Bacterial Lesions of Oral Cavity 153
All rights reserved. May not be reproduced in any form without permission from the publisher, except fair uses permitted under U.S. or applicable copyright law.
Figure 1. Immunopathogenesis of sarcoidosis (a proposed model).
The so called sarcoid antigen is engulfed by circulating dendritic cells.
Dendritic cells stimulate the T cells. Activated T cells are highly polarized and
they produce IL-2 which causes monoclonal proliferation of T cells. Also,
upon TCR activation, T-bet production increases. T-bet upregulates and
enhances the production of IFNγ which enables the granuloma formation. The
future antigen clearance and increased IL-10 levels bring about disease
clearance. Disease chronicity results in a predominance of TH2 cytokines
which leads to lung remodelling by fibrosis.
Recurrent Aphthous Stomatitis
Copyright 2016. Nova Science Publishers, Inc.
Introduction
Recurrent aphthous stomatitis is a disorder characterized by recurring
ulcers in the oral mucosa in patients with no other signs of the disease.
EBSCO Publishing : eBook Collection (EBSCOhost) - printed on 5/12/2024 5:21 PM via PONTIFICIA UNIVERSIDAD JAVERIANA - BIBLIOTECA CENTRAL
AN: 1430461 ; Namboodiripad, P. C. Anila, Anuradha Sunil, E..; Pathophysiology of Oral Diseases
Account: s6670599.main.eds
154 P. C. Anila Namboodiripad and E. Anuradha Sunil
Pathogenesis
A large number of etiological factors have been suggested as the cause for
the recurrent aphthous stomatitis. The etiological factors other than ones
mentioned below cannot be pathogenetically explained as etiopathogenetic
factors, since no substantiating evidence has been found between the etiology
and the disease.
Stress has been emphasized as a causative factor in RAU.
Stress as an etiological factor in RAS patients induces parafunctional
habits in them such as lip or cheek biting that may result in trauma to
the site and the patient acquiring ulceration. But correlating stress
with RAU in experimental studies the relationship has been found
negative, thus implying that stress may only be a contributory factor
in RAS and plays no role in its etiology.
Oral organisms have been found at the site of the ulcer, suggesting
that probably the bacteria such as oral streptococci, helicobacter
pylori etc may play a role in the causation of RAS and though the role
of virus has been suggested, it is still said to be under speculation.
Viruses that have been suggested include the viruses from the herpes
family like the EBV, CMV, HSV, HSV6, etc. These organisms may
act as an antigenic stimuli initiating an immunologic reaction and
damaging the oral mucosa in the bargain.
TNF-alpha is said to play a major role in formation of the RAU. The
inciting factor may be any of the above mentioned antigens that
stimulate the production of IL-2 and TNF-alpha, following its attack
on the oral mucosal keratinocytes. This TNF-alpha causes expression
of MHC 1 which further attracts the CD 8+ cells resulting in the ulcer
formation of the oral mucosa.
Both types of immune responses humoral and acquired is said to play
a role in RAS. It is said to result in neutrophil reactivation,
complement addition, role of NK cells, B cells altered CD4+/CD 8+
ratio and T cell receptors in the peripheral blood. The Th1 is said to
play a major role in RAS formation.
There was found to be an increase in the production of the IL-2, IFN-c
and the TNF- alpha in the acute cases of RAS and also a simultaneous
reduced secretion of the TGF- beta and the IL-10. This imbalance in
EBSCOhost - printed on 5/12/2024 5:21 PM via PONTIFICIA UNIVERSIDAD JAVERIANA - BIBLIOTECA CENTRAL. All use subject to https://www.ebsco.com/terms-of-use
Bacterial Lesions of Oral Cavity 155
the pro and the anti-inflammatory cytokines may be the reason for the
ulcer formation in the RAS.
Also the increased Th1 as compared to the Th2 may also be the cause
for the RAS. The heat shock proteins are a component of the anti-
inflammatory cytokine and this is said to inhibit the differentiation of
the monocytes into the dendritic cells. This may further aggravate the
inflammatory process. The heat shock proteins are found at elevated
levels in smokers thus explaining the reduced occurrence of aphthae
in the smokers.
Autoimmunity is suggested as another etiological factor for RAS.
Here the structures of the epithelium such as the desmosomes,
hemidesmosomes get disrupted due to an auto-antibody antigen
reaction at that site.
EBSCOhost - printed on 5/12/2024 5:21 PM via PONTIFICIA UNIVERSIDAD JAVERIANA - BIBLIOTECA CENTRAL. All use subject to https://www.ebsco.com/terms-of-use
EBSCOhost - printed on 5/12/2024 5:21 PM via PONTIFICIA UNIVERSIDAD JAVERIANA - BIBLIOTECA CENTRAL. All use subject to https://www.ebsco.com/terms-of-use
