Diabetes Care 28:433-434, 2005
© 2005 by the American Diabetes Association, Inc.
Pathophysiology/Complications
Brief Report |
Relationship of Periodontal Bacterium Genotypic Variations With Periodontitis in Type 2 Diabetic Patients
Miki Ojima, DDS, PHD1,
Munehiro Takeda, DDS2,3,
Hideo Yoshioka, DDS, PHD3,
Makoto Nomura, MD, PHD4,
Noriaki Tanaka, DDS, PHD3,
Takahiro Kato, DDS, PHD2,
Satoshi Shizukuishi, DDS, PHD1 and
Atsuo Amano, DDS, PHD2
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{at}dent.osaka-u.ac.jp
 |
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 have shown that clones with type II fimA have a significantly greater virulence in vitro and in vivo (10–12). Therefore, specific P. gingivalis fimA types may be related to periodontitis associated with type 2 diabetes.
|
RESEARCH DESIGN AND METHODS
|
|---|
We selected 97 Japanese adults (53 men and 44 women) with type 2 diabetes with or without adult periodontitis according to a protocol approved by the Ethics Committee of Osaka Rosai Hospital. All of the subjects completed questionnaires and were excluded if antibiotics, corticosteroids, and/or nonsteroidal drugs had been used during the previous 3 weeks. Subjects had >10 functional teeth and had not received professional periodontal treatment during the 6-month period before the study.
Periodontal condition was determined by measuring the level of attachment loss as described previously (13). The development of periodontitis was assessed by attachment loss level, i.e., individuals who had more than a tooth with an attachment loss of >5 mm were classified into the periodontitis group and the others comprised the nonperiodontitis group. The ratio (a percentage) of teeth with an attachment loss of >5 mm among all teeth in each subject was used as an index of periodontal deterioration.
Bacterial samples were collected from subgingival pockets and analyzed using a PCR method as described previously (13–15). The target microorganisms were P. gingivalis, A. actinomycetemcomitans, T. forsythia, T. denticola, and P. intermedia. P. gingivalis fimA types were also analyzed. Statistical analyses were performed using a t test and  2 test.
|
RESULTS
|
|---|
General condition and bacterial occurrence were analyzed in relation to periodontitis development. No significant differences were found in sex, BMI (mean 23.6 ± 4.9 kg/m2), HbA1c level (9.6 ± 2.0%), and disease duration (8.5 ± 7.6 years) between the periodontitis and nonperiodontitis groups, but age was significant (Table 1). Of the five periodontal bacteria, only the occurrence of P. gingivalis was significantly different between the two groups, and its type II fimA clone was more predominant in the periodontitis group (42.0%) than in the nonperiodontitis group (35.7%) but not significantly. The ratio of teeth with an attachment loss of >5 mm, used as an index of periodontitis deterioration, varied from 3.3 to 100.0% (means ± SD 30.5 ± 27.6%) in the periodontitis group. P. gingivalis was found to be the only pathogen with a significant relationship to periodontitis deterioration (Table 1). Among the six genotypes of P. gingivalis, the occurrence of type II fimA clone was significantly associated with disease deterioration. On the other hand, type I and IV fimA clones showed a tendency to be negatively associated with the deterioration. Furthermore, a regression model was constructed to independently confirm the relationship of P. gingivalis type II fimA with deterioration of periodontitis, which included age and sex as adjusting variables. This model indicated that the occurrence of type II fimA clone was independently related to periodontitis deterioration (standard regression coefficient 0.274, P = 0.025), but age and sex were not.
|
CONCLUSIONS
|
|---|
P. gingivalis is reported to be the most frequently detected pathogen in periodontitis diseased sites of type 2 diabetic and nondiabetic populations (16,17). In the present study, P. gingivalis type II fimA was found to have a significant association with deterioration of periodontitis, whereas types I and IV clones were not related to disease progression. We previously reported that the occurrence of type II fimA clones is significantly correlated with both the development and deterioration of periodontitis in systemic healthy subjects, as compared with other fimA types, while the most prevalent fimA type in periodontal healthy sites was type I (9,14). Other studies performed in different countries with systemic healthy populations have confirmed our findings (18–20). Similar findings have been reported in Down’s syndrome patients, who are congenitally susceptible to periodontitis, and in young adults with mental disability, a major factor in determining oral hygiene (13).
Diabetic patients are at greater risk of developing periodontitis due to their high susceptibility to infection (7). The present findings also suggest that P. gingivalis clones, even with lower pathogenicity, can lead to periodontitis in diabetic patients. They hardly respond to periodontal therapy (7); thus, patients infected with the type II clone require careful attention to bacteria elimination and periodontal management by professional periodontists.
|
Footnotes
|
|---|
A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.
Received for publication October 28, 2004.
Accepted for publication October 29, 2004.
|
References
|
|---|
- Löe H: Periodontal disease: the sixth complication of diabetes mellitus. Diabetes Care 16:329–334, 1993[Medline]
- Nelson R, Shlossman M, Budding L, Pettitt DJ, Saad MF, Genco RJ, Knowler WC: Periodontal disease and NIDDM in Pima Indians. Diabetes Care 13:836–840, 1990[Abstract]
- Emrich L, Shlossman M, Genco RJ: Periodontal disease in non-insulin-dependent diabetes mellitus. J Periodontal 62:123–131, 1991
- Taylor G, Burt B, Becker M, Genco RJ, Shlossman M, Knowler WC, Pettitt DJ: Non-insulin dependent diabetes mellitus and alveolar bone loss progression over 2 years. J Periodontol 69:76–83, 1998[Medline]
- Darveau RP, Tanner A, Page RC: The microbial challenge in periodontitis. Periodontol 2000 14:12–32, 1997
- Williams RC, Offenbacher S: Periodontal medicine: the emergence of a new branch of periodontology. Periodontol 2000 23:9–12, 2000
- Genco RJ: Current view of risk factors for periodontal diseases. J Periodontol 67:1041–1049, 1996[Medline]
- Amano A: Molecular interaction of Porphyromonas gingivalis with host cells: implication for the microbial pathogenesis of periodontal disease. J Periodontol 74:90–96, 2003[Medline]
- Amano A, Kuboniwa M, Nakagawa I, Akiyama S, Morisaki I, Hamada S: Prevalence of specific genotypes of Porphyromonas gingivalis fimA and periodontal health status. J Dent Res 79:1664–1668, 2000[Abstract/Free Full Text]
- Amano A, Nakagawa I, Okahashi N, Hamada N: Variations of Porphyromonas gingivalis fimbriae in relation to microbial pathogenesis. J Periodontal Res 39:136–142, 2004[Medline]
- Nakano K, Kuboniwa M, Nakagawa I, Yamamura T, Nomura R, Okahashi N, Ooshima T, Amano A: Comparison of inflammatory changes caused by Porphyromonas gingivalis with distinct fimA genotypes in a mouse abscess model. Oral Microbiol Immunol 19:205–209, 2004[Medline]
- Nakagawa I, Amano A, Kuboniwa M, Nakamura T, Kawabata S, Hamada S: Functional differences among FimA variants of Porphyromonas gingivalis and their effects on adhesion to and invasion of human epithelial cells. Infect Immun 70:277–285, 2002[Abstract/Free Full Text]
- Amano A, Kishima T, Akiyama S, Nakagawa I, Hamada S, Morisaki I: Relationship of periodontopathic bacteria with early-onset periodontitis in Down’s syndrome. J Periodontol 72:368–373, 2001[Medline]
- Amano A, Nakagawa I, Kataoka K, Morisaki I, Hamada S: Distribution of Porphyromonas gingivalis strains with fimA genotypes in periodontitis patients. J Clin Microbiol 37:1426–1430, 1999[Abstract/Free Full Text]
- Nakagawa I, Amano A, Ohara-Nemoto Y, Endoh N, Morisaki I, Kimura S, Kawabata S, Hamada S: Identification of a new variant of fimA gene of Porphyromonas gingivalis and its distribution in adults and disabled populations with periodontitis. J Periodontal Res 37:425–432, 2002[Medline]
- Yuan K, Chang CJ, Hsu PC, Sun HS, Tseng CC, Wang JR: Detection of putative periodontal pathogens in non-insulin-dependent diabetes mellitus and non-diabetes mellitus by polymerase chain reaction. J Periodontal Res 36:18–24, 2001[Medline]
- Tervonen T, Oliver RC, Wolff LF, Bereuter J, Anderson LA, Aeppli DM: Prevalence of periodontal pathogens with varying metabolic control of diabetes mellitus. J Clin Periodontol 21:375–379, 1994[Medline]
- Missailidis CG, Umeda JE, Ota-Tsuzuki C, Anzai D, Mayer MP: Distribution of fimA genotypes of Porphyromonas gingivalis in subjects with various periodontal conditions. Oral Microbiol Immunol 19:224–229, 2004[Medline]
- van der Ploeg JR, Giertsen E, Ludin B, Morgeli C, Zinkernagel AS, Gmur R: Quantitative detection of Porphyromonas gingivalis fimA genotypes in dental plaque. FEMS Microbiol Lett 12:31–37, 2004
- Beikler T, Peters U, Prajaneh S, Prior K, Ehmke B, Flemmig TF: Prevalence of Porphyromonas gingivalis fimA genotypes in Caucasians. Eur J Oral Sci 111:390–394, 2003[Medline]
 CiteULike  Del.icio.us  Digg  Reddit  Technorati What's this?
|
|
|
TOP
INTRODUCTION
RESEARCH DESIGN AND METHODS