Periodontal disease leads to the gradual destruction of structures that support the teeth, primarily through the interaction between bacteria and the host’s immune response. Conditions like apical periodontitis, which stem from endodontic issues, can exacerbate this destruction by creating endo-periapical lesions. Recent studies have brought to light previously unidentified bacterial species that play a role in the progression of periodontal disease. Advanced laboratory techniques, including real-time polymerase chain reaction (PCR), have enabled the identification of these microorganisms.
In mature dental plaque, pathogenic bacteria dominate the microbial community. One such bacterium, Mogibacterium timidum, has gained recognition as part of the microbial flora in dental plaque. This rod-shaped, anaerobic, and gram-positive bacterium, identified in 2000, is considered to contribute to the severity of gingivitis and periodontitis.
Research indicates that diabetes worsens periodontal disease and serves as a significant risk factor for its progression. Numerous studies have compared plaque composition in diabetic versus non-diabetic individuals, revealing that diabetic patients tend to harbor a greater abundance of periodontal pathogens. Consequently, inadequate glycemic control and diabetes mellitus are critical contributors to periodontitis and the increased pathogenicity of subgingival microbiota. Given this context, it is plausible that Mogibacterium timidum may be associated with periodontitis, particularly in diabetic patients who may exhibit a heightened susceptibility to this bacterium in deeper periodontal pockets. However, no existing research has specifically assessed the levels of Mogibacterium timidum in diabetic patients with chronic periodontitis.
This study aims to quantitatively evaluate Mogibacterium timidum levels in subgingival plaque samples from individuals suffering from periodontitis and uncontrolled type 2 diabetes, compared to those with periodontitis but without diabetes. The specific objectives include:
Measuring Mogibacterium timidum levels in subgingival plaque samples from healthy individuals at baseline and six weeks after scaling and root planing.
Analyzing Mogibacterium timidum levels in plaque samples from non-diabetic patients with chronic periodontitis at both baseline and six weeks following scaling and root planing.
Assessing Mogibacterium timidum levels in plaque samples from diabetic patients with chronic periodontitis at the same intervals.
Comparing the quantities of Mogibacterium timidum across all three groups using real-time PCR at both baseline and six weeks post-treatment.
This investigation aims to enhance our understanding of the relationship between Mogibacterium timidum, diabetes, and periodontal disease, potentially guiding future therapeutic approaches.
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