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Introduction
(Dorlands Dic.)
Inflammation
The inflammatory
response has many
players
These include:
Circulating cells
Neutrophils
Eosinophils and
Basophils
Lymphocytes and
Monocytes
Platelets
Inflammation
Circulating Proteins :
Clotting Factors
Kininogens
Complement
components
1. Heat (Calor)
2. Redness (Rubor)
3. Swelling (Tumor)
4. Pain (Dolor)
Reversible mechanism
Induced by cytokine mediators (TNF & IL-1)
Cause structural reorganization
Cells retract
Takes 4 to 6 hrs to develop and persists for 24hrs
or more
Increased vascular permeability
Direct endothelial injury :
Seen in severe injuries (burns, infections etc.)
Leakage begins immediately after surgery and persists for
several hours. (immediate sustained response)
Increased vascular permeability
Leukocyte dependent endothelial injury :
Leukocytes may accumulate during inflammatory response.
These leukocytes may release toxic oxygen species and
proteolytic enzymes causing injury.
Increased vascular permeability
Leakage from new blood vessels :
Cellular Events
Cellular Events
Transendothelial Migration
E-selectins are expressed at low levels or are not present at
all on normal cells. They are upregulated after stimulation by
specific mediators. eg.IL-1 and TNF.
O2 - + 2H+ H2O 2
Cl -
H2O 2 Myeloperoxidase HOCl + H2O
Chemical Mediators Of
Inflammation
Vasoactive Amines
Histamine – widely distributed in mast cells; also
present in circulating basophils and platelets.
Preformed histamine is stored in mast cell granules and
released in response to a variety of stimuli :
Physical injury
Immune reactions involving binding of IgE antibodies to Fc
receptors on mast cells.
Anaphylatoxins; C3a and C5a
Leukocyte derived histamine releasing proteins.
Neuropeptides
Certain cytokines (IL-1; IL-8)
Vasoactive Amines
Histamine causes arteriolar dilatation and is the
principal mediator of immediate phase of
increased vascular permeability.
Autoimmunity
steroids
Steroids add to the analgesic effect of NSAID
Leukotriene antagonists
Montelukast & Zafirlukast
Antagonize cysLT1 mediated
bronchoconstriction, increased vascular
permeability and recruitment of eosinophils
Indicated for prophylactic therapy of mild to
moderate asthma
Omalizumab
Omalizumab
Does not bind to cell-bound IgE
Therefore, does not trigger cell activation
by crosslinking of the IgE molecules on cell
membranes.
Omalizumab
Omalizumab
Omalizumab reduces the allergen induced
late asthmatic response, airway
hyperresponsiveness and sputum
eosinophilia
Reduces both asthma exacerbations and
corticosteroid requirement
Agent may have a long-term anti-
inflammatory effect
Enzymes as anti-
inflammatory agents
Cleave the antigenic surface protein of organisms
and digest their outer coat
Reduce number and activity of receptors for
pathogen on host cells
Detoxify blood and remove viruses from circulation
Cause enhancement of immune cells to kill
bacteria, viruses, molds and fungi
Enzymes as anti-
inflammatory agents
Break down immune complexes which block the
immune cells
Accelerate the volume and fluidity of blood flow
Bromelain modulate arachidonate pathway in
such a way that thromboxane production is
decreased with no effect on cyclooxygenase
Enzymes as anti-
inflammatory agents
Powerful anti-oxidants and effectively combat the
harmful free radicals such as nitric oxide
Block pro-inflammatory metabolites that
propagate the inflammation
Possess anti-secretory and mucolytic qualities
and decrease acute phase reactions
Serratiopeptidase
Proteolytic enzyme isolated from the
non-pathogenic enterobacteria Serratia
E15 found in silkworms
Acts upon inflammation by thinning the
fluids in the body that collect around
injured areas and increases fluid
drainage
Serratiopeptidase
Enhances tissue repair and reduces pain
Ability to block the release of pain-inducing
amines from inflamed tissues
Ability to dissolve dead and damaged
tissue
Modifies cell-surface adhesion molecules
References
Robbins & Cotran. Pathologic basis of disease; 7th ed.
Harsh Mohan. Essential Pathology for Dental Students.; 3rd ed.
Henry Trowbridge. Inflammation A review of the process; 4 th ed.
Goodman & Gilman's The Pharmacologic Basis of Therapeutics -
11th Ed. (2006)
Laskin DM, Giglio JA. The use of steroids and NSAID in Oral and
Maxillofacial Surgery. Oral and Maxillofacial Surgery Clinics of
North America. 2001 Feb; 13(1): 31-41.
References
M. Soler et al. The anti-IgE antibody omalizumab reduces
exacerbations and steroid requirement in allergic asthmatics Eur
Respir J 2001; 18: 254–261
G. Hanf et al. Omalizumab inhibits allergen challenge-induced nasal
response. Eur Respir J 2004; 23: 414–418.
Shahid S . Role of Systemic Enzymes in Infections . WebmedCentral
COMPLEMENTARY MEDICINE 2012;3(1):WMC002504
Chopra et al. A randomized, double-blind, placebo-controlled study
comparing the efficacy and safety of paracetamol, serratiopeptidase,
ibuprofen and betamethasone using the dental impaction pain
model. Int. J. Oral Maxillofac. Surg. 2009; 38: 350–355