P

alate,

Lips,

Buccal

mucosa,

Gingiva

,

Palatine

tonsil, and floor of the mouth.

Salivary

glands, tonsils, and uvula are also frequently involved.

Primary

oral TB can be present as painless ulcers of long duration and enlargement of the regional lymph

nodes.

The oral lesions may be present in a variety of forms, such as ulcers, nodules,

tuberculomas

, and

periapical

granulomas

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The oral manifestations of TB can also be in the form of superficial ulcers, patches, indurated soft tissue lesions, or even lesions within the jaw that may be in the form of TB osteomyelitis or simple bony

radiolucency

.

The

ulcerative form is the most

common.

It is often painful, with no caseation of the

dependant

lymph nodes.

Oral

lesions of TB are nonspecific in their clinical presentation and often are overlooked in differential diagnosis, especially when oral lesions are present before systemic symptoms become apparent.

Primary gingival involvement is more common in children and adolescents than adults

.

It

usually presents as a single painless indolent ulcer, which progressively extends from the gingival margin to the depths of the adjacent vestibule and is often associated with enlarged cervical lymph nodes.

They

may be single or multiple, painful or painless and usually appear as irregular, well-circumscribed ulcer with surrounding erythema without induration and satellite lesions are commonly found

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When oral TB occurs as a primary lesion, an ulcer is the most common manifestation usually developing along the lateral margins of the tongue which rest against rough, sharp, or broken teeth or at the site of other

irritants.

Patients

with oral tubercular lesions often have a history of preexisting

trauma.

Deep

tubercular ulcers of the tongue are typical in appearance with a thick mucous material at the base.

These

tongue lesions are characterized by severe unremitting and progressive pain that profoundly interferes with proper nutrition and rest.

Classically

, tubercular ulcers of the tongue may involve the tip, lateral margins, dorsum, the midline, and base of the tongue. They are irregular, pale, and indolent with inverted margins and granulations on the floor with sloughing tissue

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Diagnosis

A biopsy of an oral lesion is confirmatory but in majority of the cases, a single biopsy may not suffice because the granulomatous changes may not be evident in early lesions. The lesion is eventually disclosed by repeat biopsies

.

A radiological examination of chest and a

Mantoux

skin test are mandatory to rule out systemic

TB

Fine-needle aspiration cytology is a highly specific and sensitive tool for identifying

parotitis

and/or TB in major salivary glands 

Treatment

The treatment of oral tuberculosis lesions is the same as the systemic tuberculosis. 

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Dental consideration

Dentists are at higher risk to develop tuberculosis while treating a patient suffering with tuberculosis

If a dentist suspect presence of tuberculosis due the oral presentation of the disease or previous history of the disease cell culture must be done.

Defer the treatment till patient becomes free of the disease

For emergency treatment all precaution must be taken to avoid spread of infection to the treating dentist.(like use of rubber dam etc.)

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ACTINOMYCOSIS

Actinomyces

, a saprophytic component of the endogenous flora of the oral cavity, cause a

suppurative

, granulomatous inflammatory lesion that is locally aggressive and destructive.

This

infection is anatomically and clinically divided into three

types;

Cervico

facial

,

Pulmonary

, and

Abdominalpelvic

,

Cervicofacial

is the

most common form.

The bacteria

is non-acid fast, anaerobic, and

microphilic

with filamentous branching and lives as a commensal in the human body but acts aggressively when it invades the mucosal barrier and enters the subcutaneous tissue.

This

infection is extremely unusual in the oral mucosal

membranes

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When

present, patients exhibit classical symptoms of

Abscesses

,

Sinus

tract formation,

Woody

fibrosis

.

Bacteria

of this genus include almost 30

species.

Actinomyces

israelii

is the most prevalent species isolated in humans.

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Predisposing Factors

Trauma

Breach in the continuity of mucosa due to trauma or surgery

Local factors

Cervico

facial

actinomycosis

is endogenous in origin and occur when dental plaque, calculus and gingival debris contaminates the deep wounds.

Secondary bacterial infection and hypersensitivity reaction may predispose to the disease

Clinical Features

Peak incidence in the fourth and fifth decades of life and

Male predilection with superimposition in immune compromised individuals.

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It present itself as swelling and induration of the tissue

Which will develop into abscess with discharge

Clinically there may be non healing extraction socket , granulation tissue and periosteal thickening of the alveolus

SINUS

Its very common to form with draining abscess.

Multiple sinuses are formed with perforation of skin

Tongue

Painful nodule that eventually ulcerate

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Actinomycosis

Osteomyelitis- may develop in patient with periodontal infection, non vital tooth

Diagnosis and Management

Cultures

and pathology are keystones of the diagnosis of this disease.

Specific preventive measures along with a long-term antibiotic regime are the standard line of treatment

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NOMA (Cancrum Oris )

Noma

is a “gangrenous affection of the

mouth.

It is commonly seen in

children in whom the constitution is altered

by

Bad Oral hygiene

and

Serious

illness

especially from eruptive fevers,

It begins

as an ulcer of the mucous membrane with edema of the face extending from within

out.

It rapidly destroy

the soft tissues and the bone and almost always quickly fatal”.

The

term

noma

originates from the

greek

word “

nomein

” which means to devour or to graze

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It is believed that

noma

is an extension of necrotizing ulcerative gingivitis (NUG) which is characterized by gingival edema, necrosis, bleeding and

pain.

NUG

may progress to necrotizing periodontitis (NP) and later to necrotizing stomatitis.

In

necrotizing stomatitis, NUG or NP spread beyond the

mucogingival

junction to affect the alveolar,

buccal

, lingual or palatal mucosa.

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Clinical Features

Systemic manifestations of

noma

include fever, tachycardia, lymphadenopathy, high respiratory rate, anorexia, general edema and ascites.

Medical

history reveals a parasitic or viral infection (measles, malaria) in the recent past, recurrent fever and diarrhea.

Blood

examination reveal a low hemoglobin concentration and white blood cell count, elevated erythrocyte sedimentation rate

Children

with acute

noma

suffer from linear growth retardation and are severely

affected.

The course of

noma

is very rapid and death can occur in some days. HIV patients reported with

noma

may have a very low CD4

count.

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The first recognized sign of

noma

is edema of cheek, or gingiva or both.

A

greyish black area appears on the external surface of the cheek opposite to the intraoral lesion within the next few days, which later on becomes a well-defined black necrotic zone.

This

necrotic zone acquires a cone shape and rapidly sloughs

away.

Intra-oral manifestations include sequestration of the exposed bone and teeth, halitosis,

pseudomembranes

, excessive salivation, spontaneous gingival bleeding and loss of tips of interdental gingival papilla.

Sometimes

the necrosis is very severe that both maxilla and mandible are completely destroyed extending up till the nose, upper lip, pre-maxilla and the

infraorbital

margin

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Differential Diagnosis

Differential

diagnosis for

noma

includes

leprosy,

Leishmaniasis

,

Post

kala-azar

dermal

leishmaniasis

,

Oral

cancer,

Clostridial

or streptococcal gangrene

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Complication

Mortality used to be a common complication of

noma

. With the use of modern antibiotics and better nutrition, mortality rate has reduced from 90% to 8-10

%.

Noma

can result in

Trismus

,

Sequestration

of jaws

,

Fibrous

ankylosis

of

temporomandibular

joint,

Oro-nasal

fistula,

Damage

to permanent tooth bud, early loss of

decidious

teeth and hypoplasia of maxilla or mandible.

Most

of the

noma

patients have difficulty in mastication because of loss of soft and hard tissue. Severe cosmetic disfigurement can also take place from the resulting scarring and loss of

tissue

Slide29

Tetanus

Tetanus is a severe,

life-threatening

infectious disease present worldwide

.

Tetanus is a severe toxin-mediated infection caused by bacterium Clostridium

tetani

, a noninvasive Gram-positive anaerobic and

spore forming bacterium.

Tetanus

spores remain

localized

in the infection site, often a contaminated

wound.

Once produced, a tetanic toxin called

tetanospasmin

spreads in the nervous tissue and reaches the inhibitory

interneurone

of the motor system; it prevents release of γ-

aminobutyric

acid, thus inducing blockage of inhibitory pathways and muscular spasms

.

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Transmission

Injury

Intravenous drug user

Contamination –

from contaminated soil ,dust etc.

Tetanus Neonatorum

–

I

nfection of the umbical cord due to the use of unclean instrument and dressing , may results in tetanus of newborn which is called teatnus neonatorum

TYPES

Local Tetanus

Generalised form

Cephalic form

Neonatal form

Chronic form

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CLINICAL FEATURES

More commonly seen in young male.

Incubation period is 14 days

Systemic tetanus presents three classical symptoms early in the

disease that are

Trismus due the spasm of muscle of mastication

Dysphagia

and

Neck

stiffness.

All

three symptoms are due to spasm of respective muscles

.

Some degree of fever is commonly found with temperatures up to Io3°F, profuse sweating is another feature.

Involvement

of the facial muscles gives rise to a characteristic grin known as

'risus sardonicus

'.

Slide32

Abdominal discomfort is often found and on palpation the abdominal musculature may be board-like.

Spasm

of the back muscles,

opisthotonos

, produces arching of the body supported only by the heels and occiput.

The

muscle spasms are usually short, being easily precipitated by mild stimuli, such as vibration and noise.

Spasms

may persist and if affecting laryngeal and respiratory muscles, cyanosis and even asphyxia may follow

.

Death in the early stage is usually due to asphyxia.

Diagnosis

Based on clinical findings like lock jaw with Risus Sardonicus

Treatment

Antitoxin

–

Immedtae I.V. injection of 20,000IU of antitoxin

Penicillin –

1,000,000 unit of penicillin G I.V every 6 hoursly for 10days

Sedation

- with diazepam

Slide33

MYIASIS

Invasion of living tissues by larvae of certain species of flies

The term Myiasis was first introduced by Hope in year 1840

 

refers to infestation of living tissues of humans and animals by Dipterous eggs or larvae

Predisposing Factors

Poor oral hygiene

Mentally retadred person

Cerebral palsy and hemiplegia

ORAL MYIASIS

 Oral myiasis was first described by Laurence in 1909

.

It should be considered rare owing to the fact that oral cavity rarely provides a favorable site for infestation and harboring of larvae. 

Slide34

Predisposing factor for Oral Miyasis

Conditions leading to persistent mouth opening along with poor

hygiene

Facial trauma

E

pilepsy

patients with lacerated lips following a seizure

,

Incompetent

lips and thumb sucking habits,

Advanced

periodontal disease

,

Tooth

extraction sites

,

Fungating

carcinoma of buccal mucosa

Patients

with tetanus

Slide35

Clinical features

Oral myiasis

is

a rare condition.

If present the most commomn site to

occur anteriorly around gingival crevices or extraction

sites.

Present as erythematous, edematous or granulomatous lesion

Itching or pain may be present

These lesion may pulsate with movement of larva .

An opening is present through which larva come to the surface

Slide36

Treatment

Irrigation

Irrigation of the lesion with hydrogen peroxide will flush out the larva

Surgical removal of larva may also be needed .

Slide37

Images of Oral Miyasis

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Thank you