Inflammatory mechanisms in localized aggressive periodontitis patients

Introduction. Localized Aggressive Periodontitis (LAP) has a bacterial etiology, with infection of the gingival tissues by several bacterial pathogens. However, in addition to bacterial etiology, host immune and inflammatory factors are implicated in the pathogenesis and progression of localized aggressive periodontitis. Objective. The objective of this study is to explore underlying mechanisms involved in selective sites of infection, and the subsequent inflammatory process in LAP. Methods and Materials. Ten LAP patients participated in this study (3 male and 7 female), with an age range of from 13-32 years. Samples were taken from one tooth with the deepest pocket for a test site and one tooth with healthy periodontium for a control site from each individual. Laboratory Tests. Bacterial culture was conducted to evaluate the fourteen periodontal pathogens. Also Real-Time Polymerase Chain Reaction (RT PCR) was done to analyze the presence of Aggrigatibacter actinomycetemcomitans (A.a.) RNA, Cytomegalovirus (CMV) RNA, Nuclear factor kb (NFKb), Tumor Necrosis Factor alpha (TNFa), and Inter Cellular Adhesion Molecule 1 (ICAM1). Results. No periodontal pathogens were present in the control sites. All the test teeth revealed some periodontal pathogens. A.a. was not present in any test samples. The mean percentages of other pathogens in test teeth were 5.28 for Fusobacterium species, 4.90 for Campilobacter species, 3.93 for T. forsythia, 3.53 for P. intermedia, 2.73 for P. gingivais, 1.40 for Enteric gram negative rod, 0.69 for Beta hemolytic streptococci, 0.38 for D. pneumosintes. With PCR analysis CMV RNA and A.a RNA was not present in any of the test or control samples. Measurement of NFkb and ICAM1 expression by RT-PCR showed there was marked increase in the affected sites when compared with control sites. TNFa was not present in any of the test or control samples. Conclusion. The preliminary findings of this study suggest upregulation of active NFkb and ICAM1 play an important role in LAP.