2. Definition
Stomatitis is the inflammation of the mucous membrane of the
mouth(oral cavity).
Infective stomatitis occurs due to infective microorganisms such as
fungi, viruses, and bacteria
3. Viral Infections
Laboratory diagnosis of many viral diseases is slow and difficult, therefore, most
viral infections of the oral mucosa is based on clinical mainly on clinical features.
However, 3 main laboratory methods are available:
1. Tissue culture: virus may be isolated from the lesions and identified after
cultivation in tissue culture, fertilized eggs, or laboratory animals.
2. Light/Electron microscopy: Here, virus particles or characteristic histological
changes may be found in affected tissue. Viral antigens may be demonstrated in
infected tissue by immunofluorescent, immunocytochemical or in-situ
hybridization techniques.
3. Serological studies: this demonstrates a significant rise in antibody titre (at
least fourfold) against a particular virus between the acute and convalescent
sera- IgM antibody is produced in acute infection
4. Viruses associated with infective stomatitis
VIRUS DISEASE
Herpes simplex viruses, type 1 and 2 Primary herpetic Gingivostomatitis
Varicella –zoster virus Chickenpox and shingles(herpes zoster)
Epstein-Barr virus Infectious mononucleosis
Coxsackie A virus Hand, foot, and mouth disease
Cytomegalovirus Cytomegalovirus infections
Human papillomavirus Viral warts/epithelial hyperplasias
Paramyxovirus Measles
Coxsackie A virus Herpangina
Epstein-Barr virus Hairy leukoplakia
5. Primary Herpetic Gingivostomatitis
Also known as Orolabial herpes is a combination of gingivitis and stomatitis cause by herpes simplex virus
type 1 (HSV-1), rarely type 2.
Clinical features
It is usually seen in children aged between 6 months and 6 years
The onset of the disease is abrupt and is clinically characterized by ;
High fever, headache, malaise, anorexia, irritability, bilateral sensitive regional lymphadenopathy, and
sore mouth lesions.
The affected mucosa is RED and EDEMATOUS, with numerous coalescing vesicles, which rapidly
rapture, leaving painful small, round, shallow ulcers, covered by yellow fibrin.
New lesions continue to develop during the first 3-5 days.
The ulcers heal in 10-14 days.
Both movable and non movable mucosa may be affected.
Gingival lesions are almost always present, resulting in enlargement and edematous and painful
erosions.
7. Cont..
Extra oral and systemic signs and symptoms
1-3 days of fever, loss of appetite and myalgia
Cervical lymphadenopathy is present.
After the primary infection, the virus remains latent in the nerve tissues
If reactivation occurs, it causes herpes labialis(cold sore)
Histopathology
The virus targets the epithelial cells which “ballooning degeneration”
These cells are called Tzanck cells.
Infected cells fuse, forming multinucleated cells and infected cells edema leads to formation of a
intraepithelial vesicles that rupture and develops a secondary inflammatory response with a fibro
purulent exudate.
Discrete ulcerations have a central portion of acute inflammation with exudate surrounded by
engorged blood vessels.
8. Cont..
Diagnosis
I. Established from patient history and clinical findings
II. HSV isolation by cell culture is the gold standard
III. Tzanck smear
IV. Biopsy
V. Serological tests
10. Cont...
Treatment
1. Local applications:
• Using topical lignocaine in mild cases
• Topical steroids like triamcinolone and Clobetasol application in
severe cases.
2. Systemic therapy:
• Pentoxifylline daspsone short bursts of systemic steroids and
thalidomide have been used to reduce the no. of ulcers and recurrence.
11. HERPES LABIALIS
Also known as cold sores, is a type of infection caused by herpes
simplex virus that primality affect the lip.
It’s mainly caused by herpes simplex virus type 1, rarely by type 2.
• The incubation period for herpes - 2 to 7 days.
• Persons with primary herpetic lesions are infectious for about 7 to 12
days.
• Genital, rectal, or oral herpes recurs in 60 to 80% of persons whose
primary infection was symptomatic.
• These recurrent episodes of herpes are milder and of shorter duration
than the initial outbreak.
12. Transmission
1. HSV-1- usually transmitted in saliva (kissing, sharing of glasses,
etc.)
2. HSV-2 transmitted by;
sexual contact (HSV-2 can infect genitalia, anorectal tissues, or the
oropharynx)
autoinoculation
during pregnancy and labour
3. Both types can cause oral and genital lesions.
People at risk; Neonates, Immunocompromised, Physicians, nurses,
dentists, etc. in contact with oral and genital secretions
13. Epidemiology
• HSV-1 and 2 infections are life-long.
• The virus is found in the lesions on the skin but can be present in body
fluids including saliva and vaginal secretions.
• HSV-2 is normally spread sexually and is found in the anus, rectum and
upper alimentary tract as well as the genital area.
• An infant can be infected at birth by a genitally-infected mother.
• The infant can also be infected in utero if the mother’s infection spreads.
• Highest incidence of HSV-1 infection occurs among children 6 months to 3 years
of age
• 70–90% of persons thus acquire type 1 antibodies by adulthood
• Primary infection by HSV-2 is more common in young adults
14. Clinical manifestations
• Fever blisters or cold sores, are the most common manifestation of
recurrent HSV-1 infections.
• Lesions sometimes occur on the nose, chin, cheek, or oral mucosa.
• Burning, tingling, itching, or pain 3–6 hrs before the development of
the herpes lesion.
• Painful ulcers
• Complete healing within 6–10 days.
Pathogenesis; HSV causes cytolytic infections.
• Pathologic changes are due to necrosis of infected cells together with
the inflammatory response
16. Infection types/phase
1. First Clinical Episode
• Primary infection
– First infection ever with either HSV-1 or HSV-2
– No antibody present when symptoms appear
– Disease is more severe than recurrent disease
• Non-primary infection
– Newly acquired HSV-1 or HSV-2 infection in an individual previously seropositive to the other virus
– Symptoms usually milder than primary infection
– Antibody to new infection may take several weeks to a few months to appear
2. Recurrent symptomatic infection
• Antibody present when symptoms appear
• Disease usually mild and short in duration
3. Asymptomatic/ primary infection
• Serum antibody is present
• No known history of clinical outbreaks
17. Diagnosis
• Usually based on symptoms
• Cultures from skin lesions, mouth, nasopharynx.
• Serologic tests
• PCR testing
• Cytology (Tzanck or Pap)
– Insensitive and nonspecific and should not be relied on for HSV
diagnosis
Treatment
Antivirals
Acyclovir is the treatment of choice, Famciclovir, Valacyclovir etc
18. HERPES ZOSTER OF TRIGEMINAL NERVE
• Herpes zoster(HZ) A.K.A Shingles is a very painful skin rash caused by Varicella
zoster virus.
• HZ usually appears in a band, strip, or a small area on one side of the face or body
• It’s of an acute onset.
• It is extremely painful and having incapacitating nature.
• It is characterized by inflammation of dorsal root ganglia or extra-medullary
cranial nerve ganglia, associated with vesicular eruptions of the skin or mucous
membrane in areas supplied by sensory nerves.
• Varicella zoster virus is similar to herpes simplex virus(HSV) in many respects.
• Chicken pox represents the primary infection with VZV latency ensures and
recurrence is possible as herpes zoster.
19. Cont..
• This disease is most common in adult life and affects male and female with equal
frequency.
• Although rare it does occur in children.
• The infection period is 10 – 21 days with an average of 15 days.
Predisposing factors for reactivation
• HIV infection
• Cytotoxic or treatment with immunosuppressive drugs
• Radiation
• Presence of malignancies
• Old age
• Alcohol abuse
• Stress ( emotional and physical )
• Dental manipulation
20. Pathogenesis
• After the initial infection with VZV (chicken pox ) , the virus is
transported up the sensory nerves and presumably establishes latency
in dorsal spinal ganglia.
• Similar eosinophilic intra-nuclear inclusion bodies , indicative of viral
infection occur in both the cases.
• Herpes zoster rash has healed, a debilitating complications known as
post herpetic neuralgia(PHN).
• The incidence and severity of herpes zoster and PHN increase with
age in association with an age related decline in cell-mediated
immunity to VZV
21. Clinical features
It can be grouped into three phases;
- prodrome
- acute
- chronic
During initial viral replication , active ganglionitis develops with resultant neuronal
necrosis and sever neuralgia
As the virus travels down the nerve, pain intensifies and has been described as burning,
tingling, itching, boring, prickly, or knifelike.
Approximately 10% of affected individuals will exhibit no pro-dermal pain.
The pain may be;
-sensitive teeth
-otitis media
-migraine headache
- myocardial infraction or appendicitis, depending upon which dermatome is affected
22. Cont..
Zoster sine; Conversely on occasion there may be recurrence in the
absence of vesiculation of the skin or mucosa.
This pattern is called zoster sine (zoster with out rash).
The acute phase begins as the involved skin develops clusters of vesicles
set on an erythematous base.
within 3 to 4 days the vesicles becomes pustular and ulcerate with crusts
developing after 7 to 10 days.
oral lesions;
• Occur with trigeminal nerve involvement and may be present on the
movable or bound mucosa.
• The lesions often extend to the mid-line and frequently are present on
conjunction with involvement of skin overlying the affected quadrant.
• Individual lesions manifest as 1 to 4 mm, white, opaque vesicles that
rupture to form shallow ulcerations.
24. …
Involvement of maxilla may be associated with devitalization of the
teeth in the affected area.
Several reports have documented significant bone necrosis with loss
of teeth in areas involved with herpes zoster.
It is postulated that the gnathic osteonecrosis may be secondary to
damage of the blood vessels supplying the alveolar ridges and teeth,
leading to focal ischemic necrosis.
Of the reported cases there is almost an equal distribution between
maxilla and mandible with both sexes similarly.
Ocular involvement is not unusual and can be the source of
significant morbidity, including permanent blindness.
26. James Ramsay Hunt’s syndrome
A special form of zoster infection of the geniculate ganglion, with the
involvement of the external ear and oral mucosa, has been termed
hunt's syndrome.
Clinical manifestation :-
- facial paralysis
- pain of external auditory meatus and pinna of ear.
- vesicular eruption occur in oral cavity and
oropharynx with hoarseness, tinnitus and vertigo.
27. Oral manifestations
• Herpes zoster may involve the face by infection of trigeminal nerve.
• This usually consist of unilateral involvement of skin areas supplied by
either the ophthalmic , maxillary or mandibular nerves.
• Lesions of the oral mucosa are fairly common , and extremely painful
vesicles may be found on the buccal mucosa, tongue, uvula, pharynx and
larynx.
• This generally rupture to leave areas of erosion.
• One of the characteristic clinical features of the disease involving the face
and oral cavity is the unilaterality of the lesions.
• Typically, when large, the lesions will extend up to the midline and stop
abruptly.
• Histopathologic features; The virus causes acantholysis, the formation of
numerous free-floating Tzanck cells which exhibit nuclear margination of
chromatin and occasional multinucleation.
28. Diagnosis
• Viral cultural – results take at least 24 hours.
• A rapid diagnosis can be obtain through the use of direct staining of
cytologic smears with fluorescent monoclonal antibodies for VZV.
• Molecular techniques such as dot blot hybridization.
• PCR
Treatment
• Fever should be treated with antipyretics that do not contain aspirin.
• Antipruritics such as diphenhydramine can be administrated to reduce
itching.
• Early therapy with appropriate antiviral drugs such as acyclovir,
valacyclovir and famciclovir.
• A live attenuated VZV vaccine has been approved for use in adults, 60 years
of age or older.
29. CYTOMEGALOVIRUS INFECTIONS
Cytomegalovirus is a viral genus of the viral family known as Herpes viridae or
herpes viruses. The species that infects humans is commonly known as human
CMV (HCMV) or human herpesvirus-5 (HHV-5)
Cytomegalovirus(CMV) is a herpes group virus that rarely causes disease in
immunocompetent individuals but is an important pathogen in
immunocompromised hosts e.g AIDS patients and organ transplant patients.
Subclinical is common, affecting 40-80% of adults
Uninfected transplant patients may acquire the virus from the transplanted organs
or blood transfusion.
The most common oral manifestation is non-specific oral ulceration. CMV is
infection of the salivary glands is common but asymptomatic.
CMV is strongly associated with the xerostomia seen in AIDS patients.
Also plays a role in cyclosporin-associated gingival overgrowth in transplant
patients following CMV infection of gingival fibroblasts and endothelial cell.
30. Transmission
• Person to person contact (kissing, sexual contact, getting saliva or urine on hands and then
touching eyes, or the inside of nose or mouth)
• Through the breast milk of an infected woman
• Infected pregnant women can pass the virus to their unborn babies
• Blood transfusions and organ transplantations.
Pathogenesis
• Once infected, the virus remains in the person for life and my be reactivated from time to time,
especially in immunocompromised individuals.
• The virus may be transmitted in utero, perinatally, or postnatally. Perinatal transmission occurs.
• Perinatal infection is acquired mainly through infected genital secretions, or breast milk. Overall, 2
- 10% of infants are infected by the age of 6 months worldwide. Perinatal infection is thought to be
10 times more common than congenital infection.
• Postnatal infection mainly occurs through saliva. Sexual transmission may occur as well as through
blood and blood products and transplanted organ.
31. Treatment
• Anti-CMV agents in current use are;
Ganciclovir
Forscarnet
Cidofovir
Maribavir
Valganciclovir
32. HAND-FOOT and MOUTH DISEASE - HFMD
• HFMD is a mild, but highly contagious viral infection common in
young children.
• HFMD occurs mainly in children under 10 years old but can also
occur in adults.
• Children are more likely to be at risk for infection and illness because
they are less likely than adults to have antibodies to protect them.
Cause; Coxsackievirus A type 16 (cv A16). Also HFMD has been
associated with coxsackievirus A5, A7, A9, A10, B2, and B5 strains.
Enterovirus 71 (EV-71) has also caused outbreaks of HFHD with
associated neurologic involvement.
33. Transmission
• The virus spreads through the air
• The droplets from coughs and sneezes of infected people
• spread from person to person through nose and throat secretions (such
as saliva, sputum, or nasal mucus),
• blister fluid, or stool of infected persons.
34. Signs and symptoms
• Fever
• Sore throat
• Poor Appetite
• Malaise
• Diarrhea
• Painful oral lesions
• Vomiting
• Referred ear pain
• One or two days after fever onset, painful sores usually develop in the
mouth. They begin as small red spots that blister and then often become
ulcers.
• The sores are usually located on the tongue, gums, and inside of the cheeks.
35. ..
• A non-itchy skin rash develops over 1–2 days. The rash has flat or
raised red spots, sometimes with blisters. The rash is usually located
on the palms of the hands and soles of the feet; it may also appear on
the buttocks and/or genitalia.
• A person with HFMD may have only the rash or only the mouth sores.
Contagious Period
• Infected persons are most contagious during the first week of the
illness.
• The viruses that cause HFMD can remain in the body for weeks after a
patient's symptoms have gone away.
36. Diagnosis
• Throat swab
• Stool analysis
Treatment
• There is no specific treatment for HFMD.
• Symptoms can be treated to provide relief from pain from mouth sores
and from fever and aches.
• Fluid intake should be enough to prevent dehydration (lack of body
fluids). If moderate-to severe dehydration develops, it can be treated
medically by giving fluids through the veins.
37. Prevention
Wash hands carefully
Disinfect common areas
good hygiene
Isolate contagious people
• Drink boiled water and eat cooked food only
• Thoroughly wash all eating and drinking utensils
• Avoid spoon , towel , cups , etc. sharing
• Avoid close contact such as kissing, hugging , etc with people with
hand , foot and mouth disease
38. TUBERCULOSIS - TB
Infectious disease caused by Mycobacterium Tuberculosis, which primarily
affects the lungs but is also capable of involving almost any site in the body
including the oral cavity.
Transmission
• Aerosolized droplets 5µm in diameter.
• Estimated 5-200 orgs required for infection
• Spreads through the air when a person; Sneezes, Coughs, Speaks or Talks
Diagnosis
• Chest x-ray
• Sputum analysis – AFBs
• CT scan
• Tuberculin skin test (TST or PPD)
39. Relationship of TB with Dentistry
• In dentistry, the incidence of exposure to an active TB patient is quite
low.
• Oral lesions of TB are uncommon, with most cases appearing as a
chronic painless ulcer.
• This does not mean that the dental health care worker should not
concern themselves with good diagnostic and preventive measures and
realization that patients and other HCWs may be infected with TB.
40. Safety measures by Dentists
• Patient Education; Should educate the patient regarding his/her
severe health condition and needs to make sure that the patient should
cover his/her mouth and nose while coughing or sneezing.
• Barriers; Dentist and dental nurse should wear gloves, eye glasses
and mask to prevent the possibility of microorganism from being
transferred during dental procedures.
• Sterilization; Proper sterilization of all the instruments should be
done before and after the treatment of that patient. The dentist should
also disinfect his/her hand after treatment.
41. Common Symptoms of TB Disease
• Cough (2-3 weeks or more)
• Coughing up blood
• Chest pains
• Fever
• Night sweats
• Feeling weak and tired
• Losing weight without trying
• Decreased or no appetite
• If you have TB outside the lungs, you may have other symptoms
42. Pathogenesis
• Droplet nuclei containing tubercle bacilli are inhaled, enter the lungs
and travel to the alveoli.
• Tubercle bacilli multiply in the alveoli.
• A small number of tubercle bacilli enter the blood stream and spread
throughout the body.
• Within 2-8 weeks, special immune cells called macrophages ingest and
surround the tubercle bacilli (granuloma).
• If the immune system cannot keep the tubercle bacilli under control,
the bacilli begin to multiply rapidly (TB d’se). This process can occur
in different areas in the body such as lungs, kidneys, brain, bone or
mouth.
43. Treatment
• Four drugs for two months Isoniazid – Rifampicin – Ethambutol -
Pyrazinamide
• Two drugs for four or seven months Isoniazid - Rifampicin
• DOTS (Directly Observed Treatment Short-course ) is given
44. SYPHILIS
Syphilis is a contagious bacterial infection that is transmitted through
contact with an chancre on an infected person, usually during intimate
sexual contact.
• classified as an STI (sexually transmitted infection) caused by the
bacterium Treponema Pallidum.
• Contracted through contact with a chancre during sexual contact or
passed from mother to baby called congenital syphilis
• Progresses through 4 stages; primary, secondary, latent and tertiary
stages.
• Stages get progressively worse if left untreated highly contagious
potentially fatal
45. Primary Stage
• A small painless ulcer like sore called a chancre appears at the site of
initial infection
• Chancre usually appears 2-3 weeks after the initial infection
• A rash near the chancre may also appear, the chancre may go
unnoticed because of the location in the mouth, anus, vagina or throat
• Usually disappears in 4-6 weeks without treatment
• The bacteria is still multiplying in the body and is contagious
Chancre
46. Secondary Stage
• Begins a few weeks to months after the chancre heals
• Rash with flat and raised patches - frequently on palms, soles, can be
anywhere on body
• Lesions in the mouth, vagina, penis, mucus patches; condyloma Lata
• Fever
• Swollen glands
• Loss of appetite
• Fatigue
• Aches and pains in bones or joints
• Patchy hair loss
• Chancre still present in some cases
• Here bacteria has spread to the blood most contagious stage most
contagious stage resolves in 2-6 weeks without treatment
Palm
Tongue
47. Latent Stage
• Characterized by the lack of symptoms
• No symptoms may appear for months or years
• Syphilis is still alive in the body.
• Bacteria starts to damage the internal organs; brain, heart, sexual organs.
• Damage can go unnoticed until the next stage.
Tertiary Stage
• Occurs many years later, 5 to 50 years after secondary stage symptoms disappear
• Characterized by paralysis, gradual blindness, deterioration of the brain, loss of
co-ordination , shooting pains, and death
• Gummatous syphilis - destructive lesions of bones, skin or liver
• Cardiovascular syphilis - severe damage to heart and blood vessels, inflammation
of the aorta, heart disease
• neurosyphilis - nervous system disorders; brain, eye, spinal cord.
48. Mode of transmission
1. Sexual intercourse
2. Blood transfusion
3. Contaminated needles
4. Vertical transmission
5. To hospital personnel by indiscriminate handling of infected lesions
49. Diagnosis
• Dark field Microscopy
• VDRL, RPR
• FTA-ABS, MHA-TP
• Direct Fluorescent Antibody (DFA)
Treatment
Penicillin – Benzathine
Incase allergic to penicillin, Doxycycline, Erythromycin, Ceftriaxone
50. ORAL CANDIDIASIS
Oral candidiasis is the most prevalent opportunistic infection affecting the
oral mucosa, caused by the yeast, Candida albicans.
Local predisposing factors for candidiasis
• Denture wearing
• Smoking
• Atopic constitution
• Inhalation steroids
• Topical steroids
• Hyperkeratosis
• Imbalance of oral microflora
• Quality and quantity of saliva
54. Investigations
Investigation of candidiasis, is by isolation of Candida from oral samples, by-
1. Smear: Smear from the affected area, which compromises of the epithelial cells,
creates opportunities for detection of yeasts. The obtained material is fixed in
isopropyl alcohol, and air dried, and then stained with PAS. The detection of yeast,
indicates infection.
2. Swab: Taken by rubbing cotton tipped swabs, over the lesional tissue.
3. Imprint Culture: Sterile plastic foam pads dipped into Sabouraud (Sab) broth, is
placed over a lesion for 60 seconds. Pad is pressed on Sab agar plate, and incubated.
4. Impression culture: Maxillary and mandibular alginate impressions; casting in
agar; fortified with Sab broth; incubation.
5. Salivary culture: Patient expectorates 2ml saliva into sterile container; vibration;
followed by culture on Sab agar by spiral plating; followed by counting.
6. Oral Rinse: Subject rinses for 60 seconds with Phosphate buffered saline (PBS),
at 7.2 pH, 0.1 M, and returns it to the original container. This is concentrated by
centrifugation, cultured, and counted as in previous methods.
