2- Infections of the Oral Mucosa II

7/30/2019 2- Infections of the Oral Mucosa II

1/7

Dr. Tahani Abualteen

1/7

Infections of the Oral Mucosa II

Bacterial infections: It is surprising how few bacterial infections occur in the oral mucosa despite the wide range of

species present normally in the oral cavity

This actually reflects the normal defensive mechanisms that are operating in the mouth e.g. theepithelial barrier, the mechanical cleansing and the anti-microbial (by IgA) effects of saliva, immune

phagocytic cells into the gingival crevicular fluid .

Bacterial infections and their oral manifestation:1. Necrotizing Ulcerative Gingivitis (NUG) OR Acute Necrotizing Ulcerative Gingivitis (ANUG)2. Noma (cancrum oris)3. Actinomycosis4. Syphilis5. Tuberculosis (TB)6. Leprosy7. Gonorrhea

Necrotizing Ulcerative Gingivitis (NUG) OR Acute Necrotizing Ulcerative Gingivitis (ANUG): This infection is:

o Polymicrobial (caused by different bacteria)o Endogenous (caused by bacteria already present in the oral cavity)o Opportunistic (caused by bacteria waiting for a chance "e.g. immunosuppression" to cause the

infection) Predisposing factors (local and systemic) involved in the etiology of NUG:

o Immunosuppression (decreased host resistance, depressed immune responses)o Pre-existing chronic gingivitiso Traumao Association with AIDSo Malnutrition and poverty (predisposes to NUG in children)o Smokingo Stress, fatigueo

Poor oral hygieneo Overgrowth of associated endogenous flora (fusospirochaetal complex) {F.fusifornis, T. vincentii}

NUG was common among Soldiers, as they had developed many of the predisposing factors (e.g. stress,smoking, poor oral hygiene, Malnutrition )

Occurs predominantly in young adults More common in males than in females Is now relatively uncommonexcept for HIV patients High recurrence rate if underlying cause is untreated Persistent form is associated with AIDS (all AIDS-related infections are persistent to treatment)


2/7


2/7

Clinical picture:o Sudden onset ofnecrosis and crater-like, punched

out ulceration of interdental papilla and gingival

margins

o Ulcerated areas are covered with a grey-greenpsuedomembrane which is demarcated from thesurrounding mucosa by a linear Erythema

** The psuedomembrane consists ofnecrotic tissue

debris, inflammatory exudate and bacteria

o Gingival bleedingo Pain or soreness of the gumso Halitosis (foul breath)o Salivationo Altered taste (metallic taste)o Malaise, fever and lymphadenopathy may be present in advanced cases

Diagnosis is based on:o Clinical pictureo Demonstrating the fusospirochaetal complex in a gram-stained gingival smear

Differential diagnosis:chronic marginal gingivitis (presence ofpunched-out necrotic ulcers at thetips of interdental papillae and psuedomembrane are important signs to diagnose NUG)

NUG may be an important factor to develop NOMAE.g. Gingivae of teeth may contact the buccal mucosa and necrosis may then spread to involve it causing

gangrene and loss of orofacial tissues Treatment:

o Identify and eliminate the predisposing factoro Gentle debridement of necrotic gingival tissueo Chlorhexidine mouth wash & gentle tooth brushingo Metronidazole 200 mg 3 times daily for 3 days

Noma (cancrum oris): It is a severe and rapidly destructive gangrene of the orofacial

tissue and jaws Usually preceded by NUG, and then followed by rapid spread of

necrosis from gingiva to the cheek

Almost all cases appear in developing countries (especially Africa)particularly in malnourished children whose resistance has been

lowered by concurrent infections such as measles or malaria (i.e.

immunosuppressed individuals)

Treatment:o Debridement and removal of all necrotic tissueo Followed by cosmetic rehabilitation

- Punched out ulceration of interdentalpapilla and gingival margins

- Grey-green psuedomembrane,surrounded by linear Erythema


3/7


3/7

Actinomycosis: This infection is:

o Chronic Suppurative ( pus-forming)o Polymicrobial (caused by different bacteria)o Endogenous (caused by bacteria already present in the oral cavity amongst which Actinomyces

specie, especiallyActinomyces israell i, predominate)

* *Actinomyces species areanaerobic & Gram positive bacteria

Soft tissues of the submandibular region and neckare most commonly involved and Actinomycesbacteria can gain access to this region through an infected root canal or lower third molar socket

The infection is characterized by multiple foci of chronic suppuration Clinical picture:

o Development offirm painless swelling which eventuallysoftens and suppurates(accompanied by the formation of pus

which discharges through multiple sinuses)o These sinuses may release sulphur granules in the pus

(yellowish granules composed of bacterial colonies)

o The multiple abscesses which eventually form tend to point onto the skin rather than the mucosal surface and are

accompanied by marked fibrosis of the surrounding tissues

Histopathological picture:o Actinomycotic lesions develop as areas of

granulomatous inflammation (histiocytes or

macrophages response) surrounded by

granulation tissue (immature repair tissue)

o Central area of suppurative necrosis(WBCs, debris and bacteria)

o Characteristic featurebacterial colonieswith radiating striae (rods) projecting into

the surrounding neutrophils

Treatment:o Antibiotics for 6-8 weeks

Syphilis " ": Caused by the spirochaete Treponema pallidum Usually progresses over three stages: primary, secondary and tertiary (if the disease is discovered

early and treated properly, the patient may not pass through all of these stages)

This infection has now declined significantlythanks to antibiotics (penicillin) Primary syphilis:

o Develops usually 2-3 week after the initial exposure to the bacteriao Results in an ulcer referred to as chancre which is characterized by:

Usually occurs on genitaliabut in minority of patients may present on the oral mucosa(usually the lips)


4/7


4/7

Shallow painless ulcer Indurated (firm) base Almost always associated with lymphadenopathy Heals spontaneously within 3-6 weeks

Microscopically, the ulcer shows an ulceratedgranulation tissue with dense mononuclear

infiltrate (composed mainly ofplasma cells)

** The surface of the ulcer is heavily infected with bacteria and thus transmission of the

disease might happen upon touching and examining the ulcer with bare hands

Secondary syphilis:o Develops usually about 6 weeks after the appearance

of the primary chancre (2-3 months after the initial

exposure to the bacteria)

o Characterized by: Generalized skin rash is the predominant feature May be accompanied by oral lesions, of which the

so-called "mucous patch" is the most frequent

** Mucous patch = flat areas of ulceration

Multiple areas of ulceration may coalesce toproduce lesions ofirregular outline called "snail-

track ulcers"

Tertiary syphilis (late-stage syphilis):o Develops usually many years after the initial exposure to the bacteriao May be fatal as disseminates to involve the brain, major blood vessels o Characterized by:

Gumma:- An area ofnecrosis associated with delayed type IV hypersensitivity (cell-mediated)

reactions to syphilitic antigens

- Occurs especially on the hard palate leading to perforation into the nasal cavity- Histologically, Gumma consists of a central mass of Coagulative necrosis (no pus)

surrounded by granulation tissue infiltrated by lymphocytes, plasma cells, macrophages

and occasional giant cells. Spirochetes are very little or absent

Atrophic glossitis:- Atrophy and fibrosis of the tongue musculature

resulting in breaking up thesmooth surface of

the tongue by fissures due to endarteritis

obliterans (obliteration of arteries ends)

- The epithelium is now thin and more prone tocarcinogens

- This atrophy may be followed by Syphiliticleukoplakia


5/7


5/7

Syphilitic leukoplakia:- Hyperkeratosis- A premalignant lesion which may be followed by Sequamous cell carcinoma

Sequamous cell carcinoma Congenital syphilis:

o Important cause ofmiscarriage, stillbirth or neonatal infectiono Infected mother will transmit the disease to her fetus since Treponema pallidum has the ability

to cross the placental barrier

o Characterized by : Collapse of nasal bridge due to infection and destruction of the developing nasal bones

producing the saddle deformity of the bridge and thedished appearance of the face

Hutchinson triad (Blindness, deafness, dental anomalies) Dental anomalies related to congenital syphilis are caused by infection of the developing

tooth germs of the permanent incisors and first molars and they include:- Hutchinson incisors (also called notched

teeth, screw-driver teeth):

Incisors characterized by centralnotching of the incisal edge and a

tapering "screw-driver" appearance

The maxillary central incisors are themost frequently involved

- Peg shaped laterals (conical and microdontic)- Moons or Mulberry molars:

Molars characterized by constrictedatrophic cups with globular masses of hard tissue on their occlusal surface

The first permanent molars are the most frequently involved Tuberculosis (TB) " ":

Caused by mycobacteria, usuallyMycobacter ium tuberculosis Oral infection is not common, and oral lesions of tuberculosis may present as :

o Primary oral infectiono

Secondary oral infection (associated with coughing-up of infected sputum from pulmonarytuberculosis) and it is a more likely cause of oral lesions

Results in an ulcer referred to as "Classical TB ulcer" which is characterized by:o Chronico Painlesso Induratedo Underminedo Covered with grayish-yellow slougho On the tongue


6/7


6/7

Other manifestations of Tuberculosis:o Gingival involvementgranulomatous inflammation

forming exophytic masses or granulating gingival lesions

o Tuberculouslymphadenitis most frequently affectingthe cervical lymph nodes

Diagnosis:o Biopsy, to identify:

Granulomas with central necrosis Acid Fast bacilli (either by stain or by culture)

o Chest X-ray Treatment:

o 2 antimicrobial agents (isoniazide and rifampicin) for4-8 months

Leprosy " ": Caused by mycobacteria, usuallyMycobacter ium leprae Endemic in tropical areas Two forms of infection existdepending on the immune response of the host to the organism:

o Tuberculoidlocalized infection (good immune response)o Lepromatouswidespread infection throughout the body (poor immune response)

Oral lesions occur almost exclusively in the Lepromatous type:o Can be identified in 50% of patientso Present as nodular inflammatory granulomatous masses

which tend to ulcerate and heal with fibrosis

o Hard and soft palates, maxillary anterior Gingivae andthe tongue are the most often affected

o Oral lesions are usually secondary to nasal involvement Patients may with Lepromatous leprosy may show varying

degrees of facial deformity especially in the naso-maxillary

complex

Gonorrhea " ": Caused byNeisseria gonorrhea The oral mucosa is considered somewhat resistant to this bacterium; however oral lesions do occur

in some patients

Differential diagnoses of a chronic ulcer:1. Syphilis2. TB3. SCC4. Cytomegalovirus in immune-compromised patients5. Deep fungal infection


7/7


7/7

Oral lesions are non-specific, present as Erythema, vesicles, ulcers, pain on speaking andswallowing, such lesions have been reported in any part in the oral cavity but mainly the disease

results in Tonsillar and soft palatal lesions

Granulomatous infections:

1. Actinomycosis:- Endogenous polymicrobial infection- Submandibular swelling- Chronic suppuration- Multiple sinuses draining pus- Sulphur granules in pus

2. Syphilis:- Primary chancre- Secondary snail-track ulcers, mucous patches- Tertiary Gumma, lingual leukoplakia- Congenital Hutchinson incisors, mulberry molars, dished face

3. Tuberculosis:- Oral usually secondary to pulmonary- Painless chronic lingual ulcer

4. Leprosy:- Oral lesions in Lepromatous type- Secondary to nasal involvement- Nodular masses on palate/anterior maxillary gingiva

Documents

2- Infections of the Oral Mucosa II