A presentation prepared by 3rd yr student for class presentation of Oral pathology!

1. Binaya Subedi
BDS 4th Batch (3rd year)
College of Dental Sciences, CMC

2.  Introduction
 Etiology
 Epidemiology
 Pathogenesis
 Clinical Features
 Radiographic Features
 Histopathologic features
 Diagnosis
 Tuberculine Test
 BCG Vaccine

3.  Tuberculosis is a specific infectious, chronic
granulomatous disease caused by Mycobacterium
Species.
 Primary Tuberculosis mostly affects Lungs (Primary
Pulmonary TB).

4.  Mycobacterium tuberculosis – Pulomary TB
 Mycobacterium bovis – Oropharyngeal & Intestinal TB
 Atypical Mycobacterium – Opportunistic infection
 Tuberculosis can affect any organ-system including
lungs, lymphatic, skin, CNS, Renal, Skeletal and
gastro-intestinal system.
 Skin involvement may occur, called Lupus Vulgaris

5.  M. tuberculosis is;
 Rod- shaped
 Non- sporing, Non- capsulated
 Facultative Aerobic
 Intracellular
 Acid fast bacillus
 Acid fastness is due to presence of complex long
chained cross-linked fatty acid (Mycolic Acid) and
other cell wall lipids.

6. M.
tuberculosis
Acid fast
staining of a
smear prepared
from sputum of
a patient with
tuberculosis.

7.  “Disease of Poor”
 Incidence has declined due to early & accurate
diagnosis and improved socio-economic condition.
 In developing countries, south east Asia, western
pacific and Africa accounts for 95% of cases of TB.
 HIV patients are at extremely high risk.

8.  Prevalence of Extra-pulmonary TB is increasing
nowadays.
 Most common extra-pulmonary sites in head and neck
are;
 Cervical lymph nodes
 Larynx
 Middle ear
 Less common are; nasal cavity, nasopharynx, parotid
gland, spine, esophagus and oral cavity.

10. Exposure to infected Air droplets
M. Tuberculosis bacteria is taken up by Pulmonary Alveolar
Macrophages (PAM) by receptor mediated endocytosis
In macrophages, phagosomes containg bacilli fuses with
Lysosomes; resist internal microbicidal activities and proliferates
with in macrophages
Early Phase:
Tubercular bacilli then either freely or with in macrophages are
drained into regional lymphnodes

11. Later Phase:
Tubercular antigens are presented to CD4+T lymphocytes via MHC-2
complex by Antigen Presenting cells (APC’s); Macrophages
Under influence of macrophage-secreted IL-12, CD4+T cells
differentiate into TH1 Cells which produce IFN-γ
IFN-γ are most potent activator of Macrophages.
Activated macrophages then produces:
 TNF-α; recruits monocytes which differentiate into epithelioid cells
Activation of ‘inducible Nitric oxide synthase’ (inos) gene; produces
Nitric Oxide; antibacterial activity
Generation of Reactive Oxygen Species; antibacterial activity

12. Thus;
 Epitheliod cells are formed by differentiation of activated
macrophages
Activated macrophages coalesces to from multinucleated
giant cells
Production of Nitric oxide and reactive oxygen species;
which are highly oxidative causes oxidation of cells forming
caseous necrosis
Macrophages produced chemokines causes recruitment
of lymphocytes and fibroblast

13.  Based upon history of previous exposure Tuberculosis can be:
Primary Tuberculosis
 Occurs in previously unexposed host
 Primary Pulmonary TB is most common
Secondary Tuberculosis
 Occurs in previously exposed host
 Progressive Pulmonary Tuberculosis
 Miliary Pulmonary Tuberculosis
 Endobronchial, endotracheal and laryngeal tuberculosis
 Systemic Miliary Tuberculosis
 Isolated Organ Tuberculosis
 Lymphadenitis
 Intestinal Tuberculosis

14. Primary TB
 is usually asymptomatic. Occasionally fever and cough
which may be productive or dry.
 Usually seen in children but may occur in adults.
Secondary TB
 Low grade fever, malaise, anorexia, weight loss and
night sweats
 Productive cough with hemoptysis or chest pain

15.  Episodic fever with chills and rigor
 Easy fatigability and malaise
 Gradual loss of weight
 Persistent cough with or without hemoptysis or chest
pain.
 Bilateral crackles on auscultation
 Hepatosplenomegaly
 Tubercular cervical lymphadenitis; tender, often shows
inflammation of overlying skin
 When an actual abscess exists, typically perforate and
discharge pus.

16.  Oral lesions are realtively uncommon.
 Lesions of oral mucosa are seldom primary, but rather
secondary to pulmonary disease.
 Most commonly affected is Tongue.
 Usually, an irregular, superficial or deep, painful ulcer
which tends to increase slowly in size often around the
areas of trauma.

18.  Chronic ulceration or swellings
 Non healing extraction sockets
 Areas of mucosal granularity or diffuse zone of
inflammation
 Mandibular swelling with intra bony involvement
 Gingiva, lips, buccal mucosa, soft palate, hard palate
are other affected sites in decreasing order
 Primary oral TB involving gingiva present as diffuse
hyperemic, nodular or papillary proliferation.
 Oral lesion co-exist with palpable, tender
submandibular or cervical lymphnodes; scrofula

19. Diffuse enlargement and
ulceration of labial
gingiva
Ulcerated gingiva

20.  Bones of maxilla or mandible may also be involved.
 Lesion produced is essentially periapical granuloma or
tuberculoma. These are usually painful and sometimes
involve considerable amount of bone by relatively
rapid extension.
 Tuberculous osteomyelitis usually occur in later stages
of disease and has poor prognosis.

21. Cervical lymphnodes
enlargement with
erythematous overlying
skin
Sinus formation and
discharge

22.  Nonspecific.
 Common findings in lungs include
 segmental or lobar airspace consolidation,
 ipsilateral hilar and mediastinal lymphadenopathy
 pleural effusion.
 Atelectasis may occur in primary pulmonary
tuberculosis
 Areas of nodal involvement appears as calcified
lymphnodes that may be confused with sialoliths.

23. Calcified Cervical
lymph nodes.

24.  Cell mediated Hypersensitivity
 Oral lesions are histopathologically similar to
pulmonary lesions.
 Formation of typical granuloma consisting of;
 Central caseous necrosis
 Circumscribed by epithelioid histocytes and langhans
type giant cell.
 Surrounded by a rim of fibroblast and lymphocytes

25.  Primary consolidation in lungs parenchyma is called as
Ghon’s Focus.
 Regional lymphnodes often caseate with parenchymal
involvement; called Ghon’s complex.
 In long standing cases, lymphnodes tends to calcify;
called as Ranke’s complex.

26. Photomicrograph of Histopathology of Tuberculosis
Epithelioid Cells
Langhans Type
Giant cells

27. Caseous
Necrosis
Photomicrograph of Histopathology of Pulmonary TB showing
Caseous Necrosis

28. Caseous
Necrosis
Langhans
Type giant
cell
Epithelioi
d cells

29.  Demonstration of bacilli in infected tissue or sputum
by AFB stain is gold-standard for diagnosis.
 Radiographs of affected parts like chest
 Tuberculine test
 CT scan is used to diagnose mediastinal or hilar
lymphadenopathy, cavities and intralesional
calcification.
 A high resoulation CT scan can be used to differentiate
millary TB and other diffuse form of TB from other
diffuse lungs disease.

30.  Also called as Mantoux Test
Principle:
 A cell mediated hypersensitivity reaction develops
against tubercular antigen.
Procedure:
 0.1 ml of 5 tuberculine units of purified proteins
derivatives (PPD) of siebert stabilized with Tween 80
or 1 tuberculine unit of PPDRT 23 injected
subcutaneous into the flexor aspect of forearm.

31. Interpretation
 Suggestive but not diagnostic
 Readings is taken 48-72 hours later for the indurations
Size of indurations Interpretation
More than 15 cm or ulceration Strongly positive
More than 10 cm Positive
5-9 cm intermediate
Less than 5 cm Negative

35. • Multi- Drug resistant TB (MDR-TB) is tubercular
infection that are resistant to at least two of the most
powerful first-line anti-TB (drugs), Isoniazid and
Rifampin
• Extremely Drug Resistant TB (XDR-TB) resistant to
Isoniazid and Rifampin plus any Fluoroquinolone and at
least one of three injectable second-line drugs (i.e.,
Amikacin, Kanamycin or Capreomycin).
• Treatment of these depends on antibiotics susceptibility
assay .

36.  Bacillus Calmette-Guerin (BCG) Vaccine is available to
approx. 80% of world population.
 BCG is given as a single intradermal injection at the
insertion of the Deltoid muscle.
 Except in neonates, a tuberculine skin test should
always be done before administering BCG.
 If BCG is accidentally given subcutaneously, then a
local abscess may form (a "BCG-oma") that can
sometimes ulcerate, and may require treatment with
antibiotics immediately

37.  Oral and Maxilofacial Pathology; Neville, 4TH edition
 Shafer’s Textbook of Oral Pathology; Seventh edition
 Oral Medicine and Pathology; WM Tilakaratne,
 Regezi’s Oral Pathology; Sixth edition
 Robbin’s Basis Pathology; 8th edition
 A Textbook of Microbiology; P Chakraborty,