1. Chronic inflammation is characterized by mononuclear cell infiltration and occurs over a prolonged period due to persistent stimuli. It can lead to tissue destruction, necrosis, and proliferative changes like granulation tissue formation and fibrosis. 2. Granulomatous inflammation is a type of chronic inflammation where injurious agents cause formation of granulomas, which are composed of epitheloid cells, multinucleated giant cells, lymphocytes, and may include caseation necrosis. 3. Examples of diseases involving granulomatous inflammation discussed in dentistry include tuberculosis, leprosy, syphilis, and sarcoidosis. Their pathogenesis involves a complex interplay between the causative organisms and the host immune response.

1. Basics of
Inflammation with
Applied Clinical
Aspects – part 2

3. 3

4. 4
Kowalski ML, Makowska JS, Blanca
M, Bavbek S, Bochenek S, et al.
Hypersensitivity to nonsteroidal anti-
inflammatory drugs (NSAIDs) –
classification, diagnosis and
management: review of the
EAACI/ENDA and
GA2LEN/HANNA. Allergy, 2011,
Volume 66, Issue 7, Pages: 818–
829.

5. Contents
1. Chronic Inflammation
1. Definition
2. Causes
3. General features
4. Systemic effects
5. Types of chronic inflammation
2. Granulomatous inflammation
1. Pathogenesis
2. Composition
3. Examples of granulomatous inflammation-
tuberculosis, leprosy, syphilis and sarcoidosis
3. Clinical implications in dentistry. 5

6. “ An inflammatory response of
prolonged duration provoked by the
persistence of the causative
stimulus and simultaneous
presence of active inflammation,
tissue destruction and repair.
6

7. Chronic inflammation may occur by one of
the following
7
Chronic inflammation following acute
inflammation
Recurrent attacks of acute inflammation
Chronic inflammation starting de novo

8. General features
1. Mononuclear Cell Infiltration
◂ Chronic inflammatory lesion are infiltrated by mononuclear
inflammatory cells like
◂ Phagocytes – circulating monocytes, tissue macrophages,
epitheloid cells and giant cells
◂ Lymphoid cells
8

9. Macrophages appear at site of inflammation from
1. Chemotactic factors and adhesion molecules
2. Local proliferation of macrophages
3. Longer survival rate of macrophages at the site of
inflammation
9
 Apart from phagocytosis- On activation macrophages
release several biologically active substances e.g. acid
proteases, oxygen derived reactive metabolites and
cytokines.
 These products bring about tissue destruction,
neovascularisation and fibrosis.
 Lymphocytes and macrophages influence each other and
release mediators of inflammation.

10. 10
2. Tissue destruction and necrosis
◂ Salient feature brought about by activated
macrophages which release variety of
biologically active substances

11. 3. Proliferative changes
◂ As a result of necrosis proliferation of small blood
vessels and fibroblasts is stimulated resulting in
formation of inflammatory granulation tissue.
◂ Eventually, healing by fibrosis and collagen laying
takes place. 11

12. 12
Systemic effects
Fever
Anaemia
Leucocytosis
ESR elevated
Amyloidosis

13. 13

14. Chronic non specific
inflammation
◂ Irritant substance produces a non
specific chronic inflammatory
reaction with formation of
granulation tissue and healing with
fibrosis.
◂ Variant – chronic suppurative type-
infiltrated by polymorphs and
abscess formation.
14

15. Chronic granulomatous
inflammation
◂ Injurious agent causes a
characteristic histologic
tissue response by formation
of granulomas.
15

16. Pathogenesis of Granuloma
16
Engulfment by macrophages
Macrophages and
monocytes engulf antigen
Antigen poorly
degradable- fail to digest
Instead undergo
morphogenic changes as
epitheloid cells.
CD4+ T cells
Macrophages present the
antigen to CD4+ T
lymphocytes.
These lymphocytes get
activated and elaborate
lymphokines.
Cytokines
IL-1 IL-2 proliferation of T
cells
Interferon γ activate
macrophages
TNF- α promote fibroblast
proliferation and secrete
prostaglandins
Growth factors stimulate
fibroblast growth.

17. 17

18. 18
Composition of Granuloma
Epitheloid cells
• Modified macrophages
• Slipper shaped
• Weakly phagocytic
Multinucleated giant cells
• Fusion of epitheloid cells
• 20 or more nuclei
• Produce secretory products help in removing invading agents
Lymphoid cells
• Accelerated immune response
Necrosis
• Features of few granulomas
Fibrosis
• Periphery
• Feature of healing

19. 19

20. 20
Types of granuloma
Foreign body
granulomas
eg- silica
Immune
granuloma
eg- TB

21. 21
Feature Acute inflammation Chronic inflammation
1. Onset and duration Short duration Long duration
2. Cardinal signs Invariably present Generally
imperceptible
3. Pathogenesis Vascular and cellular
changes
Recurrent attacks of
acute inflammation
4. Main inflammatory
cells
Neutrophils Lymphocytes, plasma
cells, macrophages
5. Plasma exudation Present May or may not
6. Systemic effects Leucocytosis-
neurophilic,
eosinophilic
Leucocytosis-
lymphocytic, monocytic
7. Main morphology Suppuration, ulcer Granulomatous
inflammation
8. Fate Resolution, chronicity Resolution, dystrophic
calcification
9. Common examples Cellulitis Tuberculosis

22. 22

23. Tuberculosis
◂ Communicable chronic granulomatous disease
caused by Mycobacterium tuberculosis
◂ It usually involves the lungs but may affect any
organ or tissue in the body.
◂ Typically, the centres of tubercular granulomas
undergo caseous necrosis
23

24. 24
Pathogenesis
◂ No demonstrable toxins
◂ Virulence mycobacteria reach the alveoli
◂ Macrophage – initiates phagocytosis, but
unable to do so- bacterial sulfolipids inhibit
the fusion of phagocytic vesicles with
lysosomes
◂ multiply in the pulmonary epithelium or
macrophages
◂ 2 to 4 weeks - destroyed by the immune
system, but some survive and are spread
by the blood to extrapulmonary sites
◂ Ability to survive and grow within host cell

25. 25

26. FATE OF PRIMARY TUBERCULOSIS
1. Heals by fibrosis or calcification and even ossification
2. Progressive primary tuberculosis : Spreads to
other parts of Lungs
3. Primary miliary tuberculosis : bacilli may enter the
circulation through erosion in a blood vessel and
spread to various tissues and organs. Ex: liver,
spleen, kidney, brain and bone marrow
4. Progressive secondary tuberculosis : bacilli lying
dormant in acellular caseous material gets activated 26

27. Leprosy
◂ Like tuberculosis- the immune response is T cell
mediated delayed hypersensitivity. (IV)
◂ M. leprae do not produce toxins but instead the
damage to the tissues is immune mediated.
27

28. Immunology of leprosy
◂ Antigens of leprosy- phenolic glycolipid 1 and another
surface antigen (LAM) determine immune response.
Invasion of peripheral nerves.
◂ Genotype of host- MHC class determines host
response.
◂ T cell response- CD4+ and CD8+
◂ Humoral response- high level of immunoglobulins
IgG, IgA, IgM- but no protective role against bacteria 28

29. Syphilis
◂ T- palladium does not produce any endotoxin
or exotoxin.
◂ The pathogenesis of the lesions is due to host
immune response
◂ Antibody to T. palladium
◂ Non specific reaginic antibodies- IgM, IgG
29

30. Sarcoidosis
◂ Etiology unknown but the disease has immune pathogenesis –
but the antigenic trigger that stimulates the disease process is
still unknown.
◂ However disease involves three interlinked factors
◂ Disturbed immune system
◂ Genetic predisposition
◂ Exposure to environment agent 30

31. Clinical implications
◂ Inflammations are relatively a common presentation
in dental practice.
◂ These can be both odontogenic and non
odontogenic origin.
◂ Once it extends past the apex of the tooth, the
pathophysiology may vary depending on virulence,
host resistance and other factors
◂ Sometimes it may become severe.
31

32. 32

33. ◂ Apical periodontitis-
inflammatory products
from inflamed pulp
penetrate apically
periodontal ligament in
sufficient amount-
inflammation is initiated;
no frank abscess
◂ Periapical abscess- An
abscess is a localized
collection of pus, surrounded
by an area of inflamed tissue
n which hyperaemia and
infiltration of leucocytes are
marked.
33

34. ◂ Periapical granuloma- growth of
granulation tissue with
periodontal ligament resulting
from the death of pulp tissue.
◂ due to prolonged irritation,
release of inflammatory
mediators and replacement of
bone by granulation tissue.
◂ Radicular cyst- odontogenic cell
rests of epithelium proliferate and
cyst a develop.
34

35. ◂ Dentoalveolar abscess-
raised sessile swelling with
smooth, frequently
reddened mucosa over
yellow pus.
◂ Fluctuant swelling; when
aspirated yields pus.
◂ Cellulitis- PLEGMON – non
suppurative inflammation of
the subcutaneous tissues
extending along the
connective tissue planes and
across the intercellular
spaces.
◂ When abscess is not drained 35

36. ◂ Ludwig’s Angina-
Overwhelming, rapidly
spreading, septic cellulitis
with bilateral involvement of
sublingual, submandibular
and submental space.
◂ Osteomyelitis-
inflammation of bone
marrow that produces
clinically apparent pus and
secondarily affects the
calcified components.
◂ involves periosteum, cortex
and marrow.
36

37. Acute exacerbation of a chronic lesion-
PHOENIX ABSCESS
◂ The periradicular area may
react to the noxious stimuli and
form diseased pulp with chronic
periradicular disease.
◂ At times, because of the influx
of necrotic products from the
diseased pulp or because of
bacteria and their toxins- this
apparently dormant lesion may
react and cause an acute
inflammatory reaction
37

38. Pericoronitis
◂ Inflammation of soft tissue
surrounding the crown of a
partially erupted tooth.
◂ If untreated pericoronal
abscess.
38

39. References
1. Textbook of pathology- Harsh Mohan-
7th edition
2. Pathology basis of disease- Robbins
and Cotran-volume 1
3. Textbook of oral medicine- Anil
govindrao ghom- 3rd edition
4. Burket’s oral medicine- 11th edition.
39