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A total of 30 systemically healthy subjects were selected after obtaining an informed consent. This study was carried out in the Department of Periodontics, PMNM Dental College and Hospital, Bagalkot, Karnataka, India. Hence, the aim of this study was to detect the presence of subgingival herpesviruses (HCMV and EBV-I) along with putative bacterial pathogens (Aa and Pg) in AgP patients using Hotstart PCR so as to evaluate their synergistic role in the pathogenesis of periodontal breakdown. It is relatively easy to perform and demonstrates excellent detection limits and little cross-reactivity under optimal conditions. 3 Hence, PCR assays have the potential form being an ideal detection method of periodontal microorganisms. Polymerase chain reaction (PCR) developed by Mullis in 1985 is one such diagnostic method, which is emerging as an alternative on the basis of its ability to directly and rapidly assess the microorganisms with extreme levels of sensitivity, which would be particularly helpful since some individuals may harbor periodontal pathogens at levels below that detectable by culture or other diagnostic methods. Subsequently, herpesviruses reactivation then diminishes the resistance of periodontal tissues causing local immunosupression, leading to overgrowth of periodontopathic bacteria. Presumably, herpesviruses residing in inflammatory cells enter gingival tissues with the development of gingivitis. Conceivably, herpesviruses rely on co-infection with to produce periodontitis and, conversely bacteria may develop on viruses for the initiation and progression of some types of periodontal diseases. The presence of human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) has been linked to a high occurrence of subgingival Porphyromonas gingivalis (Pg), Aggregatibacter actinomycetemcomitans (Aa) and other bacterial pathogens. Recent studies suggest that periodontal herpes viruses comprise an important source of triggering periodontal tissue destruction. A number of bacterial species have been incriminated in the etiopathogenesis of periodontitis, but a bacteriologic cause alone seems insufficient in explaining several clinical features of the disease. The events that initiate AgP have been difficult to delineate because of the complexity of the pathogenic microbiota and pathophysiologic effects of several pro- and anti-inflammatory mediators. These observations may suggest that aggressive periodontitis (AgP) in young patients require less infectious agent stimulus to trigger a progressive disease response than the more chronic type of disease.ĪgP comprises a group of rare, severe rapidly progressive forms of periodontitis often characterized by an early age of clinical manifestation and the rapid destructive tendency for cases to aggregate in families. The course of the disease in adolescents and young adults is typically aggressive and relatively brief.

Furthermore, the course of periodontitis can vary considerably between young and adults. Periodontal diseases being multifactorial in etiology encompass a variety of infectious entities with various unique microbial constellations and immune responses. Researchers of the late 19 th century acknowledged the role of these deposits in the initiation and progression of diseases of teeth and their supporting structures.

Relationship between dental disease and soft deposits on teeth has been suspected since ancient times. This makes periodontal disease one of the most common and complex disease affecting mankind and is the leading cause of tooth loss in adults. Periodontal disease affects four out of every five adults.