this seminar prepared by me will be very helpful for medical and dental students. hope u like it

2. Dr. Gaurav S.Salunkhe
PG -Student
Oral & Maxillofacial Pathology

3. Introduction
 Bacteria singular: bacterium) constitute a
large domain of prokaryotic microorganisms.
 Typically a few micrometres in length, bacteria have a
number of shapes, ranging from sphears to rods and
spirals.
 Bacteria were among the first life forms to appear on Earth,
and are present in most of its habitats. Bacteria inhabit
soil, water, acidic hot springs, radioactive waste, and the
deep portions of Earth's crust.
 Bacteria also live in symbiotic and parasitic relationships
with plants and animals.

4. What are bacteria?
Single celled organisms
Very small
Need a microscope to see
Can be found on most
materials and surfaces
E. Coli O157:H7
can make you very
sick.
Streptococcus
can cause strep
throat.
This E. coli helps you
digest food.

5. What do they look like?
Three basic shapes
 Rod shaped called bacilli
 Round shaped called cocci
 Spiral shaped
Some exist as single
cells, others
cluster together
Bacilli
Spiral
Cocci
Cluster of cocci

6. Ex: Streptococcus Ex: Lactobacillus Ex: Spirillium

8. A Closer Look – Helpful Bacteria
Pediococcus - used in
production of fermented meats
Leuconostoc cremoris – used
in the production of buttermilk and sour
cream
Lactobacillus casei – found in
human intestines and mouth to improve
digestion
Lactobacillus bulgaricus –
used in the production of yogurt
www.bioweb.usu.edu

9. 1. Syphilis
2. Tuberculosis
3. Leprosy
4. Gonorrhea
5. Noma
6. Scarlet fever
7. Actinomycosis
8. Diphtheria
9. Streptococcal tonsillitis & pharyngitis
10. Tetanus
11. Cat-scratch Disease

10. Syphilis
 Syphilis is a worldwide
chronic infection
produced by Treponema
pallidum.
 The organism is extremely
vulnerable to drying;
therefore, the primary
mode of transmission are
sexual contact or from
mother to fetus.

11. Syphilis - Treponema pallidum on
darkfield

12. Syphilis
 Although the risk of infection from blood transfusion is
negligible because of serological testing of donor,
transmission through exposure to infected blood is
theoretically possible because the organism may survive
upto 5days in refrigerator blood.
 Humans are the proven host for syphilis.
 In patients with syphilis, the infection undergoes a
characteristic evolution that classically proceeds through
three stages.
 A syphilitic patient is highly infectious during the first two
stages but a pregnant woman may transmit the infection to
the fetus, during the latent stage.

13. Syphilis
 Maternal transmission during the first two stages
mostly results in miscarriage, stillborn or an infant
with congenital malformations.
 Infection of the fetus may occur at any stage during
pregnancy but the stigmata do not begin to develop
until after the 4th month of gestation.
 The clinical changes secondary to the fetal infection
are known as congenital syphilis.

14. Syphilis
 Primary syphilis:
1. It is characterized by the chancre that develops at the
site of inoculation, becoming clinically evident 3 to 90
days after the initial exposure.
2. Progresses from macule to papule to ulcer
3. Typically painless, indurated, and has a clean base
4. Highly infectious
5. Heals spontaneously within 1 to 6 weeks
6. It could be solitary or multiple.
7. 25% present with multiple lesions

15. 8. The external genitalia and the anus are the most
common site of infection followed by the oral cavity.
9. Oral lesion are most on the lips, but the other sites
include the tongue, palate, gingiva, and tonsils.
10. Upper lip is mostly affected in males while the lower
lips is mostly affected in females.

16.  The oral lesion appears as a
painless, clean-based ulceration
or, rarely as a vascular
proliferation.
 Regional lymphadenopathy
which may be bilateral is seen in
most of the patients.
 At this time the organism
spreading systemically through
the lymphatic channels, setting
the stage for further progression.

18. Syphilis
 Secondary syphilis:
 the next stage is called secondary syphilis and is
discovered after 4-10 weeks of initial infection.
 The lesions may arise before the primary lesion has
resolve completely.
 During secondary syphilis, systemic symptoms often
arise.

19.  The most common systemic symptoms are
1. Painless lymphadenopathy
2. Sore throat
3. Malaise
4. Headache
5. Weight loss
6. Fever
7. Musculoskeletal pain
8. The consistent sign is a diffuse, painless, maculopapular
cutaneous rash which is widespread and can even affect
the palmar and plantar areas.

20.  These rashes may appear as the chancre is healing, or may
be delayed several weeks after the healing process has
completed.
 The characteristic rash of secondary syphilis is maculo-
papular (flat and slightly bumpy).
 It may appear as being rough, red, or having reddish-
brown spots on either the palms of the hands and/or the
bottoms of the feet, which is a unique characteristic of this
disease and several others. However, a rash is still a
common symptom of many other diseases, which can make
the diagnosis difficult. Sometimes rashes associated with
secondary syphilis are so faint that they are not noticeable.

23. Syphilis
 Some patients have focal
areas of intense exocytosis
& spongiosis of the oral
mucosa leading to zone of
whitish mucosa known as
mucous patch.
 Occasionally several
adjacent patches can fuse
and form a serpentine or
snailtrack pattern.

24. Syphilis
 Elevated mucous patches also may be centered over
the crease of the oral commissure and have been
termed as split papules.
 Occasionally papillary lesion may resemble HPV
infection and are known as
Condylomata lata.

25.  In patients with compromised immunity, secondary
syphilis can exhibit an explosive and widespread form
known as lues maligna.
 The symptoms are
1. Fever
2. Headache
3. Myalgia
4. Necrotic ulceration of face & scalp.

26. Syphilis
 Tertiary syphilis:
 After the secondary stage patient enters a period in
which they are free of lesions and symptoms, known as
latent syphilis.
 This period may last from 1 to 30 years.
 This stage includes the most serious complications of
vascular system, CNS, ocular region.

27. Aneurysm of the
ascending aorta.
Left ventricle
hypertrophy
Aortic
regurgitation
Congestive heart
failure
General paralysis
Psychosis
Dementia
Paresis
Tabes dorsalis
Death
Iritis
Choroidoretinitis
Argyll Robertson
pupil

28. Syphilis
 Scattered foci of granulomatous inflammation, which
may affect the skin, mucosa, soft tissue, bones, and
internal organs.
 This active site if granulomatous inflammation, is
known as gumma.
 It appears as an indurated, nodular, or ulcerated lesion
that may produce extensive tissue destruction.

29.  Intraoral lesion usually
affect the palate &
tongue.
 When the palate is
involved, the ulceration
usually perforates
through to the nasal
cavity.

30. Syphilis
 The tongue may be involved
diffusely with gummata and
appear large, lobulated, and
irregularly shaped.
 This lobulated pattern is termed
as intertitial glossitis.
 This is thought to be caused due
to contracture of the lingual
musculature after healing of the
gumma.
 Diffused atrophy and loss of the
papillae produce a condition
called luetic glossitis.

31. Syphilis
 Congenital syphilis:
 In 1858 sir Jonathan Hutchinson described the changes
found in congenital syphilis and defined the 3
pathognomic diagnostic features, known as
Hutchinsons’s traid:
1. Hutchinsons’s teeth
2. Ocular intertitial keratitis
3. Eighth nerve deafness
Few patients exhibits all the three features

32. Hutchinsons’s teeth

33.  Ocular intertitial keratitis
means corneal scarring due
to chronic inflammation of
the corneal stroma.
 It is not present at birth, it
develops at the age of 5-25 yrs.
 It may result in loss of vision.

34.  Pathophysiology
 The corneal scarring is the end result of the initial
invasion of blood vessels into the corneal stroma as
part of the inflammatory response.
 Since normal corneal tissue should be avascular and
therefore clear to allow light to pass, the presence of
blood vessel and the infiltration of cells as part of the
inflammatory process results in scarring or hazing of
the cornea

35.  Other causes
 TB
 Leprosy
 immunological response, such as a hypersensitivity
reaction.
 and parasitic infections

36. Syphilis
 This infection alters the formation of both anterior
(Hutchinsons’s incisors) & posterior dentition
(mulberry molars, Moon’s molar).
 In addition to Hutchinsons’s triad, other alteration like
1. Saddle-nose deformity
2. High arch palate
3. Frontal bossing
4. Hydrocephalus
5. Mental retardation
6. Gummas &
7. Neurosyphilis may be seen.

37. Early infections treatment:
 The first-choice treatment for uncomplicated syphilis
remains a single dose of intramuscular penicillin G or a
single dose of oral azithromycin.
 Doxycycline and tetracycline are alternative choices;
however, they cannot be used in pregnant women.
 Antibiotic resistance has developed to a number of
agents including macrolides, clindamycin,
and rifampin.
 Ceftriaxone, a third-
generationcephalosporin antibiotic, may be as
effective as penicillin based treatment.

38. Late infections treatment:
 For neurosyphilis due to the poor penetration of penicillin G into
the central nervous system it is recommended that those affected be
given large doses of intravenous penicillin for a minimum of 10
days.
 If a person is allergic, ceftriaxone may be used or penicillin
desensitization attempted.
 Other late presentations may be treated with once weekly
intramuscular penicillin G for three weeks.
 If allergic as in the case of early disease doxycycline or tetracycline
may be used but for a longer duration. Treatment at this point will
limit further progression but has only slight effect on damage which
has already occurred

39.  Primary and Secondary Stage:
 Ulcerative/ hypertrophic epithelium
 Increased vascular channels in lamina propria
 Intense chronic inflammatory reaction.
HISTOLOGICAL FEATURES

40.  Tertiary Stage:
 Pseudoepitheliomatous hyperplasia
 Granulomatous inflammation
 Coagulation necrosis with peripheral rim of fibrosis
containing fibroblasts
 Histiocytes and giant cells.

41.  Silver impregnaiton technique- Warthin Starry or
Steiner Stains shows “corkscrew like spirochaetal
organism”.

43.  Tuberculosis (TB) is an infectious disease caused
by bacteria, Mycobacterium tuberculosis.
 It was first isolated in 1882 by a German physician
named Robert Koch who received the Nobel Prize
for this discovery.
 TB most commonly affects the lungs but also can
involve almost any organ of the body.

44.  One third of the world's population is thought to have
been infected with M. tuberculosis
"Tuberculosis Fact sheet N°104". World Health Organization. November 2010.
Retrieved 26 July 2011.
 In 2007, there were an estimated 13.7 million chronic
active cases globally.
World Health Organization (2009). "Epidemiology".Global tuberculosis control:
epidemiology, strategy, financing. pp. 6–33. ISBN 978-92-4-156380-2. Retrieved
12 November 2009.
 While in 2010, there were an estimated 8.8 million new
cases and 1.5 million associated deaths, mostly occurring
in developing countries. The absolute number of
tuberculosis cases has been decreasing since 2006, and new
cases have decreased since 2002.
World Health Organization (2011). "The sixteenth global report on tuberculosis"

45.  Signs and symptoms:
 Tuberculosis may infect any part of the body, but most
commonly occurs in the lungs (known as pulmonary
tuberculosis).
 Extrapulmonary TB occurs when tuberculosis
develops outside of the lungs, although
extrapulmonary TB may coexist with pulmonary TB as
well.

46.  General signs and symptoms include
1. fever
2. chills
3. night sweats
4. loss of appetite
5. weight loss
6. Evening rise of temperature
7. and fatigue.

47. Symptoms may include chest pain and a prolonged cough
producing sputum.
Occasionally, people may cough up blood in small amounts, and in
very rare cases, the infection may erode into the pulmonary artery,
resulting in massive bleeding .

48. • Extrapulmonary TB occurs more commonly in immunosuppressed
People and young children.
•In those with HIV, this occurs in more than 50% of cases. Notable
extrapulmonary infection sites include the pleura (in tuberculous
pleurisy), the central nervous system (in tuberculous meningitis),
the lymphatic system (in scrofula of the neck), the genitourinary
system (in urogenital tuberculosis), and the bones and joints (in Pott's
disease of the spine), among others. When it spreads to the bones, it is
also known as "osseous tuberculosis". a form of osteomyelitis.
•Sometimes, bursting of a tubercular abscess through skin results in
tuberculous ulcer.
•An ulcer originating from nearby infected lymph nodes is painless,
slowly enlarging and has an appearance of "wash leather"

49.  Involvement of the skin may develop and has been
called lupus valgaris.
 The most common extrapulmonary sites in the head &
neck are the cervical lymph nodes followed by the
larynx and middle ear.
 Much less common sites are nasal cavity, nasopharynx,
oral cavity, parotid gland, & esophagus.
 Oral TB involves the gingiva, mucobuccal fold, &
extraction sites.
 Secondary lesions are more common on tongue, palate
& lip.

50.  A potentially more serious,
widespread form of TB is
called "disseminated" TB,
commonly known
as miliary tuberculosis.
 Miliary TB makes up about
10% of extrapulmonary
cases.

51. Diffuse dissemination through the vascular system may occur
and often produces multiple small foci of infection that grossly
and radiographically resemble millet seed, resulting in the
nickname, miliary tuberculosis.

52.  Drinking contaminated milk can result in a form of
mycobacterial infection known as scrofula.
 Scrofula is characterized by enlargement of the
oropharyngeal lymphoid tissue & cervical lymph node.
 Occasionally the involved lymph node may develop
caseous necrosis and form numerous sinus tracts
through the overlying skin.
 Radiographically it appears as calcified lymph node.


54.  Organism enters through sputum and reaches
mucosal tissue due to break in the surface. (primary
lesion)
 Enters through haematogenous spread and get
deposited to submucosal tissue. (secondary lesion)
ORAL MANIFESTATION

55.  PRIMARY TB
 Gingiva- most common site, and appears as diifused,
hyperemic, nodular/ papillary proliferation of gingiva.
 Mucosal lesions shows swelling, granular, nodular,or
fissured lesion.
 SECONDARY TB
 Any site in oral cavity.
 Tongue most common site.
 Irregular, deep, painful ulcer.
ORAL MANIFESTATION

56.  BONE OF MAXILLA /MANDIBLE-
 Enters by anachoretic effect/ direct migration from
open pulp chamber to periapical areas.
 Tuberculous periapical granuloma/ tuberculoma
 Painful.
 Tuberculous osteomyelitis- later case.

57.  Due to cell mediated hypersensitivity reaction
 Granuloma formation.
HISTOLOGICAL FEATURES

58. Treatment:
 Such drugs as:
1. Isoniazid
2. Rifampin
3. Pirazinamid
4. Ethambutol
5. Streptomycin (for multidrug-resistant cases)
 Combination of that drug are often used in 6-, 9-, 12-
month to 2 year.

60. Leprosy
HANSEN DISEASE
Leprosy is a chronic infectious disease produced by
Mycobacterium leprae.
Leprosy takes its name from the Latin word Lepra,
which means "scaly", while the term "Hansen's
disease" is named after the physician Gerhard Armauer
Hansen.
Because of worldwide efforts coordinated by the WHO a
dramatic decrease in the prevalence of leprosy has
been seen over the past 15 yrs.

61. Gerhard Henrik Armauer Hansen (29 July 1841 – 12 February
1912) was a Norwegian physician, remembered for his
identification of the bacterium Mycobacterium leprae in 1873 as
the causative agent of leprosy.

62. However, leprosy remains a public health problem in many area
of world.
82% of all current cases reported were from,
1. Brazil
2. India
3. Indonesia
4. Myanmar
5. Nigeria

64. Although the mode of transmission of leprosy remains uncertain,
many think that M. leprae is usually spread from person to person
in nasal droplets. Studies have shown that leprosy can be
transmitted to humans by armadillos
Although Humans are the major host , other animals like
1. Chimpanzee
2. Armadillo
3. Mangabey monkey

65.  Related to immune reaction to the organism leprosy
can be of two types:
1. Tuberculoid leprosy
2. Lepromatous leprosy
Tuberculoid leprosy- develops in patients with high
immune reaction.
Lepromatous leprosy – develops in patients who
demonstrate a reduce cell-mediated immune
reaction.

66. Clinical features
 Currently, leprosy is classified into two separate
categories, on the basis of clinical manifestations and
skin smear results.
1. Paucibacillary leprosy
2. Multibacillary leprosy
Patients showing negative smears at all sites are
grouped as paucibacillary leprosy (PB), while those
showing positive smears at any site are grouped as
having multibacillary leprosy (MB).

67. Paucibacillary leprosy – corresponds closely to the
tuberculoid pattern of leprosy .
Exhibits a small number of well circumscribed, hypo pigmented
skin lesion.
Nerve involvement usually result in anesthesia of the affected
skin, often accompanied by loss of sweating.
Oral lesion are rare in this variant.

68.  Multibacillary leprosy – correspond to lepromatous
pattern of leprosy.
 Ill-defined macules or papules on the skin that, with
time becomes thickened.
 The face is the most common site.
 Hairs including the eyebrows and lashes,
are often lost.

69.  Nasal involvement result
in nosebleeds, stuffiness,
and a loss of sense of
smell.
 The hard tissue of the
floor, septum, and
bridge of nose may be
affected.
 Collapse of the bridge of
the nose is considered
pathognomomic.

70. Oral lesions are not rare in multibacillary leprosy.
The locations affected in order of frequency are:
1. Hard palate
2. Soft palate
3. Labial maxillary gingiva
4. Tongue
5. Lips
6. Buccal maxillary gingiva
7. Labial mandibular gingiva
8. & buccal mucosa.

71. Affected soft tissue initially appears as yellow to red,
Sessile
Firm
Enlarging papules that develops in ulceration and necrosis,
followed by attempted healing by secondary intention.
Continuous infection of an area can lead to scarring & loss of
tissue.
Complete loss of uvula may occur.
Lingual lesion appears on anterior 1/3 as areas of erosion which
develops into large nodules.

72.  Facies leprosa, a term used to describe resorption of
bone in the facial region of patients with leprosy.
 It is triad of lesion consisting of
1. Atrophy of the anterior nasal spine
2. Atrophy of the anterior maxillary alveolar ridge
3. Endonasal inflammatory changes.

73. Histological features:
 Lepromatous type-
 Sheets of lymphocytes with vacuolated macrophages
called lepra cells are scattered throughout the lesion
 No well formed granulomas

75. Paucibacillary leprosy -6 month regimen

76. Multibacillary leprosy – 24 month regimen

77. Patients allergic to rifampin are treated with 24 month regimen

78. 78
Multibacillary (MB or lepromatous) is a 24-month treatment of rifampicin, clofazimine, and dapsone.
Paucibacillary (PB or tuberculoid) is a six-month treatment of rifampicin and dapsone.

79. Treatment
After resolution of
the infection, the
therapy must be
directed towards
reconstruction of
the damage , in
addition to
physiotherapy and
patient education.

80. Impetigo
 It is a highly contagious bacterial skin infection most
common among pre-school children.
 People who play close contact sports such
as rugby, American football and wrestling are also
susceptible, regardless of age. Impetigo is not as
common in adults.
 The name derives from the Latin impetere which
means to impeach.
 It is also known as school sores.

81. Impetigo
 Causes
 It is primarily caused by Staphylococcus aureus, and
sometimes by Streptococcus pyogenes.
 Either separately or together.

82. Impetigo
 Transmission
 The infection is spread by direct contact with lesions or
with nasal carriers.
 Intact epithelium is normally protective, therefore most
cases arise in area of dermatitis or previous trauma such
as abrasion, or cuts.
 The incubation period is 1–3 days.
 Dried streptococci in the air are not infectious to intact
skin. Scratching may spread the lesions.

83. Classification
Impetigo
Impetigo contagiosa Bullous impetigo
Ecthyma

84. Impetigo
 Clinical features.
Most commonly occurs on the skin of the face or the
extremities.

85.  Impetigo contagiosa
 This common form of impetigo, also called nonbullous
impetigo, most often begins as a red sore near the nose
or mouth which soon breaks, leaking pus or fluid, and
forms a honey-colored scab, followed by a red mark
which heals without leaving a scar.
 Sores are not painful, but may be itchy.
 Lymph nodes in the affected area may be swollen, but
fever is rare. Touching or scratching the sores may
easily spread the infection to other parts of the body.
 Ulcerations with erythema and scarring also may
result from scratching or abrading of the skin.

86.  Bullous impetig
 It is mainly seen in children younger than 2 years,
involves painless, fluid-filled blisters, mostly on the
arms, legs and trunk, surrounded by red and itchy
skin. The blisters may be large or small. After they
break, they form yellow scabs.

87.  Ecthyma
 In this form of impetigo, painful fluid- or pus-filled
sores with redness of skin, usually on the arms and
legs, become ulcers that penetrate deeper into the
dermis. After they break open, they form hard, thick,
gray scabs, which sometimes leave scars.
 Ecthyma may be accompanied by swollen lymph
nodes in the affected area.

88. Treatment
 Topical or oral antibiotics are usually prescribed.
 Treatment may involve washing with soap and water and
letting the impetigo dry in the air.
 Mild cases may be treated with bactericidal ointment,
such as mupirocin, which in some countries may be
available over-the-counter. More severe cases require oral
antibiotics, such as dicloxacillin, flucloxacillin
or erythromycin.
 Alternatively amoxicillin combined with clavulanate
potassium, cephalosporins (1st generation) and many
others may also be used as an antibiotic treatment.

89. Erysipelas
 Erysipelas Greek -red skin; also known as "Ignis
sacer", "holy fire", and "St. Anthony's fire.
 It is an acute infection of the upper dermis and
superficial lymphatics, usually caused
by streptococcus bacteria.
 Erysipelas is more superficial than cellulitis, and is
typically more raised and demarcated.
 Also called as SAINT ANTHONY’s FIRE- because
the lesion is similar to the French house of St.
Anthony, which has fiery red walls.

90. Signs and symptoms
 Patients typically develop symptoms including
high fevers, shaking, chills, fatigue, headaches,
vomitng, and general illness within 48 hours of the
initial infection. The erythematous skin lesion
enlarges rapidly and has a sharply demarcated raised
edge.
 It appears as a red, swollen, warm, hardened and
painful rash, similar in consistency to an orange peel.
 More severe infections can result in vesicles, bullae,
and petechiae, with possible skin necrosis.
 Lymph nodes may be swollen, and lymphedema may
occur. Occasionally, a red streak extending to the
lymph node can be seen.

92. Signs and symptoms
 The infection may occur on any part of the skin
including the face, arms, fingers, legs and toes, but it
tends to favor the extremities.
 Fat tissue is most susceptible to infection, and facial
areas typically around the eyes, ears, and cheeks.
Repeated infection of the extremities can lead to
chronic swelling.
 Butterfly shaped lesion on face, involving cheeks and
bridge of nose.
 Eyelids become edematous and shut.

93. Treatment
 Antibiotics

94. It is a highly contageous systemic infection occuring
predominantly in children.
It is similar to tonsillitis & phayringitis.
It is regarded as separate entity because of its nature
of the toxin.
A number of different strains may produce this
disease.

95. Causes
 The disease itself is caused by secretion of pyrogenic exotoxins
by the infecting Streptococcus.
 Zabriskie, J. B. (1964). "The role of temperate bacteriophage in the production
of erythrogenic toxin by Group A Streptococci". J Exp Med 119 (5): 761–780
 Most of the clinical features are caused
by erythrogenic toxin, a substance
produced by the bacterium Streptococcus
pyogenes (group A strep.)

96.  Incubation period- 3 to 5 days.
 Enters through pharynx.
 Pharyngitis, tonsillitis, headche, chills, fever,
vomiting.
 Enlargement of lymph nodes.
 Diffuse, bright, scarlet skin rash on 3rd day.
 Occur in skin folds
 Due to damage to vascular epithelium
 Dilatation of blood vessels
 Hyperemia.
CLINICAL FEATURES

97. Samall papules of normal colour erupts through these
rashes giving a characteristic “Sand paper” feel to the
skin.
 “Pasta lines”- rashes prominent in the areas of skin fold
 Sun burn with goose pimples
 Rash subsides after 6-7 days followed
by desquamation of palms and soles.

98.  Stomatitis scarlatina
 Palatal mucosa- congested,petechiae
 Palate and throat- fiery red
 Tonsils- swollen and covered with greyish white exudate.
 Tongue- early in the course of the disease the tongue
exhibits a white coat & the fungiform papillae are
edematous projecting above the surface as small red knobs-
white strawberry/ strawberry tongue.
 The coating of the tongue is soon lost and this organ
becomes deep red, smooth, except for the swollen papillae
the tongue in this phase is called the “red strawberry/
raspberry tongue”.
ORAL MANIFESTATIONS

99.  Bacterial dissemination
 Hypersensitivity to bacterial toxins
 Rhinitis
 Sinusitis
 Abscess
 Arthritis etc.
COMPLICATIONS

100. Treatment
 Antibiotics- penicillin, cephalexin
 Local applications- mupirocin relieves discomfort

101. (Strangling angel of the children)

102. Cause
 Diphtheria (Greek diphthera) "pair of leather scrolls")
is an upper respiratory tract illness caused
by Corynebacterium diphtheriae.
 A facultative anaerobic, Gram-positive bacterium.

103. PATHOGENESIS
 Diphtheria is an infectious disease spread by direct
physical contact or breathing the aerosolized
secretions of infected individuals.

104.  Bacilli at the site of entry multiply and liberates toxins.
 These toxins induce initial edema and hyperaemia
followed by epithelial necrosis and acute
inflammation.
 Coagulation of fibrin and purulent exudates produces
a pseudomembrane consist of dead cells, leukocytes,
erythrocytes, and the bacteria.

105. Signs and symptoms
 The symptoms of diphtheria usually begin two to seven
days after infection.
 Symptoms of diphtheria include
1. fever of 38°C (100.4°F), low grad fever.
2. chills,
3. fatigue,
4. bluish skin coloration (cyanosis),
5. sore throat, hoarseness, cough,
6. headache,
7. difficulty swallowing,
8. painful swallowing,
9. difficulty breathing, rapid breathing, foul-smelling
10. bloodstained nasal discharge
11. and lymphadenopathy.

106.  Diphtheric membrane- which bleeds when stripped off.
 Extends to involve soft palate, buccal mucosa, tongue, lips.
 Bull neck appearance.
 3-5 weeks- soft palate paralysed
 Nasal twang
 Nasal regurgitation
 Later cases- membrane extends to larynx- husky voice.
 If airways not cleared- suffocation.
ORAL MANIFESTATIONS

107. Diphtheritic croup
 Laryngeal diphtheria can lead to a characteristic
swollen neck and throat, or "bull neck".
 The swollen throat is often accompanied by a serious
respiratory condition, characterized by a brassy or
"barking" cough, stridor, hoarseness, and difficulty
breathing, and historically referred to variously as
"diphtheritic croup", "true croup“, or sometimes
simply as "croup“.

108. An adherent, dense, grey
pseudomembrane covering the tonsils is
classically seen in diphtheria

109. Diagnosis
 Laboratory criteria
 Isolation of Corynebacterium diphtheriae from a gram
stain or throat culture from a clinical specimen.
 Culture- Pai agar, Cystine tellurite agar.
 Histopathologic diagnosis of diphtheria by a stain
called "Albert's Stain“, Ponder’s, Neisser’s.
 Clinical criteria
 Upper respiratory tract illness with sore throat
 Low-grade fever (>102 °F (39 °C) is rare)
 An adherent, dense, grey pseudomembrane covering
the posterior aspect of the pharynx. In severe cases, it
can extend to cover the entire tracheobronchial tree.

110. Treatment
 Antibiotics are used in patients or carriers to
eradicate C. diphtheriae and prevent its transmission
to others, either:
 Metronidazole
 Erythromycin (orally or by injection) for 14 days
(40 mg/kg per day with a maximum of 2 g/d), or
 Procaine penicillin G given intramuscularly for 14 days
Patients with allergies to penicillin G or erythromycin
can use rifampin or clindamycin.
 Diphtheria antitoxin

112.  It is a chronic granulomatous suppurative & fibrous
disease caused by anaerobic or microaerophilic
gram+, non acid fast, branched filamentous bacteria.
 Commonly isolated organisms are: A. israelii,, A.
viscosus, A. odontolyticus.
 Actinomyces is a common inhabitant of the oral cavity
even in the absence of any specific infection, hence the
organism can be cultured from tonsils, carious teeth ,
non vital root canals, dental plaque, calculus, gingival
sulcus & periodontal pockets

113. CLASSIFICATION
 Actinomycosis can be classified anatomically
according to the location of the disease:
Cervicofacial
Abdominal
Pulmonary forms

114. Epidemiology
• Males > females.
• Peak incidence in middle age.
• Incidence has decreased due to improved oral
hygiene and antibiotics.
 Actinomyces is a common inhabitant of the oral
cavity even in the absence of any specific infection,
hence the organism can be cultured from carious
teeth , non vital root canals, dental plaque,
calculus, gingival sulcus & periodontal pockets

115. Pathogenesis
 It is not clearly known, it appears to be
endogenous infection and not communicable.
 It is not an opportunistic infection.
 Disruption of the mucosal barrier is the 1st step in
the invasion of bacteria.
 Initial acute inflammation is followed by chronic
inflammation.
 Lesions appears as single or multiple indurations.
 Pus from the abscess shows the presence of typical
‘sulphur granules’ and neutrophils which is
diagnostic of the disease.

116.  Occurs in association with HIV infection, organ
transplantation, chemotherapy, herpes , & in
patients with serious systemic illness.
Cervicofacial Actinomycosis

117. Clinical features
 Cervicofacial type is the
most common.
 The organism may enter
through the oral mucous
membrane, to the soft
tissue or spread to the
salivary gland, bone or
even the skin of the face
and neck.
 It produces swelling and
indurations of the tissue.

118.  These soft tissue
swellings eventually
develop into one or more
abscesses, which tends to
discharge upon a skin
surface, rarely a mucosal
surface, liberating pus
containing the typical
“sulfur granules”.

119.  The skin overlying the abscess is purplish-red,
indurated, wood feel and has drained to heal.
 Because of the chronicity of the disease, new abscess
develop and perforate the skin surface.
 The patient over a period of time, may show a great
deal of scarring and disfigurement of the skin.

120.  Infection of the soft tissue may extend to the
mandible-maxilla.
 In maxilla it may result in actinomycotic osteomylitis,
it may future result in cranium meninges or the brain
itself.
 In bones the destruction is more extensive, at the apex
of the teeth and may result in pulp-related infections
like periapical granuloma or cyst.

121.  Abdominal form-
 Its an extremely serious form and carries a high
mortality rate.
 Fever
 Chills
 Nausea
 Vomiting
 Pain
 Palpable abdominal mass

122.  Pulmonary form-
 Fever
 Chills
 Cough
 Pleural pain

123. Histological features
•Typical lesion is a granulomatous one showing central abscess formation which
shows characteristic colonies of microorganisms.
•These colonies are floating in a sea of PNL, associated with MULTINUCLEATED
GIANT CELLS & macrophages around the periphery of the lesion.
•Filaments stains with haematoxylin, whereas the ends of filament show
eosinophilia.
•The peculiar appearance of the colonies, with the peripheral radiating filaments is
called ‘ray fungus’.
•Tissue surrounding the lesion exhibits fibrosis.
•Methanamine silver stain can demonstrate the organism better

124. colonies of bacteria

125. Grocott-Gomori methenamine-silver nitrate stain (A) and hematoxylin-
eosin stain (B), both showing a sulfur granule in a patient with
actinomycosis.

126. Treatment
 Draining the abscess,
 Excising the sinus tract with high doses of
antibiotics .
 Penicillin,
 Tetracycline
 & Erythromycin.

128.  It is a Chronic granulomatous disease which was 1ST
recognized 100 yrs ago in horse.
 Caused by “Actinobacillus.

129.  Affects skin/ mucosa.
 Occur in patients with impaired immunity or systemic
disorder- diabetes, HIV.
 Can disseminate along liver, lungs, kidney.
 Mimics actinomycosis
 Chronic granulomatous mass with multiple ulcers and
sinuses.
 Tongue- nodular swelling without sinuses.
CLINICAL FEATURES

130.  Granulomatous area comprised of-
 Suppurative foci containing grains and granules
forming around microrganisms.
 Grains and granules are eosinophilic, PAS negative and
methamine negative.
 Eosinophilic peripheral club formation is absent.
HISTOLOGICAL FEATURES

131. Foci of suppuration

132.  Non specific, as the definite cause is not known.
TREATMENT

133. Also known as Pahvant Valley plague,
rabbit fever, deer fly fever, and
Ohara's fever

134.  Caused by Francisella tularensis
 Also called as- Bacillus/Pasteurella tularensis
 Gram –ve, non motile bacillus.
 Caused by contact with infected rodents and rabbits to
humans, either by eating contaminated meat, bite of
infected deer fly, or skinning freshly killed infected
animals.
CAUSE

135. Pathogenesis
 F. tularensis is a facultative intracellular bacterium
that is capable of infecting most cell types but
primarily infects macrophages in the host organism.
 F. tularensis entry into the macrophage occurs
via phagocytosis and the bacterium is sequestered
from the interior of the infected cell by a phagosome.
 F. tularensis then breaks out of this phagosome into
the cytosol and rapidly proliferates. Eventually the
infected cell undergoes apoptosis, and the progeny
bacteria are released to initiate new rounds of
infection.

136.  F. tularensis strains produce different hemolytic
agents, which may facilitate degradation of the
phagosome.
 Tularensis undergoes asexual replication. Bacteria will
divide into two daughter cells, each of which contains
identical genetic information. Genetic variation may
be introduced via mutation or horizontal gene
transfer.
 Incubation period- 7 days.

137.  6 characteristic clinical syndromes-
 Ulceroglandular (most common)
 Glandular
 Occuloglandular
 Oropharyngeal
 Pneumonic
 Typhoid
CLINICAL FEATURES

138.  Headache, nausea, vomiting, chills
 Ulcers
 A single cut or sore on the skin develops into ulcer.
 Lymphatic vessels swells, painful
 Enlarged lymph nodes.
 OTHERS- eye involvement, conjunctivitis, pneumonia,
pleuritis etc.
ULCEROGLANDULAR

139. Ulceroglandular
most common cutaneous
ulcers

140. Occuloglandular

141. Tularaemic cervical lymphadenopathy
Axillary
lymphadenopathy

142.  Necrotic ulcers of oral mucosa or pharynx.
 Sever Pain
 Generalized stomatitis.
 Regional lymphadenitis arise in submaxillary and
cervical group of lymph nodes.
ORAL MANIFESTATIONS

143.  Antibiotic- Streptomycin, gentamycin, tetracycline
 (F. tularensis is easy to aerosolize, highly infective and
no of organisms needed to infect is very less, it is
considered to be “biological weapons”.)
TREATMENT

145.  Bacillus Psudomonas Peudomallei
 Aerobic, gram –ve, non acid fast, rod shaped bacilli.
CAUSE

146.  The mode of transmission is not from man to man or
from infected animal to man, organisms are abundant
in soil and stagnant water.
 Human infection occurs through contamination of
skin abrasion by infected water or soil.
 Risk factors- diabetes
thalassemia
 It is endemic in certain parts of east countries, like
Burma, India, China, Indochina, Malaysia, Thailand.

148. Pathogenesis
 Pseudomallei is a facultative intracellular pathogen that
can invade and replicate inside various cells, including
polymorphonuclear leukocytes and macrophages and some
epithelial cell lines.
 After invasion into the cell, B.pseudomallei escapes from
endocytic vacuoles into the cell cytoplasm,and induction of
actin polymerization at one bacterial pole leads to
membrane protrusions, with cell-to-cell spread.
 Additional survival factors are the ability of B.
pseudomallei to form antibiotic-resistant small-colony
and the ability of mucoid variants with large extracellular
polysaccharide glycocalyx structures to form biofilm-
encased microcolonies that are also relatively antibiotic-
resistant.

149. Pathogenesis
 The disease can manifest as Acute, Sub acute, and
Chronic disease
 Incubation may be as short as 2 – 3 days
 Latent infections can occurs after months to years

150. Progress of Infection
 The infection starts with non specific lesion at the
inoculum, where there can be break in the skin.
 Lead to septicemia
 Most common form is pulmonary infection
 Can lead to suppurative infection and bacterimia

151.  Acute form- fever, diarrhoea, haemoptysis, pulmonary
infection
 Septicemia occurs in few days to weeks.
 Chronic form - develops in patients who survived acute
form.
 Granulomatous type
 Multiple, small abscess in viscera, lymphnodes, bones
which often leads to draining Sinus tracts.
Clinical features

152. Respiratory Infection
 The most dangerous
infection can be associated
with respiratory infection
 Can lead to suppurative
lesions.
 Consolidations of upper
lobe of the lung
 Can mimic tuberculosis.
 Progressive illness can
produce cavities

153. Spreading lesions
 Systemic infections
spread from the
primary lesions on the
skin.
 Can spread to lungs,
Myocardium, Liver and
Bone.
 Can present with
unexplained systemic
disease.

154.  Incision and drainage
 Antibiotics
 Tetracycline/chloramphenicol
TREATMENT

155. (LOCK JAW)

156.  Tetanus Ancient Greek: tetanos “taut”, and "to
stretch") is a medical condition characterized by a
prolonged contraction of skeletal muscle fibers.
 Infection generally occurs through wound
contamination and often involves a cut or deep
puncture wound. As the infection progresses,
muscle spasms develop in the jaw (thus the
name lockjaw) and elsewhere in the body.

157.  Exotoxin of anaerobic, gram +ve bacillus
 Clostridium.tetani
 Enters through deep cuts in skin and mucosa.
 Occurs always in nonimmunized individuals.
 Less often in immunized.
 Occur mainly in Asia because-
 Umbilical cord of newborn is cut with an unsterile
instrument.
 Women with unsterile handling of genital tracts.
CAUSE

158. How it forms…
 The nonencapsulated spore-forming bacterium
Clostridium tetani causes Tetanus.
 Spores that gain entry can survive for months to
years.
 Under anaerobic conditions, these spores geminate
and produce tetanospasmin. Tetanospasmin that is
released by the maturing bacilli is distributed via the
lymphatic and vascular circulations to the end plates
of all nerves. Tetanospasmin then enters the nervous
system peripherally at the myoneural junction and is
transported centripetally into neurons of the central
nervous system (CNS).

159. How it forms… (cont.)
 These neurons become unable of neurotransmitter
release. The neurons, which release gamma-
aminobutyric acid (GABA) and glycine, the major
inhibitory neurotransmitters, are sensitive to
tetanospasmin, leading to failure of inhibition of
motor reflex responses to sensory stimulation. This
results in generalized contractions of the agonist and
antagonist musculature characteristic of a tetanic
spasm. The shortest peripheral nerves are the first to
deliver the toxin to the CNS, which leads to the early
symptoms of facial distortion and back and neck
stiffness.

160.  Tetanus often begins with mild spasms in the jaw
muscle.
 The spasms can also affect the chest, neck, back,
abdominal muscles, and buttocks.
 Back muscle spasms often cause arching, called
opisthotonos.
 Sometimes the spasms affect muscles that help with
breathing, which can lead to breathing problems

161. Opisthotonos.

162. Clinical features
 Generalized tetanus
 This is the most common type of tetanus, representing
about 80% of cases.
 The generalized form usually presents with a descending
pattern. The first sign is trismus, or lockjaw, and the facial
spasms called risus sardonicus followed by stiffness of the
neck, difficulty in swallowing, and rigidity of pectoral
and calf muscles.
 Other symptoms include elevated temperature, sweating,
elevated blood pressure, and episodic rapid heart rate.
 Spasms may occur frequently and last for several minutes
with the body shaped into a characteristic form
called opisthotonos.
 Spasms continue for up to four weeks, and complete
recovery may take months.

163.  Neonatal tetanus
 Neonatal tetanus is a form of generalized tetanus that
occurs in newborns, usually those born to mothers
who themselves have not been vaccinated. If the
mother has been vaccinated against tetanus, the
infants acquire passive immunity and are thus
protected.
 It usually occurs through infection of the unhealed
umbilical stump, particularly when the stump is cut
with a non-sterile instrument.

164.  Local tetanus
 This is an uncommon form of the disease, in which
patients have persistent contraction of muscles in the
same anatomic area as the injury.
 The contractions may persist for many weeks before
gradually subsiding.
 Local tetanus is generally milder; only about 1% of
cases are fatal, but it may precede the onset of
generalized tetanus.

165.  Cephalic tetanus
 This is a rare form of the disease, occasionally
occurring with otitis media (ear infections) in
which C. tetani is present in the flora of the middle
ear, or following injuries to the head.
 There is involvement of the cranial nerves, especially
in the facial area.

166.  General measures:
 Aim is to remove –
 spores at the site of the wound
 prevent toxin production
 Neutralize unbound toxin
 Prevent muscular spasm
 Maintain sedation, airway and nutrition
 Antibiotics-
 Penicillin 10 million units IV for 10 days.
TREATMENT

167.  Antitoxin- neutralize circulating toxin
 Wound debridement
 Unimmunized individuals- Anti tetanus serum (ATS)
1500 units.
 Active immunization- 3 doses in the first year of life
and booster doses at school entry and at every 5 to 10
year intervals.

169. Causes
 Gonorrhea is primarily a venereal disease affecting the
male and female genitourinary tract and is sexual
transmitted.
 It is caused by Neisseria gonorrhoeae
 gram –ve,
 non-motile,
 Nonspore
 Grow in pairs (diplococci)

170. 170
Transmission
 Efficiently transmitted by:
 Male to female via semen
 Female to male urethra
 Rectal intercourse
 Fellatio (pharyngeal infection)
 Perinatal transmission (mother to infant)
 Gonorrhea associated with increased transmission
of and susceptibility to HIV infection
Epidemiology

171. Pathogenesis
 GC are ingested, and they evade host defense, and
spread through subepithelial tissues.
 Attachment is mediated by pili
 Divides every 20-30 minutes
 Leads to formation of submucosal abscess and
accumulation of exudate in lumen
 GC toxins damage cells

172. Clinical features
 Common age group is 15-29 yrs.
 It predominantly affects young persons.
 Males- urethritis, dysuria, urethral discharge,
prostatitis, balanitis.
 Females- trichomonal or candidal vaginits, cervicitis.
 Carrier symptom includes vaginal discharge,
discomfort and dysuria.
 It may affect the rectum, oropharynx, and the eye.

173.  Lips- painful ulcers with limited movement.
 Gingiva- erythematous with or without necrosis.
 Tongue- dry, red, swollen, painful erosions
 Pharyngitis, tonsillitis
 Vesicles or ulcers with gray or white pseudomembrane.
 Oral lesions are accompanied by fever and
lymphadenopathy.
 Gonococcal parotitis
ORAL MANIFESTATIONS

174. Treatment
 Antibiotics
 Preventive measure

175. Granuloma venereum/ donovanosis.

176.  Caused by chlamydia trachomatis.

177. Pathogenesis
 Organisms gain entry via trauma or abrasions.
 A small firm nodule containing ‘Donovan bodies’
occurs at the site of inoculation and is considered
classic for the disease.
 ‘Donovan bodies’ consist of large mononuclear cells in
which intracytoplasmic inclusion bodies contain the
bacteria.
 These inclusion bodies rupture, releasing infective
organisms to the surrounding tissue.

178.  PRIMARY LESION:
 Occur in genitalias, anus, and in the inguinal region.
 Papules, nodules which ulcerate to form clean,
granular lesion with rolled margins and which shows a
tendancy for peripheral enlargement.
 Inguinal ulcerations begin initially as fluctuent
swelling- “pseudobubo”.
CLINICAL FEATURES

179.  Occurs through autoinoculation.
 Lesion may occur in any oral location such as lips,
buccal mucosa, or palate, or diffusely involve the
mucosal surface.
 3 types- ulcerative/cicatricial/exuberant.
 Fibrous scar formation- limit mouth opening.
ORAL MANIFESTATIONS

180.  Granulation tissue with infiltration of PMN’s and plasma
cells.
 Pseudoepitheliomatous hyperplasia
 Large mononuclear phagocytes, containing tiny
intracytoplasmic cyst.
 The cyst contains “DONOVAN BODIES”-tiny, elongated,
basophilic, argyrophilic rods.
HISTOLOGICAL FEATURES

181.  Donovan bodies are rod-shaped, oval organisms that
can be seen in the cytoplasm of mononuclear
phagocytes or histiocytes in tissue samples from
patients with granuloma inguinale.
 They appear deep purple when stained with Wright's
stain. Wright- or Giemsa-stained smears show
clusters of encapsulated coccobacilli in
cytoplasm of mononuclear cells called
"Donovan bodies"

182.  Antibiotics
 Improvement occurs in 2-3 weeks.
TREATMENT

183. (CANCRUM ORIS,
GANGRENOUS STOMATITIS)

184.  Noma – to devour (a spreading sore)
 Occur in debilitated or nutrionally deficient persons.
 Thus it is secondary complication of systemic disease,
rather than a primary disease.
 It originate as a specific infection by Vincent’s
organism, which is complicated by streptococci,
staphylococci and diphtheria bacilli.
CAUSE

185. The reported predisposing factors include:
malnutrition (particularly A-and B-vitamins) or dehydration
poor hygiene, particularly oral
unsafe drinking water
proximity to unkempt livestock
recent illness
an immunodeficiency disease, including AIDS.

186. PATHOGENESIS
 Noma starts within the oral cavity progressing from
untreated Acute Necrotizing Ulcerating Gingivitis
(ANUG): - halitosis, bleeding gum, painful gum and
pseudomembranous ulcers.
 The Bacteroides produce a range of destructive
metabolites such as collagenase, fibrinolysin,
endotoxins, hydrogen sulfide, Indole ammonia fatty
acids, protease.
 The ulcers are covered with whitish- yellow or brown
fibrin and debris.
 The gangrenous necrosis progressively involves the
cheeks , the lips, and the adjacent bone, producing
catastrophic lesions on the face.

187.  Begins as small ulcer of the gingival mucosa
 Spreads to surrounding tissue of the jaws, lips, and cheeks by
gangrenous necrosis.
 Initial Site is an area of stagnation around a fixed bridge or
crown.
 Skin becomes inflamed, edematous and finally necrotic.
 Line of demarcation develops between normal and dead tissue.
 Large mass of tissue slough out, leaving jaw exposed.
 The commencement of gangrene is denoted as Blackening of
skin.
CLINICAL FEATURES

188.  Subcutaneous fat and buccal fat pad undergo necrosis,
in advance to other adjoining tissue.
 Odor- extremely foul from the necrotic tissue.
 High temperature during course of disease.
 Patient die from septicemia or pneumonia.

190.  Remove the cause
 Antibiotics may help if give before last stage.
Treatment and Prognosis

191. Cat scratch fever
Benign lymphoreticulosis
Benign nonbacterial regional lymphadenitis

192. Causes
 It is thought to arise after a traumatic break in the skin
due to the scratch or bite of the household cats.
 Rarely by dog or monkey.
 It is caused by Bartonella henselae
 A gram negative bacilli demonstrated by sliver stain.

193.  Children and young adults
 Caused by traumatic break in the skin due to scratch
or bite of the household cat.
 Primary lesion- papule, pustule, vesicle at the site of
injury.
 1-3 weeks- regional lymphadenitis without
lymphangitis.
CLINICAL FEATURES

194.  Nodes- painful, several cms, drains pus, sinus
formation.
 Overlying skin- edematous
 Lymphadenopathy may persist for 1-6 months.
 Low-grade, Fever, headache, nause, malaise,
abdominal pain.
 Maculopapular rash
 Parotid swelling
 Seizures

195.  OCULOGLANDULAR SYNDROME OF PARINAUD-
granuloma of eye and preauricular lymphadenopathy.
 Preauricular, submaxillary or cervical lymph nodes
may be involved.

196.  Initial stage- reticuloendothelial hyperplasia of lymph
node.
 Later stage- granulomas, suppuration, necrosis,
capsular thickening
 Epitheloid cells and multinucleated giant cells are
rarely seen.
HISTOLOGICAL FEATURES

197. Treatment and Prognosis
 Incision and drainage of lymph nodes
 Antibiotics- ineffective.
 Prognosis is good.

199.  It is a chronic, slowly growing, localised infection.
 Casused by Klebsiella rhinoscleromatosis.
 Slightly more females than males are affected .
 Patients are usually 10 to 30 years of age.
 Affects respiratory tract, nose, lacrimal glands, orbit, skin,
& sinus.
 Rhinitis stage- nasal obstruction, epistaxis
 Infiltrative stage- granulation tissue, larynx involvement,
anaesthesia of soft palate.
 Nodular stage- proliferation of nasal mass produce
“HEBRA NOSE”, laryngeal and tracheal obstruction.
CAUSE AND CLINICAL FEATURES

200. Hebra nose
 Destruction of the nasal cartilage are also noted.
 The damage may result in anaesthesia of the soft
palate, enlargement of the uvula, dysphonia, and
various degrees of airway obstruction.

201.  Proliferative granulomatous mass on lips, palate,
tongue.
 Enlargement of uvula.
 Anesthesia of soft palate.
 Impairment of taste sensation.
ORAL MANIFESTATIONS

202. Prognosis & treatment
 It is not lethal in nature and is responsive
to Tetracycline or Ciprofloxacin.
 However, if left untreated the disease can lead to
sepsis, hemorrhage or other chronic conditions that
can be fatal.

204. CAUSE and PATHOGENESIS
 It is a distinctive clinical entity originating as a
response of the tissues to a non-specific infection.
 It is a tumor like growth that is considered and
exaggerated conditioned response to minor trauma.
 Synonym= Granuloma Pyogenicum.
 Etiology-It is an exuberant tissue response to some
local irritants or minor trauma which provides a
pathway for microorganisms and show overzealous
proliferation of vascular tissue.

205.  It is a vascular lesion that occurs on both mucosa and
skin, and appears as an overgrowth of tissue due
to irritation, physical trauma or hormonal factors.
 Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine. (6th
ed.). McGraw-Hill.
 Jafarzadeh H, Sanatkhani M, Mohtasham N (December 2006). "Oral pyogenic
granuloma: a review". J Oral Sci 48 (4): 167–75.

206.  SITE-It occurs on the gingiva (75% cases).
Other sites are lips, tongue and buccal mucosa.
More common on the facial gingiva than the lingual gingiva.
 The granuloma can be smooth or lobulated.
The lesion is usually elevated , pedunculated or sessile
 commonly ulcerated and shows a tendency of hemorrhage.
SIZE-The lesion in diiferent cases may vary in size ranging from
a few millimeters to a centimeter or more in diameter.
GENDER-Female (70%)>>Male.
AGE-Children , young adults and pregnant women.
CLINICAL FEATURES

208. It is similar to that of granulation tissue except that it is exuberant
and usually well localised.
The overlying epithelium is usually atrophic but maybe hyperplastic
with or without ulceration.
There is usually a moderately intense infiltration of
polymorphonuclear leucocytes,lymphocytes and plasma cells but the
finding depends on the ulceration.
The connective tissue stroma is typically delicate although frequently
fasiculi of collagen fibres are noted coursing through the tissue mass.
Shows large amount of newly formed endothelial vascular spaces.
Old lesions give a fibrous appearance.
Pregnancy tumours-is histologically identical to pyogenic granuloma
of the gingiva frequently occurs during pregnancy and often has been
called the pregnancy tumour.
HISTOLOGICAL FEATURES

210. TREATMENT AND PROGNOSIS
Pyogenic granulomas can be treated by surgical
excision . The lesion occasionally recurs because it is not
encapsulated.

212.  Pyostomatitis vegetans is an
inflammatory stomatitis and most often seen in
association with inflammatory bowel disease,
 Namely ulcerative colitis and Crohn's disease.
 Uncommonly, it may be one of the features of orofacial
granulomatosis.

213.  Broad papillary projections
 Tiny vegetations/abscess in the area of erythema.
 Tiny pustules may be present beneath epithelium.
 Area of ulceration may coalesce to large necrosis-
“SNAIL TRACK ULCERS”
 BUCCAL MUCOSA SHOW- COBBLESTONE
APPEARANCE.
ORAL MANIFESTATIONS

214.  Papillary projection- hyperkeratotic stratified
squamous epithelium
 Connective tissue- plasma cells, lymphocytes,
neutrophils.
 Area of necrosis or microabscess formation seen
intraepithelial/subepithelial.
HISTOLOGICAL FEATURES

215. Treatment & Prognosis
 Topical corticosteroids
 Systemic steroids
 Dapsone
 Azathioprine