Microbiologic and immunologic characteristics of periodontal disease in Hispanic americans with type 2 diabetes
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Updated: Jul 6, 2026

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Published on: January 21, 2020
Jeffrey L Ebersole1, Stanley C Holt, Richard Hansard
1Center for Oral Health Research, University of Kentucky, Lexington, KY, USA.
Background:
The microbiology of periodontitis in type 1 diabetes has been reported, but less is known about type 2 diabetes. Moreover, these data have not linked microbial colonization, host response, and clinical presentation in type 1 or type 2 diabetes. The objectives of this study were to relate periodontal status, periodontal microorganisms, and host-response characteristics in Hispanic Americans with type 2 diabetes.
Methods:
Plaque and serum samples were obtained from 63 Hispanic American subjects with and without type 2 diabetes. The microbiology of subgingival plaque samples was evaluated using DNA checkerboard hybridization, and serum antibody to a battery of oral microorganisms was determined using an enzyme-linked immunosorbent assay.
Results:
In general, similar pathogens were present in periodontitis sites from subjects with and without type 2 diabetes, although the periodontitis sites in diabetes showed a higher frequency of Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans), and Campylobacter spp. Serum antibody to Campylobacter rectus was elevated in type 2 diabetes, whereas antibody to P. gingivalis and C. rectus were elevated in subjects with periodontitis, irrespective of diabetes status. Stratification of the population based upon antibody to P. gingivalis or C. rectus suggested a linkage between elevated antibody to P. gingivalis, increased frequency of diabetes, and significantly worse periodontitis.
Conclusion:
The increased severity of periodontal disease with type 2 diabetes may reflect an alteration of the pathogenic potential of periodontal bacteria and/or a modification of the characteristics of the host's inflammatory response that may contribute to a breakdown in the homeostasis of the periodontium.
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