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Relationship of Periodontal Bacterium Genotypic Variations With Periodontitis in Type 2 Diabetic Patients

¹ Department of Preventive Dentistry, Osaka University Graduate School of Dentistry, Suita, Osaka, Japan
² Department of Oral Frontier Biology, Osaka University Graduate School of Dentistry, Suita, Osaka, Japan
³ Department of Dentistry and Oral Surgery, Sakai, Osaka, Japan
⁴ Department of Internal Medicine, Center for Diabetes Mellitus, Osaka Rosai Hospital, Sakai, Osaka, Japan

Address correspondence and reprint requests to Atsuo Amano DDS, PhD, Department of Oral Frontier Biology, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka, Suita-Osaka 565-0871, Japan. E-mail: amanoa@dent.osaka-u.ac.jp

The first 20% of the full text of this article appears below.

	INTRODUCTION

 
Periodontitis is characterized by gingival inflammation, as well as loss of connective tissue and bone from around the roots of the teeth, which leads to eventual tooth exfoliation. Severe periodontitis often coexists with diabetes and is considered to be the sixth complication of the disease, as both type 1 and type 2 diabetic patients show a three- to fourfold increased risk of periodontitis (1–4). However, the involved factors and mechanisms are still unclear.

Periodontitis is caused by a small subset of periodontal Gram-negative bacteria that attach to the gingival margin, such as Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Tannerella forsythia, Treponema denticola, and Prevotella intermedia (5). Among them, P. gingivalis is considered to be a bona fide periodontal pathogen (5–7). P. gingivalis fimbriae are hair-like appendages on the bacterial surface that mediate bacterial interactions with and invasion of host tissues (8). These fimbriae have been classified into six types (I through V and Ib), based on the diversity of the fimA genes encoding FimA (a subunit protein of fimbriae) (9,10). Studies . . . [Full Text of this Article]

	RESEARCH DESIGN AND METHODS

 

	RESULTS

 

	CONCLUSIONS

 

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