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Historical perspective - nonspecific plaque hypothesis ..
According to this, changes in the environmental conditions leads to This ecological So, according to this hypothesis, disease can be prevented not only by targeting the putative pathogen directly, but also by interfering with the selection pressures responsible for their enrichment.The life cycle of a biofilm is characterized by attachment of to adhere cells irreversibly to the substrate, and then by additional EPS production, and , and to produce a mature, thick and spatially structured biofilm.Dental plaque forms via an ordered sequence of events, resulting in a structurally- and functionally-organized structure.
Gingivitis and periodontal disease is mainly caused by microorganisms within the subgingival dental plaque, which penetrate the gingival epithelium and elicit an inflammatory host response. The microflora associated with gingivitis is predominated by such as A. viscosus and A. naeslundii, and . Other species such as S. sanguis and S. anginosus are also found. As periodontal disease advances, Porphyromonas gingivalis, , Bacteroides forsythus, species and Treponema denticola become predominant. Two specific clinical entities, Localized Juvenile Periodontitis and Acute Necrotizing Ulcerative Gingivitis are associated with specific pathogens, namely in the former, and in addition to Treponema denticola in the latter. A unifying hypothesis postulating the microbial shift from a plaque-free tooth surface and progression to supragingival and subgingival plaque organisms and various odontogenic infections is shown in .
Specific Plaque Hypothesis (Loesche,1976
There is growing awareness of the infectious nature of dental caries, and that only certain microorganisms residing within dental plaques are cariogenic (the specific plaque hypothesis of dental caries and periodontal disease). Dental caries are primarily caused by microorganisms within the supragingival plaque composed mainly of gram-positive facultative and microaerophilic cocci and rods. The microbial aetiology of dental caries has been well characterized. There is clear evidence that the mutans streptococci group - notably and S. sobrinus, are the primary organisms associated with dental caries, both in animal models and in human studies. Root caries are associated with including A. naeslundii and A. viscosusin addition to mutans streptococci. Investigations of decayed fissures have identified high levels of these mutans streptococci, as have studies comparing the microflora of carious and non-carious teeth. Longitudinal studies also support these conclusions. These streptococci are transmissible between humans, and infants are often infected by salivary contact with their mothers.
Chemical Plaque Control - Other Agents excepts Chlorhexidine (Peridex)
Loe, Theilade, and Jensens in their famous “experimental gingivitis” study in 1965 has demonstrated the role of plaque in gingivitis and that the inflammation occurred is reversible upon removal of plaque. This lead to the development of the nonspecific plaque hypothesis which stated that all plaque are bad and are required to be eliminated in the process of periodontal disease prevention. Supragingival plaque accumulation leads to alteration of subgingival bacterial population, which leads to opportunistic proliferation of pathogenic species in the pocket and subsequently brought about tissue destruction. The importance of plaque removal has brought about many searches for an ideal chemical agent which is nontoxic and can serve the function of both supragingival plaque control (good adherent properties to the enamel and reduction of pellicle formation) and subgingival plaque control (good penetration in the pocket). Ideally, that would be an agent which provided complete elimination of plaque control upon its usage alone. Practically, the prevailing strategy seems to be to use such an agent as part of mechanical plaque control therapy, which combined the professional and home care mechanical methods. This therapy will provide not the complete elimination but the reduction of plaque level to the level of which result in acceptable clinical health, the level which is fluctuated according to the individual patient due to his own host factors. Today, the specific plaque hypothesis has indicated that only certain pathogenic organism are associated with disease, and that elimination of all bacterial microflora would exposed human host to the invasion by pathogenic organisms (Newman and Poole in 1974).
The nonspecific plaque hypothesis.
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