Periodontitis is associated with insulin resistance in adults living with diabetes mellitus in Uganda: a cross- sectional study

Kiryowa, Haruna Muhmood; Munabi, Ian Guyton; Buwembo, William; Rwenyonyi, Charles Mugisha; Mwaka, Erisa Sabakaki; Kaddumukasa, Mark

doi:10.1186/s13104-023-06473-1

Cited by 1 publication

(1 citation statement)

References 34 publications

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“…Periodontal pathogens trigger neutrophils and monocytes, producing excessive pro-inflammatory cytokines [ 129 ]. Hence, systemic inflammations are frequently linked with periodontitis and the development of IR [ 129 , 130 ] by increasing the levels of serum adipocytokines (TNF-α, IL-6, and IL-1) [ 44 , 129 ]. Additionally, these Gram-negative anaerobic periodontal pathogens produce lipopolysaccharides (LPS).…”

Section: Reviewmentioning

confidence: 99%

Role of Nonalcoholic Fatty Liver Disease in Periodontitis: A Bidirectional Relationship

Vegda,

Patel,

Girdhar

et al. 2024

Cureus

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Nonalcoholic fatty liver disease (NAFLD) and periodontitis share common risk factors such as obesity, insulin resistance (IR), and dyslipidemia, which contribute to systemic inflammation. It has been suggested that a bidirectional relationship exists between NAFLD and periodontitis, indicating that one condition may exacerbate the other. NAFLD is characterized by excessive fat deposition in the liver and is associated with low-grade chronic inflammation. There are several risk factors for the development of NAFLD, including gender, geriatric community, race, ethnicity, poor sleep quality and sleep deprivation, physical activity, nutritional status, dysbiosis gut microbiota, increased oxidative stress, overweight, obesity, higher body mass index (BMI), IR, type 2 diabetes mellitus (T2DM), metabolic syndrome (MetS), dyslipidemia (hypercholesterolemia), and sarcopenia (decreased skeletal muscle mass). This systemic inflammation can contribute to the progression of periodontitis by impairing immune responses and exacerbating the inflammatory processes in the periodontal tissues. Furthermore, individuals with NAFLD often exhibit altered lipid metabolism, which may affect oral microbiota composition, leading to dysbiosis and increased susceptibility to periodontal disease. Conversely, periodontitis has been linked to the progression of NAFLD through mechanisms involving systemic inflammation and oxidative stress. Chronic periodontal inflammation can release pro-inflammatory cytokines and bacterial toxins into the bloodstream, contributing to liver inflammation and exacerbating hepatic steatosis. Moreover, periodontitis-induced oxidative stress may promote hepatic lipid accumulation and IR, further aggravating NAFLD. The interplay between NAFLD and periodontitis underscores the importance of comprehensive management strategies targeting both conditions. Lifestyle modifications such as regular exercise, a healthy diet, and proper oral hygiene practices are crucial for preventing and managing these interconnected diseases. Additionally, interdisciplinary collaboration between hepatologists and periodontists is essential for optimizing patient care and improving outcomes in individuals with NAFLD and periodontitis.

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