1. Bacterial
1.1. ACTINOMYCOSIS
1.1.1. Chronic granulomatous, localized bacterial infection
1.1.2. AETIOLOGY
1.1.2.1. A.israelii, A. viscosus , A. Naeslundi, A.odontolyticus.
1.1.3. Types(according to location)
1.1.3.1. Thoracic actinomycosis
1.1.3.2. Abdominal actinomycosis
1.1.3.3. Cervicofacial actinomycosis
1.1.3.3.1. CF
1.1.3.3.2. HP
1.2. SYPHILIS
1.2.1. Chronic systemic venereal disease of bacterial etiology causing a granulomatous reaction.
1.2.2. AETIOLOGY
1.2.2.1. Treponema pallidum
1.2.3. Types
1.2.3.1. Acquired
1.2.3.1.1. Primary stage(((CHANCRE)))
1.2.3.1.2. Secondary stage
1.2.3.1.3. Tertiary stage
1.2.3.2. Congenital
1.2.3.2.1. Occurs as a result of transplacental transfer after 4th -5th months
1.2.3.2.2. CF
1.2.3.2.3. HP
1.2.4. TRANSMISSION
1.2.4.1. Direct contact of a healthy patient
1.2.4.2. Unprotected sexual intercourse
1.2.4.3. Transplacental (from mother to fetus)
1.2.4.4. Contaminated blood or blood products
1.3. TUBERCULOSIS
1.3.1. Chronic granulomatous systemic bacterial disease.
1.3.2. Infection by Mycobacterium tuberculosis.
1.3.3. incidence is AGAIN increasing alarmingly
1.3.4. PATHOGENESIS
1.3.4.1. Infection must be distinguished from ACTIVE DISEASE
1.3.4.2. Primary infection
1.3.4.2.1. always in lungs of previously unexposed persons
1.3.4.2.2. Lead to formation of localized, fibrocalcified nodule.
1.3.4.2.3. Immunosuppression is often responsible for reactivation of dormant
1.3.4.2.4. AIDS, old age, poverty and crowded conditions are considered risk factors for progression from primary to (((secondary disease)))
1.3.5. TRANSMISSION
1.3.5.1. Inhalation of micro-organisms
1.3.5.2. Eating or drinking contaminated milk (bovineTB)
1.3.5.3. Direct contact with body’s fluids like blood , saliva & urine
1.3.5.4. Blood transfusion
1.3.5.5. Mother to fetus (transplacental)
1.3.6. CF
1.3.6.1. Primary TB
1.3.6.1.1. Asymptomatic
1.3.6.1.2. Fever, pleural ,effusion may occur.
1.3.6.2. Secondary TB
1.3.6.2.1. In apex of lung
1.3.6.3. Extrapulmonary TB
1.3.6.3.1. common and can occur anywhere in body
1.3.6.4. ORAL LESIONS OF TB
1.3.6.4.1. manifest as chronic painless ulcer.
1.3.6.4.2. appear nodular, granular or even leukoplakic areas.
1.3.6.4.3. Primary TB lesions mostly involve gingiva or extraction sites.
1.3.6.4.4. Secondary TB lesions mostly seen on palate, tongue and lip.
1.3.6.4.5. Drinking milk contaminated with M.bovis can lead to non tubercular infections of cervical and oropharyngeal lymph nodes, called????
1.3.7. HP
1.3.7.1. formation of granuloma.
1.4. CANCRUM ORIS (Noma, Gangrenous stomatitis, Necrotizing stomatitis)
1.4.1. Acute, rapidly progressing, localized, bacterial infection of the orofacial tissues and jaws
1.4.2. Causative organisms
1.4.2.1. Fusobacterium necrophorum, F.nucleatum and Prevotella intermedia.
1.4.3. CF
1.4.3.1. Age
1.4.3.1.1. between 1 – 10 years old
1.4.3.2. Sex
1.4.3.2.1. Male
1.4.3.3. Site
1.4.3.3.1. Usually begins on gingivae as ANUG, then spreads facially / lingually to adjacent soft tissues.
1.4.3.4. Signs & symptoms
1.4.3.4.1. Disease begins initially in gingivae as ANUG
1.4.3.4.2. necrosis extends deeper over next few days, zones of bluish-black discoloration of overlying skin develop.
1.4.3.4.3. Other
2. Mycotic
2.1. CANDIDIASIS
2.1.1. infection with yeast like fungal organism (Candida Albicans).
2.1.1.1. It’s in oral fungal infection.
2.1.1.2. So component of normal oral flora.
2.1.2. Factors
2.1.2.1. Local
2.1.2.1.1. -Mucosal trauma - Denture wearers - Denture hygiene - Tobacco smoking - Carbohydrate rich diet - Drugs (Broad spectrum antibiotics, steroids, Immunosuppressant / cytotoxic agents) - Xerostomia
2.1.2.2. Systemic
2.1.2.2.1. -Iron deficiency anaemia - Megaloblastic anaemia - Acute leukaemia - Diabetes mellitus - HIV infection - Other immunodeficiency states
2.1.3. Classifications
2.1.3.1. Group 1(Condition to oral mucosa)
2.1.3.1.1. Acute
2.1.3.1.2. Chronic
2.1.3.2. Group 2(generalised candidates)
2.1.3.2.1. Chronic mucocutaneous candidiasis
3. Viral
3.1. HERPES SIMPLEX INFECTION
3.1.1. DNA virus.
3.1.1.1. Belongs to human herpesvirus (HHV) family, also called Herpetoviridae.
3.1.1.1.1. Other members of this family are
3.1.2. Types
3.1.2.1. HSV 1
3.1.2.1.1. Spread through saliva
3.1.2.1.2. Lesions above the waist
3.1.2.1.3. oral, facial and ocular areas including pharynx, and skin.
3.1.2.2. HSV 2
3.1.2.2.1. Transmitted through sexual contact
3.1.2.2.2. Involves genitalia and skin below the waist
3.1.3. PATHOGENESIS
3.1.3.1. 1-primary infection
3.1.3.1.1. Initial exposure to virus, no antibodies are produced.
3.1.3.1.2. Occurs in young age, often symptomatic
3.1.3.1.3. Virus taken up in sensory nerves and transported to associated ganglia.
3.1.3.2. 2-secondary/recurrent infection
3.1.3.2.1. Virus residing in ganglia is reactivated.
3.1.3.2.2. Not always symptomatic
3.1.3.2.3. sometimes patients only shed the virus through saliva.
3.1.4. Predisposing factors for reactivation of virus
3.1.4.1. Age
3.1.4.2. UV light
3.1.4.3. Emotional stress
3.1.4.4. Trauma
3.1.4.5. Menstruation
3.1.4.6. Systemic diseases or malignancy
3.1.5. Type
3.1.5.1. ACUTE HERPETIC GINGIVOSTOMATITIS (Primary herpes)
3.1.5.1.1. Commonest pattern of primary HSV infection.
3.1.5.1.2. Incubation period is 3 – 9 days.
3.1.5.1.3. CF
3.1.5.2. HERPES LABIALIS (Recurrent Herpes)
3.1.5.2.1. Can occur either at primary site or in adjacent areas.
3.1.5.2.2. Commonest sites – vermilion zone and adjacent area of lips.
3.1.5.2.3. Multiple, small, erythematous papules develop and form ((clusters ))of fluid filled vesicles.
3.1.5.2.4. Vesicles rupture and crust within 2 – 3 days and heal within 7 days.
3.1.5.2.5. HP
3.1.5.2.6. DIAGNOSIS
3.2. VARICELLA (Chickenpox)
3.2.1. similar to HSV in many respects.
3.2.2. Chickenpox represents primary infection with VZV
3.2.3. Herpes zoster or Shingles represents??
3.2.3.1. reactivation of the latent VZV residing within the ganglia.
3.2.4. spreads through droplets or direct contact with infected persons.
3.2.5. Incubation period is 10 – 21 days.
3.2.6. CF
3.2.6.1. Age
3.2.6.1.1. 5-9 years
3.2.6.2. Sex
3.2.6.2.1. Nil
3.2.6.3. Site
3.2.6.3.1. Face
3.2.6.3.2. Trunk
3.2.6.3.3. Extremities
3.2.6.4. Signs & symptoms
3.2.6.4.1. All lesions pass through phases of erythema > vesicle > pustule > crusting.
3.2.6.4.2. surrounded by zone of erythema.
3.2.6.4.3. vesicles continue to erupt for 3 – 4 days.
3.2.6.4.4. old crusted lesions are mixed with new vesicles.
3.2.6.4.5. Oral manifestations
3.2.7. HP
3.2.7.1. Same Herpes zoster are identical with those of Herpes simplex.
3.2.8. COMPLICATIONS
3.2.8.1. Children
3.2.8.1.1. Secondary skin infections
3.2.8.1.2. Encephalitis
3.2.8.1.3. Pneumonia
3.2.8.2. Adults
3.2.8.2.1. Varicella pneumonitis
3.2.8.2.2. Encephalitis
3.2.8.2.3. Pneumonia
3.2.8.2.4. Early pregnancy
3.2.9. DIAGNOSIS
3.2.9.1. H/o exposure to VZV within last 3 weeks.
3.2.9.2. cytopathological changes
3.3. HERPES ZOSTER (Shingles)
3.3.1. Herpes zoster infection occurs by reactivation of the VZV.
3.3.2. Unlike HSV, there is usually a single recurrence.
3.3.3. PREDISPOSING FACTORS
3.3.3.1. Immunosupression
3.3.3.2. Treatment with cytotoxic drugs
3.3.3.3. Radiation
3.3.3.4. Presence of malignancy
3.3.3.5. Alcohol abuse
3.3.3.6. Dental manipulation
3.3.4. CF
3.3.4.1. Age
3.3.4.1.1. Middle age to old
3.3.4.2. Sex
3.3.4.2.1. Nil
3.3.4.3. Site
3.3.4.3.1. affected sensory nerve (dermatome).
3.3.4.4. Signs & symptoms
3.3.4.4.1. Prodromal phase
3.3.4.4.2. Acute phase
3.3.4.4.3. Chronic phase
3.3.4.4.4. Oral manifestations
3.3.5. HP
3.3.5.1. Same previously
3.4. RECURRENT APHTHOUS STOMATITIS
3.4.1. known as canker sores and aphthous ulcers
3.4.2. common ulcerative disease characterized by?
3.4.2.1. development of painful, recurring, solitary or multiple ulcerations of the oral mucosa.
3.4.3. ETIOLOGY
3.4.3.1. 1. Allergies 2. Genetic predisposition 3. Hematologic abnormalities 4. Hormonal influences 5. Immunologic factors
3.4.4. Pathogenesis
3.4.4.1. Primary immunodysregulatio
3.4.4.1.1. Reduction of CD4+ T lymphocytes
3.4.4.2. Decrease in mucosal barrier
3.4.4.2.1. Trauma
3.4.4.2.2. Nutritional deficiency
3.4.4.3. Increase antigenic exposure
3.4.4.3.1. Increase cytotoxic destruction of mucosa
3.4.5. Types
3.4.5.1. RECURRENT APHTHOUS MINOR
3.4.5.1.1. CF
3.4.5.2. RECURRENT APHTHOUS MAJOR
3.4.5.2.1. CF
3.4.5.3. RECURRENT HERPETIFORM ULCERATIONS
3.4.5.3.1. CF
3.4.5.3.2. HP
3.4.5.3.3. CYTOLOGICAL SMEAR
3.5. (AIDS)
3.5.1. ROUTES OF TRANSMISSIO
3.5.1.1. Sexual contact
3.5.1.2. Infected blood / blood products
3.5.1.3. Intravenous drug abuse
3.5.1.4. Transplacental transfer
3.5.2. PATHOGENESIS
3.5.2.1. <—Virus enters body
3.5.2.1.1. DNA incorporated into primary target cell(CD4+)
3.5.2.2. Abs to virus are formed but are not protective
3.5.2.3. Virus can remain silent or cause cell death
3.5.2.3.1. as a result, decrease in helper T- cells occurs, leading to???
3.5.2.4. Asymptomatic stage lasting for about 8 – 10 years after which the final symptomatic stage develops.
3.5.3. CF
3.5.3.1. patient may be asymptomatic or develop acute response similar to infectious mononucleosis.
3.5.3.1.1. After inoculation
3.5.3.2. fever, generalized lymphadenopathy, sore throat, myalgia, diarrhea, maculopapular rash
3.5.3.2.1. Acute response—>
3.5.3.3. opportunistic infections (pneumonia, CMV, HSV, TB etc) and neoplastic processes (Kaposi sarcoma, Non-Hodgkin’s lymphoma)
3.5.3.3.1. Symptomatic phase
3.5.4. ORAL MANIFESTATIONS
3.5.4.1. Group 1 (lesions strongly associated with HIV):
3.5.4.1.1. 1. Oral candidal infections
3.5.4.1.2. 2. Hairy leukoplakia
3.5.4.1.3. 3.HIV associated periodontitis
3.5.4.1.4. 4. Kaposi sarcoma
3.5.4.1.5. 5. Non-Hodgkin’s lymphoma
3.5.4.2. Group 2 (lesions less commonly associated with HIV):
3.5.4.2.1. 1. Aphthous ulcers (oropharyngeal region)
3.5.4.2.2. 2. Idiopathic thrombocytopenia
3.5.4.2.3. 3. Salivary gland disorders
3.5.4.2.4. 4. Viral infections (apart from EBV)
3.5.5. DIAGNOSIS
3.5.5.1. Screening test (ELISA)
3.5.5.1.1. most commonly used test. But it can show false positive results.
3.5.5.2. Western Blot test
3.5.5.2.1. a test to detect viral antibodies. More accurate than ELISA.
3.6. HAIRY LEUKOPLAKIA
3.6.1. chronic, localized viral infection
3.6.2. Caused by Epstein-Barr virus.
3.6.3. CF
3.6.3.1. Age
3.6.3.1.1. Young age
3.6.3.2. Sex
3.6.3.2.1. Males
3.6.3.3. Site
3.6.3.3.1. Lateral borders of tongue, bilaterally
3.6.3.4. Signs & symptoms
3.6.3.4.1. Asymptomatic, slowly spread
3.6.3.4.2. Non scrapable
3.6.3.4.3. papillary, greyish-white lesion.
3.6.4. HP
3.6.4.1. hyperparakeratosis & acanthosis.
3.6.4.2. peripheral margination of nuclear chromatin is seen, called nuclear beading