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1. INFLAMMATION (II).
GUIDED BY :
Dr.S.R.Godbole.
Dr.Mithilesh Dhamande.
Presented By:
Apurva Deshmukh.

2. CONTENTS (PART I):
 Introduction
 Definition
 Causes
 Signs of inflammation.
 Inflammatory cells
 Types of Inflammation – Acute Inflammation.
 Fate of acute inflammation.
 Conclusion
 References

3. CONTENTS (PART II):
 Introduction.
 Definition.
 Chronic inflammation.
 Chemical mediators of inflammation.
 Prosthodontic aspects of inflammation.
 Summary
 References.

4. Introduction:
 “Inflammation is defined as the local response of living
mammalian tissues to injury due to any agent.”
- Harsh Mohan Essentials of pathology 6th Edition.
 The agents causing inflammation are Infective, Immunological,
Physical, Chemical agents or Inert materials.
 The cardinal signs of inflammation are Rubor, Calor, Tumor,
Dolor and Functio laesa.

5.  In acute inflammation, if the injurious agent persists for a
longer duration, then chronic inflammation will occur as a
result.
 It is characterized by dominating presence of macrophages
in the injured tissue.These cells are powerful defensive
agents of the body.
 As a result, it is always accompanied by tissue destruction,
as the toxins produced by them are injurious to the
organism's own tissues as well as invading agents.

6.  Chronic inflammation is defined as inflammation of prolonged
duration (weeks or months) in which
 active inflammation
 tissue destruction and
 attempts at healing
proceed simultaneously.
- Harsh Mohan, Textbook of Pathology,6th edition.
DEFINITION:

7.  Chronic inflammation is characterised by :
1. Infiltration with mononuclear cells including macrophages,
lymphocytes, and plasma cells which indicates persistent reaction to
injury.
1. Tissue destruction largely induced by the products of the
inflammatory cells.
1. Repair involving new vessel proliferation and fibrosis which are
attempts to replace lost tissue.

8.  Causes :
a) Persistent infections.
b) Immune-mediated inflammatory diseases.
c) Prolonged exposure to non-degradable but potentially toxic
substances.

9. Cells of Chronic Inflammation:
 Histologically chronic inflammation includes:
1. Macrophages,
2. Lymphocytes,
3. Plasma cells,
4. Eosinophils,
5. Multinucleate Giant cells,
6. Fibroblasts,
7. Collagen secreting cells.

10. Macrophages:
 Functions :
 Phagocytosis.
 Production of toxic
biologically active
substances such as oxygen
metabolites.
 Cause fibroblast
proliferation and collagen
deposition.

11.  The ways in which macrophages accumulate in the inflammed
area are :
– Continued recruitment from the circulation, secondary to
chemotactic factors.
– Division.
– Prolonged survival &
immobilisation.

12.  Lymphocytes:
Comprise of 20-45% of all WBCs. T-cells are the characteristic cells
that activates macrophages.
 Plasma cells:
Even though these develop from lymphocytes they are larger in
size. Abundant cytoplasm, eccentric nucleus, cart wheel
pattern of chromatin. Secrete antibodies against specific
antigens.
 Eosinophils:
They can destroy parasites and certain cells as they are rich in
Myeloperoxidase. Comprise of 1-6% of all WBC's.

13.  Multinucleate giant cells:
Huge cells with many nuclei formed by fusion of
macrophages when macrophages fail to deal with
inflammatory particles.
 Fibroblasts and collagen secreting cells:
Collagen production is a common feature of chronic
inflammation. Chemical mediators stimulate
collagen secreting cells and promote fibrosis via
fibroblasts.

14. PROSTHODONTIC ASPECTS OF
INFLAMMATION:
1) Traumatic ulcers.
2) Denture Stomatitis.
3) Inflammatory papillary hyperplasia.
4) Inflammatory fibrous hyperplasia.
5) Peri-Implant diseases :
a) Peri-implant mucositis.
b) Peri-implantitis.

15. 1. TRAUMATIC ULCERS.
 They are caused in the denture wearers due to friction between
the tissue surface of the denture and mucosa.
 Primary line of treatment includes discontinuation in wearing
dentures and application of topical benzocaine 20% and
benzalkonium hexachloride.
 In cases of severe inflammation, kenacort gel is indicated.

16. 2. DENTURE STOMATITIS.
 Denture-related stomatitis indicates an inflammatory process of
the mucosa that bears a complete or partial removable dental
appliance, typically a denture.
 It stands for a mild chronic erythematous candidiasis.
 Lesions more frequently found in the upper jaw, especially on the
palate. The absence of denture stomatitis in the lower jaw is due
to the washing action of saliva.

17.  It is frequently asymptomatic but patients may complain of halitosis,
slight bleeding and swelling in the involved area, or a burning
sensation, xerostomia, or taste alterations.
 Classification for denture stomatitis : Newton in 1962, (based on
clinical criteria) :
1. Newton ́s type I: Pin-point hyperaemic lesions (localised
simple inflammation).

18. 2. Newton ́s type II: Diffuse erythema confined to the mucosa contacting the
denture (generalised simple inflammation)
3. Newton ́s type III: Granular surface.

19.  Treatment :
1. Local therapy with nystatin, amphotericin B, miconazole, or
clotrimazole should be preferred to systemic therapy with
ketoconazole or fluconazole because resistance of Candida
species occurs with them regularly.
1. Treatment should continue for a minimum of 4 weeks along
with meticulous oral hygiene maintenance.

20. 3. INFLAMMATORY PAPILLARY HYPERPLASIA.
 It is hyperplasia of soft tissue, usually beneath a denture. It is
associated with poor denture hygiene, denture overuse, and ill-
fitting dentures.
 First reported by Berry in 1851.The lesion results from a
combination of chronic, mild trauma and low-grade infection
by bacteria or candida yeast.

21.  The condition results in selective but severe edema and
eventual inflammatory fibrosis of the connective tissue
papillae of the palatal epithelium.
 It is found in three of every 1,000 adults.

22.  Clinical features :
1. Papillary hyperplasia is seen in middle-aged and older persons
and there is a strong female predilection (2 females:1 male).
2. The disease occurs on the bone-bound oral mucosa of the hard
palate and alveolar ridges.
3. It presents as a cluster of individual papule or nodules which
may be erythematous, somewhat translucent or normal in
surface coloration.

23. 4. White cottage cheese-like colonies of candida may be seen in
clefts between papules.
5. There is seldom pain, but a burning sensation may be produced
by the yeast infection.
6. Early papules are more edematous while older ones are more
fibrotic and firm.

24.  Treatment :
1. Early lesions may completely disappear with cessation
of denture use for 2-4 weeks, perhaps aided by topical
antibiotic or antifungal therapies.
1. Persistent lesions must be surgically removed or laser
ablated if a proper base is to be prepared for a new and
better-fitting denture.

25. 4. INFLAMMATORY FIBROUS HYPERPLASIA.
 Benign hyperplasia of fibrous connective tissue which develops as a reactive
lesion to chronic mechanical irritation produced by the flange of a poorly
fitting denture.
 Excess folds of firm tissue form inside the mouth as a result of rubbing on
the edge of dentures that do not fit well.

26.  Clinical features :
1.The usual appearance is of two excess painless tissue folds in the sulcus,
with the flange of the denture fitting in between the two folds.
1.May occur in maxillary/mandibular sulci, anterior regions being more
common.
1.The swelling is firm and fibrous, with a smooth, pink surface and
may/may not show ulceration or erythema.
1.The size of the lesion varies from less than 1 cm to involving the entire
length of the sulcus.

27.  Treatment :
1. Surgical excision of the fibrous tissue overgrowth.
2. Common techniques : Removal with a surgical scalpel,
electrical scalpel, or laser excision with a laser scalpel.
3. The poorly fitting denture can be adapted to fit better
(relining) or a new denture constructed.
4. Alternatively, the section of flange that is sharp/over-
extended can be smoothened or reduced.

28. 5. PERI-IMPLANT DISEASES.
A) PERI-IMPLANT MUCOSITIS :
 Mucositis describes a bacteria-induced, inflammatory
process of the peri-implant soft tissue with reddening,
swelling and bleeding on periodontal probing
 It is a reversible inflammatory change of soft tissues without
bone loss.
 It is a precursor to peri-implantitis.

29.  Treatment : Non-surgical
– Curettes ( Teflon, carbon, plastic and titanium
curettes)
– Air polishing systems (hydroxylapatite/tricalcium
phosphate, hydroxylapatite, glycine, titanium
dioxide, phosphoric acid).
– Ultrasonic and Laser therapy.
– Photodynamic therapy : It generates reactive
oxygen species with a high-energy single-frequency
light (e.g. diode lasers) in combination with
photosensitizers (e.g. toluidine blue) to generate
bactericidal effects against aerobic and anaerobic
bacteria.

30. B) PERI-IMPLANTITIS :
 Inflammatory reactions associated with loss of supporting bone
around an implant in function.
 Clinical features :
1. Crestal bone loss
2. Deepening of the peri-implant pocket
3. Bleeding and/or pus after probing
4. Swelling and redness of gingiva
5. Gingival recession
6. Implant mobility.

31. 1) Non-surgical treatment: Same as for Peri-implant Mucositis.
2) Surgical treatment :
 Resective therapy :
-- The basic principles include the elimination the
periimplant osseous defect using ostectomy and
osteoplasty as well as bacterial decontamination.
-- Additionally, smoothening and polishing of the
supracrestal implant surface (implantoplasty)
may be applied.
 Regenerative therapy :
-- regeneration of defects using various graft
materials and/or resorbable membranes.

32. Stage Result Therapy
Pocket depth<3mm, no plaque or
bleeding
No therapy.
A
PD<3mm, plaque or bleeding on
probing
Mechanically cleaning,
polishing.
B
PD 4-5 mm, radiologically no bone
loss
Mechanically cleaning,
polishing, oral hygiene
instructions plus local anti-
infective therapy e.g.
Chlorhexidine.
C
PD>5mm, radiologically bone
loss<2mm
Mechanically cleaning,
polishing, oral hygiene
instructions plus local and
systemic anti-infective therapy.
D
PD>5mm, radiologically bone
loss>2mm
Surgical and regenerative
surgery.
TREATMENT PROTOCOL :

33. Criteria. Acute Chronic
1. Duration Short (days) Long (weeks/months)
2. Onset Acute Insedious
3. Inflammatory cells Neutrophils, macrophages. Lymphocytes, plasma cells,
macrophages, fibroblasts
4. Vascular changes Active vasodilation, increased
permeability
New vessel formation
(granulation tissue)
5. Cardinal clinical signs. + -
6. Fibrosis - +
7. Systemic manifestations Fever, often high. Low grade fever, weight loss,
anaemia.
ACUTE VERSUS CHRONIC INFLAMMATION:

34. CHEMICAL MEDIATORS:
A) CELL DERIVED :
1) Histamine
2) Serotonin
3) Prostaglandins.
4) Leukotrienes.
5) Platelet activating factor
(PAF).
6) Reactive oxygen species.
7) Nitric oxide
8) Cytokines.
9) Chemokines
B) PLASMA DERIVED :
1) Complement system.
2) Kinins.
3) Proteases activated during
coagulation.
 Definition: A chemical messenger that acts on blood vessels, inflammatory cells or
other cells to contribute to an inflammatory response is termed as a chemical
mediator.

35.  A) CELL DERIVED MEDIATORS:
1) Histamine :
– PRINCIPAL SOURCES : Mast cells, Basophils, Platelets.
– ACTIONS : Vasodilation, Increased vascular
permeability, Endothelial activation.
2) Serotonin :
– PRINCIPAL SOURCES : Platelets.
– ACTIONS : Vasodilation, Increased vascular permeability.

36. 3) Prostaglandins :
– PRINCIPAL SOURCES : Mast cells, leukocytes.
– ACTIONS : Vasodilation, pain, fever.
4) Leukotrienes :
– PRINCIPAL SOURCES : Mast cells, leukocytes.
– ACTIONS : Increased vascular permeability, chemotaxis,
leukocyte adhesion and activation.

37. 5) Platelet Activating Factors :
– PRINCIPAL SOURCES : Mast cells, leukocytes.
– ACTIONS : Vasodilation, increased vascular permeability,
leukocyte adhesion, chemotaxis, degranulation, oxidative
burst.
6) Reactive oxygen species :
– PRINCIPAL SOURCES : Leukocytes.
– ACTIONS : Killing of microbes, Tissue damage.

38. 7) Nitric Oxides :
– PRINCIPAL SOURCES : Endothelium, macrophages
– ACTIONS : Vascular smooth muscle relaxation, killing of
microbes.
8) Cytokines :
– Cytokines: (TNF, IL -1)
– PRINCIPAL SOURCES: Macrophages, endothelial cells, mast
cells.
– ACTIONS: Local endothelial activation, fever, pain, anorexia,
hypotension, decreased vascular resistance (shock).

39. 9) Chemokines :
– PRINCIPAL SOURCES : Leukocytes, activated
macrophages.
– ACTIONS : Chemotaxis, leukocyte activation.

40. B) PLASMA PROTEIN DERIVED
 Complement system(C5a, C3a, C4a), Kinins and Proteases
activated during coagulation.
 PRINCIPAL SOURCE: Plasma (produced in liver).
 ACTIONS : Leukocyte chemotaxis and activation, vasodilation,
Increased vascular permeability, smooth muscle contraction,
vasodilation, pain, endothelial activation and leukocyte recruitment.

41. SUMMARY:
 Inflammation is a body defense reaction which acts in order to
eliminate or limit the spread of injurious agent as well as to
remove the consequent cells and tissues.
 Acute Inflammation when not treated progresses in the form
of chronic inflammation which has more deleterious effects
over an individual.
 It is necessary for the oral surgeons to have knowledge about
inflammation to diagnose inflammatory diseases and
inflammatory lesions and to treat them in conservative or
surgical approach.

42. REFERENCES:
 Kumar, Cotran, Robbins - basic pathology - 8th and 9th edition.
 Harsh Mohan - essential of pathology - 3rd and 6th edition.
 Jagadeeshwaran.A.R et al: Pharmaco-prosthodontics revisited
:J Pharm Bioallied Sci. 2012 Aug; 4(Suppl 2): S338–S340.
PMCID: PMC3467929 doi: 10.4103/0975-7406.100297
 Smeets.R.et al: Definition, etiology, prevention and treatment of
peri-implantitis – a review: Head & Face Medicine 2014, 10:34
 Fardal o, johannessen ac, olsen i. Severe, rapidly progressing
peri-implantitis. J clin periodontol 1999;26:313-17.

43. THANK YOU.