Oral Pathology

1. A B AC T E R I A L I N F E C T I O N I S T H E I N VA S I O N O F
B O DY T I S S U E S B Y D I S E A S E - C AU S I N G B AC T E R I A ,
T H E I R M U LT I P L I C AT I O N A N D T H E R E AC T I O N O F
B O DY T I S S U E S TO T H E S E M I C RO O RG A N I S M S A N D
T H E TOX I N S T H AT T H E Y P RO D U C E .
Bacterial Infection

2. Topics
 Leprosy
 Tularemia
 Botryomycosis
 Actinomycosis
 Syphilis
 Gonorrhoea
 Tuberculosis
 Cat-Scratch Disease
 Scarlet fever
 Diphtheria
 Meliodosis
 Tetanus
 Rhinoscleroma
 Noma

3. Leprosy
 Also called as Hansen’s Disease.
 Caused by Mycobacterium leprea.
 Affects skin, peripheral nerves, upper respiratory tract,
eyes, testes, bones and joints.
 It is unique in exhibiting dopa oxidase activity.
 Staining smears taken from skin and nasal mucosa with ZN
method demonstrate the presence of the bacilli.

4. Tuberculoid Type Lepramatous Type
 Lesions are characterised by
single or multiple macular,
erythematous eruptions.
 Peripheral nerves are involved
with loss of sensation
accompanied by loss of
sweating of affected skin.
 These develop early
erythematous macules or
papules that lead to progressive
thickening of skin and
characteristic nodules.
 Facial nerve paralysis occurs
due to facial nerve involvement.
Types

5. Histopathology
Well formed granulomatous
inflammation demonstrating
clusters of histiocytes and
macrophages

6. Pathogenesis
 Host’s defenses are crucial in determining patient’s
response to disease.
 Tuberculoid type of leprosy is characterized by
strong CMI, positive lepromin test, granuloma
formation, paucity of bacilli.
 Lepromatous type of leprosy is characterized by
suppressed CMI, negative lepromin test, no
granuloma formation and multiple bacilli.

7. Diagnosis and Treatment
 Tests for humoral responses are monoclonal antibodies,
ELISA, PCR, etc.
 In children sweat function test is used.
 MDT is used which includes rifampicin, dapsone and
clofazimine is used for treatment.
 Tuberculoid type rifampicin + dapsone for 6 months.
 Lepramatous type rifampicin + dapsone + clofazimine

8. Tularemia
 Also called Rabbit Fever.
 It is highly communicable and transmitted from
infected mammals to humans.
 It occurs more frequently in adults.

9. Clinical Features
 Based on site of infection, tularemia has 6 clinical
symptoms:
a). Ulceroglandular(most common)
b). Glandular
c). Oropharyngal
d). Pneumonic
e). Oculoglandular
f). typhoidal

10. Treatment
 Disease responds to antibiotic therapy.
 Streptomycin is the drug of choice.
 Also responds well to adequate doses of gentamicin
and tetracycline.

11. Botryomycosis
 It is a chronic granulomatous infection.
 A number of common bacteria such as
staphylococcus, streptococcus, Escherichia,
pseudomonas and probably many others may serve
as etiologic agents of the disease.

12. Histopathology

13. Treatment
 This condition may be caused by a variety of
different micro organisms of low virulence.
 Therefore, pathogenesis may be related more to a
modified host resistance or tissue hypersensitivity
than to a specific micro organisms.
 Treatment is non specific, however surgical
invention aids in cure.

14. Actinomycosis
 It is a chronic, granulomatous, suppurative and fibrosing disease
caused by anaerobic or microphilic gram positive, non acid fast,
branched filamentous bacteria.
 They are a normal flora of oral cavity, colon and vagina.
 It is characterized by formation of abscesses that tend to drain by
formation of sinus tracts.
 They are classified according to the location of lesions as-
-cervicofacial
-abdominal
-pulmonary forms
It appears to be an endogenous infection and not communicable.

15. Histopathology
Tongue lesions
Tonsil lesions

16. Treatment and Prognosis
 Long standing fibrosis cases are treated by draining the
abcsess, excising the sinus tract with high doses of
antibiotics.
 Surgical drainage of abcsesses and excision of sinus tract is
necessary to accelerate healing.

17. Syphilis
 It is a veneral i.e. sexually transmitted disease caused
by spirocheates, treponema pallidum.
 It is transmitted by following routes:
Coitus
Transfusion of infected blood
Mother to foetal transmission

18. Acquired syphilis Congenital syphilis
 Mainly contracted as a
veneral disease.
 It may also be acquired by
dentists while working on
infected patients in a
contagious state.
 Its divided into 3 types
based on their appearance
and type of lesions:
a).Primary
b).Secondary
c). Tertiary
 It is only transmitted
from infected mother to
foetus only.
 It is a very rare disease.
 Morphological features
are :
a). Saddle nose
b). Bony lesions,
mucocutaneous lesions
c). High palatal arch
d). Mulberry molar
Types

19. Demonstration of
treponemas Serological test
 Dark ground microscopy
 Direct flourescent
antibody staining for
T.pallidum.
 Treponemas in tissue by:
a). Silver impregnation
method
b). Immunoflourescent
staining
 Non treponemal test
 Treponemal test
Diagnosis
VDR
L
RPR
TPI TPH
A

20. Histopathology

21. Prophylaxis
 Early syphilis: Benzathine benzyl penicillin 24 lac
units i.m. in a single dose after sensitivity test.
 Late syphilis: Benzathine benzyl penicillin 24
lacs units i.m. once weekly for 3 weeks.

22. Hutchinson's Triad
 Hypoplasia of incisor and molar teeth.
 8th nerve deafness and interstitial keratitis.
 75% of congenital syphilis patients suffer from one
or more components of Hutchinson's triads.

23. Gonorrhoea
 It is a veneral disease affecting the male and female
genitourinary tract.
 It is caused by gram negative diplococci Neisseria
gonorrhoea.
 The bacterium is a strict parasite and dies rapidly
outside the host in 1 to 2 hr in exudates and in 3 to
4 days in culture.

24. Oral Manifestations
 Extra genital infection of the oral cavity occurs as a result of
oral-genital contact or inoculation through infected hands.
 Lips may develop acute painful ulceration, gingiva may
become erythematous with or without necrosis.
 Tongue may present red, dry ulcerations or become glazed
or swollen with painful erosions.
 Gonococcal pharyngitis and tonsilitis are also well
recognized.

25. Diagnosis and Treatment
 Diagnosis is established by bacteriological
examination of smear or culture.
 Organism is sensitive to large doses of penicillin or
doxycycline.

26. Tuberculosis
 It is an infectious, granulomatous disease caused by
mycobacterium tuberculosis.
 Primarily affects lungs but also affected are intestines,
bones, joints, meninges, lymph glands, skin and other
tissues.
 The bacterium is a facultative intracellular parasite.
 It causes pulmonary or generalized infection in
immunocompromised patients.

27. Pathogenesis
Bacilli-host interaction: droplet nuclei inhaled by patient
Most bacilli are exhaled by ciliary reaction and 10% enters the alveoli
Initial stage is asymptomatic but 2 – 4 weeks after infection, specific
immunity develops and accumulation of a large number of activated
macrophages at the site of primary lesion.(granulomatus or
tubercles are formed).
Lesion consists of epithelioid cells, langerhans cells, plasma cells and
fibroblasts
Central part of the lesion contains caseous necrosis (dry cheesy,
granular and yellow in appearance).
Ranne complex necrotic material may undergo calcification(in lung
parenchyma or hilar lymph nodes.
Sometimes necrotic material may liquefy, discharging in the lungs leading
to cavity formation.

28. Histopathology
Tuberculosis granulomas
demonstrated by ZN stain

29. Oral Manifestations
 Most commonly affected site is tongue. Others are
palate, lips, buccal mucosa, gingiva and frenula.
 Usual presentation is irregular superficial or deep
painful ulcers which tend to increase in size slowly.
 It may also involve the bone of the maxilla and
mandible.
 Microorganisms may enter the pulp chamber and
root canal of the tooth with an open cavity.

30. Treatment
 Isoniazid (NPH) combined with rifampicin for 9
months
 INH and rifampicin and pyrazinamide for 2
months followed by INH and rifampicin for 4
months.
 Other drugs used are streptomycin and
ethambutol.

31. Cat-Scratch Disease
 It is a condition caused by Bartonella lenselae a
gram negative bacillus demonstrable with silver
stain.
 It occurs at any age most commonly in children and
young adults by a traumatic break in the skin by
scratch or by household bite of cat, dog or monkeys.

32. Histopathology
Lymph node necrosis
Swelling due to
inflammation

33. Treatment and Prognosis
 Prognosis is good since the disease is self limiting
and regresses within a period of weeks or months.
 Incision and drainage of involved node may be
necessary.
 Antibiotic therapy is ineffective

34. Scarlet Fever
 It is a highly contagious, systemic infection.
 It occurs predominantly in children.
 It is caused by β-heamolytic streptococci, streptococcus
pyogens which produces a pyrogenic exotoxin
 These organisms produce clear heamolysis around colonies
on blood agar plates.
 Scarlet fever may reflect a hypersensitivity reaction
requiring prior exposure to the toxin.

35. Histopathology
Necrotic conective tissue

36. Oral Manifestation
 Chief manifestations are termed as ‘Stomatitis scarlatina’.
 Small, red macules may appear in the hard and soft palate and uvula which are
called Forchheimer spots.
 Palate and throat is often fiery red.
 Tonsils and faucial pillars are usually swollen and sometimes covered with a grayish
exudate.
 In early course of the disease, tongue exhibits a white coating and the fungiform
pappila are edematous and hyperemic. This phenomenon has been described
clinically as ‘strawberry tongue’.
 Later, the tongue coating is lost and appears red and glistening and smooth except
the pappliae this is called as ‘raspberry tongue’.

37. Diptheria
 It is an acute, life threatening infection and
communicable disease of skin and mucous membrane.
 Caused by toxemic strains of corneybacterium diptheria.
 Characterized by local inflammation and formation of a
graying adherent psuedomembrane which bleeds on
removal.
 Also referred as ‘The strangling angel of children’.

38. Clinical Features
 Signs and symptoms arise 1 to 5 days after exposure.
 Swelling of neck (Bull neck).
 Onset is gradual.
 Manifestations are fever, sore throat, weakness,
headache, change of voice.

39. Of patients Of tonsils
 Diptheria cases:
Pseudomembrane present
 Diptheria carriers:
Pseudomembrane absent
 On the basis of location of
pseudomembrane:
a). Pharyngeal
b). Laryngeal
c). Tracheal
d). Tonsillar
e). Nasal
f). Conjunctival
g). Cutaneous
h). Genital
Classification

40. Oral Manifestations
 Formation of ‘Diptheric Membrane’.
 In oral cavity, appears as non specific ulcers.
 Soft palate is temporarily paralysed.
 Patients have peculiar nasal twang.
 If infection spreads unchanged in repiratory tract:
a). Larynx becomes edematous, covered by pseudomembrane.
b). Husky voice
c). Suffocation if airways is not cleared.

41. Meliodosis
 Specific infection in man and animals.
 Caused by burkholderia pseudomallei.
 It is endemic in certain areas of far east including
Burma, India, Indo-china, malaysia and thialand.

42. Diagnosis and Treatment
 Diagnosed by culturing the organism from clinical and
throat sample.
 Treatment involves:
 Incision and drainage accompanied by massive antibiotic
therapy.
 Tetracycline alone or in combination with chloremphenicol
is drug of choice.

43. Acute Chronic
 Fever
 Diarrhoea
 Acute pulmonary
infection
 Death as a result of
septicemia
 In those patients who
have survived acute type.
 It is of granulomatous
type, characterized by
multiple, small, non
specific abscesses.
Clinical Features

44. Tetanus
 Tetanus is an acute infection of the nervous system
characterized by intense activity of motor neurons and
resulting in severe muscle spasms.
 It is caused by exotoxin of the anaerobic gram positive
bacillus clostridium tetani.
 Most commonly occurs in non immunized, partially
immunized or even fully immunized people.
 In infants were umbilical cord is cut with unsterile
instrument or in children with otorrhea.
 After acute trauma.

45. Pathogenesis
 Suitable anaerobic conditions favour the spores of
clostridium to enter the wounds and germinate.
 These produce tetanospasmin(potent neurotoxin)
 It binds to the peripheral motor nerve terminals and enters
the axons cell body in the brain stem and spinal cord in
a retrograde direction.
 Toxins migrate to the synapse where they block the
receptors of glycine and GABA which increases the resting
state of locomotor neurons thereby producin rigidity.

46. Generalized Tetanus Local Tetanus
 Lock jaw due to the spasm of
masseter is the first symptom.
 Dysphagia, stiffness or pain in
the neck, shoulder or back
muscles occurs concurrently.
 Laryngeal spasm leading to
asphyxia.
 Spasm of muscle near the
wound is uncommon.
 Cephalic tetanus characterized
by spasm of muscle and facial
palsy is rare.
 Acute oral infection, trauma,
TMJ dysfunction and even
hysteria may be manifested.
Types

47. Prophylaxis
 Wound debriment and booster doses of tetanus
toxoid.
 For unimmunized indivisuals, anti-tetanus
serum(ATS) 1500 units or TIG 250 units should be
given.

48. Rhinoscleroma
 It is a chronic, slowly progressive, localized infectious,
granulomatous disease caused by bacillus klebsiella
rhinoscleromatus which is a gram negative, non motile
bacillus.
 Mode of infection is through nasal exudates.
 Granulomatous lesions are chiefly found in upper
respiratory tract involving nose, lacrymal glands, orbit, skin
and paranasal sinuses.
 Oral lesions impair taste, anesthesia of the soft palate and
enlargement of the uvula and upper lip are described.

49. Treatment
 Administration of tetracycline or ciprofloxacin.
 If left untreated, outcome is fatal.

50. Noma
 It means a rapidly spreading mutilating, gangrenous
stomatitis that occurs usually in debilitated or
nutritionally deficient persons.
 Occurs chiefly in undernourished persons.
 The condition is usually seen around the gingiva and
progressed to destruction of the mouth and the lower
lip.

51. Clinical Features

52. Treatment
 The prognosis is considerably better if antibiotics are
administered before the patient reaches the final
stage.
 Immediate treatment of any existing
malnourishment further improves the probability of
saving the patient.