PERIODONTAL DISEASE RESEARCH CENTER

本中心的主要目标是制订下列方式

The major objectives of this Center are to develop modalities for diagnosis, treatment, and prevention of periodontal diseases. A series of related clinical, microbiological, and immunological studies have been designed to address these objectives. The clinical component is designed to detect early disease activity utilizing highly sensitive detection methods such as an electronic constant-force probe which has been shown to be highly sensitive and reproducible. Microbiologic and immunologic studies are designed to investigate the microbial etiologies of refractory and suppurative periodontal diseases and to define the interrelationship between specific microorganisms and the host's immune response. Clinical measurements will be performed to verify that individual sites are in an actively progressing state of disease prior to therapy and in a state of remission after therapy. The composition of the microbiota and the immune response will be examined longitudinally in each patient to determine the overall effects of different therapeutic regimens. Determination of the effect of different periodontal therapies on the clinical response the host's microbiota, and the immune response, should lead to more rational approaches in the treatment of these diseases. By thoroughly investigating the multiplicity of interrelated factors associated with the periodontal disease process, it hoped that bases for rational prevention and therapy will be established. The objective of the squirrel monkey (Saimiri sciureus) study is to develop an in vivo model for colonization with suspected periodontal pathogens (e.g., B. gingivalis, H. actinomycetemcomitans) and then to examine the effects of immunization on colonization. The specific aims are: (1) establish an association between one or more subgingival bacteria (e.g., B. gingivalis) and disease; (2) define the relationship of immunity to suspected periodontal pathogens; (3) investigate the mechanisms of infection and oral colonization of monkeys with pathogens; (4) identify and characterize the antigens from pathogenic bacteria against which normally infected and immunized monkeys make antibody; and (5) test the effect of immunization on colonization of subgingival plaque with pathogenic bacteria. From these studies, the microbiota involved in disease as well as the humoral immune response to these bacteria will be defined. A model of colonization of subgingival plaque by identified pathogens will be developed. This model will then be used to study the potential of the humoral immune response to modulate the oral colonization by suspected pathogens. Information of this type will provide valuable knowledge to our understanding of periodontal diseases and possibly provide a basis for a rational approach to immunologic prevention of periodontal diseases.