bacteria causing pulpitis
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Microbiological Aspects and Immunity Response of Bacteria Causing Pulpitis Deepak Dwivedi1, Sapna Kushwah1, Vinod Singh1 1Department of Microbiology, Barkatullah University, Hoshangabad Road, Bhopal, M.P., India
Abstract
Oral cavity is a very wide distributed ecosystem in which several hundred microbial species normally cohabit harmoniously. Under special conditions some micro-organism with a potential is promoted, leading to inflammation & infection by induced demineralization of dental enamel that normally constitutes an impermeable barrier that protects the underlying dentin and the connective tissue situated in the centre of the tooth & dental pulp such as pulpitis, dental caries, periodontal infection. In inflammation process in the dental pulpitis the immunity response against oral infection follow leading infection & it is resulting in high level of morbidity and economic burden to society.
Introduction
The human tooth is the target of a substantial number of oral bacteria agents that are responsible for the development of oral inflammation. These agents induce demineralization of enamel that normally constitutes an impermeable barrier that protects the underlying dentin and the connective tissue situated in the centre of the tooth, and dental pulp ( Love and Jenkinson 2002 ). When the enamel barrier is disrupted the dentin exposed to the oral environment. The pulpitis tissue is mainly composed of cells, loose connective tissue and ground substances. The main components are fibroblast, odontoblast, undifferentiated cells and defence cells. Dental pulp is also consists of nerves and blood supply
Corresponding Author
Dr. Vinod Singh Asso. Professor & Head, Department of Microbiology, Barkatullah University, Hoshangabad Road, Bhopal, M.P., India, Phone no. +91755-4242852, Mobile No.-+919425712910
E-mail: [email protected]
.
Figure-1, Structural overview of Pulp
Invasion of the pulp and the periapical areas can promote the development of pulpitis and dento-alveolar abscess and spread of the infection to other anatomical areas. Pulpitis can occur when caries progresses deeply into the dentin, when a tooth requires multiple invasive procedures, or when trauma disrupts the lymphatic and blood supply to the pulp. Untreated pulpitis may lead to pulp necrosis,
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Figure-2, Mechanism of inflammation in pulp
associated with the root canal infection finally lead to apical periodontitis, destruction of the bone surrounding the root apex of affected tooth. Pulpitis begins as a reversible condition in which the tooth can be saved by a simple filling. It becomes irreversible as swelling inside the rigid encasement of the dentin compromises circulation Several oral acid producing aerobic and anaerobic bacteria.
There is a chamber in the centre portion of each tooth, and that chamber contains a mix of nerves, blood vessels and soft, spongy tissue called pulp. Healthy pulp causes no sensations, but when it is attacked by bacteria, pressure builds up in the chamber and you experience pain.
Pulpitis is typically caused by untreated caries (decay) that has inched its way down into the pulp chamber. Your “simple toothache” could have also been the result of a loose filling, periodontal disease, an injury to the tooth or an extensive, invasive dental procedure that came close to the pulp chamber.
Predominant isolated bacteria from necrotic infected pulp
Obligate anaerobic bacteria
Genus Common species
Gram negative rods
Porphyromonas P. gigivalis , P.endodolis
prevotella P.oralis, P.oris, P.intermidius
Fusobacterium E.alactolyticum, E.lentum,
Propionibacterium P.propionicus Lactobicillus L.catenaforme
etc. Actinomyces A.naeslundii
etc. Gram positive cocci
Peptostreptococcus P. anaerobius
Gram negative cocci
Veillonella V.parvula
Facultative anaerobic bacteria
The interaction between micro flora and eukaryotic cell is highly complex and involves active processes allowing both type of partner to co-exist. The microbes encounter with the host and bacterial surface protein termed “adhesions” mediate this step. Bacteria also secret mediators that bind or invade the host, he microbial attachment as well as the encounter with the secreted protein serve as signals that are deciphered through multi mediator cascades ultimately affecting gene expression in the host.
Many receptors recognizing the pathogens and mediating the host response, as well as the variety
Gram positive cocci
streptococcus S.mitis, S.oralis etc.
Enterococcus E.faecalis Gram negative cocci
Neisseria
Gram positive rod
cornibacterium
Gram negative rod
Eikenella
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of microbial molecular triggering the host response have been demonstrated.
Toll like receptor and bacteria present in pulpitis –
Host defence against invading microbial pathogens is elicited by the immune system, which consists of two components: innate immunity and acquired immunity. Both components of immunity
recognize invading microorganisms as non-self, which triggers immune responses to eliminate them
As above described in caries causing pulpitis both gram positive and gram negative bcteria are present and TLRs function as signal transducers that mediate innate immunity and inflammatory response to pathogen through pattern recognition of virulence molecules. Mammalian innate immune system recognizes bacteria and their cell wall components through and pattern recognition receptors CD14 and TLR 2and 4, Although the exact mechanism of immune activation by Gram-positive bacteria remains unknown, recent studies of immune activation by bacterial LPS provide a clue. TLR2 recognizes a variety of microbial components. These include
lipoproteins/lipopeptides from various pathogens, peptidoglycan and lipoteichoic acid from Gram-positive bacteria. Whereas TLR4 seems to serve as the primer LPS receptors. Some researchers have shown that TLR 2 may not be exclusively pattern recognition receptors for LPS from Gram negative bacteria (Schwandner et al 1999).
To study the expression of TLRs by odontoblasts, we used a pure population of cells generated in vitro that are similar in many aspects to in vivo odontoblasts ( Couble et al 2000,Lucchini et al 2002).We observed the constitutive expression of TLR1–6 and 9 genes but not TLR7, 8, and 10 genes. This large range of TLRs expressed by odontoblasts appears comparable to what has been reported for cultured epithelial cells, including
keratinocytes intestinal epithelial cells , bronchial epithelial cells (sha et al 2004)and gingival epithelial cells . Interestingly, the pattern of TLRs expressed by odontoblasts was similar to the one reported for gingival fibroblasts in primary cultures . Whether a common TLR expression profile exists for all oral mesenchymal cell types remains to be determined.
Thus, odontoblasts might be involved in the recognition of bacterial products such as triacetylated lipoproteins (TLR1+TLR2), LTA
(TLR2), diacetylated lipoproteins, peptidoglycans (TLR2+TLR6), LPS (TLR4), flagellin (TLR5), and unmethylated CpG motif-containing DNA (TLR9), and also of viral dsRNA through TLR3 (Takeda et al 2002, Iwasaki 2004).
Indeed, we found in the present work that odontoblasts responded in vitro to the TLR2 ligand LTA but also to TLR3 and TLR4 ligands (our preliminary data). It remains to be determined whether these cells can actually detect and react to TLR5 and 9 ligands.
Although the dental pulp is equipped with cells of the immune system (Jontell 1986), the immune response in the pulp to caries pathogens is poorly understood.
The basis for the earliest step in innate immune response to Gram positive bacterial infection is poorly understood. We hypothesized that Gram positive bacteria might also be recognized by TLRs.
Although the exact mechanism of immune activation of Gram positive bacteria remains unknown, recent studies of immune activation by bacterial LPS provide a clue. Like Gram negative bacteria, major component of the gram positive bacterial cell wall employ CD14 for immune recognition. Both peptidoglycan and lipoteichoic acid have been demonstrated to activate macrophages in a CD14-dependent manner (Gupta 1996)
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